Sunday, June 15, 2014

Cholesterol: Do chylomicrons clog your arteries? (2)

I'll keep this brief.

The comments on the last post are awash with people trying to help my resident lipophobe out of his lipophobia. This is admirable but misguided and ultimately doomed.

Many years ago I looked at the Copenhagen Heart Study. This observational study generated two hypotheses. One is that chylomicrons kill you. That seems enough for a lipophobe and, if you have this mindset, for goodness sake add carbs to your diet and avoid post prandial hyperlipidaemia. The choice is yours. Go for it. The lack of stress will help you no end.

My own hypothesis is that elevated post prandial triglycerides, here in a population on a mixed diet, is a surrogate for insulin resistance. That is rather similar to an elevated HbA1c under the same circumstances. These are both superficial markers for a failure of complex I of the electron transport chain to effectively deal with the amount of NADH being provided by processing of the diet.

The solution from a Hyperlipid point of view is to concentrate on supplying FADH2 to the ETC via beta oxidation of maximally saturated fatty acids and to minimise NADH input via chronic normoglycaemia, possibly assisted by the inhibition of glycolysis by ketones.

I have no interest in converting lipophobes to lipophiles. We all have our problems, we just have to live with them.

But some gems are coming out of chylomicrons and endotoxin reading. I especially enjoyed this one (among many), all quotes from the same paper:

"Therefore, on the basis of current information, lipoproteins modulate the host response to endotoxin by inhibiting the activation of macrophages, monocytes, and other LPS-responsive cells; promoting the catabolism of LPS by the hepatic parenchymal cells; and inhibiting the response of hepatocytes to pro inflammatory stimuli"

"Early in the course of this work, we found that chylomicron increases the clearance of LPS by the liver while decreasing overall TNF-α production"

"These most recent studies are focused on cells that express the low-density lipoprotein receptor and are critical to the innate immune response to infection, including adrenocortical cells and vascular endothelial cells. The postulated series of events, whereby a foreign molecule (i.e., LPS) serves to both trigger and attenuate a programmed cellular stress response, is unprecedented"

My emphasis.

Now, a functional LDL-C receptor is utterly necessary for the anti-inflammatory effect of the chylomicron/endotoxin complex. If someone's ears don't prick up on this one they have clearly never heard of homozygous familial hypecholesterolaemia. The focus on elevated lipids (sigh) might just have missed the core of the problem, which is the failure to internalise lipoproteins. Interesting idea? It certainly is to me.

Peter

56 comments:

George Henderson said...

There's a lot of useful stuff in those lipoproteins, ubiquinone, carotenoids and retinol, all things cells need for metabolic normalcy.

This is a book a man could get lost in - http://tinyurl.com/kem75mo

Nigel Kinbrum said...

"My own hypothesis is that elevated post prandial triglycerides, here in a population on a mixed diet, is a surrogate for insulin resistance."
It's a plausible hypothesis (like your other hypotheses), but it's wrong and here's why (I already explained why on the previous thread).

In Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, there's no association between fasting TG's and the RR for CHD. Fasting TG's are a surrogate for insulin resistance, therefore there would have been an association between non-fasting and fasting TG's and the RR for CHD, if the cause had been insulin resistance. There wasn't, so it isn't. Q.E.D.

Nigel Kinbrum said...

The post that you linked to many years ago had an interesting comment. Emphasis, mine.
"Gretchen said...

Keep in mind that although the increases in the postprandial lipid levels were slightly lower in the people who had been on a ketogenic diet in Volek's study, they still weren't zero. Not sure how high they were as the axis is mislabeled.

And not everyone sees the reduction that he saw.

What we need is studies that show *why* high PP lipids are related to heart disease."
Studies like Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling?

Nigel Kinbrum said...

P.S. I drink Gold Top milk and eat fatty meats like pork belly strips. Lipophobe, moi?

However, I do believe that eating sticks of Kerrygold butter to achieve "Nutritional Ketosis" is stupid. I hate stupidity, so that makes me a stupophobe.

Oliver Magoo said...

My postprandial TG is still lower on low carb than even my fasting TG was when I was McDougalling.

Oliver Magoo said...

And I see the same thing in Volek's study. The keto dieters TG levels after the fat bolus is still lower than their pre-keto fasting TG.

Nigel Kinbrum said...

Oliver Magoo said...
"My postprandial TG is still lower on low carb than even my fasting TG was when I was McDougalling."
Are you eating sticks of Kerrygold butter to achieve "Nutritional Ketosis". Do you drink "Bulletproof coffee"?

See Traditional Bulletproof Coffee Technique. ;-)

Purposelessness said...

Nigel is fighting windmills made out of strawmen

Oliver Magoo said...

I've had bulletproof coffee before but it's not a daily thing. And yes, I am in ketosis. I average about 1.5 - 2.0 mmol.


One thing about chylomicrons is they contain Apo A1 which they pass off to HDL. Apo A1 is a good guy. It's the main apo that gives HDL its protective qualities.

Charles Grashow said...

@Oliver

Have you had your ApoB, LDL-P measured? What was your last LDL-C and what were your TG's pre and post?

I'm not against saturated fat - I consume full fat raw goat milk, full fat goat milk yogurt/kefir, etc as well as fruit/veggies, nuts, seeds, 100% dark chocolate, etc. and my last fasting TG was 43. I'm probably not in NK because 1) I don't measure and 2) I really don't care.

"My own hypothesis is that elevated post prandial triglycerides, here in a population on a mixed diet, is a surrogate for insulin resistance."

Any proof for that theory?

IcedCoffee said...

@Nigel, from your study:
"Elevated postprandial levels of triglycerides, via higher peak concentrations or delayed clearance, also might represent an abnormal response to an oral fat load that reflects insulin resistance"

Nigel Kinbrum said...

Purposelessness said...
"Nigel is fighting windmills made out of strawmen."
I don't know what I'm fighting, half the time. I'm definitely not a lipophobe.

Nigel Kinbrum said...

Oliver Magoo said...
"I've had bulletproof coffee before but it's not a daily thing. And yes, I am in ketosis. I average about 1.5 - 2.0 mmol."
You didn't answer the Kerrygold question. Does that mean you don't eat sticks of Kerrygold butter?

Nigel Kinbrum said...

IcedCoffee said...
"@Nigel, from your study:
"Elevated postprandial levels of triglycerides, via higher peak concentrations or delayed clearance, also might represent an abnormal response to an oral fat load that reflects insulin resistance""
Yup. It might.

In a healthy person, it takes ~1 hour before an OFTT starts to affect TG's, due to delayed gastric emptying. It takes a further ~1 hour for TG's to reach a peak. TG's stay high for ~2 hours before starting to reduce, so significant clearance doesn't even start until ~4 hours have elapsed. Ref: http://ajcn.nutrition.org/content/75/3/505/F3/graphic-4.large.jpg

Oliver Magoo said...

Charles,

My last test results:

TC 177
TG 68
HDL 77
LDL Calc 86 (76.5 Iranian)


I didn't have particles tested. When I tested my TG they were in the 70s fasting and peaked to the 140s postprandial.

Nigel, I get most of my calories from nuts. I'm not afraid of saturated fat though. I just like nuts.



Purposelessness said...

"I don't know what I'm fighting, half the time."

I think that was the most genuine thing you ever said, Nigel. Thank you.

Nigel Kinbrum said...

Oliver Magoo said...
"Nigel, I get most of my calories from nuts. I'm not afraid of saturated fat though. I just like nuts."
Thanks for replying. What's your opinion of adding humongous amounts of fat to the diet to achieve "Nutritional Ketosis"? This is what I'm warning people about. I have no problem with "standard" LC & LCK diets.

Nigel Kinbrum said...

Purposelessness said...
"I think that was the most genuine thing you ever said, Nigel. Thank you."
Thank you for your thank you. I'm hit with so many logical fallacies in the course of "discussions", that it's really grinding my gears. The 3 favourites are:-

1) Appeal to Authority: You don't have any relevant qualifications, therefore you don't know what you're talking about.

2) Ad Hominem: You're over-fat and under-muscled, therefore you don't know what you're talking about.

3) Strawman: LC & LCK diets are safe, therefore you don't know what you're talking about. I'm not attacking "standard" LC & LCK diets. I'm attacking extremist behaviour like eating sticks of Kerrygold butter.

I feel a blog post coming on!

tremendo said...

>> My own hypothesis is ...

> Any proof for that theory?

Oy

Ilaine Upton said...

Oliver, if you are in the US, you can order an NMR and a VAP online, they cost about $100 each, lots of providers, I use mymedlab. Once you pay for the test, go to a nearby lab and get a draw. You will get the results in a week or so. You don't need a physicians order in most states. You don't need to be fasting for most of the parameters except triglycerides, really, but do it fasting so you get the triglycerides. It is entirely possible to have normal LDL-C (calculated) but abnormal particle count and/or particle size. A smallish but substantial percentage of people eating low carb/Paleo develop an extremely high LDL particle count. Dr. Thomas Dayspring thinks it might be genetic.

My own particle count went way down when I started the resistant starch/soil based probiotic hack. Maybe a coincidence? Maybe something to do with recycling bile acids? Dunno. Also getting hypothyroid under control, taking female hormones (I'm post-menopausal, Type 2 diabetic). Too many moving parts to really know why.

At any rate, if your LDL particle count is elevated, and your LDL particle size is small, you will want to work on that. Saturated fat increases LDL particle size.

Oliver Magoo said...

Ilaine,

Thanks. I'll consider getting an NMR or VAP.

Does Dr. Dayspring consider Apo A1? The ratio of Apo B to Apo A1 is a much stronger predictor than either alone. Low carbers should have plenty of Apo A1 from chylomicron production.

Dr. Attia has said that some who go on a low carb diet don't see a fall in LDL-P, which is correlated with Apo B, but they do have a reduction in PAI-1, a marker of arterial inflammation. Having an increase in Apo A1 might explain it.

Glad you are doing better. I eat a raw potato a day myself.

OldTech said...

"This is a book a man could get lost in - http://tinyurl.com/kem75mo"

And I am getting lost in it. It seems perhaps a bit out of date, but I need the background.

Galina L. said...

I guess the mentioning of the eating the whole stick of a Karrygold butter with eggs for a breakfast is mostly the reference to the latest diet practices of Jimmy Moore who also has a significantly elevated TC. Most if not all the people who comment here are not in his situation - his initial weight was 400 lbs, he lost 180 lbs then kept yo-yoing not to regain too much, now he straggles to be under 250 lbs. Somehow his story is used by some people as the illustration about the flows of LCarbing (in my opinion it is mostly the illustration about the degree to which human body hates to loose fat). I wonder , is it possible to eat too much fat if you eat only once a day. My guess once a day most people could eat anything and be healthy, if it is not a starvation diet. As a person with a removed gallbladder, I have no intentions to practice something like that, just curious what lipophiles may say. I got adapted to a fat eating, but the lack of a gallbladder still sort-of limits my fat consumption abilities, however when travel, I live on a coffee with a heavy cream. Ketosis is the perfect state for a traveler.

George Henderson said...

Gurr, page 42 -
It is not uncommon to find an exaggerated
lipaemic response (43) in which the postprandially raised TAG concentration
persists for much longer (Figure 1.3C). An important reason for TAG
persistence may be a reduced activity of lipoprotein lipase resulting in slower
clearance of TAG-rich particles. Such ‘TAG intolerance’ is frequently observed
in people with maturity onset diabetes (so-called non-insulin dependent, or
type 2 diabetes). In this type of diabetes, insulin production is not a problem
but lipoprotein lipase (whose activity is controlled by insulin) is less able to
respond to insulin under these conditions and so the removal of chylomicrons
is sluggish. Lipaemia is further exaggerated because the partially hydrolysed
remnant particles are poorly taken up by the receptors on the surface of the liver
cells.

http://tinyurl.com/kem75mo

What is the "first cause" of hyperinsulinaemia?

Normal insulin response = rapid first phase release on exposure to glucose (this is enhanced by extra copies of salivary amylase, inhibited by PGE2, an omega 6 prostaglandin) and short phase 2 release (this is suppressed by efficiency of phase 1, and prolonged by omega-6 metabolite 12-HETE).
So we have two conditions besides excess carbohydrate that help DM2 develop; salivary amylase genetics, and omega 6/3 imbalance (or maybe just excess omega-6).
Plus any inflammatory or pro-oxidant milieu that also helps drive prostaglandins.
http://hopefulgeranium.blogspot.co.nz/2014/05/diabetes-as-iatrogenic-disease-indian.html

marie said...

Galina L., "...when travel, I live on a coffee with a heavy cream. Ketosis is the perfect state for a traveler."
Yes, exactly. I've found the same.

Frankly, I think that even long term, fasting (as in IF) is the state that renders the most benefits, the ensuing ketosis being secondary to that. This assumes no extravagance of starches/sugars in between.
However, that is just a personal experience.

Galina L. said...

Marie,
Probably, I had to say that ketosis is perfect for emergency situations and stressful periods. I have a tendency to have migraines after anything stressful, and a very long plane trip or a long (more than two hours) car driving used to be a migraine-producing with 100% accuracy. My resistance to stress is way better in ketosis, and just a long-distance travel is not enough to make me sick any longer. Not everybody has a migraines, but many people could use some extra protection against life troubles.

marie said...

Better at handling stress in ketosis, or specifically when fasting eg. just having coffee and cream?

I find it fascinating either way, I am like that both ways. Yet, people persist on claiming higher stress and lower energy 'in ketosis' . Why, it even induces hypothyroidism doncha know?

This makes no biochemical sense whatsoever and it's also not my experience. More 'calmness' and more, steady energy instead.

Is there a bunch of hypochondriacs or liars, or perhaps do some people not really achieve it or not stay long enough to get adapted? It's not an easy state to maintain nutritionally, it's easier if significantly hypocaloric and guaranteed if fasting.

George Henderson said...

Just noticed this post:
http://high-fat-nutrition.blogspot.co.at/2008/06/ihd-and-ghee.html
about this study
http://www.ncbi.nlm.nih.gov/pubmed/9212571
Which fits with my previous comment.
Ghee = low PUFA %, which preserves n-3:6 balance when n-3 is low (e.g. no fish in diet).

Nigel Kinbrum said...

George Henderson said...
"Gurr, page 42 -
It is not uncommon to find an exaggerated lipaemic response (43) in which the postprandially raised TAG concentration persists for much longer..."
As I discussed in I'm NOT a lipophobe, I'm a very naughty boy!, TAG persistence doesn't significantly affect TAG level in the 2 to 4 hour period. Tag level in the 2 to 4 hour period is determined by the amount of fat in the bolus. Particle number is also dependent on the amount of fat in the bolus.

Nigel Kinbrum said...

marie said...
"Yet, people persist on claiming higher stress and lower energy 'in ketosis' . Why, it even induces hypothyroidism doncha know?

This makes no biochemical sense whatsoever and it's also not my experience. More 'calmness' and more, steady energy instead."
Hi marie,

Hypercortisolaemia on a KD can cause problems for some people (most likely the very active, as their muscles are burning carbs at a higher rate than the sedentary). Hypercortisolaemia can also lower T3 & raise rT3.

George Henderson said...

@ Nigel,
hypercortisolaemia is a finding in anorexia nervosa.
http://www.ncbi.nlm.nih.gov/pubmed/1889142
I thought we were talking about excessive consumption of sticks of kerrygold butter.
Anyway, while we're on the butter tip,

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3347809/

Ghee oil is an important dietary fat in India and other South Asian countries,42, 43 which contains high amounts of SFAs (about 59% of its whole fatty acids). SFAs, except for stearic acid, increase serum TC,44 and therefore, ghee oil, that are high in cholesterol and SFAs, are considered as harmful. On the other hand, ghee is a good source of oleic acid which is capable of protecting LDL-C particles from oxidation and prevents atherosclerosis.45, 46 Furthermore, according to Asgary et al, the average TFA content in ghee produced by Bakhtiari nomads (the kind of ghee that was used in this study) is 8.3 ± 0.7 which is 1.4 times less than the amount of existing TFA in hydrogenated oils.41

Kumar's study indicated that consumption of ghee in the diet even at high intakes does not increase serum lipids. A strong idea was also made to link the consumption of anhydrous milk fat such as ghee with increased risk of heart diseases.47 Kumar's study with experimental animals did not show any linking between ghee consumption to hypercholesterolemia and hyperlipidemia, which are considered to be risk factors for heart diseases. Interestingly, consuming increased levels of ghee reduced serum TC and TG levels.47 However, use of excess intake of ghee as a means for lowering serum TC is not recommended, but the study indicates that there is no reason for apprehension for consuming ghee in the diet, which is an age-old practice that is relished in Indian culinary.47 Mozaffarian et al obtained that substituting 8% of energy intake from TFA with SFA cause to decrease CVD by modifying TC/HDL-C ratio.48 So, it confirms the proper effect of ghee on serum lipid profile.

marie said...

Nigel, thanks, I'll look into that (not British-english ;) )

tess said...

Marie, i'm with you.... My understanding is that the "LC is stressful" argument is a jump to conclusions: put together "high cortisol promotes glucose release" and "VLC requires GNG" made some people assume that GNG=high cortisol ... which is not true ALL ACROSS THE BOARD. Not to mention, KD diet as studied for epileptic children doesn't have much in common with VLC for health and weight loss. If Peter has taught me anything, all these years I've been reading his blog, it's that you have to look at exactly WHAT the test-subjects are eating, not assume the experimenters are putting the appropriate label on them! :-)

Galina L. said...

When some people report that they find ketosis stressful, I tend to believe them. It is rude and aggravating to declare everybody with a different experience to be delusional. In my case I find ketogenic state beneficial for doing physical activities as well, not only when I travel sitting on my butt, but I am well adapted to ketosis. I like food and I enjoy cooking, so living on coffee is not my normal routine, but I consume my vegetables and carbohydrates during the second part of the day. I found that exercising in the morning after only cup of a coffee is comfortable enough. My preferable routine includes nowadays movements against my own body weight, like climbing pole and hanging on hands.

Nigel Kinbrum said...

George Henderson said...
"@ Nigel,
hypercortisolaemia is a finding in anorexia nervosa. http://www.ncbi.nlm.nih.gov/pubmed/1889142 "
Any situation where the liver has insufficient glycogen to produce the necessary glucose raises cortisol. Jimmy Moore has hypercortisolaemia, but doesn't know why. Hmmm!

"I thought we were talking about excessive consumption of sticks of kerrygold butter."
marie changed the subject! :-D

Nigel Kinbrum said...

tess said...
"Marie, i'm with you.... My understanding is that the "LC is stressful" argument is a jump to conclusions: put together "high cortisol promotes glucose release" and "VLC requires GNG" made some people assume that GNG=high cortisol ... which is not true ALL ACROSS THE BOARD."
Exactly. It's insufficient carbs for the level of exercise in the presence of insufficient protein that raises cortisol level. See RQ plots from Vogt et al. As long as RQ >0.7 , there is carb-burning. At max intensity, carb-burning can reach ~4g/min.

marie said...

Galina! Did you just call me rude? :)

It's ok, I certainly didn't mean anyone's delusional, instead I suggested that if they find it stressful, they likely didn't maintain ketosis long enough to ever get adapted.

As for those who hypothesize a biochemical/ physiological pathway to define the state as stressful, they are mix-matching effects to get to that conclusion just as Tess describes.

It's not about validating anyone's experience ;)
It has to make biochemical sense otherwise there's some explanation for the mismatched experience. I just think non-adaptation is a likely explanation.

marie said...

Tess, thanks, your breakdown of that aspect of the 'ketosis is stressful' hypothesis makes sense to me too.

Nigel, ditto :)

Galina L. said...

No, Marie, I was not calling you rude, when I was writing my comment I was thinking about the people who were trying to deny my experience and telling me I couldn't feel calm and energetic in a ketogenic state. I don't want to do it to them in return. If they are sure their thyroid gland go into hibernation without "safe starches" and practicing"moderation", so be it. I am glad to meet others , like you, who share my experience.

marie said...

Galina, thanks, we are alike in that too.

George Henderson said...

I'm tempted to agree with Nigel's theory after reading this:

http://www.ncbi.nlm.nih.gov/pubmed/124686012335

Accumulation of postprandial triacylglycerol-rich lipoproteins is generated by assimilation of ingested dietary fat and has been increasingly related to atherogenic risk. Nevertheless, the influence of different kinds of dietary fatty acids on postprandial lipid metabolism is not well established, except for (n-3) polyunsaturated long-chain fatty acids. Our goal was to evaluate the effects of test meals containing a common edible fat source of saturated (butter), monounsaturated (olive oil) or (n-6) polyunsaturated (sunflower oil) fatty acids on postprandial lipid and triacylglycerol-rich lipoprotein responses. After a 12-h fast, 10 healthy young men ingested mixed meals containing 0 g (control) or 40 g fat, provided as butter, olive oil or sunflower oil in a random order.

The butter meal induced a lower postprandial rise of triacylglycerols in serum and chylomicrons (incremental AUC, mmol.h/L: 0.72) than the two unsaturated oils (olive oil: 1.6, sunflower oil: 1.8), which did not differ. Circulating chylomicrons were smaller after the butter meal than after the two vegetable oil meals. We conclude that butter results in lower postprandial lipemia and chylomicron accumulation in the circulation of young men than olive or sunflower oils after consumption of a single mixed meal.

Now, where's my stick of Kerrygold...

Sam Knox said...

Amber at Ketotic has some thoughts about the cortisol issue:

Here

IcedCoffee said...

Losing weight is going to raise cortisol almost invariably. Natural bodybuilders diet on as high a carb content as possible, but still have a linear rise in cortisol as they lose weight.

Ilaine Upton said...

Oliver, re: Dr. Dayspring. He is a MD, PdD, medical school professor, with a specialty in lipidology, and a penchant for teaching via new media, and I would not dream of trying to explain what he thinks about anything.
http://www.fhit.org/faculty.html

As far as I can tell, when it comes to explaining lipids as is commonly understood by the uncommonly educated man, Dr. Dayspring is the guru, although Peter is the guru for pushing the envelope. I try to never miss anything either of them puts online.

I am on the email list for whenever Dr. Dayspring puts up a new lecture on Lecturepad, and try to grasp what is being said as hard as I can. Free registration. Priceless.
http://www.lecturepad.org/

mnature said...

Chylomicrons? Is that similar to Midichlorions?
[Yes, I'm bad. I'll go sit in the corner now]

marie said...

mnature,
they must be! Since we know that "without the Midichlorians, life would not exist...."

(Make some room in that corner... ;-) )

marie said...

Sam Knox,
thanks for the link, Amber's very informative.

Tess,
she breaks the Cortisol=>GNG causation, quite nicely.

Oliver Magoo said...

Like anything else, cortisol can be pathogenic or physiological.

I get the same response from a ketogenic diet that I did from taking ephedra:

1. Decreased appetite
2. Calmness; sense of well-being
3. Increased energy
4. Mental clairity

What I don't get from keto are the side-effects. My blood pressure is reduced on keto and no GERD. Ephedra made both worse.

Sam, thanks for linking to Amber's post. In the link to her more personal blog ( http://www.empiri.ca/2014/02/red-light-green-light-responses-to.html ), she talks about how longevity researchers view cortisol in the context of calorie restriction. What's most interesting to me is the study showing that reducing cortisol by removing adrenals in these animals results in some lost benefits of CR. Injecting them with the hormone restored the benefits.

George, That is interesting. My TG would have less than doubled with a bulletproof coffee then. :)

Ilaine, thanks. After a tentative search, I see he does talk about Apo A-1 but he's cautious about infering it from HDL levels as HDL can have 1 or several Apo A-1 proteins. I would be surprised if someone producing lots of chylomicrons had a deficiency of Apo A-1.

People eating lots of sugar would have an increase in ApoB through VLDL production without any of the Apo A-1 that chylomicrons offer.

Chylomicron... chylomicron... chylomicron... That word is starting to sound quite strange. ;)

George Henderson said...

A common finding in dairy fat experiments is that Apo A goes up (with HDL) and Apo B comes down (with TAG).
A more arcane finding is that long chain omega 3 increases in proportion to long chain omega 6 with higher dairy fat. Maybe an effect of odd-chain SFAs competing selectively for elongation enzymes.
My thinking is that butter should be considered, in nutrition terms, as a marrow surrogate.

Nigel Kinbrum said...

George Henderson said...
"I'm tempted to agree with Nigel's theory after reading this:

Butter differs from olive oil and sunflower oil in its effects on postprandial lipemia and triacylglycerol-rich lipoproteins after single mixed meals in healthy young men."
Your link doesn't work - here's one that does. I feel sorry for the poor beggars who were guzzling up to 600g/day of corn oil in Kasper et al (1936).

Nigel Kinbrum said...

Sam Knox said...
"Amber at Ketotic has some thoughts about the cortisol issue:

Here"
Amber's post is refuting the hypothesis that hypercortisolaemia induces metabolic syndrome. She's not denying that keto diets produce hypercortisolaemia.

Chronic hypercortisolaemia also adversely affects the hippocampus.

As hypercortisolaemia turns LBM into substrate (e.g. glutamine) for hepatic & renal GNG, people cutting their dietary protein intake because their BG is too high on a keto diet aren't doing themselves any favours.

Paging Jimmy Moore & Fred Hahn. Please go to aisle Hyperlipid. :-D

Ilaine Upton said...

George, Dr. Dayspring doesn't like inferring any lab value from any other lab value, he's all about direct testing and measurement.

With new technology, direct testing and measurement is reasonable in price.

Inferring used to make some sort of sense back in the day before the new technology.

altavista said...

So Peter, which one is it? These guys make me dizzy after 50+ comments. Help a brother with no med cred :)

Nigel Kinbrum said...

altavista said...
"So Peter, which one is it?"
If by "it" you mean "my resident lipophobe", that's me he's referring to, which is hilariously funny as I'm NOT a lipophobe, I'm a very naughty boy!

Oliver Magoo said...

Actually, Dr. Dayspring has no problem inferring ApoB from LDL-P since each LDL-P will only have one Apo B. Apo A1 cannot be inferred from HDL-P since one HDL-P may have anywhere from 1 - several Apo A-1. It looks like he focuses on only LDL-P for this reason. My contention is that someone eating lots of fat will have lots of Apo A-1 from chylos, which would allow for a higher Apo B. We can test for Apo A-1 and Apo B, so why not?

Oliver Magoo said...

This study is interesting. It looks like chylomicrons themselves may be responsible for a great deal of reverse cholesterol transport.

"We examined whether postprandial (PP) chylomicrons (CMs) can serve as vehicles for transporting cholesterol from endogenous cholesterol-rich lipoprotein (LDL+HDL) fractions and cell membranes to the liver via lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities. During incubation of fresh fasting and PP plasma containing [(3)H]cholesteryl ester (CE)-labeled LDL+HDL, both CMs and VLDL served as acceptors of [(3)H]CE or cholesterol from LDL+HDL. The presence of CMs in PP plasma suppressed the ability of VLDL to accept [(3)H]CE from LDL+HDL. In reconstituted plasma containing an equivalent amount of triglycerides from isolated VLDL or CMs, a CM particle was about 40 times more potent than a VLDL particle in accepting [(3)H]CE or cholesterol from LDL+HDLs. When incubated with red blood cells (RBCs) as a source for cell membrane cholesterol, the cholesterol content of CMs, VLDL, LDL, and HDL in PP plasma increased by 485%, 74%, 13%, and 30%, respectively, via LCAT and CETP activities. The presence of CMs in plasma suppressed the ability of endogenous lipoproteins to accept cholesterol from RBCs. Our data suggest that PP CMs may play an important role in promoting reverse cholesterol transport in vivo by serving as the preferred ultimate vehicle for transporting cholesterol released from cell membranes to the liver via LCAT and CETP."

http://www.ncbi.nlm.nih.gov/pubmed/15102891