Hi David.
I am absolutely not a medical physician, but have done a lot of medical research. I suspect that I have been personally dealing with the beginnings of athlerosclerosis, so have been researching that very recently. I like a physician in Georgia named Sten Ekberg. He has a video on cholesterol and statins you may want to watch: https://youtu.be/Swc4ps4iPXs
Basically, the crux of it is that high cholesterol numbers alone should not concern the patient. Modern medicine has been obsessed with high cholesterol, but Sten (and the most recent evidence) shows that it is really oxidized cholesterol that is the major culprit. Because it is oxidized at the apoB protein layer, it causes the cholesterol particle not to be reabsorbed by the liver, so it builds up in the blood stream while it actually gets smaller. It tends to get embedded in the arterial walls, which is the start of the atherosclerosis process. If a patient simply has a high number of normal LDL cholesterol, Sten says not to be worried. He believes what happens is that excess sugar and seed oils cause more free radicals and oxidation and this is what ends up oxidizing the LDL cholesterol, and ultimately causing the problem. Well, the modern ketogenic diet basically eliminates these dietary insults. He explains the side effects of statins, and why dealing with cholesterol from a dietary standpoint is preferable.
As a matter of fact you (I see you live in the UK) may want to consider seeking Sten out as your physician with a telephone/video consult, because you seem to present a complex medical picture. I am sure he would advise you to continue with a ketogenic diet, but like me, he emphasizes cruciferous vegetables, and not just meat.
If you still have cardiovascular concerns, you may want to consider getting a CAC score, which will show any significant plaque if it is calcified.
Unhappy with Progress so far please advise
Regardless of whether or not oxidised apolipoproteins are a problem (and Iâm not entirely convinced by the studies on their role in cardiovascular disease), cholesterol itself is irrelevant, except for its role in the bodyâs efforts to deal with arterial damage (think of the plaque as a scab over a wound, and the cholesterol as part of the bandage). To say that reducing cholesterol will reduce the incidence of cardiovascular disease is very much like claiming that cutting back on municipal fire engines will reduce the number of fires.
One of the most telling statistics is that well over 50% of patients presenting with their first cardiac event have normal or low cholesterol. Another is that 50% of people with familial hypercholesterolaemia never develop cardiovascular disease and die of other causes at perfectly normal ages. It has been shown that their relatives who do develop cardiovascular disease all share variants of clotting factors (primarily fibrinogen and factor VIII) that make their blood much more likely to clot. So itâs clearly not the cholesterol that causes the problem
Thanks for your insights Paul.
Well, maybe. I am convinced that oxidized cholesterol is a problem, although clearly there can be others. I am not saying oxidized cholesterol is the only problem, but I do believe it is probably the major problem causing cardiovascular disease. However, anything that causes cracks in the endothelial layers can be looked at as a probable cause of the disease. Whatever it is, I believe the vast majority of it is going to be linked to the SAD. Eliminate the SAD, and cardiovascular disease seems to disappear. Wherever the SAD goes, diabetes, cardiovascular disease and other metabolic diseases are sure to follow. The most recent examples are found in Polynesia and India. Clearly, I donât believe modern medicine has shown one, single cause of cardiovascular disease.
A clarification, if you donât mind, sorry: when they talk about oxidised particles, they are talking about the oxidation of the lipoprotein envelope, not oxidation of the cholesterol molecules inside.
And there is so much evidence to show that cholesterol cannot possibly be the cause of cardiovascular disease, that it is odd how much resistance there is to accepting the evidence. We can understand the statin manufacturers not wanting to stop believing that cholesterol is bad, but everyone else? Given that several large, well-funded studies show a negative correlation between cholesterol level and cardiovascular risk (including, by the way, Ancel Keysâs own Minnesota Coronary Study), we can safely conclude that whatever causes cardiovascular disease, it ainât cholesterol. A positive correlation is not proof of causality, but a negative correlation is sufficient proof of lack of causality.
I am partial to Ravnskov and Diamondâs hypothesis that arterial damage is occurring all the time, but in healthy people, the repair mechanisms keep up with it. However, when metabolic dysfunction interferes with the repairs and accelerates the rate of damage, that is when arterial plaque occurs. Given that people on a keto diet have been able to reduce their coronary arterial calcification, it is clear that carbohydrate intake is implicated in the cause (and there are a number of mechanisms shown to be at work).
Diabetes and heart disease became a problem in the population only at the point where cheap refined sugar and grains began to permeate the food supply. And after the U.S. dietary guidelines, the rate of increase steepened. This is correlation, of course, so we canât definitely assume causation just yet, but a couple of the Bradford-Hill criteria (dose-response and plausible mechanism) have already been met. And given that 88% of the population is metabolically damaged, that means that it serves us ill to follow an outdated hypothesis that was never founded on solid science to begin with (since Keys fudged his data), and which has been contradicted by almost all of the studies designed to confirm it. We need to admit that our prejudice against fat and cholesterol is prejudice and not science.
This is true I am talking about the oxidation of the apoB protein molecule enclosing the cholesterol ester inside. This is because LDL-C is used as a measure of the blood cholesterol level. The cholesterol ester is not a problem. It is simply part of the particle that ends up getting trapped. It is appaently the apoB remnants that are the major antagonists. They donât go away. They end up becoming part of the plaque. There are several studies showing apoB ends up in the plaque, and may be considered as a biomarker for atherosclerotic risk. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6380558/
apoB100 is made in the liver. It forms the wall of the LDL particle. How does it end up in plaque without the LDL cholesterol delivering particle taking it there? My belief is that it is oxidized, and becomes âresistantâ to uptake for recycling by the liver. Thus, the damaged LDL particles tend to accumulate. They shrink, and become more likely to lodge into arterial walls. This process has been seen, and we know it happens. That is hard to refute. However, HDL can become oxidized too. There are several other cholesterol delivery particles which may be involved. I admit that it is still very much not completely known or understood what is going on in the plaque formation process. There appear to be at least several stages involved, and perhaps several vectors of possible progression of the disease. Nevertheless, it does not appear to typically happen without oxidized LDL particles, which I was calling cholesterol just because they are the standard unit of measure.
I know about the studies showing a correlation between decreased cholesterol and increased coronary heart disease. However, that may be because normal LDL is protective, so decreasing it increases risk of coronary disease. It is all very perplexing, and I am the first to admit that I do not fully understand what is going on - but then it seems no one does. or we would have better answers. Right now the best answer seems to be to avoid the SAD - esp sugar, simple carbs, and processed seed oils.
Again, I am not claiming Keys was right. He was wrong. That much is clear. I am not blaming normal LDL or cholesterol for causing heart disease. Sorry, I needed tobe more clear. What I am saying is that normal particles become damaged through oxidation, and there is good reason to believe the oxidation is a result of the SAD - excess sugar, easily oxidized PUFAs or seed oils, and excess simple carbs overloading the system and causing ROS to escape into the blood. Indeed, that appears to be the mechanism for disease in the unpublished Keys study - Corn oil caused ROS which damaged the LDL, so even though there was lower LDL overall, the risk of disease and death went up. Note that the risk of disease in the saturated fat group did not drop to zero though, and this is probably because of sugar.
You may be right about what causes the initial arterial damage which allows particles to enter the aterial wall, and start accumulating. I currently do not even have a working hypothesis there.
It was actually this dude who âtalked me intoâ keto in the first place. One of his videos popped up in my feed a few years ago where he was talking about foods people really should avoid, and at that time I was in complete denial about my general state of health and not at all ready for the truth so I wrote him off as a nut xD
When he showed up again earlier this year though, I gave him another shot and found it all so fascinating that I started chaining his videos⌠and here I am now : )
Paul, you just said something that hit me like a brick!!
I installed a carb tracking app and it insisted on telling me my calorie needs based on my infoâŚit actually told me 1,460 calories per day???
I uninstalled it!!
But question remains, why is those particles found in the plaque? Are they causing the problem, or are they part of the healing? Do we know for sure?
Myself, I see the focus on cholesterol and apolipoproteins as part of the ongoing attempt to vilify dietary fat. At first they were saying itâs the saturated fat, then it was oops, sorry, itâs actually the cholesterol. Then it became oops, hereâs the bad cholesterol we need to worry about, and now itâs oh, sorry, itâs not the cholesterol, itâs the lipoproteins. Iâve watched this progression over a lifetime, and I suspect that we are completely on the wrong track.
In any case, saying something is a marker for a condition is no guarantee that it has a causal role. And the danger of manipulating markers is that it leaves the actual cause untreated. For example, shoe size is a marker for reading comprehension, but buying larger shoes isnât going to improve your reading score. The reason is that shoe size is actually a surrogate for age, and age is actually a surrogate for years of schooling, which is what really improves reading. So even if LDL-P size and count have some association with cardiovascular risk, Iâll be very surprised if someone manages to show that LDL-P actually causes cardiovascular disease.
Weâve known since the 1960âs, for example, that the elevated cholesterol in people with familial hypercholesterolaemia is definitely not the cause of the cardiovascular problems experienced by 50% of them, because we know that the cause of their cardiovascular problems is abnormalities that make their blood clot more readily. The elevated cholesterol by itself clearly causes no problems, because it doesnât affect the 50% who lack the clotting abnormalities.
The authors of a paper on FH from back then explicitly state in their conclusion that their data clearly contradicted the diet-heart hypothesis being pushed by Ancel Keys and his friends at the time, but Keys and his buddies were already too wedded to their hypothesis to consider alternatives, and too influential to be overcome. Keys was already in the process of destroying the career of John Yudkin, for daring to suggest that sugar might be more causal in cardiovascular disease than saturated fat. (It has since been revealed that several of Keysâs friends were being paid by the sugar industry at that time to emphasise the dangers of fat and mimimise the dangers of sugar.)
Well, this we can certainly agree on. There are several known mechanisms that explain this, plus the fact that glycated haemoglobin is much more likely to clotâanother mechanism by which too much sugar damages the body. Not to mention that the interference of elevated insulin with the production of nitric oxide makes arterial walls stiffer, thereby raising blood pressure and increasing the likelihood of arterial damage leading to plaque formation in response. If only (he says sarcastically) there were some way of minimising the damage in the first place!
That app was probably set to Weight Loss mode. Youâd likely have gotten a better amount from setting it to Maintenance mode. Most of these apps are based on the âcalories in, calories outâ model of weight loss, which is contradicted by the carbohydrate-insulin model that underlies how a ketogenic diet works.
In any case, the more Iâve learned, the more irrelevant calories seem as a measure of food intake. What does the energy release from burning food have to do with the actual amount of energy utilisable by the body? At the time calorimetry began, burning food was all we knew how to do, there was no understanding of the roles of protein, fat, and carbohydrate in the diet, yet. Now we know that, first of all, our energy comes from fat and carbohydrate, protein being used for structural purposes (except in emergencies). And secondly, we know about ATP, glycolysis, and the Krebs cycle (which is central to fatty-acid metabolism). Itâs really ATP yield that counts, as far as energy is concerned. And in any case, since fatty acids and glucose yield about the same amount of ATP, the body chooses which to metabolise on the basis of other considerations.
Was this âcalculatorâ including your daily energy expenditure, body-fat %, your goals (weight goal etc)? 1460 is about what I used to get when I was up at 140 lbs, and the calc. was including all the above. I do eat much less at times but do need to get about 1300 Iâm finding, now at 113 lbs. I am 5â2", 113, small-boned doing walking 4 miles per hour, and weight-training last 5 months.
I can tell if Iâm not eating enough (always keto foods) so Iâll grab more, often in larger portion of meat, maybe an extra egg, fatbomb, but almost always upping my protein cooked in extra fat.
you need to heal. point blank from what ails you âright nowâ and could be life threatening and you are in a massive âcombo of I got results when healthier from Keto Plan and then I got hurt to this level and things are offâ. Darn right they will be off 
Key now is time. Heal the issue with the infection and take the pills to do just that and heal and recoverâŚall the while eating real whole foods, holding your Keto Plan to 20g and for me this is all about time and who you are ya know. You got nailed man, literally nailed here, but you WILL walk thru it and heal more if you hold plan and âforget goalsâ they mean nothing in that gain a bit thru med intake etcâŚyour goal now is heal point blank and get âin that healthier zoneâ off this infection and let lifeâ then move forward.
this is you ILL right now ya know. the body while we change is âmaking ya off cause we are changingâ and healing/repairing but at this point it is ALSO fighting a big injury.
My personal take is just eat well on Keto. Hold your plan. Let the pills and more do their thing for healing as you needâŚwaitâŚthen re-evaluate it all. Rest all you can, this is OK 
Do what you need to heal this injury and âthink all that otherâ stuff later kinda.
You got time You donât have to do anything overnight and you wonât where the body is concerned with an injury like you mentioned so put yourself in âsmart Keto Planâ mode and wait.
You desire forward movement and more but ya got slammed here kinda, but that is OK, you must give that time for it to pass, forcus on that healing as it has to go down all the while just eat the Keto Plan as you need and time will handle the rest, along with ALL the body functions to do just that
Your mode of thinking canât now be overthink with the issues you are facing. Heal first. Breathe. Relax. ALL IS OK truly if we just allow the time we need to get thru things we seem and feel so wrong ya know that get âin the wayâ of our progress but ya got time truly
wishing you only the best!!
Tracking apps and sites are for tracking. I care about the data mine has about items, couldnât care less about its silly assumptions 
Our energy need canât be calculated. I am a mere mortal and even among them, simple regarding fat-loss, I just need a cute calorie deficit to lose fat, itâs enough and needed too - but even that is way more than 1460 kcal! I donât want quick fat-loss, I just donât have the energy need for that, among other things.
I typically donât even have target/minimal/maximal macros. I eat as much as I feel like or consider right if it wouldnât be good enough at that time, experiment a bit and I just look at my various data afterwards and try to figure out what works best for me. It canât be calculated or scientifically showed what exactly works well for our individual body so for many of us a lot of self-experimenting happens.
My working theory certainly explains a few things. It explains why vegans and vegetarians suffer from atherosclerosis as well, and even increased risk of stroke over meat eaters together with your theory about NO being a main driver. Vegans and vegetarians may well have higher insulin over time leading to less NO and stiffer arteries which are bad for strokes. Sugar and PUFA oils are vegetarian, and many substitute PUFA oils for saturated animal fats under the old mistaken belief you are talking about that saturated fats are the root cause of cardiovascular disease. We know that vegetarians do not eliminate cholesterol. Their livers are going to make it anyway or they would be dead. So, they too are subject to some mechanism which causes their cardiovascular disease, and again, I believe it is oxidation of their normally good LDL. Denying that because you suspect some ulterior motive doesnât make much sense to me. Science can often be slow - especially in the world of nutrition - but the evidence is just becoming overwhelming. It is no longer just subjective correlation studies. Thanks again for your input.