Cholesterol

[CCCustom]

Heart disease is still the number one killer in Singapore.
But load up on seed oils and swallow your statins, healthcare industry gospel, they say.

Polyclinic medicines switching more and more to India pharmaceuticals btw … my Atorvastatin they switched to simi Dr Reddy brand that has history of multiple recalls specifically for Atorvastatin … every time I crack open for 1 pill there is this disgusting car engine oil smell that I never had with the old brands they used.

 

[cyke69sg]

Basically if you have a lifestyle disorder, you try your best with conventional advice first.

Stick with it if you think its beneficial and sustainable.

Otherwise, pick a diet that is sustainable and can give you good mental health.

Personally I think it's also marketing. Selling krto diet for example is to cater to people who like meat and fat and are ok with not eating carbs.

 

[Checkyrmed]

Their rate of plagues progression is like someone with metabolic disorder.

Nobody wants that kind of outcome.

I don't follow keto diet. I'm eating a balanced diet and my insulin sensitivity is just perfect without skyhigh LDL.

https://www.reddit.com/r/ScientificNutrition/s/SV642H9gT7

Soto-Mota et al. omitted their primary outcome because it showed an increase in NCPV of 18.8 mm³ which indicates stunningly rapid plaque progression in the LMHRs.

They spun the rest of the paper around an analysis that wasn't even mentioned in their pre-registration, a correlation between rates of plaque progression and LDL-C.

Variability in Progression: The study found that not all LMHR participants behaved the same way. Some showed plaque progression, some had no progression, and some even showed regression. The average increase of 18.8 mm³ represents the mean across the entire group, which can be influenced by individuals with significant progression.

"Plaque Begets Plaque": A key finding was that individuals who already had existing coronary plaque at the beginning of the study were more likely to show greater or faster plaque progression. This suggests that pre-existing plaque, rather than high ApoB levels within this population, was a stronger predictor of future plaque development.

In essence, the study indicated that while some LMHRs did experience plaque progression, their high ApoB (LDL) levels were not the correlating factor for that progression

It’s important to note that participants were not screened for insulin resistance or underlying inflammation level. These unmeasured factors could mean that some individuals might have fared worse had they not been on a low-carb diet.

 

[KakiMeow]

tis one easy ...

... every thing can do ... just dun overdo

kiang dio hoh ... mai keh kiang ...

by right cannot ... by left can

all these is do ok ok can riao dun do too much ...

dat why some pple smoke can live very long ...

no nid sciencetists to tell us sia

 

[Checkyrmed]

I already said you can achieve the same level of health without skyhigh LDL keto diet.

 

[orpisia]

How to reduce bad cholesterol?

I got

 

[Checkyrmed]

How to reduce bad cholesterol?

I got

To reduce oxidized cholesterol levels, restrict dietary intake of unsaturated fats and omega-6 fatty acids while monitoring serum omega-6 to omega-3 ratios through linoleic acid measurement to gauge your body omega-6 level. Concurrent laboratory evaluation should include assessment of insulin resistance (HOMA-IR), inflammatory markers (high-sensitivity C-reactive protein), and LDL cholesterol particle phenotyping (Pattern A versus Pattern B).

 

[rogze79]

Their rate of plagues progression is like someone with metabolic disorder.

Nobody wants that kind of outcome.

I don't follow keto diet. I'm eating a balanced diet and my insulin sensitivity is just perfect without skyhigh LDL.

https://www.reddit.com/r/ScientificNutrition/s/SV642H9gT7

Soto-Mota et al. omitted their primary outcome because it showed an increase in NCPV of 18.8 mm³ which indicates stunningly rapid plaque progression in the LMHRs.

They spun the rest of the paper around an analysis that wasn't even mentioned in their pre-registration, a correlation between rates of plaque progression and LDL-C.

How do you know you are insulin sensitive?

What's LDL to you?

 

[Mecisteus]

How do you know you are insulin sensitive?

What's LDL to you?

I shared here I calculated my Homa IR.

Post in thread 'High cholesterol' https://forums.hardwarezone.com.sg/threads/high-cholesterol.7003688/post-156357810

 

[rogze79]

I shared here I calculated my Homa IR.

Post in thread 'High cholesterol' https://forums.hardwarezone.com.sg/threads/high-cholesterol.7003688/post-156357810

You checked for homa ir. What's the test called?

 

[huphoe]

triglycerides

 

[Mecisteus]

You checked for homa ir. What's the test called?

So you are doubting my value ? lol

I don't need to prove to you.

 

[Checkyrmed]

You checked for homa ir. What's the test called?

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is used for insulin resistance.

HOMA-IR = (Fasting Insulin (µU/mL) x Fasting Glucose

It's the most important blood check but MOH completely ignores it.

 

[rogze79]

So you are doubting my value ? lol

I don't need to prove to you.

You have shared your blood results for discussion before. And I'm just asking what's the name of the blood test for checking homa ir.

I wonder why not this time.

 

[Mecisteus]

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is used for insulin resistance.

HOMA-IR = (Fasting Insulin (µU/mL) x Fasting Glucose

It's the most important blood check but MOH completely ignores it.

The fun part is I was being paid for all these tests which include CT scan and MRI of my heart.

 

[rogze79]

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is used for insulin resistance.

HOMA-IR = (Fasting Insulin (µU/mL) x Fasting Glucose

It's the most important blood check but MOH completely ignores it.

Thanks. your sharing of the formula is not complete though. And that omission makes the difference.

 

[cyke69sg]

Variability in Progression: The study found that not all LMHR participants behaved the same way. Some showed plaque progression, some had no progression, and some even showed regression. The average increase of 18.8 mm³ represents the mean across the entire group, which can be influenced by individuals with significant progression.

"Plaque Begets Plaque": A key finding was that individuals who already had existing coronary plaque at the beginning of the study were more likely to show greater or faster plaque progression. This suggests that pre-existing plaque, rather than high ApoB levels within this population, was a stronger predictor of future plaque development.

In essence, the study indicated that while some LMHRs did experience plaque progression, their high ApoB (LDL) levels were not the correlating factor for that progression

It’s important to note that participants were not screened for insulin resistance or underlying inflammation level. These unmeasured factors could mean that some individuals might have fared worse had they not been on a low-carb diet.

same with people who still eat omega 6 oils.

Variability is huge in humans.

 

[Checkyrmed]

same with people who still eat omega 6 oils.

Variability is huge in humans.

 

[cyke69sg]

All these you can find an opposing critic.

See below. Everything got its advocate and critics.

 

[Mecisteus]

Variability in Progression: The study found that not all LMHR participants behaved the same way. Some showed plaque progression, some had no progression, and some even showed regression. The average increase of 18.8 mm³ represents the mean across the entire group, which can be influenced by individuals with significant progression.

"Plaque Begets Plaque": A key finding was that individuals who already had existing coronary plaque at the beginning of the study were more likely to show greater or faster plaque progression. This suggests that pre-existing plaque, rather than high ApoB levels within this population, was a stronger predictor of future plaque development.

In essence, the study indicated that while some LMHRs did experience plaque progression, their high ApoB (LDL) levels were not the correlating factor for that progression

It’s important to note that participants were not screened for insulin resistance or underlying inflammation level. These unmeasured factors could mean that some individuals might have fared worse had they not been on a low-carb diet.

By the way, I hope you read the arguments in the post on reddit which I posted above.