High cholesterol on a lchf

Oldvatr

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Sam Feltham, previously of Smash The Fat and now with the UK Public Health Collaboration: https://phcuk.org/
I can see pictures of her, but cannot find any way to view the story that B is talking about. The blogs showing today that she gives are not connected to this topic. Nice to see @Southport GP is listed as a founding member. Hi.

Edit: OOPs. The two pictures that the site displays in the blog section in connection with Sam Feltham both show a blonde lady, but B's video shows a guy. Confused....... Sam is obviously not shown as a founding member, so unable to confirm either way. Please advise.
 
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Indy51

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I can see pictures of her, but cannot find any way to view the story that B is talking about. The blogs showing today that she gives are not connected to this topic. Nice to see @Southport GP is listed as a founding member. Hi.

Edit: OOPs. The two pictures that the site displays in the blog section in connection with Sam Feltham both show a blonde lady, but B's video shows a guy. Confused....... Sam is obviously not shown as a founding member, so unable to confirm either way. Please advise.
Sam Feltham is male. His Twitter profile refers to him as "Director of @PHCukorg helping as many people as possible to obtain and maintain a healthy lifestyle :)"

The link in @Brunneria's post leads to a Youtube playlist:

https://www.youtube.com/watch?list=PLZvITiygC4TbAMvSyTnG8d1fogchxlJTP&v=WvycTi6Ta7Y
 

Oldvatr

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Hope you don't mind me jumping in, but my experience is a bit different.

The way i look at it, the body cannot lay down fat without insulin (and cortisol, but lets not muddy the water :) )
So, if you keep the carbs low enough, you cannot gain weight even while eating a lot of fat - because you keep your insulin so low that there isnt enough floating around to lay the fat down into the cells.

I think of it as a seesaw. Get the carbs low enough and you can eat LOTS of fat, and not gain.

I bet, @Oldvatr that your current carb intake is teetering on your personal carb tolerance, in a zone where you can gain on fat.
However, if you dropped your carbs lower then you could eat more fat without weight gain, because your insulin would drop proportionate to the even-lower-carbs, and you would not be able to gain.
(Not suggesting you do it, since you seem happy with your current situation, but just suggesting it as a possibility)

This is a working theory that i have been applying to myself for a couple of years, and it REALLY works on my body.
- have no references to support it, just 2 years of varying carbs by teensy amounts, and watching my 'immunity' to fat intake vary with it.

Mind you, now i come to think about it, there was that guy who ate huge amounts of just meat and fat - and didnt gain. 5000 cals, i think per day. Then he repeated the experiment with 5000 carb calories and ballooned like a whale. All about the insulin, you see.

Can anyone remember the guy's name?
If you count up his daily carb intake, it is way up above 20 g /day according to his description. It seems to be way above my own current intake, and I am not in deep ketosis. So is the explantion you give still valid?
Breakfast
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
200g of salmon; 374 calories, Carbohydrate=0.4g, Fat= 19.8g, Protein=48.2g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
220g of eggs; 367 Calories, Carbohydrate=9.6g, Fat=53.8g, Protein=48.8g

Total; 936 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of walnuts; 1,058 Calories, Carbohydrate=4.6g, Fat=102.75g, Protein=25.95g

Lunch
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
240g of river cobbler; 293 calories, Carbohydrate=0g, Fat=5.28g, Protein=61g

Total; 488 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of pecans; 1,059 Calories, Carbohydrate=8.25g, Fat=105.15g, Protein=16.35g

Dinner
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
400g of topside beef; 576 calories, Carbohydrate=0g, Fat= 15.6g, Protein=108g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g

I total carbs at 58.25g assuming he repeats daily as he stated in the description. Keto? Suppressing insulin?
 
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Brunneria

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If you count up his daily carb intake, it is way up above 20 g /day according to his description. It seems to be way above my own current intake, and I am not in deep ketosis. So is the explantion you give still valid?
Breakfast
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
200g of salmon; 374 calories, Carbohydrate=0.4g, Fat= 19.8g, Protein=48.2g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
220g of eggs; 367 Calories, Carbohydrate=9.6g, Fat=53.8g, Protein=48.8g

Total; 936 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of walnuts; 1,058 Calories, Carbohydrate=4.6g, Fat=102.75g, Protein=25.95g

Lunch
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
240g of river cobbler; 293 calories, Carbohydrate=0g, Fat=5.28g, Protein=61g

Total; 488 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of pecans; 1,059 Calories, Carbohydrate=8.25g, Fat=105.15g, Protein=16.35g

Dinner
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
400g of topside beef; 576 calories, Carbohydrate=0g, Fat= 15.6g, Protein=108g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g

I total carbs at 86.25g assuming he repeats daily as he stated in the description. Keto? Suppressing insulin?

This is the reason that I feel counting carb g is often misleading.
There is a vast difference between eating 16g carbs as white bread, and 16g carbs as green beans.
It is digested differently, is processed differently, releases glucose differently... the comparison becomes meaningless.

We use is as a handy label, but any T1 knows that they risk hypoing if they switch to low carb and continue to inject simply based on carb grams. They have to time the insulin differently, and sometimes spread the dose. Their body has very different insulin requirements when keto. The same applies for T2s, the difference being that we have no measure of insulin units to measure it.

Also remember that he is young, fit, active and non diabetic (much lower IR). His muscle mass will be pulling sucking in any stray glucose very easily (mopping it up) while remaining fat adapted and keto (I prefer the phrase fat adapted, because it allows for dual fuel usage if the glucose is around to use). And his personal carb threshold will be dramatically different from you or I. More muscle. More activity. So yes, I think with his level of activity he was in ketosis. He MUST have been well below his personal carb threshold, or he would have gained.

Its been a long time since I watched those videos, so I can't remember if he measured insulin, but that protein/fat diet will have minimised his insulin level to the point he doesn't gain weight - for his body - as shown, which was my original point.

Did you watch the second video on there - when he eats 5000 cal of carbs.
I need to watch that one again too. :D
 
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Indy51

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Agreed re carb counting @Brunneria, especially in non-diabetics with healthy metabolisms. There is also exercise-induced ketosis.
 

Oldvatr

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@Brunneria, you are quite correct that storage of fat into cells requires insulin. Sudden weight loss is one symptom that insulin dependant diabtics report when diagnosed. Indeed, there have been many threads on this site where the OP declares that they are witholding insulin in order to control their weight. It is the diabetic equivalent of bulemia. Sadly these posters have a real pride in their weight loss achievements, and try to encourage us to agree and praise them too as if it is a sensible course of action that can be fully justified. Sadly they seem blind to the advice we give to them, and quite often there are reports here and in the press where sadly they took it too far. We should be careful about posting this data without also including warnings that this is a potentially lethal practice.

As a T2D, I would have difficulty in suppressing my insulin. I would have to be very sick indeed if my Insulin resistance prevented cell storage of fat or glucogen. That is why I take Metformin, and use an LC diet - to reduce IR. If cell storage is suppressed such that weight cannot be put on, then ketosis will still drop weight and gradually I will waste away. I am not sure this is what happens.

There is another mechanism that may be at play. Triglycerides require glycogen, which in turn needs glucose. Suppress glucose by low carbs, then less glycerides are made (in theory ?) so less fat gets made. This may be how lipids reduce on LCHF. But, the processes of gluconeogenesis and lipogenesis normally ensure that minimum glucose is produced even if carb input is zero. So normally fat production is not inhibited even under LC conditions, but there may be other metabolic conditions that interfere with these other pathways.

I think the following link is relevant too.
http://www.dietdoctor.com/what-happens-if-you-eat-5800-calories-daily-on-an-lchf-diet
 
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Brunneria

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The whole suppressing-insulin issue is a right royal pain in the a*rse. I am looking at it now, in a speculative attempt to lose more weight myself.

We (T2s) seem to have 3 main factors re insulin levels (prob many more!) which kick in (i am assuming carb reduction is already achieved)
- insulin resistance (drops through exercise, fasting, keto eating)
- hormone imbalances, mainly thyroid, cortisol and insulin (tackled through diet, medication, lifestyle such as stress reduction and getting more sleep)
- background insulin - which we all have, but T2s and the obese have more than nonT2s and slim ppl - tackled through keto and fasting

Working on all of these will lower hormone (insulin) resistance leading to reduced insulin production

I seem to have hit a wall with LC weight loss (after a loss of 20 pounds in 10 months of keto eating), due to a combo of the things listed above and high insulin resistance. Sigh.
Am v happy with my bg control (below pre-D), but the weight wont drop due to insulin resistance.

So am planning a multi pronged attack.
Still in info gathering phase, Fung and Eric Berg being main info sources at the moment.

Fung's book discusses in depth the hormone/insulin situation and quotes the most amazing studies on how to reduce insulin production, with all the attendant health benefits. The book is called 'The Obesity Code' but he should really have called it 'The Insulin Code' although that probably wouldn't have sold it as well.

I am convinced that while suppressing insulin is a bad idea, reducing insulin production by creating an environment where v little insulin is needed, is the key to my situation, and is doable. Most people find low carb enough. Some people find keto enough. A few need fasting too. A very few (yay! i am a special little snowflake) need to rope in the Big Guns of all of those, plus some extra hormonal work too. At which point the knock on reduction in insulin resistance should permit further weight loss.

Of course, the real issue is the insulin resistance, not the weight - so this thinking applies to any T2 with insulin resistance - which brings me back to the idea of why weight gain is well nigh impossible until you get your insulin production down and your insulin resistance drops. And why weight loss is only possible when the same thing happens...

Hope that made sense. :)
 
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SunnyExpat

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If you count up his daily carb intake, it is way up above 20 g /day according to his description. It seems to be way above my own current intake, and I am not in deep ketosis. So is the explantion you give still valid?
Breakfast
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
200g of salmon; 374 calories, Carbohydrate=0.4g, Fat= 19.8g, Protein=48.2g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
220g of eggs; 367 Calories, Carbohydrate=9.6g, Fat=53.8g, Protein=48.8g

Total; 936 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of walnuts; 1,058 Calories, Carbohydrate=4.6g, Fat=102.75g, Protein=25.95g

Lunch
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g
240g of river cobbler; 293 calories, Carbohydrate=0g, Fat=5.28g, Protein=61g

Total; 488 Calories, Carbohydrate28=g, Fat=88.6g, Protein=99g

Snack
150g of pecans; 1,059 Calories, Carbohydrate=8.25g, Fat=105.15g, Protein=16.35g

Dinner
15g of coconut oil; 135 calories, Carbohydrate=0g, Fat= 15g, Protein=0g
400g of topside beef; 576 calories, Carbohydrate=0g, Fat= 15.6g, Protein=108g
180g of green beans; 60 calories, Carbohydrate=18g, Fat= 0g, Protein=2g

I total carbs at 58.25g assuming he repeats daily as he stated in the description. Keto? Suppressing insulin?

He only did the diet for three weeks.

It takes about that long for the body to adapt to any major diet change.
It would be very interesting to see if his theories could hold out to a lifestyle change scenario.
Say if he maintains his 5000 calories for 1 year?
 

lindisfel

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Ezitemide has a list of horrid side affects worse than some statins! :) They are all poisons we live on a fragile knife edge with our need for them.D.


I think I have similar problem. so far my TC and LDL are rising, my HDL fell slightly on my recent test.
I consulted my GP about one of my meds in connection with a ketogenic diet. I was taking Ezetimibe which is a gentle med that reduces LDL, but does so in a different manner to a statin. As a ketogenic diet is fat burning, I queried whether I should be cutting down on fats in the blood (LDL), and if it was safe.
My GP did some research into this, and has replied that it seems to be ok with ketosis. so I will continue with it and see if I can reduce my TC. Also I expect better lipids since previous I was not actually triggering ketosis, but now that I am it should raise HDL and drop Trigs.
Might be worth considering Ezetimibe? It apparently also reduces the risk of gallstones, dissolves existing gallstones , protects against Nonalcoholic fatty liver disease, and reduces artheriosclerosis. I need that I do!

Good luck with your review.
 

Oldvatr

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Ezitemide has a list of horrid side affects worse than some statins! :) They are all poisons we live on a fragile knife edge with our need for them.D.
Having tried most of the common statins, and also plant stanols, I find Ezetimibe to be totally unexciting. Looking at the list of side effects for this med, they seem standard for any medication nowadays, and I think you will find worse listed for aspirin or any other OTC painkiller. Even placebo pills probably carry safety warnings. Half of these symptoms could be caused by brussel sprouts!
 

Bluetit1802

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Having tried most of the common statins, and also plant stanols, I find Ezetimibe to be totally unexciting. Looking at the list of side effects for this med, they seem standard for any medication nowadays, and I think you will find worse listed for aspirin or any other OTC painkiller. Even placebo pills probably carry safety warnings. Half of these symptoms could be caused by brussel sprouts!

and beware ...... they may contain nuts. Even a jar of peanuts has that warning on these days. ;)
 

Oldvatr

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Messages
8,470
Type of diabetes
Type 2
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The whole suppressing-insulin issue is a right royal pain in the a*rse. I am looking at it now, in a speculative attempt to lose more weight myself.

We (T2s) seem to have 3 main factors re insulin levels (prob many more!) which kick in (i am assuming carb reduction is already achieved)
- insulin resistance (drops through exercise, fasting, keto eating)
- hormone imbalances, mainly thyroid, cortisol and insulin (tackled through diet, medication, lifestyle such as stress reduction and getting more sleep)
- background insulin - which we all have, but T2s and the obese have more than nonT2s and slim ppl - tackled through keto and fasting

Working on all of these will lower hormone (insulin) resistance leading to reduced insulin production

I seem to have hit a wall with LC weight loss (after a loss of 20 pounds in 10 months of keto eating), due to a combo of the things listed above and high insulin resistance. Sigh.
Am v happy with my bg control (below pre-D), but the weight wont drop due to insulin resistance.

So am planning a multi pronged attack.
Still in info gathering phase, Fung and Eric Berg being main info sources at the moment.

Fung's book discusses in depth the hormone/insulin situation and quotes the most amazing studies on how to reduce insulin production, with all the attendant health benefits. The book is called 'The Obesity Code' but he should really have called it 'The Insulin Code' although that probably wouldn't have sold it as well.

I am convinced that while suppressing insulin is a bad idea, reducing insulin production by creating an environment where v little insulin is needed, is the key to my situation, and is doable. Most people find low carb enough. Some people find keto enough. A few need fasting too. A very few (yay! i am a special little snowflake) need to rope in the Big Guns of all of those, plus some extra hormonal work too. At which point the knock on reduction in insulin resistance should permit further weight loss.

Of course, the real issue is the insulin resistance, not the weight - so this thinking applies to any T2 with insulin resistance - which brings me back to the idea of why weight gain is well nigh impossible until you get your insulin production down and your insulin resistance drops. And why weight loss is only possible when the same thing happens...

Hope that made sense. :)
I am having real difficulty with this. Googling LCHF and weight brings up loads of complaints of not being able to lose weight, or of plateauing. But virtually nothing on how to put on weight. I know I read somewhere that excess lipids get stored in the adipose tissue as body fat, but I have read many learned and geeky treatises on how LDL gets used in the cell for energy, but not how trigs get stored except in the blood andthings called adipocytes. I have seen a diagram of one, but no description except that it is a specialist fat cell.
The boffins see to be shying away from this. Even Sikaris seems to gloss over it. But I did read a well described process in one of them, but I cannot find it, This question is one I raised when I started LCHF. I still cannot answer it,

Maybe it is as you say, LCHF reduces insulin resistance to the point where the limited carbs and protein is enough to get lipids stored. But if you go VLC ketosis then the glucose gets vacuumed up and theres nothing left for trig manufacture.
One thing I did find is that lipids are very sensitive to Leptin, rather than insulin. and leptin deficiency disorder may be linked to obesity. (From a nutrition body builder health blog).

The following article is close to the one I remember, and is a description of how the adipose system is used, Its a bit heavy, but it seems to back up the other research I did, which was when I was looking at sdLDL problems. No mention of Leptin though.
http://www.sportsci.org/encyc/adipose/adipose.html
 

Brunneria

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Interesting article! I particularly resonate with the discussions on hormones and the effect on obesity. :) pity some of their other info is outdated, but then it was written in 1998. Thanks for pointing it out though. Had forgotten about Lipase.

I am sorry I have sent you off chasing what may be Wild Geese. I only mentioned the whole personal carb tolerance/insulin seesaw as a potential other perspective for you.

I am in the situation where my body works this way, so I am trying to find the reasons, and then tweak things to get a bit of weight loss. However, I most other people don't have my hormonal issues, so they may never be in the situation where they see the 'seesaw' in action, or need to act on it.
 

Oldvatr

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We seem to have strayed from topic here, so I am starting a new thread under DISCUSSIONS called Trying to Gain Weight on LCHF. I thought I had an answer to this that was simple, but it seems I know nuttin. As a T2D at my optimal weight, I want to keep it that way, but use LCHF to control BGL and lipids. So I invite anyone interested in this new topic to join me there.
 
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AtkinsMo

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An Ischaemic stroke is caused by a block in an artery in the brain, caused by a blood clot. A haemmorhagic stroke is caused by a blood vessel bursting (haemorrhage). The degree of damage depends on the location and extent of the bleed / block. Generally speaking, an Ischaemic stroke has a better outcome (better chance of recovery). Ischaemic strokes are more common than haemorrhagic.
 

Oldvatr

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Hi, Oldvatr,

Could you please explain the difference in the kinds of strokes?
Hemorragic stroke is basically when a blood vessel in the brain ruptures, and ischemic stroke is when a blood vessel feeding the brain becomes obstructed by a blood clot. Both lead to brain cell death, Either can be fatal, and certsinly disabling. There is another type of stroke that is related to arrythmia in the heart (e,g, atrial fibrillation)
 

Kristin251

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TIA attack is a temporary lack of oxygen to the brain. Often called a mini stroke. Symptoms can be as small as staring off into space.

A CVA ( cerebral vascular attack) is a blood clot or larger longer lack of oxygen to the brain. Causes death of brain cells due to lack of oxygen to the brain and CAN cause more permanent damage such as limited use of limbs or paralyzed body parts.

I was a medic for a few years. TIA's can be a sign of up coming CVA 's.
 

Kristin251

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TIA attack is a temporary lack of oxygen to the brain. Often called a mini stroke. Symptoms can be as small as staring off into space.

A CVA ( cerebral vascular attack) is a blood clot or larger longer lack of oxygen to the brain. Causes death of brain cells due to lack of oxygen to the brain and CAN cause more permanent damage such as limited use of limbs or paralyzed body parts.

I was a medic for a few years. TIA's can be a sign of up coming CVA 's.

If you are fortunate to get TPA ( tissue plasminogen activator ) within 3 hours of onset you have a good chance of reversing the damages