Wednesday, August 12, 2009

Shazia and Dr Clifton

The following is pure fantasy. If it's too offensive I'll take it down. Blame George for forwarding the link to me. Better read the original text before going on to my travesty.

Here's the original.

Here's the travesty:

Dr Peter Clifton, a human nutrition researcher from Adelaide, has recently made surgical history as the first nutrition researcher to receive a functional human brain.


The newly implanted brain, inserted during a 15 hour neurosurgical procedure, has allowed him perceptive thought for the first time in his life. Looking back on his most recent research presentation using his newly acquired brain, he was interviewed by Shazia Qureshi for DGDispatch.

Qureshi: Dr Clifton, what do you now think about the elevation in LDL cholesterol that was found in the low carbohydrate, high saturated fat arm of your study?

Dr Clifton: Well Shazia, I can't believe I've been such a berk. We've known since the 1980s that saturated fat increases the size of LDL particles, to give the large fluffy non atherogenic type, which can typically give an increase in calculated LDL of 20% or more but with a marked reduction in cardiovascular risk. Of course, before my brain implant I simply assumed a 19% rise in LDL implied 19% more bad stuff. I'd never read the literature and had no idea there could be good LDL. Just stupidity, pure and simple. I'm so embarrassed.

Qureshi: How about the change in HDL cholesterol? Was this adversely affected by the saturated fat diet?

Dr Clifton: God no, Shazia, it improved dramatically, by 21%, on the saturated fat diet, that's over 4 times as much as the low fat group who only achieved a 5% increase. Now I can see the low fat group only managed their pityful 5% rise because they were accessing their own supplies of saturated fat due to weight loss. If we'd not starved the poor buggers their HDL would certainly have dropped. Now I realise that HDL always drops on low fat diets unless there is weight loss. What a pillock I've been!

Quershi: Tell me more about the weight loss.

Dr Clifton: Well of course it was greater in the low carbohydrate group, but luckily the difference didn't make statistical significance. Sheesh, at least I didn't come over as such a drongo on that one. Bit of a relief really.

Qureshi: What about the flow mediated dilation?

Dr Clifton: Well again, bit of a pillock on this one. Of course we've known for decades that flow mediated arterial dilation is blunted by free fatty acids. And, because I have always recommended low fat diets, the only way anyone could have any amount of free fatty acids in their circulation is if they are in advanced metabolic syndrome and have started to spill un-needed and uncontrolled free fatty acids from their adipose tissue. Of course these people are in trouble cardiovascular wise. I should know, I've gotten them there by telling them that fructose is great stuff as it's low in fat and a bit is found in fruit, so a giant Pepsi is fine... If only I'd had this brain sooner.

With a brain all you have to do is ask yourself: What substance is a low carbohydrate dieter going to run their metabolism on? It's not going to be glucose is it? And if they are loosing adipose tissue as free fatty acids and getting even more fat from their diet, it's obvious that there is going to have to be a higher level of free fatty acids in their bloodstream. God knows why I didn't measure them. Oh, guess that's because I didn't have a brain... It's not clear why free fatty acids blunt flow mediated dilation. I guess that's mostly because the research on this subject was done by people like me. I should have realised my boo boo when we got the pulse wave velocity results.

Qureshi: Yes, you measured the stiffness of the aorta using the time taken for the pressure wave from the heart beat to reach the lower limbs. This must have been much worse in the saturated fat group, with all that elevated LDL cholesterol clogging everything up and no ability to dilate arteries after they've had a tourniquet on their arm.

Dr Clifton: You'd have thought that I'd have realised I was talking a load of bollocks about cholesterol and flow mediated dilation when the low carbohydrate group improved their pulse wave velocity as much as the low fatters. But don't forget, I had no brain in those days. This is so embarrassing. I actually said long-term consumption of a low-carb diet may have detrimental effects on cardiovascular risk.

Do you think anyone might have noticed?

Qureshi: I hope not.

68 comments:

Thackray said...

Peter,

That is SO funny!!

I'm hearing Gunther words from the comment section of the last post. But as you said to him:

"There is no conspiracy. Repeat after me, There is no..."

Regards,

Philip Thackray

Kurt G. Harris MD said...

Peter

A brilliant piece of Swiftian sarcasm. Don't take it down.

I have been planning a post on how Flow-Mediated Dilatation (sorry, "endothelial function", they call it) is no more a real proxy for atherosclerosis that total cholesterol- that's why the cardiologists love it.

Thanks for the encouragement!

Connie said...

I love it too. Please leave it up?

gunther gatherer said...

Just to add more insult to our marginalization as crazed conspiracy theorists, did you guys know that we high-fatters are ALSO all stupid and lazy?

http://news.yahoo.com/s/livescience/20090812/sc_livescience/highfatdietmaymakeyoustupidandlazy

Richard A. said...

gunther gatherer,

The abstract to the study that the article makes reference to can be found at--
http://www.ncbi.nlm.nih.gov/pubmed/19667117

gunther gatherer said...

Thanks Richard A. Unfortunately the abstract doesn't say what kind of fat was used on the rats.

And I'd love to know how the article deduced that humans would become stupid based on a rat study. Any rat that runs 35% less on a treadmill for the researchers is getting MORE intelligent in my book...

Peter said...

Richard and Gunther,

Thanks for the links, the high fat diet is pretty certain to be 30% sucrose. They do say Western diet, which is a synonym for sucrose/fat combo. Ultimately this comes down to semantics, a research high fat diet has nothing to do with us unless it is ketogenic. That's the only term that might have any relevance to LC eaters, and studies using real high fat diets are as rare as hens teeth and are generally positive, unless performed by idiots of course!

Peter

Anna said...

Too funny. Please leave it up!

Richard A. said...

For the past few months I have been drinking about 150 Calories of coconut milk in the morning and 150 Calories at night. In the past, at night I usually get so tired and sleepy and end up going to bed early. Drinking the coconut milk at night has been keeping me alert and awake late into night.

What I suspect is that at night my brain begins losing the ability to use glucose and uses ketones generated from MCTs from the coconut milk.

George must lose weight said...

No serious comment on the original study?

Stan (Heretic) said...

Hi Peter, please keep it posted, you can't please everyone, for some it may be too offensive for others too conciliatory...

I have an even better candidate for brain transplant (as long as they won't try using abnormal brain like the last time... )

http://jama.ama-assn.org/cgi/content/abstract/290/7/912

(Dr. Kwiterovich)

This guy managed to obtain a miraculous DECREASE of HDL and an INCREASE of triglyceride on a "ketogenic" diet! Good job!

Regards,
Stan

Peter said...

Hi Kurt,

Go for it, I've just spent several hours trying to make sense out of FMD. I've also failed to find what NEFA do to basal blood flow to muscles. I suspect these might be related....

Got some reading to do on your blog. Did you know Solpadeine (paracet/codeine) is a serious issue here in the UK? Pretty much like Vicodin in the states. Simply fighting off the withdrawal headache, on a chronic basis, can lead to liver failure from the paracet...

Peter

Peter said...

George,

The study showed that a high fat diet increased HDL by 21%. This is GOOD. It increased LDL by 20%. We have known since 1984 (!!!!!!) that the increase in LDL seen on feeding saturated fat is due to increased diameter and decreased density of LDL particles. This is fully accepted as GOOD. Aortic stiffness decreased. This is GOOD. The only problem was that FMD dropped in the high fat group. We know that NEFA always decrease FMD. What we don't know is whether a blunted FMD response, when produced by a normal physiological increase in NEFA, signals vascular pathology. Personally I doubt it and Kurt is going to post soon on it (yes please Kurt).

Personally I suspect FMD is bollocks, but then I would!

So we have a study, performed by a moron, which is still highly supportive of high fat eating, being wrongly reported, by the same moron, as indicating that it increases CV risk.

Now, either Dr Cliford knows this (GUNTHER!!!! Repeat after me, again, "There is no....") and isn't saying or he doesn't know it and he's a moron.

Personally I favour the moron hypothesis.

Peter

Peter said...

Stan,

You can't make anything idiot proof because idiots are so clever.

Peter

Drs. Cynthia and David said...

I vote leave it up. Somebody needs to set it straight with these guys. But I suspect they only care about their grant reviewers though- the ones who keep paying them to do crappy studies and toe the party line.

George must lose weight said...

So the significance of this:

http://jama.ama-assn.org/cgi/content/abstract/290/7/912

is....

I thought it was usually medically used to treat epilepsy!

Meanwhile you can buy this NEW book on self-healing from Rodale for £30:

http://www.secretsofselfhealingbook.com/uof/secretsofselfhealingbook/?keycode=105048&mktOfferId=BKS23144&product_code=042030&smartcode=1064250000060601000013246146220090813

or buy it new from amazon (Jun 2008) for about £11....http://www.amazon.co.uk/Secrets-Self-Healing-Ailments-Vitality-Wellness/dp/1583332960/ref=sr_1_1?ie=UTF8&qid=1250245860&sr=8-1

Peter said...

Cynthia,

Perhaps we should call this the "Small" Conspiracy Theory. Clifton does have a functional brain, knows exactly what he has found and is deliberately distorting/hiding the facts for personal career reasons. Multiple minute acts of personal avarice. That's how we got where we are! I'll buy that.

George,

It's very difficult to see how anyone can get the changes in lipids reported in the abstract. Quite how they did it is the mystery, especially as one of the authors is Miller, a major proponent of the diet. However, the diet is very extreme and does have a number of catastrophes, including death, in it's record. Atkins induction is probably as effective (Stan has the paper and probably I do too somewhere) and possibly even the minimally ketogenic Optimal Diet Stan and I eat to would work. All improve lipids dramatically. The only LC study to show deterioration in lipids was performed by the guy who's name I forget but he was the same person who got Dr Atkins' death certificate by fraud. Oh, and I have one aussie paper on diabetes which shows a deterioration in EVERYTHING on LC. Maybe by Clifton! Have to hunt it out some time

Peter

Thackray said...

Peter said: “you can’t make anything idiot proof because idiots are so clever”.

That lead me to one of my favorite sayings:
“Never argue with an idiot, they will bring you down to their level and beat you with experience”.

Regards,
Philip Thackray

George must lose weight said...

OK, more research

http://www.ncbi.nlm.nih.gov/pubmed/7644455

"whereas combined animal foods (excluding fish) were directly correlated (R = 0.798) with CHD death rates. Multivariate stepwise analysis selected butter, lard+margarine and meat as significant predictors and produced an R2 of 0.922."

comments?

Peter said...

Observational. Most CV researchers only ask about fat, especially those as awful as this crowd! Fat intake and sucrose intake go together. If arsenic intake and fat intake went up together, death from arsenic poisoning would be associated with fat intake. No doubt Blackburn and his crowd would blame the fat!

These people are directly carrying on the work of Ancel Keys. They never measure sucrose (after Keys did and found it was associated with CVD and then ignored this because it didn't fit his preconceptions). It goes up in step with fat. It's lethal.

Peter

George must lose weight said...

I don't understand the point about 'fat intake and sucrose intake go together'. From the abstract:

"Univariate analysis showed significant positive correlation coefficients for butter (R = 0.887), meat (R = 0.645), pastries (R = 0.752), and milk (R = 0.600) consumption, and significant negative correlation coefficients for legumes (R = –0.822), oils (R = –0.571), and alcohol (R = –0.609) consumption."

George must lose weight said...

And a separate study:

"We found that a higher dietary intake of long-chain saturated fatty acids, including 12:0, 14:0, 16:0, and 18:0, was associated with an increased risk of CHD, whereas intake of short- to medium-chain saturated fatty acids (4:0–10:0) "

However, these data do suggest that replacement of long-chain saturated fat with polyunsaturated fat is likely to reduce substantially the risk of CHD. Our results also support recommendations to substitute poultry and fish and low-fat dairy products for red meat and high-fat dairy products to reduce the risk of CHD."

http://www.ajcn.org/cgi/content/full/70/6/1001

Peter said...

George,

The only info in the abstract about sucrose is pastries. There just might be other sources of sucrose in the diet! Fat plus sucrose = hyperglycaemia = CHD. Fat without sucrose = health.

Second study is again observational and suggests the hypothesis that saturated fat is bad, using risk factors derived from the cholesterol hypothesis, which is garbage. Observational studies suggest things which need checking. This is intrinsic to observational studies. They cannot, by their nature, ever prove anything. When you do intervention studies, like the one by Clifton, saturated fat, LC diets win every time. Saturated fat, or any other fat, plus sucrose is the Western diet, and gives the Western diseases. No surprise there.

Peter

George must lose weight said...

You say: "The only info in the abstract about sucrose is pastries. There just might be other sources of sucrose in the diet! Fat plus sucrose = hyperglycaemia = CHD. Fat without sucrose = health."

What the study claims to show is that Fat (eg meat) = CHD. You just saying there 'must be' sucrose' is the same approach as various bodies who when i say 'high carb = CHD' they say 'there must be saturated fat!'

The paper quoted from claims a correlation. The butter, meat correlation?

From the second paper they say "We found that a higher dietary intake of long-chain saturated fatty acids, including 12:0, 14:0, 16:0, and 18:0, was associated with an increased risk of CHD" Are you saying a) the data is wrong or b) the inference is wrong?

Jacqueline said...

George
I don't know about Peter, but my interpretation (of the AJCN Hu et al paper, which is the one which actually refers to types of foods) is that their inference is wrong and not justified by their data.
For example, their statement

We found that a higher dietary intake of long-chain saturated fatty acids, including 12:0, 14:0, 16:0, and 18:0, was associated with an increased risk of CHD

is quite unsupported by their Table 5. In the first place, the supposed increased risk of CHD largely disappears once a multi-variate relative risk model is applied and the confounding variables are removed. No, I take it back - it's even better than that - once they also adjust for the confounding dietary variables ALL the significant relative risks disappear and ALL the increased risks are non-significant. It's only by further data torturing that they nearly manage to extract a 19% increase in risk for stearic acid but it's snatched away at the last minute by another adjustment....
In the second place, I'm always suspicious of anything where data is divided into quintiles - it suggests a lot of prior data torturing went on when the desired correlation didn't just leap out at them. Just two examples: in Table 5, the difference between the median values of the bottom quintile and the top quintile is 2.3% of energy for stearic acid. Are you telling me that having just 2.3% more stearic acid intake is what makes the difference in CHD? In Table 7, eating almost no high-fat dairy products is mysteriously (it's certainly mysterious if you think high fat dairy's bad) worse for you than eating up to 2 serves per day, but golly gosh, don't eat more than 2 serves a day - could be fatal!

Stan (Heretic) said...

Here it is:


Efficacy of the Atkins diet as therapy for intractable epilepsy


and the recent follow up:

A modified Atkins diet is effective for the treatment of intractable pediatric epilepsy.

Stan (Heretic) said...

Dear "George must lose weight",

I used to dissect many papers like that thrown at me on various vegan fora (until they banned me even before I got tired).

Every single time without exception, I found the same what Jacqueline has just written above. Not only the correlations tend to disappear but those that remain are typically marginal left after some heavy data dredging.

Beware of every paper when they list, analyze and correlate every possible food item except sugar and starch, with CVD or anything! As yourself why is that the study focuses on something that consitutes 20-40% of the calories while omitting or playing down carbohydrates that constitute typically 50-70% of the calories? Please notice that many of those studies did not even mention the word "sugar"!

&nbsp &nbsp &nbsp - Why is that?

Often there are as many favorable as unfavorable correlations with various food stuffs, and only those favoring the present orthodox doctrine that animal produce such as fat, dairy, meat or fish are supposed to be harmful, seem to make it to the abstract while the rest gets tucked away to the bottom of the paper, costing you 30 bucks to find out.

I wish you good luck,
Stan (Heretic)

----

"Technology is in a race with the Universe to create bigger and better idiot-proof devices, while the Universe is trying to create bigger and better idiots. So far the Universe is winning."

(found on some proggie's forum)

Bris said...

"The greater (numerically, but not statistically) weight loss in the low-carb group may have in part led to the larger positive impact on HDL cholesterol, according to the researchers."

The only way this is possible is if the low-carb subjects were initially more obese than the high-carb subjects.

Sabio Lantz said...

I have done 7 months on low-carb, high fat diet. My labs are back and cholesterol is 337 !

I was hoping readers here could give me the top 5 links they think I should read to address my reflexive concerns. I need to get educated on this Cholesterol Myth issue but would like some direction.
Thought I’d check in with experienced folks and ask for advice and education. This link takes you to my labs.

Bris said...

Sabio:

You have nothing to worry about. Your cholesterol values will seem much higher than they actually are because your triglycerides are low. This effects how the LDL and HDL values are calculated.

Kiwi Geoff said...

Sabio Lantz said...
---------------------
My labs are back and cholesterol is 337 !
---------------------

Sabio, I recently wrote a little Cholesterol Calculator, have a play:

http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

where you can see your LDL drops from 242 down to 201 mg/dL.

Your LAB is clearly using the Friedewald equation to "estimate" LDL levels.

Regards, Kiwi Geoff (NZ)

Sabio Lantz said...

Wow, Kiwi Geoff,
That is incredibly helpful. Thank you.
Now, risk factors for plaque deposit (heart disease) were base on the Friedewald model, no? So does this really solve the dilemma? Do you see my point?

George must lose weight said...

Kiwi Geoff

That's an interesting calculator

I put my profile in:

Total: 6.2
HDL: 1.2
Trig: 2.47

(all mmol)

This gave me LDL 3.9

On your calculator this means in the UK we're using Friedewald.

Iranian gives: 6.1885

At the time I was NOT on a low carb diet. I ate piorridge and cinnamon every day, stacks of fruit...

So, any comments on the blood test results - and what should I be aiming for?

George must lose weight said...

Stan (Heretic)

Do you know of any well-written book that explains about the interpretation of tables, observational v intervention studies etc etc?

Take for example this:

http://www.numberwatch.co.uk/September%202000.htm

I didn't understand most of that page.

I know the owner of the site has written a book about statistics - but it has been panned in Amazon over its mistakes and general layout.

Jacqueline said...

George
There are some good resources on the internet. Sandy at Junkfood Science suggests:The Little Handbook of Statistical Practice
http://www.tufts.edu/~gdallal/LHSP.HTM
it's pretty comprehensive, but I'd suggest you'd have to start at the beginning and plough through it.
I've got both John Brignell's books and they're really good. Sure, they are cheaply produced - they were published with a grant from the EU of all people! - but I don't think they are full of mistakes at all.
Sandy's page also suggests the following book:
'How to lie with statistics' by Darrell Huff

Peter said...

Bris, I think they would have had to have said if there had been a weight difference at the start (though not necessarily, see the diazoxide posts and insulin levels after randomisation, not mentioned!). So Clifton thinks a NS weigh loss difference accounts for a 4 fold difference in HDL rise? Thinks is not the correct word!

Jacqueline, Thanks for doing the donkeywork for me while I was enjoying my weekend with the family!

Stan and Thackray, I just love idiot sayings!

Hi Sabio, Your TC is almost exactly the same as mine and just above that of Barry Groves. This whole thing about numbers comes down to correlations based on a huge number of people eating to the SAD or equivalent and says nothing about people eating a paleo high fat diet. I would agree with comments that the effect is probably due to a reasonable number of very large LDL particles.

Even when you read papers suggesting LDL particle number is all that matters, size doesn't, you have to bear in mind that this information comes from people who live on sucrose spiked with fructose. Here LDL will be oxidised and so long as oxLDL correlates with apoB count the count will give the poor prognosis. But if you have a large number of large fluffy LDLs... well, who knows? The the AHA cannot do this without using Torcetrapib, so there is no data except that torcetrapib kills. Hardly surprising if you artificially inflate someone's HDL while feeding them high fructose corn syrup! So does a high apoB count matter if all of the lipoproteins are large fluffy? That would need lots of people like you, I and Barry Groves to be studied.... Not everyone eating LC/high sat fat gets TCs above 8mmol/l.

George, perhaps having your trigs lower than your HDL, while ignoring your LDL, would be a good start. Trigs of 2.5 suggests fructose poisoning.

Peter

Peter said...

Sabio, those links...

THINKCS
http://www.thincs.org/

Weston A Price, especially articles by Mary Enig on the lipid hypothesis
http://www.westonaprice.org/

Stephan
http://wholehealthsource.blogspot.com/

Barry Groves
http://www.second-opinions.co.uk/

Hold on to your hat if you try Dr BG's blog!
http://drbganimalpharm.blogspot.com/

Michael Eades is worth a read too
http://www.proteinpower.com/drmike/

Sabio Lantz said...

Peter, you are most kind. Thank you much. I will be working through that stuff and posting links on my own little Paleo diary site.
These look very helpful.
I have so much to learn.
I am a health care provider and know nothing about this stuff.

Of course I have never treated lipids, so my confession is not too embarrasing (smile).

mark said...

Hey Peter.

Is this true?

Small, dense LDL = apoprotein B-48 and large fluffy LDL = apoprotein B-100?

Mark.

JB said...

Likely, some of you have seen this:

http://www.youtube.com/watch?v=dBnniua6-oM

A clip (over an hour) regarding the evils of fructose. This doctor calls it poison.

I am uncertain whether he is covering anything that hasn't been discussed here on Hyperlipid by Peter, but he does give a pretty in-depth comparison regarding how cells and the liver handle and differentiate between ethanol, glucose and fructose... if someone is interested in the biochemistry of it all.

Cheers! Brad

mtflight said...

lol. very nice. So sad he actually needs a transplant! Maybe his body used up the fat in his brain, and he is on a statin to get his own cholesterol down (no cholesterol for the brain)?

Lynn M. said...

Perhaps the majority of people with low Trigs and high HDL have large LDL, but you can't assume that is always true.

On a low carb diet, I have a HDL-C of 55, Trigs of 62, LDL-P of 1458, yet 75% of my LDL-P is small. Sabio's HDL is 28 points higher than me, Trigs 3 points higher. I wouldn't be sure that he has large LDL.

George must lose weight said...

Jacqueline

Thank you for the links...I will peruse.

If anyone cares to comment in the blog itself on this post:

http://slob30days.blogspot.com/2009/08/colorectal-cancer-and-fibre-intake.html

in particular the final point, your comments would be welcome....

mtflight said...
This comment has been removed by the author.
Peter said...

Hi Mark,

sdLDL is the end remnant of a VLDL, an LDL formed from an intracelluar hepatic fat droplet rather than from dietary saturated fats (these form IDLs or large LDLs). The sdLDL are particularly prone to oxidation (no explanation for this) so form sd and ox LDL particles. These are considered bad. Fructose and alcohol are the best generators of the fast droplets that form VLDLs to become sdLDLs to oxidise easily.

Apo(a) is attached to LDL which is either oxidised already or subsequently receives ox phospholipids from other LDL particles. So Lp(a) seems to be a concentrated form of oxLDL. So far all of this is in apoB100 particles from the liver.

I've not chased apoB48 labeled chylomicrons much, but chylomicron remnants seem to behave like oxsdLDLs and are the same marker of eating poisons like fructose. ApoB48 glycates like apoB100 and cannot be taken up by the liver. You then influence your health by how much linoleic acid you put in to your chylomicron remnants...

There's quite a bit about this in the AGE, RAGE and ALE series which never got finished....


JB,

It's spot on until he gets lost in the beauty of fibre... Oh, and plants too, towards the end if I remember correctly.

Lynn,

So, do you think sdLDL matters? Do you feel you personally are at risk of IHD? If so, do you feel that for some people IHD is inevitable? Is a person eating an evolutionarily appropriate diet in trouble if they have sdLDL? I keep trying to drop out of lipid parameters and come back to what we are eating as mostly this is what matters. To me high HDL is a surrogate for fat intake. If your body doesn't give you that nice surrogate of an HDL of 90, but you are still eating the fat, does the lowish HDL matter?

These are very deep questions. I'd be interested on your take.

Alex, the liver producing apoB48 is news to me and quite interesting. The liver is shipping out fat labeled as if it came from the gut. I guess if you are using a particle as a fat delivery system, rather than a cholesterol delivery system, using the B48 label is sensible.

So, is apoB48 evil, as B100 is evil, or is hepatic B48 secretion a marker you are doing something very stupid with your diet????

Peter

PS Alex, where'd the comment go?

mtflight said...

mark:

small, dense LDL is associated with apoB48 presence. The common factor: insulin-resistance


and..

"Long-term insulin treatment selectively stimulates secretion of the truncated form of apolipoprotein B (apoB), apoB-48, from primary rat hepatocytes in culture. Chronic treatment with insulin at 400 ng/ml causes a 3-fold increase in total apoB secretion, with apoB-48 making up about 75% of that increase."

-Insulin promotes the biosynthesis and secretion of apolipoprotein B-48 by altering apolipoprotein B mRNA editing.

http://www.ncbi.nlm.nih.gov/pubmed/8202496

mtflight said...

I corrected myself, because although apoB48 branded particles were produced in the liver of these lab specimens, it was not confirmed they were shipped out as small, dense LDL.

I didn't want to leave a blooper :-)

gunther gatherer said...
This comment has been removed by the author.
gunther gatherer said...

JB, thanks for that clip.

I had limited my carbs to a fair amount of high fat 80% chocolate every day up until now, but this video scared me so much, I think I'm going to switch to starch (read potato) instead for my daily sugar.

Of course, in my avoidance of fructose, I eat no fruit anyway, but why not just load up a baked potato with butter instead of giving your liver the added fructose burden? According to Lustig, starch and glucose don't seem to end up with as much or any de novo lipogenesis...

Bris said...

gunther:

I think carbohydrate is entirely unnecessary.

I tried 80% cocoa chocolate because I like the taste. It still gave me gastric reflux.

My total carbs are only ~10g a day. I eat "Inuit ice cream" -100g of frozen High Antioxidant Berry Mix (bilberries and wild blueberries <5% carbohydrate and 25x as much antioxidants as tomatoes) with 200ml cream.

Lynn M. said...

Peter,

I'm no expert on all this, so I'm surprised you're asking my opinion. I read the mainstream stuff first, and for several years have been reading a lot of alternative-thinking health blogs (yours, Stephan's, TYP, AnimalPharm, Chris Masterjohn's, PaleoNu, Dr. Eades, NephroPal, Free the Animal, Barry Groves, JK and others).
I've read Weston Price, Taubes' GCBC, and Uffe Ravnskov, belong to WAPF, follow that diet, and read Wise Traditions. So I have formed some opinions, but I can't point back to specific sources.

I did NMR testing 6 months ago because I have been totally dependent on thyroid supplementation for 60 years (I'm a 62 yo female), and I wanted to know if various periods of undersupplementation had affected my heart. I had a EBCT in 2008 and my CAC score was zero. I have zero family history of heart disease. So I didn't have much concern about IHD before my NMR.

I am now perplexed about my 75% sdLDL, given my lowish trigs, and concerned enough to eat even more low-carb, quality high-fat and consider IF. Based a lot on the studies I have read that are linked to at TYP, I think high sdLDL is a strong risk factor, very high hdLDL a rather minor risk factor, high trigs a strong risk factor, low HDL a risk factor, and lp(a) a risk factor

I think for some people with the wrong genetic makeup that a pattern of eating certain types of foods will make IHD evitable, but not otherwise. I haven't figured out how necessary exercise is.

Like you, I prefer to focus on eating an evolutionary appropriate diet rather than focusing on lipid parameters. I'll watch my lipid values and fine tune my diet and exercise accordingly.

I think stress levels, lifestyle, personal fulfillment, and social interaction are also big players, and because they're not so easily quantified, we don't pay enough attention to them.

Unfortunately my at-home husband is at stage 6 dementia, so I would attribute any decline in my health to the stress and limitation that imposes on me.

George must lose weight said...

"cooked animal fats are as bad as processed vegetable oils"

Source: http://www.carnivorehealth.com/main/2009/5/20/video-saturated-fat-is-good-for-you.html

Why?

Peter said...

George,

I don't believe this, so I'm not in a position to explain it. Presumably I've missed a whole lot of published research...

Peter

Stan Bleszynski said...

George wrote: "Do you know of any well-written book that explains about the interpretation of tables, observational v intervention studies etc etc?"

No, I just use general maths knowledge. As a rule of thumb, an estimate of the statistical standard deviation of a given result subject to random (Gaussian) fluctuations is STD = sqrt(n) , this is also called "one sigma", where n is the number of samples. For example, if in a population of 2800 patients 100 had a breast cancer, then n=100 thus the risk of cancer was 100/2800 = 3.6% and the error of that number was +/-10/2800 which is +/-0.36%. Thus the risk range is 3.2% to 4%. Now, in literature it is generally accepted to consider two results that are closer than three sigma from each other, to be statistically marginal and the results within one-sigma to be insignificant.

Bris said...
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Bris said...
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Bris said...

Hydrogenated vegetable oils weren't originally developed as foods. They were developed to make cheap candles. Electricity killed candle sales so these fats were instead diverted to the food supply. There was no real evidence to suggest that TF were harmful for another 80 years.

Hydrogenated vegetable oils were very widely used for 40 years before anyone was worried about cholesterol and saturated fat. HVO were used because they were cheap, extremely stable, had good baking properties and were bland-tasting. They sold because they provided an excellent cheap cooking solution not because animal fats were being vilified.

Margarine was invented in 1870 - 40 years before heart attacks were even an issue.

The Weston Price Foundation tend towards extremism, unfounded conspiracy theories and ancient and discredited fringe science IMHO. Their message is far too simplistic as human health has a vast number of significant genetic and lifestyle contributing factors not just processed foods.

What the WPF ignore is that all traditional pre-industrial societies were mostly free of modern diseases regardless of what they ate. The Irish peasantry were healthy eating almost nothing but boiled potatoes - 81% carbohydrate, 5% protein and a tiny 1% fat.

Bris said...

Hydrogenated vegetable oils weren't originally developed as foods. They were developed to make cheap candles. Electricity killed candle sales so these fats were instead diverted to the food supply. There was no real evidence to suggest that TF were harmful for another 80 years.

Hydrogenated vegetable oils were very widely used for 40 years before anyone was worried about cholesterol and saturated fat. HVO were used because they were cheap, extremely stable, had good baking properties and were bland-tasting. They sold because they provided an excellent cheap cooking solution not because animal fats were being vilified.

Margarine was invented in 1870 - 40 years before heart attacks were even an issue.

The Weston Price Foundation tend towards extremism, unfounded conspiracy theories and ancient and discredited fringe science IMHO. Their message is far too simplistic as human health has a vast number of significant genetic and lifestyle contributing factors not just processed foods.

What the WPF ignore is that all traditional pre-industrial societies were mostly free of modern diseases regardless of what they ate. The Irish peasantry were healthy eating almost nothing but cabbage, a very small amount of fish and milk and boiled potatoes (6kg/day!) - 81% carbohydrate, 5% protein and 1% fat.

Peter said...

Bris,

My own personal feeling is that while Weston A Price are not correct on everything I learned a great deal from them. You have to decide where you go by faith and where by logic. A lot of their ideas are good.

Peter

Bris said...

Peter, I agree some of their ideas are quite valid eg animal fat is harmless.

However what everyone seems to ignore is the fact that just 120 years ago relatively few people anywhere in the world suffered from lifestyle diseases no matter what they ate. This included Inuits eating boiled seal blubber, Australians eating only white flour, mutton and jam or Irish eating just boiled potatoes and cabbage. In this context the whole "evil vegetable oil is killing everybody" hypothesis just seems implausible.

Stan Bleszynski said...

Re: If anyone cares to comment in the blog itself on this post:

http://slob30days.blogspot.com/2009/08/colorectal-cancer-and-fibre-intake.html

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Interesting! Barry Groves' uncorrected raw numbers for cancer risk vs fiber consumption by Table 3 work out as: 0.012, 0.011, 0,012, 0.015, 0.019 and 0.025. That is cancer risk doubled in the highest fiber group, with a statistical error of +/-2 to 3%.

Since the corrected number are all flat the correction factor must have been very large in order to reduce for example the relative risk ratio of 0.025/0.012 = 2 down to what they quoted 0.9 or 1.

I am skeptical about the validity of such a large adjustment since it is model dependent. I am curious if the correction has gone the other way around would they be also quoting the corrected numbers or rather use the raw numbers in their conclusion?

trinkwasser said...

Brilliant stuff!

Yes, it's a little known secret that brain transplants have been carried out for many years now.

Here's one of the many post-operative brain donors

http://www.fsascience.net/2009/02/10/the_appliance_of_science

George must lose weight said...

Anyone know the two studies referred to:

http://www.dailymail.co.uk/news/article-1208833/Low-carbohydrate-Atkins-style-diets-increase-risk-heart-disease-stroke.html

Peter said...

There's nothing out to get a look at, press releases are for the press...

Peter

George must lose weight said...

One study was in 2005 - I hardly think that was a press release.

Anyway here are more details on the study released today:

http://www.physorg.com/news170346116.html

"Rosenzweig said: "This issue is particularly important given the growing epidemic of obesity and its adverse consequences. For now, it appears that a moderate and balanced diet, coupled with regular exercise, is probably best for most people." "

Nostril Damus said...

Respectfully, "George must lose weight" should change his nick to "George must only quote facts not brainless opinions".

Jordi

George must lose weight said...

Right..obesity is not important. OK...taxes...health services...

Anyway, the study is there if you wish to look.

trinkwasser said...

""Rosenzweig said: "This issue is particularly important given the growing epidemic of obesity and its adverse consequences. For now, it appears that a moderate and balanced diet, coupled with regular exercise, is probably best for most people."

Obviously it isn't, or there wouldn't BE growing epidemics of obesity etc. just like there weren't before Ancel Keys was beamed down from the planet Carb.