I understand that this one study found the ratio to be a good indicator. But good science requires a repetition of results as well as controlling for the factors I mention. We've been through this process with LDL particle size, which ultimately proved to be irrelevant. Let's not make the same mistake again.

You mean like taking apoB without regard to insulin or ApoA1? That would be a mistake, AJ.

Anyway, apoA-1 all by itselsf is inversely associated with CVD. ApoB all by itself is associated with disease. Why is it such a stretch to understand that the ratio of one to the other would be a better predictor?

By the way, I was wrong about Dr. Dayspring. He does indeed aknowledge that the ratio is the best predictor:


http://www.lipidcenter.com/pdf/Unde...pid_Profile.pdf

I went to a lipidologist, and she had a full and in depth blood test done that included hereditary markers. Like you, all of my numbers were shining except for my LDL-p which was very high.

She told me my hereditary markers indicated high LDL-p, and said that no amount of diet or exercise would matter. I started on Atorvastatin and those numbers dropped to normal almost overnight. No side effects at all, and I feel great. Still doing LCHF with her blessing.

My aunt actually said the same thing. She quit taking her statins after finding out about that joint pain and muscle pain are possible side effects because she has problems with arthritis. She's also a cancer survivor so she flat up told me that she'd rather just drop dead of a heart attack than die slowly if the cancer comes back.

Just keep one thing in mind, everyone:

STATINS DO NOT PREVENT HEART ATTACKS.

The ONE thing they have been shown to do is very slightly bring down the chance of another heart attack in middle-aged men who have already had a heart attack.

PERIOD.

That's it, that's all, and there's a highly significant chance (at least 1 in 3 and most studies think it's much higher) of very dangerous side effects, which may, or may not, end when you stop taking them.

If this was Vegas, I wouldn't put a nickel on those odds.

That just keeps coming back in small print, and doctors do not read small print.

Like you WereBear, not even a wooden nickel.

Is this correct? LDL particle size has been proven to be irrelevant? I must have missed this one.

Dear zmktwzrd,

I have the same issue. The idea one of the people presented in this thread that if ldl-p changes so quickly, is it something to even worry about; I argue then, why worry about triglycerides?

I have read somewhere that Niacin can raise an inflammatory marker after some time. Might look into that.

After reading Dr. Spencer's results of going from low carb to high carb (and a few others) I tried it too. I've only been on it for two weeks. In just 10 days on the diet (where I lowered saturated fat and upped carbs like potatoes, rice, and oatmeal) my total cholesterol went from 258 to 207. I got the second reading from giving blood...after eating two eggs that morning I might add.

I still need to do another ApoB test in a few months to make sure this is actually working to lower the number. I might add that I lost 7lbs on this change.

I believe that for us, there's something in our genetics causing this. From reading the book The 10,000 Year Explosion, I learned that there have been just as many genetic/epigenetic changes in the last 10,000 years as there were the previous 100,000 years.

The idea is that a dramatic changes put a great strain on the species causing a much more rapid changes to our genetics (i.e. lactose tolerance and hemochromatosis).

It would stand to reason that some of us out here in the world of today would actually be eating more attuned to our genetics if we ate more carbs and maybe even grain.

The death of Seth Roberts had me re-thinking all this given that he ate nearly a stick of butter a day.

I know that my tendency for AFIB and heart ectopic beats is greatly reduced if I eat enough dietary calcium. I'm blond with blue eyes, so my genetics may favor more dairy.

Just a thought,

Good luck!

Forgot to add that on my advanced lipid panel in 2012, my insulin was 19, LDL-p was 1750, ApoB 97. This time a few weeks ago, only getting a normal lipid panel along with ApoB, my ApoB was 117.

The doctor didn't seem to be worried about my fasting insulin being high, but I've read since then that the increased cortisol levels (especially fasted) of the low carb diet can increase fasting insulin in some.

I know that my morning glucose went from ~120 down to ~100 in a couple of days of adding carbs back. And, I have issues with some carbs raising my glucose too high after meals.

Isn't this what is supposed to happen for everyone if they add back in carbs, at least at first? After all, this is exactly what low carbers are told to do if they are going to take the glucose tolerance test. Add at least 150g of carbs for several days so the pancreas 'knows' to get busy again handling the glucose load. I don't think the fact that one's fasting glucose goes down after a couple of days of adding carbs means any more than this.

I do agree that some of us may be better off eating 'healthywholegrains' and other carbs. My DH is a runner who lives on huge amounts of bread, fruit, yogurt, beans, potatoes, and assorted veggies. He eats a little bit of fish or chicken a couple of times a week. He is skinny as a rail and completely healthy.

Turtle2003,

Yes, I've read that too. My fasting glucose seems to stay lower (by around 15-25pts) when I eat more carbs--especially at night--compared to when I'm going strict low carb or even ketogenic. Even after months of low carbing, my morning glucose numbers stay in the 115-125 range.

I definitely don't believe low carb is healthy for me, despite fully believing it was after reading Taubes in 2008. Not only were my numbers worse, but I actually felt worse in many ways.

I think genetically speaking, people from modern societies started eating more (in most cases mostly) carbohydrates at various times between 20,000 and even as late as 4,000 years ago in the case of some people in England/Scotland/Ireland. That's a big variation in agricultural adoption dates which I believe can greatly affect genetic/epigenetic morphology.

I would really like for someone to answer this question for me.

If recent (i.e. since the adoption of agriculture) genetic/epigenetic changes don't affect what diet we should be eating, then please explain hemochromatosis? A person with that issue would greatly increase his chance for heart disease if he ate a low carb paleo diet...especially if it were a substantial meat-based diet.

It only seems reasonable to me that if hemochromatosis accidentally popped up in the genome and later allowed people eating predominantly grain diet to stave off anemia, then how many other much less visible changes (that could affect what diet is best) have occurred in the genome that we don't even know about yet?

Loren Cordain states that we've been eating the same way for tens of thousands to even up to 2.5 million years. Well by that logic, shouldn't we all be eating fruit and/or leaves since our ancestors from 2.5 million years back to 8 million years ate that way. It was a much longer time frame than 2.5 million or 100,000 years, whichever you chose.

Mutations populate much more rapidly in a stressed population. That has been seen in the apparent supplanting of the hunter gatherers by the dairy pastoralists. That occurred within a few thousand years. http://www.nature.com/news/archaeol...olution-1.13471

autoimmune--do you have any insulin readings for while you were eating carbs vs. when they were restricted? Have you tried eating more on the ketogenic end of things--lowering protein a little? I have no glucose issues on low carb at any level of protein myself--but my blood glucose is still a bit lower when I'm ketogenic--low 70s to mid 80s instead of low 80s to low 90s, sort of thing. Too be clear, I'm not questioning the idea of individual variation, or the possibility that you respond poorly to a low carb diet--but if all you have to judge by is that lower fasting glucose, and a single data point for serum insulin, I'm not sure you should be certain that low carbohydrates in and of itself is bad for you.

Hey Teaser,

I only had the one insulin test unfortunately. My morning blood sugar didn't seem to change much the more ketogenic I tried to get (i.e. under 20g of carbs a day), but I never went that low for longer than two to three weeks at a time. Perhaps it might have changed had I gone longer.

For me, the morning blood sugar was a bit of a challenge, but the high and rising ApoB/LDL-p was the real worry. Maybe some day they'll figure out that a high LDL-p isn't an issue when otherwise healthy. For now, I'm too spooked to hedge my bets any further with high fat/low carb.

Another thing low carb did that I wasn't fond of was that my desire for exercise (the way I like to do it which is daily including aerobics and weightlifting) plummeted. It didn't seem to matter how long I was on the low carb diet (except that I didn't go past three weeks on ketogenic to see), I just didn't have the energy that I do on a higher carb diet.

The great thing about these forums is the free exchange of information. A couple of older pubmed documents aside, I shutter to think how long it would have taken for people to recognize that a high fat/low carb diet might adversely affect some people's ApoB/LDL-p without forums like this one.

Okay. That's good. I just didn't want to see some sort of "low-carb causes an increase in fasting insulin vs. a higher carb diet" meme start going around. At least not without evidence that includes enough testing of insulin on and off of a low carb diet to show a repeatable effect. These things can have a life of their own. All sorts of people--Dave Asprey, Ben Greenfield, Paul Jaminet--are going around saying that very low carb diets cause a mucin deficiency--based on little but conjecture on Jaminet's part.

Cortisol-->glucose-->insulin makes perfect sense to me--but this rise in insulin via a low carb diet, is it documented, or only conjectured?

I don't doubt that it's possible to actually raise the carbohydrate in a person or a lab animal's diet, lower the fat, and also lower the fasting insulin. There's an awful lot of context when it comes to nutrition. I just don't want the diet (spectrum of diets, to use Dean Ornish's word)--the full range of low carb diets--to get thrown under the bus again. Or to be judged guilty of anything that hasn't actually been established. I think a lot of people's health depends on that.

I'll throw in this as well--so far as I can tell, Jimmy Moore knows how to either have a high ApoB count, high hdl, low triglycerides, and low glucose/high ketones, presumably low insulin--on a ketogenic diet, or low hdl, high triglycerides, high glucose, high insulin--and for all we know, ApoB count wasn't normally tested back when Jimmy was on a high carb diet, that may have been high as well. I doubt he's the only person given this choice, between a rock and a hard place. I do know this--the first option sucks, it killed his brother Kevin. The second option--well, it at least might be all right. Sometimes our best option has a degree of uncertainty.