13 replies to this topic

[Seeker3]

Hi everyone! My first post here after becoming a member. Hoping to get responses from you.

 

My LDL came out to be very high according to my doctor - 175.

 

Just as a background, I am a 48 years old south east asian male.

 

Remaining cholesterol stats:

 

Total cholesterol 246 mg/dL

HDL: 51 mg/dL

LDL: 175 mg/dL

Cholesterol to HDL ratio: 4.8

Triglycerides: 99 mg/dL

 

I am otherwise not overweight.  I do have other issues - undermethylation, high histamine, kidney stones, chronic fatigue, body pain, and tinnitus.

I lead a moderately active lifestyle including half an hour of exercises and running every day, and moderate hikes on weekends.

 

The cardiologist I went to, said that for my ethnicity and at this age, having a 175 LDL is "very risky". She added that I can suffer a stroke or heart attack any time.  She said that there is not much I can do except to take statins for the rest of my life.  Not just temporarily.  But forever.  Because according to her I will not be able to reverse my LDL.  She told me to go on statins ASAP.

 

My first question is - Would you agree to her recommendation?

 

My second question is - If you don't, then what would you suggest?

 

I personally would prefer not to go on statins, at least not until I have tried out lifestyle changes and any effective supplements.  Or do you think I am being impractical here and that I should just follow the recommendation of cardiologist?

 

Here is what I am thinking of - Radically cutting down on meat and sat fats (from 4 times a week to 2 times a week - only grassfed meat not cooked in high sat fats), trying out couple of supplements like hawthorne berry, sytrinol, or red yeast rice, continue with my exercises, and any other changes I could do.  After trying this for 3 months, I will once again check my lipid levels.  If there are no changes, maybe I should just heed to her advice then.

 

Thoughts?

Edited by Seeker3, 30 April 2021 - 02:17 AM.

[pamojja]

 

My first question is - Would you agree to her recommendation?

 

My second question is - If you don't, then what would you suggest?

 

I don't give medical advise. However, I too was recommented a statin, asperin and invasive surgical intervention for a very severe PAD 12 years ago. Therefore I looked at the risks/benefits analysis, found out of in average 84 persons with previous heart-attack who took stantins only 1 person experienced the benefit for 5-year mortality. Its effect longer than 5 years had never been trialed in RCTs. And for primary prevention - if one didn't already had a heart-attack - the benefits are astronomically low.

 

For more details and food for thought you can read my whole story here: https://www.longecit...nal-remissions/

 

Killing LDL is like killing fireman at a burning house to save the building. Which are only the bodies way to initiate repair, for example by being the carrier for all those damage-limiting fat-solubles vitamins: K2, D3, A. Without proper load from nutrition all its efforts wasted. LDL during its life-cycle becomes more more smaller, denser and oxidised, is thereby less likely to be recycled in the liver, and therefore sticks out much longer in the blood and becomes the more dangerous kind. The LDL number doesn't tells this difference. What indicates if all LDL are in the large fluffy harmless kind is a tryglycerides close to 50 mg/dl. Close to 150 most would be small-dense dangerous kind. So a mixed bag in your case, where I would try to lower tryglycerides further.

[Turnbuckle]

Before you get suckered into the statin scam and have your mitochondria destroyed, look at the following study:

 

https://www.ncbi.nlm...les/PMC3303886/

 

They don't break out the cholesterol types, but for total C, your all cause risk of dying is presently 3 times higher than others in your age group. (See Fig. 1) But that is a relative risk, which is low to begin with. The risk becomes dramatically higher when you reach sixty, and at that point high total C is protective. Your chance of dying from all causes is then only half of that if you had a total C of under 213 (assuming you are a non-smoker and aren't hypertensive). 

 

So to answer your questions: 

1. No.

2. Do nothing other than giving her a copy of the above paper. If she's a certified member of the statin cult, she will throw it into the trash, but at least she may stop nagging you about it.

Edited by Turnbuckle, 30 April 2021 - 04:57 PM.

[Seeker3]

I don't give medical advise. However, I too was recommented a statin, asperin and invasive surgical intervention for a very severe PAD 12 years ago. Therefore I looked at the risks/benefits analysis, found out of in average 84 persons with previous heart-attack who took stantins only 1 person experienced the benefit for 5-year mortality. Its effect longer than 5 years had never been trialed in RCTs. And for primary prevention - if one didn't already had a heart-attack - the benefits are astronomically low.

 

For more details and food for thought you can read my whole story here: https://www.longecit...nal-remissions/

 

Killing LDL is like killing fireman at a burning house to save the building. Which are only the bodies way to initiate repair, for example by being the carrier for all those damage-limiting fat-solubles vitamins: K2, D3, A. Without proper load from nutrition all its efforts wasted. LDL during its life-cycle becomes more more smaller, denser and oxidised, is thereby less likely to be recycled in the liver, and therefore sticks out much longer in the blood and becomes the more dangerous kind. The LDL number doesn't tells this difference. What indicates if all LDL are in the large fluffy harmless kind is a tryglycerides close to 50 mg/dl. Close to 150 most would be small-dense dangerous kind. So a mixed bag in your case, where I would try to lower tryglycerides further.

 

@Pamojja, thank you for your helpful response.  Great to hear your story! It may be possible that I am one of those people who has the protein mutations that react poorly to dietary fats and sat fats.

 

The reason I mention that is because my LDL problems started when I went full board Keto two years ago (should have said that in my original post, not that it matters too much)

 

Back then, two years ago, my LDL jumped to 190 after 6 to 8 months of keto or so.  Hoping that maybe I have the more favorable LDL subtype and particle sizes, I did the advanced lipid tests. No such luck.  The LDL particle number was pretty high 1750 (greater than 1400 is considered "high"), LDL medium and LDL small were both high (380 and 235), while LDL large which should have been higher, was in fact smaller (5140).

 

This was two years ago.  My LDL now is 175. I am planning to do another advanced lipid test as my baseline reference before starting with changes in lifestyles so I can document this journey properly (assuming I don't get a CVD event as my cardiologist has warned me about, in the meantime).

 

So given the above, any more thoughts?  Maybe I could still have unsat fats and just lay off with sat fats?  Which is what I am planning to do.  (I know I did a few things wrong with keto in hindsight.  Regularly consumed coconut oil, butter and eggs - all possible culprits of sat fats.)

 

On the topic of my new lifestyle program, do you or others have a thought on whether initially, I have to go full board aggressive - meaning ZERO sat fats and then slowly add some sat fats after a couple of months?  That would be very tough thing to do, btw. Or can I still live with just a little bit of sat fats per day as I make the planned changes to diet and lifestyle?

 

 

You mentioned that I should focus more on lower triglycerides.  But aren't the methods to reduce triglycerides same as those to reduce LDL?

[Seeker3]

Before you get suckered into the statin scam and have your mitochondria destroyed, look at the following study:

 

https://www.ncbi.nlm...les/PMC3303886/

 

They don't break out the cholesterol types, but for total C, your all cause risk of dying is presently 3 times higher than others in your age group. (See Fig. 1) But that is a relative risk, which is low to begin with. The risk becomes dramatically higher when you reach sixty, and at that point high total C is protective. Your chance of dying from all causes is then only half of that if you had a total C of under 213 (assuming you are a non-smoker and aren't hypertensive). 

 

So to answer your questions: 

1. No.

2. Do nothing other than giving her a copy of the above paper. If she's a certified member of the statin cult, she will throw it into the trash, but at least she may stop nagging you about it.

 

@Turnbuckle, thank you for sharing. That's a great article.  I went through it. It is heartening to see that it is hopefully not as dire as I thought initially.  Nevertheless, as I explained in my latest post, I may be one of those people who are poor responders to fat.  Do you think people like me may fall into the higher risk categories highlighted in this study.?  Given that the study didn't consider this factor, I was just wondering about it.

[Turnbuckle]

@Turnbuckle, thank you for sharing. That's a great article.  I went through it. It is heartening to see that it is hopefully not as dire as I thought initially.  Nevertheless, as I explained in my latest post, I may be one of those people who are poor responders to fat.  Do you think people like me may fall into the higher risk categories highlighted in this study.?  Given that the study didn't consider this factor, I was just wondering about it.

 

If your doctor believes you have a significantly higher risk factor due to below average triglycerides and slightly higher than average LDL, then she should be able to show you data supporting that position. And if she can (I doubt it), then clearly you should change your diet instead of taking these dangerous drugs. The best thing to do, though, is to change your doctor.

 

Statins can cause tremendous damage, and recovery can be very slow. There are genetic factors, and these are greater in Asians.

https://www.ncbi.nlm...les/PMC7242232/

[pamojja]

@Pamojja, thank you for your helpful response.  Great to hear your story! It may be possible that I am one of those people who has the protein mutations that react poorly to dietary fats and sat fats.
 
The reason I mention that is because my LDL problems started when I went full board Keto two years ago (should have said that in my original post, not that it matters too much)

 
Well as aleady outlined, we are all different. In my case my low fat vegetarian diet for 30 years culminated in the disaster. Adding up 70% fats to my diet cleared the walking-disability from it up.

 

And as Turnbuckle also mentioned, LDLs aren't really the culprit. The best predictor of cardiac adverse event would by a coronary calcium score (CAC) or detecting plaque with other imaging techniques (MRI, CIMT).
 

Back then, two years ago, my LDL jumped to 190 after 6 to 8 months of keto or so.  Hoping that maybe I have the more favorable LDL subtype and particle sizes, I did the advanced lipid tests. No such luck.  The LDL particle number was pretty high 1750 (greater than 1400 is considered "high"), LDL medium and LDL small were both high (380 and 235), while LDL large which should have been higher, was in fact smaller (5140).

 
Just as predicted from your triglycerides.
 

So given the above, any more thoughts?  Maybe I could still have unsat fats and just lay off with sat fats?  Which is what I am planning to do.  (I know I did a few things wrong with keto in hindsight.  Regularly consumed coconut oil, butter and eggs - all possible culprits of sat fats.)
 
On the topic of my new lifestyle program, do you or others have a thought on whether initially, I have to go full board aggressive - meaning ZERO sat fats and then slowly add some sat fats after a couple of months?  That would be very tough thing to do, btw. Or can I still live with just a little bit of sat fats per day as I make the planned changes to diet and lifestyle?
 
 
You mentioned that I should focus more on lower triglycerides.  But aren't the methods to reduce triglycerides same as those to reduce LDL?

 
Not at all, Statins don't move triglicerides down. If you go back to my story and scroll down to the long quoted list of 113 supplements, those which also might lower triglycerides are indicated respectively.

 

For me it was mainly high dose fish-oil and low-carb. High glucose levels in the blood-stream is which raises triglycerides. And thereby small-dense LDL.

 

THE biggest danger of low-carb is, that calories have to come from somewhere else when lowering blood-glucose. And that for the most parts can only be from healthy fats. Like you mentioned: coconut butter, MCT oil, ghee, organic eggs, wildcaught fish and some nuts. Completly avoiding omega-6 seed oils (also too many nuts with high unsatfat-content). Only monosaturated fats like from organic olive or macadamia oil are beneficial. But fats TOGETHER with high-glucose levels are really dangerous.

Therefore the biggest mistake could be low-fat while not reducing blood-glucose levels by low carb.

 

 

With testing you're on the good path to find what will work for you. But also do regular blood-glucose testing with a cheap blood-glucose monitor. Initially fasted and 1 hr postprandial after each meal to find those foods which raise yours the most, for reducing or eliminating those foods.

[Seeker3]

 
And as Turnbuckle also mentioned, LDLs aren't really the culprit. The best predictor of cardiac adverse event would by a coronary calcium score (CAC) or detecting plaque with other imaging techniques (MRI, CIMT).

 

 

I am planning to do a CT-calcium scoring this week, again as my baseline to work with.  Honestly, I am scared to do it about what it reveals. But better to know the full truth now. What is weird is this - my stress test, EKG was normal.  But I do feel numbness in my left hand from time to time and my shoulders, hands and legs pain.  So guessing that may be from the atherosclerosis?

 

 

But fats TOGETHER with high-glucose levels are really dangerous.

Therefore the biggest mistake could be low-fat while not reducing blood-glucose levels by low carb.

When I had pretty high LDL at that time I was on keto and low carb, but like I said before I did have high sat fats.  So maybe too much high sat fats (instead of higher unsat fats) there was a culprit? 

 

Speaking of which, is there such a thing, like with other therapies in other health related problems, as going full detox first before reintroducing healthy fats?  Meaning, do I need to completely swear off sat fats for like few weeks before reintroducing the healthier ones gradually?  I was specifically thinking of grass fed red meat and wild caught salmon.  Or can I continue to eat these meats now?  What would you do if you were in my shoes?

 

By the way, I was going over your journey I was trying to find out if exercises helped you.  I see that you briefly mentioned it.  Was there any specific exercise that you would recommend over others?

[Phoebus]

 

 

NEW STUDY – VITAMIN K2 LOWERS CORONARY HEART DISEASE RISK

May 28, 2020

New prospective cohort study identifies K2 as cardio-protective while K1 intakes are not.

Oslo, Norway and Edison, NJ (28 May 2020) — The British Medical Journal recently published an observational study that examined the association between intakes of vitamins K1 and K2 and incidence of coronary heart disease (CHD). The 11-year Norwegian community-based prospective cohort did indeed show a link between K2 intakes and a lower risk of subsequent CHD events, building the evidence that K2’s impact on calcification can greatly improve health outcomes.

According to “Association of dietary vitamin K and risk of coronary heart disease in middle-age adults: the Hordaland Health Study Cohort”1, the role of vitamin K in the regulation of vascular calcification is established, and that patients with both medial and intimal calcification have a higher cardiovascular risk when compared with similar patients without calcification. Therefore, an inverse association between vitamin K intake and coronary heart disease (CHD) could be expected. The purpose of the current study was to evaluate the association between intake of both K1 and K2 and subsequent CHD events among community-living middle-aged adults in Norway.

The researchers concluded “a higher intake of vitamin K2 was associated with lower risk of CHD, while there was no association between intake of vitamin K1 and CHD.”

The paper is significant because it not only adds to the growing body of evidence substantiating vitamin K2 as a cardiovascular-support nutrient, according to NattoPharma Chief Medical Officer Dr. Hogne Vik, but it helps to clarify the confusion that “vitamin K is vitamin K,” also confirming the need for a K2-specific recommended daily intake (RDI)

“NattoPharma has driven the research confirming vitamin K2’s important health benefits, showing in human studies with healthy2 and patient participants that the progression of hardening of the arteries can be halted and even regressed with daily supplementation of MenaQ7 Vitamin K2,” says Dr. Vik, noting that this study builds on the body of evidence linking vitamin K status to health concerns such as peripheral arterial disease (PAD)3, coronary calcification4, dementia5, vascular stiffness in chronic kidney disease patients (CKD)6 and more. “The common link is calcification and the need for adequate vitamin K2 intakes to inhibit this in our circulatory system and tissues. Due to its very molecular structure, vitamin K2 can move beyond the liver to support other systems of the body, such as the bones and vasculature, where K1 cannot. There remains a great deal of confusion that K1 supports both bone and heart health, and this paper helps to identify the difference between the two in that K1 is not linked to cardiovascular health, whereas K2 is linked to both.

“These results mirror what we have seen in epidemiological studies, where populations who consume a lot of dietary Vitamin K2 have healthier hearts and more flexible arteries,” Vik adds. “Recognition of vitamin K2’s benefits as strong and significant elucidated inhibitor of vascular and soft tissue calcification is one of the core reasons a separate RDI should be established.”

Researchers followed participants (2,987 Norwegian men and women aged 46-49 years) in the community-based Hordaland Health Study from 1997 – 1999 through 2009 to evaluate associations between intake of vitamin K and incident (new onset) CHD. Baseline diet was assessed by a past-year food frequency questionnaire. During a median follow-up time of 11 years, we documented 112 incident CHD cases.

In the adjusted analyses, there was no association between intake of vitamin K1 and CHD (HRQ4vsQ1 = 0.92 (95% CI 0.54 to 1.57), p for trend 0.64), while there was a lower risk of CHD associated with higher intake of energy-adjusted vitamin K2 (HRQ4vsQ1 = 0.52 (0.29 to 0.94), p for trend 0.03). Further adjustment for potential dietary confounders did not materially change the association for K1, while the association for K2 was slightly attenuated (HRQ4vsQ1 = 0.58 (0.28 to 1.19)).

Given the limited number of epidemiological studies, and the fact that dietary vitamin K sources and content differ between countries, the researchers noted that further research is warranted.

References:

1 Haugsgjerd TR, Egeland GM, Nygård OK, et al. Association of dietary vitamin K and risk of coronary heart disease in middle-age adults: the Hordaland Health Study Cohort. BMJ Open 2020;10:e035953. doi:10.1136/bmjopen-2019-035953.

2 Knapen MHJ, Braam LAKJLM, Drummen NE, Bekers O, Hoeks APG, Vermeer C. Menaquinone-7 Supplementation Improves Arterial Stiffness in Healthy Postmenopausal Women. A Double-Blind Randomised Clinical Trial. Thromb Haemost. 2015 May;113(5):1135-44.

3 Vissers LET, Dalmeijer GW, Boer JMA, Verschuren WMM, van der Schouw YT, Beulens JWJ. The relationship between vitamin K and peripheral arterial disease. Atherosclerosis 252 (2016) 15e20.

4 Wei FF, Thijs L, Cauwenberghs N, Yang WY, Zhang ZY, Yu CG, Kuznetsova T, et al. Central Hemodynamics in Relation to Circulating Desphospho-Uncarboxylated Matrix Gla Protein: A Population Study. J Am Heart Assoc. 2019;8:e011960. DOI: 10.1161/JAHA.119.011960.

5 Cui C, Sekikawa A, Kuller LH, Lopez OL, Newman AB, Kuipers AL, Mackey RH. Aortic stiffness is associated with increased risk of incident dementia in older adults. J Alzheimer’s Dis. 2018;66(1):297-306.

6 Thamratnopkoon S, Susantitaphong P, Tumkosit M, Katavetin P, Tiranathanagul K, Praditpornsilpa K, Eiam-Ong S. Correlations of Plasma Desphosphorylated Uncarboxylated Matrix Gla Protein with Vascular Calcification and Vascular Stiffness in Chronic Kidney Disease. Nephron. 2017;135(3):167-172.

.

 

 

 

https://www.ncbi.nlm...les/PMC5381086/

Conclusion

Daily consumption of 3 g of soluble fiber from 70 g of oats leads to beneficial effects on the lipid parameters, specifically total cholesterol and low-density lipoprotein cholesterol in hypercholesterolemic Asian Indians. Large scale studies over a longer period of intervention are required to further establish the cholesterol-lowering effect of oat fiber.

 

 

Edited by Phoebus, 03 May 2021 - 06:47 AM.

[pamojja]

I am planning to do a CT-calcium scoring this week, again as my baseline to work with.  Honestly, I am scared to do it about what it reveals. But better to know the full truth now. What is weird is this - my stress test, EKG was normal.  But I do feel numbness in my left hand from time to time and my shoulders, hands and legs pain.  So guessing that may be from the atherosclerosis?

 
Don't be scared of a CAC. Only once you know the extent of a problem you really can address it. LDL for that is useless, you could have sky-high but still no calcification. EKG was normal for me too. Numbness could be a sign of PAD, but other things too.
 

When I had pretty high LDL at that time I was on keto and low carb, but like I said before I did have high sat fats.  So maybe too much high sat fats (instead of higher unsat fats) there was a culprit?

 

As far as I understand, the only way sat-fats could contribute is in the presence of high blood-glucose.

 

Speaking of which, is there such a thing, like with other therapies in other health related problems, as going full detox first before reintroducing healthy fats?  Meaning, do I need to completely swear off sat fats for like few weeks before reintroducing the healthier ones gradually?  I was specifically thinking of grass fed red meat and wild caught salmon.  Or can I continue to eat these meats now?  What would you do if you were in my shoes?

 

Think fats, expecially the oxidized unsaturated fats in cell-membrans, take many months or even years to replace. With fasting those essential fats are propably are even more difficult to let go of.

 

In my shoes I don't think sat-fats are a problem (only their complete lack which let to the problem), and would continue. But ramp up the fat-soluble vitamins (K2, D3, A, Es, CoQ10).

 

By the way, I was going over your journey I was trying to find out if exercises helped you.  I see that you briefly mentioned it.  Was there any specific exercise that you would recommend over others?

 

With PAD and walking-disability the standard of care recommendation was to increase pain-free walking-distance by daily exercise. Tried it for 5 months, but pain-free walking-distance only got worse (down to 3-400 meters only). Therefore quit again.

 

For my case with real difficulty walking any distance, swimming was a godsend. Along with sweating and bathing in the sun, cold-adaptation in a river, and a short bike-ride. Sleep-hygiene too was very important.

 

In fact, this winter I missed my about 200 hrs in the sun on a South-Indian beach. And indeed, slight symptoms of pain in my left leg started. The first time since my remission from the walking-disability 4 years ago. Only the first week of daily sunbathing (and swimming) this spring reversed it again.

 

 

 

Edited by pamojja, 03 May 2021 - 11:02 AM.

[yz69]

I recommend you search Paul Mason and Dave Feldman's videos on youtube.  My doctor tried to put me on statin and I ditched her.

Edited by yz69, 04 May 2021 - 01:00 AM.

[Groundhog Day]

It's absolutely amazing doctors still recommend statins after that massive study two or three years ago that highlighted the ineffectiveness of statins. See Peter Attia's work/thoughts on cholesterol. 

[Perunyol]

Hi, Seeker3.

 

I won't comment on the statins thing but I will tell you about my case.

 

I have had high cholesterol stats all my life. Currently they are:

 

Total Cholesterol     : 557 mg/dL

HDL                         :   70 mg/dL

LDL                          : 468 mg/dL

VLDL                       :   19 mg/dL

Triglycerides           :    94 mg/dL

 

Besides that:

 

C-Reactive Protein: 0.9 mg/L

Basal Insulin          : 3.7 mcrU/mL

Basal Glucose       : 79 mg/dL

 

I have never taken statins in my life (to the horror of every cardiologist that I have ever consulted with).

 

After several years on a quite strict Paleo diet, I am currently, and have been for at least 24 months, on a 95% carnivore diet. So, as you can imagine, very high on saturated fats. That (changing from Paleo to Carnivore) multiplied by 2 (two) my total cholesterol and reduced  by a 25% my VLDL and Triglycerides. If you haven't done already, I would recommend you to listed to the series on Cholesterol that Peter Attia has on his podcast (www.peterattiamd.com). It clarifies (to the extent that it can be clarified) the key stats to be measured when trying to asses cholesterol derived CVD risk. Mind you, it's several hours long and they get really deep into detail. 

 

I have a CAC score of 0 (zero) and my carotids appear pristine on ultrasound. I am 59. 

 

Make of that what you will. 

 

Saludos,

 

S.

 

Edited by Perunyol, 09 July 2021 - 07:54 PM.

[Turnbuckle]

Another study of 25,000 Asian men and women showing that the best total cholesterol is around 210.

 

And yet another study showing if you have high HDL (>40 mg/dL in men or >50 mg/dL in women), optimal triglycerides and high LDL -- as in the OP -- you have 30% lower risk.

 

 

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Edited by Turnbuckle, 11 July 2021 - 08:10 PM.