Our first guest: Dr. Thomas Dayspring...

[Julie G]

I'm looking forward to learning more after your consult, George Good for you for making the appt.

I was browsing Dr. Dayspring's site and found his detailed commentary on a case study of a woman who experienced high LDL-P after eating a very low carb diet. Although she's never identified as an E4, her lipids indicate that may be the case. I thought his comments might prove helpful for some who are dealing with similar issues: http://www.lecturepad.org/index.php/com ... experience

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[LA18]

Thanks for posting this link. I am struggling with this issue and reading this made me realize that it’s probably time for me to consult a lipidologist.

[LanceS]

I was browsing Dr. Dayspring's site and found his detailed commentary on a case study of a woman who experienced high LDL-P after eating a very low carb diet. Although she's never identified as an E4, her lipids indicate that may be the case. I thought his comments might prove helpful for some who are dealing with similar issues: http://www.lecturepad.org/index.php/com ... experience

FWIW, she is a 3/3, from her blog. It is an interesting point in and of itself. If you believe the statistics, which are mostly hidden behind paywalls and never satisfactorily expressed IMHO, doctors should be differentiating the way they treat 4/4s as they get older. As more theories become actionable/acceptable, they may even treat them differently at a younger age. I don't know that I've heard any doc but Gundry (and I think that was my inference) say he treats 4/4s differently. I would not be surprised if Dayspring did as well.

Felt very roughed up by Dayspring's website on my first go through there. Found his asides to be difficult to understand why they were there, as they just seemed to complicate the learning. But he focuses on problem cases. I'm not sure you can understand exactly how things work unless you look at the problem cases. I am shocked at what scientists learn from these little bits of nothing. The fact that he does these asides is something that I now feel very comforted by. If you want to know and understand this, you have to assimilate these "problem cases" into your framework.

Interesting the dialogue... too bad some enterprising doc hasn't tried to figure this out for low carbers. Seems like so much is anecdotal, N=1 without really good labs. 1 really good lab could have made an interesting ending to this... closing some doors... probably opening others... leaving some open. As it is... tastes great, less filling.

[Stavia]

Ive been going through Dayspring's excellent lipid lectures for doctors. Not for the faint hearted. Im doing the hyperabsorption one now. I had forgotten most of this from my biochemistry three decades ago but luckily still have the context and the basic science to understand.
http://www.lecturepad.org/index.php/201 ... ds-to-know

Take home points for those with a non science background or not yet up with the details:
Ive got half way and need to write down my thoughts.
Background: Dont confuse cholesterol with other fats. Hyperabsorption of this and related molecules such as the phyotosterols are a separate issue from "fat" in diet. Sterols are a subgroup of fats. There are a few. The mos famous is cholesterol which is of animal origin. The other sterol molecules are called campesterol sitosterol etc. and they are of plant origin.. Hyperabsorption only pertains to cholesterol and other sterol molecules.

The overwhelming bulk of the cholesterol in the gut comes from SYNTHESIS IN LiVER CELLS which is excreted into the bile and thru the bile duct into the intestine and reabsorbed. Food sources of cholesterol are a very small contributor to this pool available for absorption. We cannot change our LDL significantly by reducing our cholesterol intake (remember cholesterol is not synonymous with saturated fat for instance. We are only talking sterols here)
Then there is a balance between two membrane bound proteins on the guts cells and on the liver cells. One pulls sterols in and the other pushes them out. If the one that pushes them out doesnt work so well then we have the hyperabsorption state. Hyperabsorption doesnt mean the pulling in protein is stronger. It means the pushing out one is weaker. The pushing out protein might be absent or defective. E4s ***might*** be associated with weaker pushing out proteins in some of us. This is a very very new area of research so its not certain yet what the implications are and how big a problem it is. The study he cites had only 78 patients and 14 e4s ( mixedhetero and homo). And it was just a snapshot blood level. Nothing clinical, not correlated to any outcome. But we are unlikely to be able to increase our pushy out protein by diet. The plant sterols Dayspring was talking about in his answers to us are higher in the blood in hyoerabsorbers cos the pushy out protein ***might*** be weaker in us. Ezetimibe blocks the pulling in protein, thus makes both proteins equally weaker so they are balanced again.
Plant sterols are thought not to be good for humans. ie campesterol sitosterol etc. we need our pushy out protein to excrete them.

Ok. Onto second half.
But take home message so far is...
Like bowties, eggs are cool. (Dr Who allusion for the non-nerd)
Ezetimibe might be needed if this is the problem IN AN INDIVIDUAL cos there aint another option at this stage. But its individual. Some ppl havent got the pushy thing at all and some ppl have a weaker one. But its a separate gene to apoe4 completely

[Ski]

Thanks for breaking this down Stavia to us lay folk. Very informative! Did they cite which snp is responsible for these under achieving pushy proteins?


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[Stavia]

Second half:
Omg post hoc analysis of the famous 4S trial, the landmark that proved simvastatin reduced coronary events. The divided the people into quartiles of absorption. The statin had huge event reduction in the hypoabsorbers, and the effect decreased across the quartiles until there was no effect on the hyperabsorbers in terms of events. Wow.

Othe modalities to reduce absorption
1. Fibrates. Work very well in diabetics.
2. Cholestyramine
3. Lactobacillus reuteri, a functional food. Looks from the graph to only have a modest effect
4. Now we get to the phytosterol and phytostanol food spready stuff and the phytosterol foody stuff and stanol foody things. Now be very very careful. A STANOL is NOT a STEROL. Both compete with cholesterol at the molecule that pulls in sterols into the body. Both will lower LDL by a significant amount 8 to 9%. But stanols are neutral. They are safe (we think). Benecol is a stanol. Phytosterols like campesterol and sitosterol we dont think are safe. Higher levels correlate with CVD and there is a disease called sitosterolaemia (Lances brother?) where things are not good. Products containing phytosterols you buy in health stores have magnitutides more phyosterols than a vegan will eat in a day from plants. They will lower your LDL cholesterol but raise your LDL phytosterols whic is correlated with not good CVD outcomes. LDL measurements are a very very blunt tool.

Ok. Phew. There was no bloody way Dayspring was going to be able to explain all this in a short answer. I absolutely dont expect him to have taken the time. Its all on his fabulous website. The lecture is exceptional in detail and clarity. He is a brilliant educator. He reminds me of my biochemistry professor who worked with Krebs himself. Each slide flows beautifully logically from the last. This has taken me over two hours to tease out. The devil is in the detail. Its very complex.

Ps. I feel awful about chunkygate. IMO he is the most objective and reasoned of all the experts we have discussed. Pity for us he is primarily CvD focussed. He only touched on the tiny phytosterol trial of AD cos it overlapped a smidgen with his primary focus.

[Stavia]

Thanks for breaking this down Stavia to us lay folk. Very informative! Did they cite which snp is responsible for these under achieving pushy proteins?


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Unfortunately not. But IMO easy to find out in the US by doing a blood campesterol and sitosteol level. There shouldnt be much in your blood. If there is, your pushy out protein aint working well. Its really simple to find out but IMO critical in terms of therapy because a statin aint enough in a hyperabsorber ( aka under excretor) as per the 4S post hoc analysis

[RichardS]

Another sort-of lay explanation of the sterol testing story:
http://www.bostonheartdiagnostics.com/s ... e_test.php

[Stavia]

Another sort-of lay explanation of the sterol testing story:
http://www.bostonheartdiagnostics.com/s ... e_test.php

Yes, I saw this. Am I able to access this while Im in the US? Ill be in NYC, Orlando and SanFran. My nephew is a US MD, Baltimore based, can he sign a labform for me?

[Tincup]

Stavia,

Why not? When I order online through a company like walkinlabs or directlabs, I get a lab order signed by some doc in Timbuktu that I've never seen or met.