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Type 2 Will higher fat harm my good cholesterol readings?

You've lost me. I though you said that you hadn't studied Keys, you certainly seemed to think that he had reduced a study from 22 to 7 countries. The data on both those papers comes not from Keys or his critics but from public organisations.(FAO and WHO).
If you do want to find out more, The methodology and published data from the Seven countries study forms a huge library of information and there is also an Archive at the University of Minnesota. If you look at the sample available of this book you will see a history of how and where the data from the Seven Countries study has been stored in section 1.2.Unfortunately you will have to either purchase the book or borrow it from a library to read the rest. There are also many available papers online and the monographs make take some time to get but should be available through the inter library loan scheme.
 
Anyone had a look at this interesting study of CETP inhibitor, evacetrapib or have the details?
http://www.nytimes.com/2016/04/04/h...-drug-has-no-benefits.html?smid=tw-share&_r=0

http://www.eurekalert.org/pub_releases/2016-04/cc-eic033116.php

"Those receiving evacetrapib saw their LDL cholesterol levels reduced by 37 percent and their HDL levels increased by 130 percent. Still, the improvements in cholesterol did not result in any reduction in the occurrence of cardiovascular death, heart attack, stroke, coronary artery bypass surgery or hospitalization for chest pain due to unstable angina."

Seems to do all the right stuff for cholesterol except changing the end-points...so that bags the question...do we really know what is good cholesterol numbers? Does it really matter?
 
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It answers the question quite well.

The good fats, don't have a bad track record. My cholesterol is good with them
The bad guys still have a bad track record. My cholesterol reflects the expectations of them.

So for me, there is a clear cause and effect, and a clear solution.
 
Is it possible to get high trigs on a low carb diet?
 
A supporter of Ancel Keys and his work would say YES. I , having now seen at least 3 seperate recent studies that show that lowering cholesterol has no effect on morbidity (i.e Atorvastatin gives us less than 1 day prolongation of life for every year we take it, if you work the figures out.) then I say Probably Not. In the blue corner we have Killer Cholesterol, and in the red corner we have Meta Study. Box clean.
As an Old Farty, I thinkI want my cholesterol to be high, and I will not take any statins. I already take Ezetimibe, that in your report was actually the placebo, and it does nothing except keep my GP off my case.
 
SunnyExpat said:
Is it possible to get high trigs on a low carb diet?
Click to expand...
Good Question. I think the LCHF mantra requires us to run it in ketosis mode to burn up the increased fat. If like me you do lower carb and not LOW carb, then I suspect that I will a) put on weight, and b) possibly not get the low trigs. But I have no proof yet. It will also maybe depend on how much HF is consumed, and how much of that is saturated fat. As ever, too much protein might also prevent ketosis mode.
 

I shall have to look again.
I thought trigs where a product of excess carbs being processed through the bloodstream.
So by definition impossible to have in excess on low carb, not specifically ketosis.
 
SunnyExpat said:
I shall have to look again.
I thought trigs where a product of excess carbs being processed through the bloodstream.
So by definition impossible to have in excess on low carb, not specifically ketosis.
Click to expand...
Trigs are the actual fat content that the LDL and HDL transport around thebody. Trigs are like the parcels in the parcel post van. They can come from stored fat or ingested fat, but are not directly related to carbs. What I 6hink is confusing you is the Sikaris video (et al) where he talks about damage occurring through collisions between LDL, or VLDL and the glucogen giving rise to small dense LDL which is the dangerous bit that clogs the arteries. Because sdLDL is damaged it does not get cleaned up and excreted, so it remains in the blood and sticks to the arterial walls. It is this damaged LDL that the trig test is picking up. Normally LDL and HDL get used up and get returned to the liver to get the next load of fat for delivery. In ketosis, glucogen levels in the blood is low so fewer collisions occur and less rogue trigs are made.
 

I can't find the paper I read but

https://professional.heart.org/idc/...op/@smd/documents/downloadable/ucm_425988.pdf
 
SunnyExpat said:
I can't find the paper I read but

https://professional.heart.org/idc/...op/@smd/documents/downloadable/ucm_425988.pdf
Click to expand...
Although this paper is dated 2011, the info in it seems to be quite dated.Some of the links I shared in this thread are more recent, and show that our understanding of the endocrine system and lipids is changing.
What you can take as being common ground is that the trig readings need to be reduced in fact below 0.8 mmol/l if possible. The amount of carbs (and protein) need to be reduced since this reduces the creation of rogue LDL by collisions between LDL and glucogen.

Studies have shown that a low carb high fat diet is better at reducing trigs than a low carb low fat diet, A high carb diet is the worst. Note: as pointed out earlier in this thread, saturated fats from animal meat ahould still be avoided, but from dairy and fish it seems to be good.

There are many anecdotal claims that the LCHF diet used on this site will lead to reduced trig levels. Some report slightly higher LDL and HDL levels, but this is not surprising due to more fat parcels being transported and used, and this may be a transient effect as body fat is being used up. Another thread I posted here shows that higher LDL and HDL does not lead to higher risk of death.

Some of the recommendations for reducing trig levels in your report are not really suitable for a diabetic. Such as increasing fruits, but reducing fructose. The impact of protein on blood glucose is not mentioned, and the concentration on carbs does show a misundertanding of basic metabolism.

Smoking is a major factor in damage to LDL leading to increased rogue LDL by oxidation, but only got a one liner mention,
 

From the great man himself.

https://drmalcolmkendrick.org/2015/06/23/what-happens-to-the-carbs/
 
SunnyExpat said:
From the great man himself.

https://drmalcolmkendrick.org/2015/06/23/what-happens-to-the-carbs/
Click to expand...
http://www.ncbi.nlm.nih.gov/pubmed/9405898

OK I can see what is happening here, Kendrick is talking about Palmitic acid, which is a primary constituent of Palm oil. It is an industrial chemical added to low fat milk to supplement Vitamin A. What he should be talking about is the amino acid Palmitoleic acid.

Yes Lipogenesis is indeed a process by which excess carbohydrate is converted into trigs (actually acetyl_CoA) and this provides a higher energy storage mechanism than just glucogen, However, lipogenesis, like the protein equivalent process, requires certain things to be in place. Firstly the normal glycogen storage cells need to be full to bursting. Then you need insulin working. If you are insulin resistant, then this prevents lipogenesis working properly, and so blood sugars do not reduce as they would normally. So this is IMO a problem for morbidly obese people, but if you are controlling your blood sugars and weight , then you should not be reacting to lipogenesis. (This is Step2 in the Kendrick article)
Why do trigs go up when high carbing? Well, then blood system is acting as a storage battery when our fat cells are full. this charges up instead. I would suggest that this is not a good place to be since the LDL / glucogen collision rate is going to be high, leading to more harmful sdLDL particles and potential cardiovascular problems.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240601/
 
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Of course, if you actually eat saturated fat, this gets nowhere near the liver. It is digested, packed into chylomicrons, and these very large lipoproteins enter the bloodstream directly through the thoracic duct. Which is a secret passage from the gut that opens out in one of the veins in your neck. When chylomicrons encounter fat cells, the fats/triglycerides are sucked out, and the chylomicron shrinks down to virtually nothing. Chylomicrons, however, do not convert to LDL and have nothing whatsoever to do with heart disease – even according to those who think saturated fat in the diet is deadly.

the above is a quote from the link in post 112. Says it all really.
 
My Trigs reduced from 0.8 to 0.4 by following low carb high fat diet. The fats include lots of dairy (butter, double cream , creme fraiche , lots of cheese etc), animal fats, coconut oil, olive oil, oily fish, avocados etc. I do not use processed vegetable oils and in particular I avoid rapeseed oil (highly processed oil as rapeseed is poisonous). My carb in take varies but not always or even that often in ketosis I don't think. I do keep carbs low - never count so can't tell how low.
So for me whether it was decreasing carbs that decreased trigs I don't know but I can certainly say the sat fat has not increased trigs.

I think this is the bit from Kendrick that resonated most with me:

"What happens to the carbs is that they are all turned into saturated fat. This then raises VLDL levels and these, in turn becomes LDL. Yet eating carbs is supposed to be healthy, and eating saturated fat is unhealthy. Go figure."

So people won't eat saturated fat which is used by the body and never goes near the liver but they will eat Carbs which in excess are stored as saturated fat. And the NHS encourages this madness.

Have never and will never touch a statin and of the opinion that cholesterol is not causal in heart disease. Each to their own as long as you're happy.
 
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I find generally I get better trigs when I'm not overeating, in fact they appear to be a reasonable reflection of my bmi, so any spare calories seem to push the trigs up.
 
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