52 replies to this topic

[TheFountain]

Take this with a grain of salt.

 

Almost every single expert in the appropriate fields that I can think of maintain that keeping LDL below the Threshold of 100 is ideal for future health outcomes. 

 

So, since I have been a member of this forum in 2008, I have been experimenting left right and mid-ways with everything. Only about 3-4 years ago did I begin to peripherally monitor my Blood work, before that I got it tested every 3 years or so.

 

But I wanted to really nail it this past couple of years so I did an experiment.

 

Now, you can either give a shit or not give a shit about this either way does not effect my personal outcome.

 

But I started about 4 Years ago really being a strict paleo dieter, before that I was meandering back and forth with paleo vegan, vegetarian and Paleo-ish diets. But I listened to the strict vernacular of posts by Scott Miller (Duke) and others who proclaimed so much with regard to "Doing paleo properly".

 

So I decided to really try to hit a home run with my blood work numbers here.

 

Entering into my strict Paleo diet, I did that for about a year and a half and decided to hit true keto for a while before monitoring my lipids, So I did.

 

After about two years on strict Paleo and about a year on Keto I got my lipids checked and was quite disappointed with the results. My Total Cholesterol was 237 and my LDL was spiked at 130! Now, as pointed out earlier every expert in the field of lipids claims that the basic threshold of healthy future sees your LDL at 100 or below. So I did some research here and elsewhere and came to a post on Bergamot extract, which I then began to incorporate into my regimen WITHOUT changing my Keto diet. After 3 months on Bergamot, got my Lipids tested again and TC went down to 220, while HDL was about 85, But my LDL stayed around 130 stubbornly. So, I went ahead, did further research and started taking red yeast rice, WITHOUT altering my strict keto diet. Red yeast rice got my total down to 205 and my LDL to about 100 even! Great right? Yea except I needed Beragot and RYR to do it! I was not pleased that Keto was not adequate enough to accomplish this so I went another route.

 

I decided to alter my diet completely and ditch the red yeast rice temporarily at least. I cut out 85% of fats, the most noteworthy of which was SFAs and made it mostly vegetables, plant based whole food with healthy carbs and no added sugar as I did on Keto also. And 3 months later had my lipids tested again.

 

An astonishing thing occurred. My Total cholesterol was now 145 and my LDL was 70! Trigs remained below 100 as on the other diet. HDL was about 60 but that's to be expected with the total number lowers. 

 

So, my take away from all this is, after having read this forum for so many years and doing self-experimentation based on available knowledge and claims that span multiple directions, do it yourself. Don't rely on studies or what Duke or anybody else claims here. Just do it yourself. 

 

Try both ways, see what both results are. Give each diet at least 6 months and see. 

 

And that is all. 

Edited by TheFountain, 02 April 2020 - 09:04 AM.

[StephCThomp]

A friend of mine experienced something similar.  For her, high fat keto (included plenty of veg) sent her cholesterol figures very high.

 

Another friend has great numbers on a 95% carnivorous diet with no veg.

 

There must be some genetic differences between people.  Would be very interesting to understand this better - including whether these cholesterol figures (high or low) actually translate into particular health outcomes for the sub-groups.

[TheFountain]

Had my lipids re-tested again a couple weeks ago. 

 

Same strict plant based diet. No added sugar, healthy carbs. No red yeast rice.

 

Total Cholesterol 145.

 

HDL 75

LDL 60

Trigs 60

 

A1C 4.8

 

My Global filtration rate and BUN scores also improved significantly.

 

Keto paleo dehydrated me, raised my cholesterol and also saw me gain weight.

 

On Strict Paleo-Keto at 6 feet tall, I was about 170 pounds on average. I worked out about 6-8 hours a week, struggled to barely see my abs.

 

On This strict plant based diet, believe it or not, my weight remains between 145 and 150 pounds even when my plates of food are large. 

 

I work out about 2-3 hours a week and my abs are now "Out there" with much less effort.

 

Again, test it, re-test it, do it yourself. 

[Mind]

Just one comment, there are no strict/definitive lines between various diet hacks. Many paleo and keto-dieters eat a lot of vegetables. My impression is that most people think keto and paleo = carnivore diet, which is not the case. It is probably the case that some high profile keto/paleo people get a lot of press/clicks by saying they eat bacon all the time, and this skews the public impression.

[Vitalist]

Had my lipids re-tested again a couple weeks ago. 

 

Same strict plant based diet. No added sugar, healthy carbs. No red yeast rice.

 

Total Cholesterol 145.

...

Just a heads up, but your low cholesterol puts you in the high risk group for total mortality. 

 

P. D. Mangan breaks it down for us on his blog, with links to the studies:

 

Older People with High Cholesterol Live Longer

"the total mortality in the low-TC (Total Cholesterol) group was 1.7-fold higher than that in the high-TC group."

 

and

 

Higher Cholesterol Is Associated with Longer Life

"The cohort with an average cholesterol of 252 mg/dl, the highest, had the lowest death rates."

 

[TheFountain]

Just one comment, there are no strict/definitive lines between various diet hacks. Many paleo and keto-dieters eat a lot of vegetables. My impression is that most people think keto and paleo = carnivore diet, which is not the case. It is probably the case that some high profile keto/paleo people get a lot of press/clicks by saying they eat bacon all the time, and this skews the public impression.

 

 

Hey Mind,

 

I agree. However the common denominator I have read into, when I was more naive, is the idea of consuming very high amounts of dietary fat equalling optimal health results, so long as carbs were kept low. I did exactly that when on my paleo-keto diet and my results are exactly what my posted blood work had resulted in. I was definitely not anywhere near a carnivore diet, I wouldn't touch that diet with a 20 foot pole. 

Edited by TheFountain, 14 July 2020 - 05:13 AM.

[TheFountain]

 

Just a heads up, but your low cholesterol puts you in the high risk group for total mortality. 

 

P. D. Mangan breaks it down for us on his blog, with links to the studies:

 

Older People with High Cholesterol Live Longer

"the total mortality in the low-TC (Total Cholesterol) group was 1.7-fold higher than that in the high-TC group."

 

and

 

Higher Cholesterol Is Associated with Longer Life

"The cohort with an average cholesterol of 252 mg/dl, the highest, had the lowest death rates."

 

 

With all due respect, I respect the science of these studies however I do consider these fringe results. Any group anywhere can come up with a 'study' that shows anything they want it to show.

 

Everything can be shown to increase all cause mortality if you dig deep enough. 

 

Are we going to say there is no absolute association with +200 cholesterol and increased risks of disease factors?

 

That would not be what the meta-data analyses reveal at all. Nor the epidemiology. 

 

As imperfect as these last two data points are we have over 100 years of it to go by. At this time I choose that over fringe results, as much as I will keep an open eye on those fringe results. They are however, isolatory in design. 

I Strongly feel more comfortable with medical meta-data showing inverse associations with lower LDL and disease factors and formation. 

Edited by TheFountain, 14 July 2020 - 05:19 AM.

[Zaul]

With all due respect, I respect the science of these studies however I do consider these fringe results. Any group anywhere can come up with a 'study' that shows anything they want it to show.

 

Everything can be shown to increase all cause mortality if you dig deep enough. 

 

Are we going to say there is no absolute association with +200 cholesterol and increased risks of disease factors?

 

That would not be what the meta-data analyses reveal at all. Nor the epidemiology. 

 

As imperfect as these last two data points are we have over 100 years of it to go by. At this time I choose that over fringe results, as much as I will keep an open eye on those fringe results. They are however, isolatory in design. 

I Strongly feel more comfortable with medical meta-data showing inverse associations with lower LDL and disease factors and formation. 

 

Yes!

 

[RWhigham]

Statins are one of the most commonly used drugs worldwide, with sales estimated to approach $1 trillion by 2020. The $1 trillion pecuniary motivation causes most published cholesterol guidance and studies as well as medical meeting talks to be the work product of pharmaceutical company sales departments, which attempt to subvert everything and everybody to maintain and boost statin sales in what amounts to a gigantic and extremely well financed criminal conspiracy with professional scientists and doctors bought in every venue. One cannot trust cholesterol promotions no matter the accreditation.

 

The reduction in fatalities in heart patients on statins may be from effects other than lowering cholesterol. For example, A Low-Dose Combination of Fluvastatin and Valsartan shows that Fluvastatin 10 mg with Valsartan 20 mg daily for 30 days lowers arterial "age" by 10 years.

 

Personally, many years ago I quit a vegetarian diet because my 170 cholesterol was too low.  I wanted 240 for minimum mortality, where I am today.

 

I suspect high blood pressure is the number 1 cause of CHD (veins don't get atherosclerosis). My BP averages 96/60 now. It used to be 120/70 which may be too high to prevent CHD. I think my low BP reflects extremely clean and flexible arteries resulting from a long list of expensive supplementation for many years, including among other things high vitamin D3, vitamin K's, and CoQ10. I don't have a prescription for nor do I take BP medication.

Edited by RWhigham, 14 July 2020 - 05:39 PM.

[TheFountain]

Statins are one of the most commonly used drugs worldwide, with sales estimated to approach $1 trillion by 2020. The $1 trillion pecuniary motivation causes most published cholesterol guidance and studies as well as medical meeting talks to be the work product of pharmaceutical company sales departments, which attempt to subvert everything and everybody to maintain and boost statin sales in what amounts to a gigantic and extremely well financed criminal conspiracy with professional scientists and doctors bought in every venue. One cannot trust cholesterol promotions no matter the accreditation.

 

The reduction in fatalities in heart patients on statins may be from effects other than lowering cholesterol. For example, A Low-Dose Combination of Fluvastatin and Valsartan shows that Fluvastatin 10 mg with Valsartan 20 mg daily for 30 days lowers arterial "age" by 10 years.

 

Personally, many years ago I quit a vegetarian diet because my 170 cholesterol was too low.  I wanted 240 for minimum mortality, where I am today.

 

I suspect high blood pressure is the number 1 cause of CHD (veins don't get atherosclerosis). My BP averages 96/60 now. It used to be 120/70 which may be too high to prevent CHD. I think my low BP reflects extremely clean and flexible arteries resulting from a long list of expensive supplementation for many years, including among other things high vitamin D3, vitamin K's, and CoQ10. I don't have a prescription for nor do I take BP medication.

 

For the record I am not a vegetarian but a strict vegan. Most of my meals are large plates (approximately 80%) of vegetables, mostly of the green variety with some cruciferous included. 

 

And interestingly, my blood pressure has only gone up slightly when consuming moderate amounts of caffeine, which is a known vaso-constrictor. 

 

Otherwise my BP always measures the low end of normal, if not slightly lower than normal. But always within healthy range.

 

The ratio of LDL to HDL is not mentioned in this U shaped association pattern interestingly. I wonder why?

 

What about trigs?

 

Don't you think that LDL is of the utmost import according to 100+ years of medical meta-data?

[TheFountain]

Yes!

 

 

So, you're asking me to trust a singular fringe data set alongside a video from one doctor that has 245 views over 100+ years of medical meta-data?

 

Why?

[TheFountain]

Also, I am not utilizing statins. 

[RWhigham]

What about trigs?

 

Fasting Trig/HDL ratio is important.  Trigs  < HDL is excellent. Trigs > 100 mg/dL is undesirable. Trigs can take up to 16 hours to reach fasting level after consuming a high fat meal. Failure to wait long enough can give erroneous results.

 

Don't you think that LDL is of the utmost import 

 

Yes, but there is bad LDL and there is good LDL. See Patrick Theut's  Reversing Your CAC Score and Heart Disease.

 

For the record I am not a vegetarian but a strict vegan. Most of my meals are large plates (approximately 80%) of vegetables, mostly of the green variety with some cruciferous included.

 

 People vary. There is no one right diet. I too eat 80% vegetables. In my case, slathered in butter from grass fed cows. I avoid canola and soy based vegetable oils like the plague, and the fat of animals fed these oils. The following explains how the official USA dietary advice replacing saturated fat with vegetable oil has caused a deadly worldwide epidemic of obesity.

 

Fire In A Bottle...the layperson's guide to Hyperlipid

• One must click on a different link at the bottom of each page to follow the exposition.
• Hyperlipid is a technically difficult, over most people's head, blog written by English veterinary anesthesiologist Peter Dobromylsky supporting a low-carb high-fat diet and high LDL with biochemistry. 
• His "Proton" series explains how mitochondria control nutrient inflow, and stop it during satiation by generating reverse electron flow out Complex I of their ECTs (electron transport chains). This reverse flow creates ROS which signals the cell to stop nutrient uptake.
• Substitution of canola or soy vegetable oil for saturated fats prevents this satiation signal.
• When unnatural canola and soy oils are consumed the fat storage is changed and the subsequent metabolism is messed up. Getting rid of this unhealthy fat is not easy.
• The saturated fat palmitic acid requires a small amount of oleic acid to properly metabolize. Mammalian fat cells normally store the ideal mixture of palmitic and oleic acid, but not when canola or soy oil is consumed.
• Animal fat is not healthy unless the animal had a healthy diet. This includes you and me.

Edited by RWhigham, 15 July 2020 - 06:57 AM.

[TheFountain]

 

Fasting Trig/HDL ratio is important.  Trigs  < HDL is excellent. Trigs > 100 mg/dL is undesirable. Trigs can take up to 16 hours to reach fasting level after consuming a high fat meal. Failure to wait long enough can give erroneous results.

 

 

Yes, but there is bad LDL and there is good LDL. See Patrick Theut's  Reversing Your CAC Score and Heart Disease.

 

 

 People vary. There is no one right diet. I too eat 80% vegetables. In my case, slathered in butter from grass fed cows. I avoid canola and soy based vegetable oils like the plague, and the fat of animals fed these oils. The following explains how the official USA dietary advice replacing saturated fat with vegetable oil has caused a deadly worldwide epidemic of obesity.

 

Fire In A Bottle...the layperson's guide to Hyperlipid

• One must click on a different link at the bottom of each page to follow the exposition.
• Hyperlipid is a technically difficult, over most people's head, blog written by English veterinary anesthesiologist Peter Dobromylsky supporting a low-carb high-fat diet and high LDL with biochemistry. 
• His "Proton" series explains how mitochondria control nutrient inflow, and stop it during satiation by generating reverse electron flow out Complex I of their ECTs (electron transport chains). This reverse flow creates ROS which signals the cell to stop nutrient uptake.
• Substitution of canola or soy vegetable oil for saturated fats prevents this satiation signal.
• When unnatural canola and soy oils are consumed the fat storage is changed and the subsequent metabolism is messed up. Getting rid of this unhealthy fat is not easy.
• The saturated fat palmitic acid requires a small amount of oleic acid to properly metabolize. Mammalian fat cells normally store the ideal mixture of palmitic and oleic acid, but not when canola or soy oil is consumed.
• Animal fat is not healthy unless the animal had a healthy diet. This includes you and me.

 

 

 

I also avoid Soy and vegetable oils and have been doing so for years. The whole thing started the first time I tried veganism, I realized I did it wrong and was consuming far too many soy products. I was moody and weak all the time. I read an article on line which, though little more than a mere opinion piece, opened my eyes. It was basically a man speaking about how his son was 'castrated' from soy consumption. That set me off on a brand new quest of avoiding soy.

 

In my case Saturated fat raised my LDL dramatically to 130 and my total cholesterol to like 236. I felt as a young man this was totally unacceptable and embarrassing. 

 

So I took control, decided to try veganism the "right way" this time, and last reading was as I stated earlier, total 145 HDL 75 and LDL 60 while trigs are at 60 also. And I had not even fasted 15 hours, maybe 9 hours or so.

 

The only way for me to alter my cholesterol on Keto was with Red yeast rice which is a weak statin itself containing variable amounts of monacolin K which is what they put in prescription statins. 

 

I ditched it and took the dietary approach and am happy I did. Still detoxing from that misguided Keto trip but feeling better by the month. 

[Zaul]

So, you're asking me to trust a singular fringe data set alongside a video from one doctor that has 245 views over 100+ years of medical meta-data?

 

Why?

 

Denial is a hell of a drug, btw 13 million subjects are not a singular fringe data, and i couldn't care less if you trust him or anyone else. 

[TheFountain]

Denial is a hell of a drug, btw 13 million subjects are not a singular fringe data, and i couldn't care less if you trust him or anyone else. 

 

What am I denying? 100+ years of medical Meta-data Association which cutting edge doctors in preventive care facilities are still touting? Or one singular data point that could be caused by who knows how many confounding factors? 13 million people? Wow. That's sooooo many people for one study to keep control of. I am guessing a lot of the results were through oral reporting and deductive analyses? 

 

Am I also to deny feeling better now and having Abs now, on less than half the physical effort as when I was on Keto?

 

Really?

[RWhigham]

What am I denying? 100+ years of medical Meta-data Association which cutting edge doctors in preventive care facilities are still touting?

 

In the PURE study of 135,335 individuals followed for 7 years, dietary intakes were categorized as carbohydrates, proteins, and fats. Fats were sub categorized as saturated or unsaturated.  RESULT:  Higher Intake of total fat and each type of fat was associated with lower risk of total mortality. Higher carbohydrate intake was associated with an increased risk of total mortality.  This study was based on food questionnaires, so there was no lipids data.

 

In Dave Feldman's analysis of NHANES lipids data and mortality, for those with the trigs (<100) and HDL (>60) or thereabouts as is typical for a low-carb paleo diet, the higher the LDL the lower the mortality.  Dave Feldman is a "hyperresponder"--one who develops extremely high LDL on a low-carb diet. Dave has found that people who look "lean and fit" are likely going to be "hyperresponders".

Edited by RWhigham, 18 July 2020 - 04:29 AM.

[Matt]

 

Just a heads up, but your low cholesterol puts you in the high risk group for total mortality. 

 

P. D. Mangan breaks it down for us on his blog, with links to the studies:

 

Older People with High Cholesterol Live Longer

"the total mortality in the low-TC (Total Cholesterol) group was 1.7-fold higher than that in the high-TC group."

 

and

 

Higher Cholesterol Is Associated with Longer Life

"The cohort with an average cholesterol of 252 mg/dl, the highest, had the lowest death rates."

 

 

 

Low total cholesterol and low-LDL caused by a healthy diet is not the same as low cholesterol caused by an underlying condition.

 

A drop in cholesterol can occur even 10-years prior to cancer diagnoses and it's not that T-Chol or low LDL is the cause, but they can be a preclincial marker of a disease and ill health (even if it hasn't become apparent yet). One study showed changes in cholesterol levels years prior to diagnoses of lymphoma (see study).

 

For example, a big drop in cholesterol in response to CR is a normal response to CR and that doesn't elevate cancer risk or all-cause mortality as far as I'm aware. On a personal note: my total cholesterol went as low as 108 mg/dl at one point in and CRON was the cause it.  

It's like the increased risk of hemorrhagic stroke from having low LDL-C. But when you have very low blood pressure and have extremely low levels of chronic inflammation, this increased risk is totally ameliorated. Plus you are protected from ischemic stroke.

 

Another example is inflammatory diseases, which often cause a drop in cholesterol as the disease becomes apparent:

 

TCh and LDL levels and the prevalence of abnormal TCh or LDL measures decreased significantly during the 5 years before RA incidence/index date in RA patients as compared to non-RA cohort. These trends in lipid profile in RA are unlikely to be solely due to lipid-lowering therapy (see study).

 

How many people have super low cholesterol because of their incredibly healthy diet? Very few.

How many have low cholesterol due to an underlying condition like intestinal issues, malnutrition, depression, or cancer (and many more conditions). A lot more I suspect.

 

They're not the same and they won't have the same outcome on mortality either. 

 

 

"Hence, it seems reasonable to postulate that, when low LDL-C points to increased non-cardiovascular mortality, it is simply serving as a marker for incipient pathologies, associated with inflammatory elevation of IL-6, which are driving the increase in mortality risk".

 

"Importantly, meta-analysis has now confirmed that increased plasma IL-6 in the elderly is associated with a notable increase in all-cause and cardiovascular mortality; an increase in non-cardiovascular mortality can also be inferred from the data. Hence, it is proposed that when low LDL-C in the elderly predicts increased non-cardiovascular mortality, this low LDL-C is serving as a marker for inflammation-linked incipient pathologies, entailing increased production of IL-6, which are responsible for this increased mortality".

Edited by Matt, 18 July 2020 - 04:07 AM.

[TheFountain]

In the PURE study of 135,335 individuals followed for 7 years, dietary intakes were categorized as carbohydrates, proteins, and fats. Fats were sub categorized as saturated or unsaturated.  RESULT:  Higher Intake of total fat and each type of fat was associated with lower risk of total mortality. Higher carbohydrate intake was associated with an increased risk of total mortality.  This study was based on food questionnaires, so there was no lipids data.

 

In Dave Feldman's analysis of NHANES lipids data and mortality, for those with the trigs (<100) and HDL (>60) or thereabouts as is typical for a low-carb paleo diet, the higher the LDL the lower the mortality.  Dave Feldman is a "hyperresponder"--one who develops extremely high LDL on a low-carb diet. Dave has found that people who look "lean and fit" are likely going to be "hyperresponders".

 

I think we all know well enough that simply breaking down the macronutrient consumption is totally inadequate in terms of making red lights on dietary outcomes or for touting any be all, end all diet such as paleo. 

 

There is black, white and grey areas. We all should be living within the grey area of health, which is technically the safest, but most of us seem to occupy the black or white zones of dietary macro consumption. And this is just in relation to the  totality of ones dietary schematic. 

 

You can't ignore micronutrients, you can't ignore other lifestyle co-factors. You can't assume people with higher fat consumption do not also do X Y OR Z, or that people with higher carb consumption do not do A, B or C.

 

It just doesn't work.

 

My numbers prove it. At least to myself, that when all things are equal between high fat Keto and Lower fat Plant based, the latter is the winner. 

Edited by TheFountain, 18 July 2020 - 05:14 AM.

[RWhigham]

My numbers prove it. At least to myself, that when all things are equal between high fat Keto and Lower fat Plant based, the latter is the winner. 

Sure, if low lipids is how you measure success.  I'm not convinced one way or the other.

 

I suspect we are well adapted to the diet we had while we were evolving as hunter-gatherers. On the other hand, those of us who believe that aging evolved so you don't eat your children's food find it easy to believe that nature may delay aging during hard times to ensure species survival--hard times such as bad hunting or famine. Thus its understandable that eating plants--not too many--and fasting could delay aging. But health spans appear to have declined with the discovery of agriculture. Egyptian mummies were decrepit by age 50.

 

The best diet may vary with age. For example, high protein in your 40's can cause problems, but higher protein in your 80's is highly recommended.

Edited by RWhigham, 18 July 2020 - 05:03 PM.

[aribadabar]

And there is also the genetic component - ApoE 3/4, and especially 4/4, carriers would not fare better on keto or any other high fat diet due to impaired lipid metabolism.

3/3 or 2/3 ones, on the other hand, may thrive on it.

 

So there is no one-size-fits-all diet that is good for everyone.

[TheFountain]

So, another significant change.

 

I had my Lp (a) tested before and after keto and plant based. 

 

Now this is interesting.

 

Before, on super clean higher fat Keto, and whilst on Red yeast rice and bergamot, my LP (a) was slightly elevated at 90 nmol/l

 

So, after doing the above protocol (from original post), after ditching red yeast rice, and being on super clean plant based ala Esselsyn with some small modifications, and using Niacin for 4 months my current reading is 65 nmol/l which is now in normal range (anything under 75 nmol/l).

 

Another win for plant based?

 

Any of you swearers of Keto and high fat diets have your LP(a) checked recently?

 

Just curious. 

[RWhigham]

When last measured in 2017 my high fat diet Lp(a) was 6 nmol/L.  I take astaxanthin 12 mg/day, have lower iron levels, and  genetically have the longest sticky molecule on my Lp(a).

 

From my notes:

• Phospholipid membranes have a mix of saturated and unsaturated fats. The mix is highly regulated and largely independent of diet. The mix is required for the proper function of the membrane. Just saturated fats would pack too tightly and block trans-membrane transport.
• The unsaturated fats oxidize over time. Lp(a) collects the oxidized molecules for disposal.
• The liver makes Lp(a) to control oxPhos. You will have high Lp(a) if you have high levels of oxidation in your blood stream.
• Lp(a) differs from regular LDL by having a sticky molecule that collects oxidized phopholipids.
• The sticky molecule that makes LDL into Lp(a) genetically occurs in 3 different lengths, short, medium, and long. It takes a lot more short Lp(a) to remove oxPhos than long Lp(a), so one's Lp(a) level is largely genetically determined.
• Lp(a) and its load of oxPhos is removed by healthy kidneys, instead of by the liver like regular LDL.
• Lp(a) is associated with CHD, but it may be more protective than damaging. Medication to lower Lp(a) while leaving oxidation elevated may do more harm than good.
• (Students of medical history know there are often errors in accepted practice that take a long time to get corrected)
• Lp(a) will be minimized if the oxidation of membrane lipids is minimized.
• Keeping iron levels low will reduce oxidation.
• Astaxanthin likely reduces oxidation of membrane lipids and presumably lowers Lp(a).

Edited by RWhigham, 30 July 2020 - 04:07 PM.

[aza]

 

So, another significant change.

 

I had my Lp (a) tested before and after keto and plant based. 

 

Now this is interesting.

 

Before, on super clean higher fat Keto, and whilst on Red yeast rice and bergamot, my LP (a) was slightly elevated at 90 nmol/l

 

So, after doing the above protocol (from original post), after ditching red yeast rice, and being on super clean plant based ala Esselsyn with some small modifications, and using Niacin for 4 months my current reading is 65 nmol/l which is now in normal range (anything under 75 nmol/l).

 

Another win for plant based?

 

Any of you swearers of Keto and high fat diets have your LP(a) checked recently?

 

Just curious. 

 

 

Now i could be wrong here, but doesnt niacin lower lpa. Would that not be a win for niacin rather then a plant based diet?

[Turnbuckle]

Statins are one of the most commonly used drugs worldwide, with sales estimated to approach $1 trillion by 2020. The $1 trillion pecuniary motivation causes most published cholesterol guidance and studies as well as medical meeting talks to be the work product of pharmaceutical company sales departments, which attempt to subvert everything and everybody to maintain and boost statin sales in what amounts to a gigantic and extremely well financed criminal conspiracy with professional scientists and doctors bought in every venue. One cannot trust cholesterol promotions no matter the accreditation.

 

 

I couldn't agree more. The statin industry is on the same moral plane as the prison industry. They've done tremendous damage for which they will never be held to account.

 

I suspect high blood pressure is the number 1 cause of CHD (veins don't get atherosclerosis). My BP averages 96/60 now. It used to be 120/70 which may be too high to prevent CHD. I think my low BP reflects extremely clean and flexible arteries resulting from a long list of expensive supplementation for many years, including among other things high vitamin D3, vitamin K's, and CoQ10. I don't have a prescription for nor do I take BP medication.

 

 

That is astonishing. I assume that D3, K, and CoQ10 are not sufficient. Is there something else you recommend? 

[RWhigham]

 

That is astonishing. I assume that D3, K, and CoQ10 are not sufficient. Is there something else you recommend? 

 

Hi TB, I'm a fan of your protocols. I suspect its just the length of time and the high dosages of D3 and K2 I've taken, although I also take a long list of other supplements in an effort to slow aging, but none would be expected to reverse hardened blood vessels. I hope Harold Katcher & AkShay's Elixir will work someday.

 

My long term use of high dose vitamin D3 and vitamin K is rather a matter of luck than of astute planning. I first started 5,000-10,000 iu D3 in the 1980's because it helped prostatitis. I stumbled on Jarrow MK7 90 ug qd when it first became available in the 1990's because my older brother happened to mention something about it in passing, thus I luckily avoided arterial calcification from the D3. I now also take Koncentrated k, but I don't trust it enough to stop taking Jarrow MK7.

 

I believe the maximum D3 one can safely take is that which drives their parathyroid hormone to the bottom of its test range. For me that occurs at a 25-OH of about 110. I'm also a fan of the high dose vitamin C proponent Jeff T. Bowles and his anti-aging strategies.

Edited by RWhigham, 02 August 2020 - 12:48 AM.

[Turnbuckle]

Hi TB, I'm a fan of your protocols. I suspect its just the length of time and the high dosages of D3 and K2 I've taken, although I also take a long list of other supplements in an effort to slow aging, but none would be expected to reverse hardened blood vessels. I hope Harold Katcher & AkShay's Elixir will work someday.

 

My long term use of high dose vitamin D3 and vitamin K is rather a matter of luck than of astute planning. I first started 5,000-10,000 iu D3 in the 1980's because it helped prostatitis. I stumbled on Jarrow MK7 90 ug qd when it first became available in the 1990's because my older brother happened to mention something about it in passing, thus I luckily avoided arterial calcification from the D3. I now also take Koncentrated k, but I don't trust it enough to stop taking Jarrow MK7.

 

I believe the maximum D3 one can safely take is that which drives their parathyroid hormone to the bottom of its test range. For me that occurs at a 25-OH of about 110. I'm also a fan of the high dose vitamin C proponent Jeff T. Bowles and his anti-aging strategies.

 

So --

 

Koncentrated K (25 mg of MK-4, 0.5 mg of MK-7, 5 mg of K1 and 2 mg of Astaxanthin)

D3 (5,000-10,000 iu)

Jarrow MK7 (90 mcg)

Vitaman C (4 g?)

CoQ10 (?)

 

And adding these up I get --

 

MK-4 (25 mg)

MK-7 (0.6 mg)

K1 (5 mg)

Astaxanthin ( 2 mg)

D3 (5,000-10,000 IU)

Vitamin C (4 grams, split dose)

CoQ10 (200-400 mg)

 

This will take a while, I suppose. Six months?

 

 

Edited by Turnbuckle, 02 August 2020 - 01:59 AM.

[aribadabar]

 

So --

 

Koncentrated K (25 mg of MK-4, 0.5 mg of MK-7, 5 mg of K1 and 2 mg of Astaxanthin)

D3 (5,000-10,000 iu)

Jarrow MK7 (90 mcg)

Vitaman C (4 g?)

CoQ10 (?)

 

And adding these up I get --

 

MK-4 (25 mg)

MK-7 (0.6 mg)

K1 (5 mg)

Astaxanthin ( 2 mg)

D3 (5,000-10,000 IU)

Vitamin C (4 grams, split dose)

CoQ10 (200-400 mg)

 

This will take a while, I suppose. Six months?

 

 

 

 Astaxanthin at 2mg/d is insignificant amount for therapeutic purposes. Anything sub 5mg/d is.I'd stick to 12mg/d for this proposed 6-month period if we are to believe that Astaxanthin is an integral part of the regimen.

I would add garlic extract, tocotrienols and pomegranate extract as very important too.

 

 

The attached regimen concurs with the above for someone who has documented 75% regression of CAD.

Attached Files

•  SLIMJOHN'S_SUPPLEMENT_LIST.pdf   100.68KB   14 downloads

[TheFountain]

 

When last measured in 2017 my high fat diet Lp(a) was 6 nmol/L.  I take astaxanthin 12 mg/day, have lower iron levels, and  genetically have the longest sticky molecule on my Lp(a).

 

From my notes:

• Phospholipid membranes have a mix of saturated and unsaturated fats. The mix is highly regulated and largely independent of diet. The mix is required for the proper function of the membrane. Just saturated fats would pack too tightly and block trans-membrane transport.
• The unsaturated fats oxidize over time. Lp(a) collects the oxidized molecules for disposal.
• The liver makes Lp(a) to control oxPhos. You will have high Lp(a) if you have high levels of oxidation in your blood stream.
• Lp(a) differs from regular LDL by having a sticky molecule that collects oxidized phopholipids.
• The sticky molecule that makes LDL into Lp(a) genetically occurs in 3 different lengths, short, medium, and long. It takes a lot more short Lp(a) to remove oxPhos than long Lp(a), so one's Lp(a) level is largely genetically determined.
• Lp(a) and its load of oxPhos is removed by healthy kidneys, instead of by the liver like regular LDL.
• Lp(a) is associated with CHD, but it may be more protective than damaging. Medication to lower Lp(a) while leaving oxidation elevated may do more harm than good.
• (Students of medical history know there are often errors in accepted practice that take a long time to get corrected)
• Lp(a) will be minimized if the oxidation of membrane lipids is minimized.
• Keeping iron levels low will reduce oxidation.
• Astaxanthin likely reduces oxidation of membrane lipids and presumably lowers Lp(a).

 

 

There's a group of individuals who have genetically elevated LP (a) and supposedly not effected by lifestyle changes but this is a relatively new development so there's things we do not know.

 

I joined a research group, assuming my Lp (a) is 'high' when it was slightly over 75 nmol/l and the longer I watched this group of people in the group talk about their numbers, the more I realized mine was just ever so slightly elevated. These people spoke of numbers ranging from 200 nmol to 800 nmol and it just astonished me.

 

I figured at that point that mine was not high but slightly elevated and that I should count myself fortunate it isn't higher.

 

I feel ecstatic that it is now in the 'normal' range (below 75 NMOL/L). 

 

What is the entirety of your Lipid context? What did your total cholesterol, LDL, HDL and trigs look like when receiving that measurement?

 

What is your history?

Edited by TheFountain, 02 August 2020 - 03:38 AM.

[TheFountain]

Now i could be wrong here, but doesnt niacin lower lpa. Would that not be a win for niacin rather then a plant based diet?

 

 

But here's the other wrench in that system.

 

Supposedly Monocolin K rises Lp(a) and at the time of my initial testing, I was taking a relatively high dose of red yeast rice. So for all I know it might have inadvertently helped to raise it even though it somewhat regulated the LDL number as far as to be expected while I was stuck in thats stupid Keto mindset, assuming it was doing all that good. 

 

It's very telling with my last Lipid reading being off both Niacin and Red yeast rice, that my total Cholesterol was 145, LDL 70 and HDL at 75 trigs 60. That was before starting the Niacin regimen. 

 

Those Lipid numbers are the same on or off Niacin. So THAT is a win for Plant based at least. And I am sure high fat diets effect LP(a) also.

Edited by TheFountain, 02 August 2020 - 03:45 AM.