Diet help. Please post what is working for you!

[TheresaB]

I’m not saying anyone is wrong, I’m not even saying I’m right, I'm not an expert, I'm still learning. I agree with Julie,

I think our understanding regarding the role of LDL and how it impacts health is still evolving

But I thought I'd share how I’ve come to understand the “good” and “bad” of LDL. I should add I’ve been educated by low carb science. I also admit this is simplistic, but anyway, here it goes…

All LDLs are atherogenic, so focus on keeping LDL low.

• atherogenic -- having the capacity to initiate, increase, or accelerate the process of atherogenesis. (formation of abnormal fatty or lipid masses in arterial walls)

LDL, VLDL, HDL, such an alphabet soup, ugh, I need a picture:

17_07_07 cholesterol components.PNG

Big or small, it all enters the artery wall, so try keeping it low.

But I understand it’s the subintimal layer. The below graphic was taken from http://www.nofructose.com/introduction/damage-process/
This website explains:

The LDLs are what I call the ‘Goldilocks’ size. Just the right size to sneak through the endothelial wall of every blood vessel and then sit in the subintimal layer between the endothelium and the smooth muscle of a blood vessel wall.

17_07_07 LDL oxidizing in subintimal layer.JPG

The article continues to say,

It is in this area that the trapped LDLs become oxidised and the inflammatory process then occurs creating a combination of macrophages and foam cells, ultimately leading to what we know as atherosclerotic plaque.

So my simplistic understanding: the small dense LDLs (sdLDLs) are the ones that get trapped in the subintimal layer, if they become oxidized and inflamed, this creates the plaque. The extent of oxidation is influenced by diet. Genetic composition (ApoE4) also seems to influence the oxidation of sdLDLs (still working on wrapping my head around this one, I think it's because we tend to keep our sdLDLs longer than other genotypes that we tend to get more oxidation). HDLs can cross in an out and help clear things out. The big fluffy LDLs just float by.

[david lerner]

Hi George and anyone else,

I'm curious to hear how folks are integrating Gundry's new book suggestions in the Plant Paradox, with his original recommendations in his earlier book (Diet revolution), which was more geared to lower saturated fat for ApoE 4's. I haven't read the new book, but from the little I know about it, seems like it creates a difficult integration if one is minimizing animal based saturated fats, and would naturally gravitate towards a low glycemic Mediterranean type diet, that likely is quite high in lectins.

Thoughts?

Thanks!
David

Thank you everyone for your discussions and explanations.

The question about the Bullet Coffee, was because I didn't think I could make it through my exercise class after 14-15 hrs of fasting. I'm very used to drinking a lot of strong coffee. So someone suggested that I just drink a cup of Bullet Coffee ( i.e. with a tablespoon or more of coconut oil) to stay in Ketosis until I returned home for breakfast after exercising.

One last question ( for tonight anyway) I just purchased a book on the Ketogenic Diet and it indicates that it takes 4-6 weeks of strict adherence for one's body to acclimate to converting to Ketones and using them. Is this correct? Also, it said that once acclimated, you can be a little more flexible. What are your thoughts on this?

So if I want more ketones, I fast more/eat less. I don't add fat or MCT's. I consider myself to be operating in "dual fuel mode" now and seamlessly transition from a carb based metabolism to a fat/ketone based metabolism. The fat is from my fat stores and the ketones are made from my body fat. Less carbs and protein = more ketones for me. Obviously not eating at all gives the strongest result.

All exercise I do is fasted. Most at least 18 hours. I've skied > 34,000' vertical off piste and on the steeps at 12,000' starting at 40 hours fasted. I've rock climbed in the sun for 6 hours on the 3rd day of a fast. And as I've linked below, I've gone to the gym on the 5th day of a fast. If you are well adapted, fueling is not an issue, in my experience.

As to adaptation, it is likely individual. I did it the Atkins way (20g carbs/day with modest protein) in October 2009. It took about two weeks as I recall. This isn't to say there isn't ongoing adaptation after that, there is, maybe for a long time, just more subtle. I've never had to re-adapt. I also didn't know to add electrolytes, which is standard knowledge when adapting now. My wife and Stavia both adapted over a period of time and didn't go through the "low carb flu" like I did.

I've fasted 22 hours a day for over two years. If I test urine or serum ketones, I'm almost always making some at 12 hours after eating. I do eat a fair amount of resistant starches, so my carb intake ranges from ~80 to ~180 g/day with an average of 122 g/day in a two week detailed analysis I did using a gram scale in March. On a couple of random serum ketone measurements during the two weeks, my ketones ranged from 0.5 - 2.0 mmol/L.

Currently I'm doing fasting/refeeding cycles as detailed here. On the fifth day of my 4th fasting cycle, my serum glucose was 31 mg/dL (1.7 mmol/L) and my serum ketones were at 6.2 mmol/L. I then went to the gym as detailed here

If I want to spike my lipids (including LDL-P), I fast for multiple days. The easiest way to knock them down for me is to eat carbs. We are Gundry patients. He has an excellent track record of keeping patients out of CVD trouble. He discounts LDL-P (though it is measured on our labs) and has us keep sdLDL-C <30 mg/dL, oxLDL in range and also TG/HDL <1 in mg/dL units. He looks at many other metrics in our 19 pages of labs we get for each of our consult. This post has links to all of our 4 consult transcripts and redacted labs.

[Tincup]

Hi George and anyone else,
I'm curious to hear how folks are integrating Gundry's new book suggestions in the Plant Paradox, with his original recommendations in his earlier book (Diet revolution), which was more geared to lower saturated fat for ApoE 4's. I haven't read the new book, but from the little I know about it, seems like it creates a difficult integration if one is minimizing animal based saturated fats, and would naturally gravitate towards a low glycemic Mediterranean type diet, that likely is quite high in lectins.

David, I've always considered "Matrix" which we follow (now rebranded and slightly updated as "Plant Paradox") as an extension of Phase 3 of his diet in the Diet Evolution book. As E4's, there are parts of the Matrix list we don't eat - mainly animal, poultry, dairy or fish with the exception of omega 3 or pastured eggs, white fish and shell fish. We also con't eat coconut oil. The book is consistent with what he has prescribed to us a patients.

Also, he's said that the food lists in Diet Evolution were a compromise between what he prescribed at the time and what the publisher thought would sell. As an example, he said he had a whole chapter on fasting in that book which got published as a few paragraphs.

The way he has worked and continues to work is to gather a very extensive set of serum metrics on all his patients (which we've posted in my linked post above). He has done this for ~15 years and sees what happens when he tells people to do "x". Clearly his ideas evolve as he gathers more information.

I can assure you that our diet is low in lectins (as demonstrated by our serum test results), following his food lists.

These are the updated food lists:

PLANT PARADOX FOODS (1).pdf

KETO PLANT PARADOX FOODS.pdf

[Tincup]

From a project in late March, using a gram scale:
Total grams consumed 14 days (except eggs & yolks which are number of)
Sauerkraut 2381
Jicama 1754.5
Guac 1742
Avocado 1045
EVOO 1036
Asparugus 898.5
Portabella Mushrooms 693
Pecan 578
Carrots 554
Walnut 507
Hazelnut 499
Chard 490
Pistachio 448
Kovita Kefir 407
Kimchi 403
Artichoke 399
Spinach 370
Balsamic Vin 364
Quorn 340
Cauliflower 329.5
Kale 305
Wine 289
Red Onion 286
Shrimp 270.5
Tomato 264.5
Beets 258
Arugula 257
Yucca Fries 237.6
Tempeh 227
Cod 223
Broccoli 183
Raddish 135
HempTofu 113
Plantain 110.5
Cilantro 110
Purple Sweet Potato 108
Green banana 103.8
Palm Heart 100
Miracle Noodles 99
Brussel sprouts 86.5
Chocolate 86
Black Olives 82
Broccoli 60
HempHearts 60
Green onion 53
Beet Leaves 50
Radicchio 47
Macadamia Nuts 30
Cassava (tapioca) flour 29.3
Flax 21.5
Garlic 18.5
Blueberries 15.6
Baking Powder 12
Vanilla 12
Psyllium Husk 10
Cinnamon 9.6
Ginger 5
Eggs (whole) 4.9
Tumeric 4.5
Corriander 4
Salt 4
Cumin 3.8
Pepper 3.5
Egg yolk (whole) 2.4
Sweet Leaf Stevia 2.4
Rosemary 2
Tumirc Root 1.5
Ginger Root 1
Agar Agar 0.5

[swampf0etus]

This website explains:

The LDLs are what I call the ‘Goldilocks’ size. Just the right size to sneak through the endothelial wall of every blood vessel and then sit in the subintimal layer between the endothelium and the smooth muscle of a blood vessel wall.

The article continues to say,

It is in this area that the trapped LDLs become oxidised and the inflammatory process then occurs creating a combination of macrophages and foam cells, ultimately leading to what we know as atherosclerotic plaque.

Please understand that ALL ApoB carrying lipoproteins are atherogenic (i.e. capable of attaching to the artery wall within the sub-endothelial space and being turned into foam cells by a maladaptive macrophage process). This includes VLDLs, which are 40-70nm in size. The endothelium lining of the blood vessel wall accommodates particles up to 75mn in size. LDLs range from 23.5 to 27.5nm (< 24.5nm are considered small-dense type B and >24.5nm are type A). So as you can see, all LDLs are all very capable of entering the sub-endothelial space.

Notice how the No Fructose website doesn’t offer any scientific reference to back up the images? This is because the ‘goldilocks size’ idea is a myth. Don’t be fooled into thinking large and fluffy LDLs are fine, they’re not when you have too many of them.

I think our understanding regarding the role of LDL and how it impacts health is still evolving. LDL provides support to all of our cells. To demonize it, makes no sense. LDL is a surrogate endpoint that correlates badly with actual atherosclerosis. Have you been following the experimentation of Dave Feldman? Our group will be meeting with him next month in San Diego to learn more.

Of course, LDLs and their contained cholesterol are important for life. However, your body is capable of making all the LDL it needs. Any excess just ends up hanging around in your blood, oxidising and ending up in your artery walls. As ApoE4 carriers, we convert more IDL to LDL and our livers don’t take up as much LDL, which is why we suffer higher LDL and heart disease than those without the ApoE4 gene.

If you think having too little LDL can cause health problems, then this is not the case. Just look at those that suffer the genetic condition Hypobetalipoproteinemia. Studies on suffers of this condition show them to live into and beyond their 90s without any traces of heart disease. Only those with no detectable level of LDL require treatment.

From http://www.msdmanuals.com/en-gb/profess ... olipidemia ;

Hypobetalipoproteinemia
Hypobetalipoproteinemia is an autosomal dominant or codominant condition caused by mutations in the gene coding for apo B. Heterozygous patients have truncated apo B, leading to rapid LDL clearance. Heterozygous patients manifest no symptoms or signs except for TC < 120 mg/dL (< 3.1 mmol/L) and LDL cholesterol < 80 mg/dL (< 2.1 mmol/L). TGs are normal. Homozygous patients have either shorter truncations, leading to lower lipid levels (TC < 80 mg/dL [< 2.1 mmol/L], LDL cholesterol < 20 mg/dL [< 0.52 mmol/L]), or absent apo B synthesis, leading to symptoms and signs of abetalipoproteinemia.

Diagnosis is by finding low levels of LDL cholesterol and apo B; hypobetalipoproteinemia and abetalipoproteinemia are distinguished from one another by family history. People who are heterozygous and people who are homozygous with low but detectable LDL cholesterol require no treatment. Treatment of people who are homozygous with no LDL is the same as for abetalipoproteinemia.

Loss of function mutations of PCSK9 are another cause of low LDL levels. There are no adverse consequences and no treatment.

LDL levels don't correlate with heart disease because heart disease progresses over many decades, whereas a cholesterol test gives you one measurement for a single point in time. Imagine someone who's been eating fatty foods their entire life until the age 50, with lots of atherosclerosis, but decides to go to the doctors for a cholesterol test. If they'd been eating low fat, healthy foods for a week or two in the lead up to that test then the LDL score would probably be low and misleading. In population studies that have followed individual and recorded their LDL scores, LDL does track with disease. The Framingham data shows this.

As to Dave Feldman’s experiments, I really don’t see how they are relevant to anyone in the real world trying to by healthy. He jacked up his LDL score by eating a high fat diet. He then showed that he can make his LDL score jump up and down by adding and taking fat from his diet, with some strange results. Either way, if you look at the lowest score on the experiment, this is still considered high LDL. He even admits this is higher than his score before he started his high fat diet. And, of course, none of this tells us if any of this LDL is actually collecting in his arteries. At the end of the day, Dave is just a software engineer, not a lipidologist. He’s just someone who has found faith in a low carb diet because he felt better when he lost weight on it. And, like many others (including myself), he’s tried to find any explanation out there to cling to and make him feel better about his high LDL caused by the low carb diet. We should really ignore this. This is not real science. Real lipidology science is performed by real lipidologists with PHds. These scientists have won Nobel prizes researching this. These scientists number thousands across the globe and their expertise spans decades. Are we really going to trust the crazy experiments of someone who has no relevant qualifications in this area over the advice of health institutions across the globe that have come to a consensus view based on over 100 years of research?

Additionally, maintaining high HDL for reverse cholesterol transport is vital for E4 carriers. Some suggest that's the closest thing we have to a small molecule corrector at this point. Lastly, ensuring a high fiber intake via lots of non-starchy vegs also hastens transport. Great discussion, Swamp. There are so many misconceptions and fears surrounding cholesterol.

Do you have a reference for this? I’d like to investigate this further, as I’ve not heard about the importance of HDL for ApoE4 other the usual ‘good cholesterol’ argument. My view on HDL is that you don’t need to worry about it if your LDL is low.

Fiber is good for many reasons, one being that it lowers LDL. Especially cereal fiber like that found in oats. And I don’t see a problem with starchy foods if your carbohydrate metabolism is functioning fine. Wholefood carbohydrates, including starch, won’t break your carbohydrate metabolism. If you think they will, try finding any studies that show this. Remember, Nigerians with ApoE4 eat starchy carbs but don't get AD or heart disease.


I know I keep linking to these videos, but I strongly encourage you to watch them. The amount of evidence covered in them is staggering and should clear up any confusion around these matters.

This one covers small-dense/large-fluffy myth and what the research really say (i.e. not what low-carb blogs say). Again, skip the first 10 minutes if you don’t want to listen to the Lustig bashing (it is actually relevant, though). All the studies are presented after this: https://youtu.be/_wmidN8rYkU?list=PLv3Q ... 2oYyAFZDBA
Transcript: http://plantpositive.com/25-cholesterol ... ion-8-a-l/

This one covers how much LDL is required for life. It pulls apart Chris Masterjohn’s arguments about Smith-Lemli-Opitz syndrome before going through research papers on those with extremely low LDL due to genetic disorders, such as Hypobetalipoproteinemia described above: https://youtu.be/RjSmmEzxK7Y?list=PLv3Q ... 2oYyAFZDBA
Transcript: http://plantpositive.com/22-cholesterol ... ion-5-cho/

Another video that covers low LDL is this one, which also covers inflammation. It shows that inflammation is actually secondary to the disease process and that high LDL in itself is inflammatory: https://youtu.be/6bSdnQ1MKGo?list=PLDBBB98ACA18EF67C
Transcript: http://plantpositive.com/blog/2012/3/26 ... h-ldl.html

I really hope I’m not coming across as a troll in these comments. I certainly don’t mean to. I’m just trying to get across what I’ve learned. I do have a real, genuine concern for the misinformation that is out there, which only serves to confuse people and risk health.

[Tincup]

Here is my simplistic approach to the cholesterol issue. I'm a Gundry patient. He has an excellent track record keeping patients from having CVD events. He told us that there is an "East Coast" vs. "West Coast" approach in the lipidology community for this topic. Says there are doc/researcher forums where they "yell at each other" discussing this. He told us not to worry about LDL-P or LDL-C (he specifically said the NMR was designed to get patients to want to take statins), but to focus on TG/HDL, sdLDL-C and oxLDL, as well as the other non-lipid measures he collects. Seems to work and it is why I pay him. As an aside, have two friends with LDL-P's in the 1700 range with CAC scores of 0 (one is 54 the other is 68, both male).

A 57 year old female 4/4 who's LDL-P dropped from 2400 to 1700 after starting Gundry's program has a CAC score of 3.5 & she likely had the high LDL-P her entire life.

I'm certainly not qualified to argue the biochem, as I say, that's what I pay Gundry for.

[circular]

swampf0etus I just want to say that I suspect there are many quiet members here who may agree with you. Thank you for voicing their perspective too, because many of the more vocal members are often exploring the merits of other perspectives. That could unintentionally be intimidating or just not welcoming to people with your views. I also think you sincerely want the best for us.

Meanwhile, looking at it from new angles is understandable given that the traditional dietary advice with respect to fats and cholesterol doesn't seem to have stemmed Alzheimer's disease. I don't agree or disagree with any perspective on cholesterol because I feel, as with any complex topic, that I'd really need my own PhD in it to have a strong opinion. But I appreciate learning more about why people do still have your perspectives on cholesterol, and it does encourage me to keep an open mind, just as you did both in trying high fat and then abandoning it.

One of your points that is sticking with me is that the large LDLs are sized to and do easily enter the bad zone, in contrast to the notion that large LDLs merrily bounce off the vessel walls and go their way. Not sure how to reconcile these. I don't have time for the videos at present (and really should not be typing this post at all for all the paperwork on my desk)

I frankly think science is as much belief as it is evidence, so I think using the word 'faith' in this context, as if science is without it and pro-HFLC dieters are based in it, is misleading. To use two simple examples, one from history and one from recent times, the world was once flat and the brain didn't have its own lymph system. Faith in science leads scientists to forget or ignore that they don't know what they don't know. For these reasons I really am not particularly influenced by whether someone has degrees or is part of a dominant thought culture, and I think it benefits everyone to always ask: 'Is there possibly something I don't know that would change my view', even if they feel they've already done thorough research into all sides of a question.

[Julie G]

I love your passion, Swamp. I want to learn all I can about how ApoE4 intersects with what we know about lipidology and health. Since learning I'm an E4 homozygote, it's become a strange hobby of mine- LOL. I'm very curious about this stuff.

Of course, LDLs and their contained cholesterol are important for life. However, your body is capable of making all the LDL it needs.

Most resources suggest that the body makes up about somewhere between 2/3 and 80% of the cholesterol we need to stay healthy. The rest comes from food. My understanding is that’s the reason we need essential fatty acids- precisely because our bodies CAN'T make them.

f you think having too little LDL can cause health problems, then this is not the case. Just look at those that suffer the genetic condition Hypobetalipoproteinemia. Studies on suffers of this condition show them to live into and beyond their 90s without any traces of heart disease. Only those with no detectable level of LDL require treatment.

It’s interesting to consider hypobetalipoproteinemia. When I look up "symptoms," however, I see that they vary vary widely among sufferers of this disorder. Some are quite severe including neurological problems, blood clotting issues, vitamin deficiencies, fatty liver disease, failure to thrive, etc. Hardly the picture of health .

As to Dave Feldman’s experiments, I really don’t see how they are relevant to anyone in the real world trying to by healthy.

I haven’t been following closely, but I’ve not yet seen Dave make any conclusions or recommendations for heath based upon his N=1 experimentation. Instead, he’s methodically demonstrated how our current thinking regarding cholesterol metabolism is backwards. Dave has shown that a very low fat diet drives his LDL-P dramatically upwards and conversely, a hypercaloric high fat diet drives his LDL-P downwards. This demonstrates a very tight homeostatic mechanism for LDL with drivers that operate inversely from mainstream recommendations. And, As you correctly point out, Dave has shown that LDL is very labile. He can very predictably manipulate his numbers for a test. I’m really intersted in hearing more about his insights. To my knowledge, no one has done more diet/cholesterol interaction investigations.

I’d like to investigate this further, as I’ve not heard about the importance of HDL for ApoE4 other the usual ‘good cholesterol’ argument. My view on HDL is that you don’t need to worry about it if your LDL is low.

Functional HDL aids in reverse cholesterol transport and abeta clearance; both problems already associated with the E4 allele. Additionally, HDL delivers antioxidants to protect our slower transiting LDL from oxidation. You can play with our search engine to find topics surrounding this.

[Stavia]

great discussion. Swamp thank you for detailing your thinking, its a lot of work.
I personally am listening carefully to all sides. Currently I do not ignore LDL in my work with patients and factor it in when assessing cardiovascular risk. What is very interesting is that the coronary calcium score my patients do is not always concordant with LDL or even insulin resistance. I am convinced that there are other unknown genetic factors at play.
I have just had two patients in their late 50s in a row recently with total cholesterols of 350 and LDL of nearly 200. Both elected to have a coronary calcium scan so as to inform management over the next 20plus years. One had a coronary calcium score of 18. The other was over 400. Both lean and fit. Both have chosen a statin.
It's not that simple as both sides of the argument might present. I believe that total LDL is one of the risk factors for heart disease. But I believe that it is an inadequate and inaccurate risk assessment tool if taken by itself.
Loving the discussion.

Sent from my SM-G930F using Tapatalk

[swampf0etus]

Most resources suggest that the body makes up about somewhere between 2/3 and 80% of the cholesterol we need to stay healthy. The rest comes from food.

Do you have any references for “most resources”? I can’t find any evidence to suggest that we need any dietary sources of cholesterol. There are no lower limits set on dietary cholesterol. The European Food Safety Authority certainly doesn’t set a lower limit: http://onlinelibrary.wiley.com/doi/10.2 ... .1461/epdf I’m sure we’d see a lot of health issues in vegetarians, especially vegans, if this was the case.

My understanding is that’s the reason we need essential fatty acids- precisely because our bodies CAN'T make them.

It is true that we need essential fatty acids, of which there are two: alpha-linolenic acid (omega-3 PUFA) and linoleic acid (omega-6 PUFA). There is no requirement for saturated fatty acids or MUFAs, as the body can make these. Also, essential fatty acids don’t seem to be a part cholesterol synthesis. There is no mention here: https://en.wikipedia.org/wiki/Essential_fatty_acid, here: https://en.wikipedia.org/wiki/Essential ... teractions or here: https://en.wikipedia.org/wiki/Cholesterol

My belief is that your essential fatty acid needs can be met by eating wholefoods, without the need to add extra oils, otherwise how did our ancestors manage? That said, our ancestors would have a got a lot of omega-3 from eating insects, so it may be best to supplement this if you don’t eat oily fish (or insects!). Vegetarians/vegans can use algal dha omega 3, but milled flax seeds can also provide AHA, which is converted into DHA.

It’s interesting to consider hypobetalipoproteinemia. When I look up "symptoms," however, I see that they vary vary widely among sufferers of this disorder. Some are quite severe including neurological problems, blood clotting issues, vitamin deficiencies, fatty liver disease, failure to thrive, etc. Hardly the picture of health.

Only homozygotes with undetectable LDL levels have these problems. Heterozygotes are asymptomatic. Please understand that no matter how hard you try, you will never get your LDL as low as these people, probably not even via the use of drugs. The bottom line; unless you are a hypobetalipoproteinemia homozygote with virtual zero LDL or suffer Abetalipoproteinemia (again, virtual zero LDL) then you do not need to worry about low LDL.

...he’s methodically demonstrated how our current thinking regarding cholesterol metabolism is backwards.

Do you really trust this one person, who has obvious biases, with his n=1 experiments, over thousands of research centres, universities and public health institutions across the globe? Is it really plausible that the entirety of the research community and the hundred years of accumulated research is all wrong, but yet he is right?

Do you know of Brown and Goldstein? In 1985, they won the Nobel Prize in physiology and medicine for their research into cholesterol and discovering the mechanisms of our LDL receptors. Their research has spanned over 40 years. Dave Feldman is software engineer that went on a low carb diet two or three years ago. Do you really trust this guy or think he’s more qualified on this topic than the likes of Brown and Goldstein?

Dave has shown that a very low fat diet drives his LDL-P dramatically upwards and conversely, a hypercaloric high fat diet drives his LDL-P downwards.

I don’t know of Dave’s low-fat experiments, nor how they were composed. When I spoke to him recently he said he was trying to set up a low-fat vegan experiment, which I’ll be interested to see. From my understanding of the literature, LDL-P improves on low-fat, wholefood diets. In this paper, 73 participants on a low fat (< 10%) diet was shown to make significant changes to lipoprotein subclasses in the right direction. I recommend you look at the graphs in this paper;

Effects of cardiovascular lifestyle change on lipoprotein subclass profiles defined by nuclear magnetic resonance spectroscopy

https://lipidworld.biomedcentral.com/ar ... -511X-8-26

Effects of lifestyle changes on lipoproteins
The lifestyle intervention led to significant changes in NMR-defined lipoprotein subclasses, in particular, clinically important LDL variables that contribute to CAD risk (Figure 1). There was a clear beneficial effect on the total number of LDL particles, which decreased 8.3% overall in participants (p < 0.05 compared to controls). Likewise, sdLDL particles, which have been associated with CAD risk in several studies, decreased 9.5% during the program (p < 0.05 versus controls). Lifestyle changes also were effective in increasing both HDL (+1.0%; p < 0.01) and LDL (+0.8%; p < 0.05) particle size, while decreasing very-low-density lipoprotein (VLDL) size (-9.7%; p < 0.01) and large VLDL and chylomicron concentrations (-29.4%; p < 0.05)

And in this study, comparing two low carb diets, one high in saturated fat and the other low in saturated fat, everything was worse for the high saturated fat group;

Changes in Atherogenic Dyslipidemia Induced by Carbohydrate Restriction in Men Are Dependent on Dietary Protein Source

http://jn.nutrition.org/content/141/12/2180.full

Interestingly, small LDL concentrations were significantly reduced following the LCLSF diet period compared to the LCHSF diet period.

Total cholesterol, LDL-C, nonHDL-C, apoB, and total LDL were reduced following the LCLSF diet period compared to both the baseline and LCHSF diet periods.

But as I’ve mentioned before, you don’t need to worry about LDL-P if you’re not suffering metabolic syndrome. LDL-P is really only relevant in those suffering metabolic syndrome, something you very probably wouldn’t be suffering from if you have a healthy body weight and following a low-fat lifestyle.

But if LDL-P is decreased on a high fat diet and LDL-C is high then you are still in trouble. You’ve got less LDL particles, but the ones you do have are large and jam-packed full of cholesterol. As I’ve also mentioned, all LDLs are atherogenic, so do you really want big LDLs crashing into your artery walls, dumping their huge cargo?

In Brown and Goldstein’s work, they explain the workings of the LDL receptor and how it pulls back into the cell once the cell has received enough cholesterol. Cells can only accept so much cholesterol and can actually die if they receive too much. So what happens when your cells have all the cholesterol they need? There will be no or few cells accepting LDLs, so the LDLs just end up floating around in your arteries for extended periods, oxidizing and attaching to artery walls. And remember, SFA down regulates the liver’s LDL receptor activity. No cells taking up cholesterol and the liver not taking up cholesterol is a recipe for disaster. And, of course, this is even worse in ApoE4 carriers as our liver’s LDL receptors see impaired activity as well as increased LDL synthesis.

Just think about FH suffers, their liver’s LDL receptors function poorly, resulting in very high LDL and heart attacks at an early age. They tend to have low LDL-P with larger, ‘fluffy’ LDLs. Doesn’t sound too different to what I’ve described in the paragraph above, does it?

Evan A. Stein is another lipid researcher that, like Brown and Goldstein, has over 4 four decades of expertise in this area. This is a quote by him, which I got from the video I linked, and I pasting it here as it’s brilliant and very relevant here;

For the practicing clinician, however, the major argument for extending measurement of subclasses into the mass market is the hypothesis that one subclass is more atherogenic than another. Because evidence clearly indicates that all Apo B–containing particles are atherogenic, this reasoning is akin to the argument that an Uzi submachine gun is more deadly than an M16 or an AK47. Obviously all are potentially lethal, and although this assertion may interest gun aficionados, it matters little to law enforcement or to general public safety if the sole objective is disarmament!

Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents, especially when the LDL-C or Apo B reducing ability of their drug was less competitive. Although these studies have created more heat, they provide little additional light.

To my knowledge, no one has done more diet/cholesterol interaction investigations.

There are hundreds of metabolic ward studies that have studied the effects of SFA on lipids. Here is one meta-analysis of 395 of them: https://www.ncbi.nlm.nih.gov/pmc/articl ... 006469.pdf The scientific community have done this to death. I really don’t see how Dave has done anything in his n=1 experiments that hasn’t already been done in the vast body of lipid research, spanning circa 100 years.

I’ve talked to Dave over social media and, to be honest, he seems like nice guy. More than I can say for the rest of the low-carb/keto crowd, as he does seem to be a little open to contrasting ideas. But I have to say, he has all the hallmarks of someone who has been misled by low carb pseudoscience and has become personally and emotionally invested in the low carb ideology. For example, he mentioned Ancel Keys in one of his videos, describing him as a cherry picker and the reason for the unfounded demonization of saturated fat. If he’d bothered to properly research this topic, he’s understand that virtually everything stated about Keys in the low carb community is just misrepresentation and complete lies. Anyone, including doctors, who mention these falsehoods about Keys should be immediately viewed with scepticism because either they haven’t done their research on this or they are using it as a way to confuse you and sell you a diet book. The worst of these lies were propagated by Gary Taubes and Nina Teicholz, but they seem to have their origin in Uffe Ravnskov’s book, The Cholesterol Myths. All of these authors have been completely debunked by various sceptics. If anyone reading this believes in the lies about Keys, then let me know and I’ll send you everything I know of that completely debunks these claims. (Sorry, went off on a bit of a tangent there).

Functional HDL aids in reverse cholesterol transport and abeta clearance; both problems already associated with the E4 allele. Additionally, HDL delivers antioxidants to protect our slower transiting LDL from oxidation. You can play with our search engine to find topics surrounding this.

I do understand the role and importance of HDL. However, having lower HDL in a low LDL environment doesn’t seem to be a problem. This hasn’t shown to predict heart disease or events. High LDL combined with low HDL is definitely a problem and, combined with high triglycerides, usually represents metabolic syndrome.

Ok, I’ve spent a lot of time on this now, so I really need to get back to spending time with my family. I wish everyone on these forums the best of health.