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Eating Saturated Fat doesn't increase fats in blood

you have to be happy with your bloods
it sounds like your 180g carb is below your body's trigger point to lay down fat, some people dont even have a trigger point and can eat 400-500g of carbs and be skinny.
some people will lay down fat at 60g a day

I think I will continue on a low dose statin, even when my trigs are good because of the vascular benefit
 
noblehead said:
another reason why he didn't want me to take a statin, after speaking with th If and when the time comes I'd happily take a statin,
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What would be the reason to go on a statin @noblehead?

My LDL were in the 70s and HDLs in 80s. When I had diabetes my HDL went to 109 and HDL stayed the same. They put me on a statin.

All my brothers and 85-year old father ( who had a heart attack at 52 ) are on them. I sorta think I need to can't really get the handle on what is best from all the reading
 
To comment on a study you can't even be bothered to read shows very poor forum taste. Perhaps you should avoid these types of threads in future if they cause such irritation.
 
@ Jack I like the trigger point range it helps explain a lot of different observations.

The vascular benefits of statins I believe from my family history but I've read that unless you have a specific genotype there is no benefit, what's your thouhgts
 

Yes possibly that true. TBH it's not a subject that I try and get involved in too much as the subject of cholesterol is a minefield, I think if your results are fine then there's no reason to change things, my current Endo thinks that the fact that I exercise daily ( just mainly walking the dog for 60-90 mins) helps to keep my cholesterol levels under control.

btw, I don't blame you for keeping on the statin, which one do you take Jack?
 


One would be family history of CVD as in your fathers case, for most people its to reduce cholesterol levels, providing your not suffering any side-effects I wouldn't stop taking them.
 
******, I didn't know that. back to the books, aka google
yes insulin resistance varies, and they say it's for life, so someone high IR and obese, and say triggers at 100g, goes on a 50g keto diet and looses a stack of weight, afterwards, they will keep the weight off as long as they stay under their 100g forever, 150g and they will be fat again
I took 10mg rosuvastatin after 3 mths TC was 2.7 and my ldl is under 1, a silly small number,
I've cut it back to 5 mg now, I need my trig lower and hdl and ldl higher ..I will see what has happened in the last 6 mths on lchf, I've lost another 5kg..so fingers crossed
 
jack412 said:
I'm getting my test results this week, they started over 2 and were last 1.2 ish ..I'm hoping for under 1 and eventually join the 0.6 mob, either that or I'm putting you both on ignore so I don't have to be reminded of my high trigs
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Since low-carbing I've never had triglycerides over 1.0 - they are normally about 0.7.

My consultant, who is a very nice man, but wholly convinced by the current dietary guidelines for diabetes (to the extent that he has to 'forget' that I'm on a low-carb diet when discussing my diabetes) said that my blood lipids showed that my diet 'was perfect' but he still wanted to give me a statin. Now, according to him I should be on a low-fat multi-grain type of diet which I am not and which I flag up to him every time I see him. It's cognitive dissonance really.

Best

Dillinger
 
I'm expecting trigs to be under one and will be disappointed if they aren't,
lowfat multigrain is the bestest and it's the patients fault they have diabetes, they're lazy and eat too much
 

I totally understand WHY this happens, but heck, it is madness, MADNESS, I say!
 
When the British medical council announces this glaring fact, is when the theory will be accepted. We have had at least 3 generations of being told the opposite, so I don't think it's going to happen anytime soon.

BUT...I'm sure all of us with heart issues must have wondered....what if....what if I'm wrong and we are long term exacerbating the issues.

Just a thought
 


Sensible to keep on a low dose Jack if you don't suffer side-effects and believe it is doing you some good in the long-term, good luck with your next set of results.
 
noblehead said:
Sensible to keep on a low dose Jack if you don't suffer side-effects and believe it is doing you some good in the long-term, good luck with your next set of results.
Click to expand...
I think I'm the only one on the forum that wants their LDL higher
 

Jack - thank you so much for those videos; the Volek one is completely on point for me; I've just had another badgering by my consultant to go on statins and I am having to carefully think about the situation; so this video is very helpful.

Best

Dillinger
 
don't thank me..I'd take a very low dose
https://www.google.com.au/#q=statin microvascular inflammation

http://cpr.sagepub.com/content/21/4/464.full.pdf

Results: Among 14 primary prevention trials (46,262 participants),

statin therapy increased diabetes by absolute risk of 0.5% (95% CI 0.1–1%, p¼0.012),

meanwhile reducing death by a similar extent: 0.5% (0.9 to 0.2%, p¼0.003).

In the 15 secondary prevention RCTs (37,618 participants), statins decreased death by 1.4% (2.1 to 0.7%, p<0.001).

There were no other statin-attributable symptoms,

although asymptomatic liver transaminase elevation was 0.4% more frequent with statins across all trials. Serious adverse events and withdrawals were similar in both arms.


Conclusions:

Only a small minority of symptoms reported on statins are genuinely due to the statins:


almost all would occur just as frequently on placebo.


Only development of new-onset diabetes mellitus was significantly higher on statins than placebo; nevertheless only 1 in 5 of new cases were actually caused by statins. Higher statin doses produce a detectable effect, but even still the proportion attributable to statins is variable: for asymptomatic liver enzyme elevation, the majority are attributable to the higher dose; in contrast for muscle aches, the majority are not.


this study looked at the history of 60,000 Diabetics after av. 2.7

http://www.thelancet.com/journals/landia/article/PIIS2213-8587(14)70173-1/abstract

retinopathy HR=0.6 [decrease of risk]

neuropathy HR=0.66

gangrene of the foot HR=0.88

diabetic nephropathy HR=0.97

[neutral..........HR=1.0 ]

diabetes HR=1·17 [increase of risk]



the way I look at it ..if nothing else take statin for neuropathy, retinopathy and gangrene of the foot
 
..@jack412
The APO genes that are involved in the production of the protein bit of the lipoprotein
These genes have various common variants .

APO E is one that is most often mentioned, The 3 common variants code for different amino acid at two places so the final protein has slightly different properties.
E3 is the most common allele , E2 and E4 the others
Since you have 2 chromosomes (one from each parent ,you can have 6 genotypes .
E2/E2, E3/E3, E4/E4
E2/E3, E2/E4 or E4/E3
These particular two alleles said to be 'co dominant ' or perhaps blending ie they interact together so the amount of the protein produced is dependent upon on the particular combination you have
I won't go into detail of why but E2 and E4 have opposing effects, E2 leads to a decreased in cholesterol and increase in trigs. E3 is normal and leads to 'normal' cholesterol levels, E4 leads to higher total cholesterol, ldl and trigs.
People with some combinations of alleles may have more propensity to higher levels of total cholesterol., LDL or Trigs Some trials suggest that E4 carriers have a higher susceptibility to saturated fat..
This is what the European Epic trial found for the levels of cholesterol in the different genotypes

.The epic trial (around 22,000 subjects using diet diaries). Unlike other trials** they didn't find, in general, that different phenotypes responded very differently to increasing sat fat or fibre or un sat fat, (ie all phenotypes had higher levels with increased sat fat and lower with increased fibre and un sat fat) .
However these effects of diet were doubled in those with the E2/E4 combination but people with this genotype constituted only 3% of the population (so may still be due to chance, research with even bigger groups needed! )
The alleles are present in different proportions in the population depending on ethnicity.
chart here: http://www.gbhealthwatch.com/GND-High-Cholesterol-APOE.php
**.Lots of detail https://www.lipidcenter.com/pdf/Apo_Ev2.pdf
there are other genes though
APO C2 inherited mutations associated with high trigs. This is recessive ie problems arise when you are homozygous inheriting a mutation from both parents. (one could have been a sufferer and the other a carrier(heterozygous) or both could have been carriers )
http://ghr.nlm.nih.gov/gene/APOC2
APO B (mutations in this one may cause familial hypercholesterolemia; ie a condition that can result in really high cholesterol and heart attacks even in childhood) It may be that some common variants (as distinct from mutations) are associated with higher than normal cholesterol and heart disease
http://ghr.nlm.nih.gov/gene/APOB
 
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I love it when you say "I won't go into detail" lol !!!!!
 
Thank you. It's lucky you had a picture for me
at a guess, I'm e2 e2

thank god we all eat 50-55% carb, that makes it easy
 
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@jack412, I meant to say don't look at the diet bit at the end of that article, I think I must have edited it out. That one was just for the ethnic distribution of the alleles. The long article does have some evidenced based diet/lifestyle comments at the end.
You can't though tell what you are without having your DNA tested and unfortunately that costs (123andme isn't too expensive for the testing but the postage charges from Europe are horrendous and I suspect it's even more from Australia)
 
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