How do we stop heart disease (Atherosclerosis, Arteriolosclerosis, Arteriosclerosis, calcification)

[prioris]

Just for the record

Here's my recent test
HDL 48.6
LDL 164
CHOL/HDL RATIO 4.7
TRIGLYCERIDE 67.0
CHOLESTEROL 226

HA1C% 4.4 (normal 4.0-5.7)
I will start checking blood glucose levels soon

 

[Gondwanaland]

HA1C% 4.4 (normal 4.0-5.7)

Short lived RBCs? I know this was the case for me when my HbA1c was 4.8 under a high carb diet and already taking warfarin.

Congrats on the lower Trig though.

 

[prioris]

One test that may be worth getting in future is the Lipoprotein Particle Number and Size and Lipoprotein Subfractions until I can manage to get to location for ultrafast calcium scan.

who knows about ha1c ... could be short lived

P.S.
My kidney seems to be very slowly getting better. Hopefully by end of month it will be better. I thought my lab tests would be an absolute horror show but everything came back normal although BUN was towards high end at 18 and GRT was 81. Need to improve those especially the BUN. I think what caused my kidney problem was a perfect storm of events and kidneys maybe under some stress already. I was doing phosphoric acid for cleansing gall bladder for 5 days, plus taking Modified Citrus Pectin and that Spinach combined with inflamed liver all combined to cause a cascade of events that became very painful kidneys and flank. That spinach is what really became the final nail. I ate the most spinach I ever ate in my entire life. All that oxalate hurt my kidneys. Vitamin C will definitely pull more oxalate into ones urine. Hopefully I get back healthier. I never count my chickens until they all hatch so will just continue healing and hope for no more roadblocks.

 

[Gondwanaland]

I was doing phosphoric acid for cleansing gall bladder for 5 days, plus taking Modified Citrus Pectin

These have a highly acidifying effect on urine, add oxalates to the party and boom. Also if you cut carbs all of a sudden there would be ketonuria - more acidity = stones.

 

[prioris]

P.S. I've been puzzled about my urinary irritation that doesn't go away. A light bulb went on today - i got interstitial cystitis I think even though I am male. Just another disease to throw on top of huge pile. It's a murky disease. At the rate I'm going, I should have personal experience with every known disease to mankind...LOL

 

[Gondwanaland]

interstitial cystitis

This could be oxalate dumping. A few years ago when I had no idea about oxalates, just by drinking apple juice my bladder would instantly be completely filled with stinging oxalate crystals. Cranberries help with that - it seems to stop the dumping.

 

[prioris]

This could be oxalate dumping. .

P.S. (means non heart disease related )
Interesting. I think I will assume it is degeneration via aging. Bladder lining is becoming compromised. I will try to regenerate the lining probably hyaluronic acid (active ingredient in Cystistat) with collagen along with maybe some retinoic acid. will continue to research.

 

[prioris]

Here is what the results of my Lipoprotein LDL large and small particle test results look like. Many tests that require doctor approval can be bypassed by going online without doctor approval then going to lab. I used www.requestatestdotcom.


LIPOPROTEIN LDL Large and Small particle size Test

Total Particles
HDL 27353 (21837-45671 n/mol/L)
NON-HDL 2326 (1485-2986 n/mol/L)

HDL Particle Subfractions
SMALL 21446 (17503-335394 n/mol/L)

LDL Particle Subfractions
VERY SMALL-d 62 (88-187 n/mol/L)
VERY SMALL-c 71 (86-203 n/mol/L)
VERY SMALL-b 61 (73-236 n/mol/L)
VERY SMALL-a 64 (49-249 n/mol/L)
LARGE-b 357 (123-332 n/mol/L)
LARGE-a 608 (123-402 n/mol/L)

IDL Particle Subfractions
SMALL 344 (93-225 n/mol/L)
LARGE 141 (152-319 n/mol/L)

VLDL Particle Subfractions
SMALL 37 (57-124 n/mol/L)
MEDIUM 36 (42-110 n/mol/L)
LARGE 5 (9-36 n/mol/L)



Lipoprotein Subfractions (RISK)
LDL PARTICLE NUMBER 1763 (HIGH) (optimal <1260)
LDL SMALL 192 MEDIUM (optimal <162)
LDL MEDIUM 348 (HIGH) (optimal <201)
HDL LARGE 5907 (HIGH) (optimal <6996)

LDL PATTERN A
LDL PEAK SIZE Angstrom 224.2 (A>222.5) (HIGH)



Not sure how to interpret LDL yet.

My vitaminD25 result was 50. I've been meaning to get this tested for so long. Finally I can cross this off my - Things to do while i'm still alive on earth - List

I have come across more people questioning the vitamin D level thing. Vitamin A is an antagonist to Vitamin D so the more A you take could supposedly effect the Vitamin D storage level and vice versa. I take fat soluble A.


P.S. On other fronts, the kidney inflammation thing is still puzzling me so continue to experiment

 

[pamojja]

Not sure how to interpret LDL yet.

Small LDL looks really good, as would to be expected from that almost perfect triglyceride level. Congratulations. The explanation in TrackYourPlaque, 2nd edition:

Small LDL particles are a powerful cause for plaque growth. Smaller particles more readily penetrate artery walls and deposit material into plaques. Small LDL’s are also more adherent to the material that resides in plaque. Small LDL is more prone to oxidation that leads to inflammatory responses. Because they are poorly recognized by the liver LDL receptor, they also hang around in the blood longer than larger particles, providing more opportunity to do damage (Julius 2007). In the Track Your Plaque approach, we aim to keep small LDL particles at no more than 30% of total LDL...

In Track Your Plaque, we try to keep your large HDL at least 15 nmol/L by NMR, or 30% HDL2b by electropheresis (Berkeley HeartLab), or 30% HDL2 by VAP, aiming for a total HDL of 60 mg/dl or greater. (The differences derive from different definitions of HDL size.) You can increase the proportion of large HDL by using the same treatment strategies as those used to correct the small LDL abnormality (above). A lack of large HDL is a relatively easy abnormality to treat, but you just have to recognize whether it’s present and whether it is fully corrected with your treatment efforts...

Also would get Lp(a), hsCRP, fibrinogen and homocysteine, if you haven't yet.

Also http://www.biomarkerbliki.org/ had good explanation of these tests, but seems offline now.

 

[prioris]

I added some more data I didn't see to previous post

 

[pamojja]

LDL particle number

Think of it this way: The more particles there are in your blood, the more likely they will enter the wall of the artery and contribute to plaque formation. Some call this a “gradient-driven” process. You might recall from high school science class that when a concentration gradient is present, it will work towards achieving equilibrium to eliminate the concentration difference. The same principle applies when a higher concentration of LDL particles is in blood compared to the artery wall: The more numerous LDL particles in the blood infiltrate the artery wall in an effort to balance the concentration gradient.

LDL particle number is one of the most powerful tools available. It can be measured directly as “LDL particle number” (by the NMR method) or apoprotein B, which is more widely available (one of the measures available through the Berkeley HeartLab as well as many local laboratories throughout the U.S.). The Quebec Cardiovascular Study is the most convincing demonstration of how LDL particle number (in this instance, measured as apoprotein B) was the best lipid/lipoprotein predictor of heart attack (St-Pierre 2005). In this study, heart attack still occurred even when LDL cholesterol was low but particle number was high. In other words, LDL particle number proved a better indicator of heart attack potential, even when LDL cholesterol was low.

You cannot predict LDL particle number by just looking at LDL cholesterol. In other words, you can have a high LDL particle number with low LDL cholesterol, a low LDL particle number with low LDL cholesterol, etc. LDL particle number or apoprotein B needs to be specifically measured. How can LDL cholesterol be low when the particle number is high? The amount of cholesterol contained per particle varies widely. If your LDL particles have less cholesterol in each particle but there are many of them, the measured LDL cholesterol can remain low— but your heart disease risk will be high (because of the high particle number and the resultant “concentration gradient.”)

There are many people with established heart disease who’ve been told their LDL cholesterol was fine and no cause for their heart disease could be identified. Many people like this have excessively high LDL particle numbers or apoprotein B.

You can still have a heart attack while being treated for high LDL cholesterol with a statin agent (Zocor®/simvastatin, Lipitor®, Pravachol®/pravastatin, Lescol®/fluvastatin, Mevacor®/lovastatin, Crestor®) if your LDL particle number is high. In other words, despite the appearance of a “good” response to a cholesterol-lowering agent, heart attack still occurs because the number of LDL particles is still excessive.

Reducing hydrogenated fats in your diet, cholesterol-reducing statin drugs, and several dietary strategies like raw nuts and flaxseed all reduce LDL particle number. These are the same treatments that reduce LDL cholesterol. (See above.) But if you rely only on LDL cholesterol and neglect to measure LDL particle number or apoprotein B, you will be groping in the dark: You won’t know if treatment is required nor will you know if treatment is sufficient. You simply need to measure LDL particle number or apoprotein B to know. For participants in Track Your Plaque, our targets for treatment that enhance likelihood of stopping plaque growth are an LDL particle number of <700 nmol/L or an apoprotein B of 70 mg/dl or less.

 

[prioris]

>Also would get Lp(a), hsCRP, fibrinogen and homocysteine ,if you haven't yet. ...

at some point i will (but first i need to survive this unknown kidney thing ... lol)

 

[prioris]

>we aim to keep small LDL particles at no more than 30% of total LDL...

so my TOTAL LDL is 1763 ... small is 192

does this mean that as long as i stay below 176x3 or 528 for current reading, that it is within the 30%

 

[pamojja]

>we aim to keep small LDL particles at no more than 30% of total LDL...

so my TOTAL LDL is 1763 ... small is 192

does this mean that as long as i stay below 176x3 or 528 for current reading, that it is within the 30%

1763 is the total LDL-particle number, for which below 700 would be considered optimal by Dr. Davis (your report says <1260).

Adding all very small LDLs up: 61+71+61+64=257, that still is below 30% of total LDL. So a mixed bag: small-LDLs are in the optimal range, LDL-particle number would still need substantial improvement.

 

[prioris]

Low TOTAL cholesterol is associated with high total mortality in patients with coronary heart disease
Same goes for cancer patients. Higher total cholesterol is associated with higher survival.

 

[Gondwanaland]

Interview on Coronary Calcification and CAC

 

[Gondwanaland]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628708/
Diabetes Care. 2009 Feb; 32(2): 361–366.
doi: 10.2337/dc08-0854
PMCID: PMC2628708
Relationship of Insulin Resistance and Related Metabolic Variables to Coronary Artery Disease: A Mathematical Analysis
David Eddy, MD, PHD,1 Len Schlessinger, PHD,1 Richard Kahn, PHD,2 Barbara Peskin, PHD,1 and Rick Schiebinger, MD3
Author information ► Article notes ► Copyright and License information ►
1Archimedes Inc., San Francisco, California
2American Diabetes Association, Alexandria, Virginia
3Eli Lilly, Indianapolis, Indiana

This article has been cited by other articles in PMC.

Abstract
OBJECTIVE—People with diabetes have an increased risk of coronary artery disease (CAD). An unanswered question is what portion of CAD can be attributed to insulin resistance, related metabolic variables, and other known CAD risk factors.

RESEARCH DESIGN AND METHODS—The Archimedes model was used to estimate the proportion of myocardial infarctions that would be prevented by maintaining insulin resistance and other risk factors at healthy levels. Person-specific data from the National Health and Nutrition Examination Survey 1998–2004 were used to create a simulated population representative of young adults in the U.S. This population was then entered into a series of simulated clinical trials designed to explore the effects of each risk factor. Each trial had a control arm (all risk factors were allowed to progress without interventions) and a treatment arm (a risk factor was held to its value in young healthy adults). The trials continued for 60 years. The effects of these hypothetical “cures” of each risk factor provide estimates of their impact on CAD.

RESULTS—In young adults, preventing insulin resistance would prevent ∼42% of myocardial infarctions. The next most important determinant of CAD is systolic hypertension, prevention of which would reduce myocardial infarctions by ∼36%. Following systolic blood pressure, the most important determinants are HDL cholesterol (31%), BMI (21%), LDL cholesterol (16%), triglycerides (10%), fasting plasma glucose and smoking (both ∼9%), and family history (4%).

CONCLUSIONS—Insulin resistance is likely the most important single cause of CAD. A better understanding of its pathogenesis and how it might be prevented or cured could have a profound effect on CAD.

 

[Gondwanaland]

My favorite carotenoid! But I am always chasing glutamate-free sources (guavas, carrots etc)

https://www.ncbi.nlm.nih.gov/pubmed/28799780
Crit Rev Food Sci Nutr. 2017 Aug 11:0. doi: 10.1080/10408398.2017.1362630. [Epub ahead of print]
Lycopene and Tomato and risk of cardiovascular diseases: A systematic review and meta-analysis of epidemiological evidence.
Cheng HM1, Koutsidis G1, Lodge JK1, Ashor AW2, Siervo M2, Lara J1.
1a Department of Applied Sciences , Faculty of Health and Life Sciences, Northumbria University , Newcastle upon Tyne , UK.
2b Human Nutrition Research Centre, Institute of Cellular Medicine and Newcastle University Institute for Ageing, Newcastle University , Newcastle upon Tyne , UK.

Abstract
BACKGROUND AND AIMS:
Worldwide, cardiovascular diseases (CVDs) remains as the main cause of mortality. Observational studies supports an association between intake of tomato products or lycopene with a reduced CVDs risk. Our aim was to undertake a systematic review and meta-analysis of the evidence on the topic.

METHODS:
Medline, Web of Science, and Scopus were searched from inception until July 2017. We included longitudinal and cross-sectional studies reporting associations between lycopene and tomato consumption and cardiovascular morbidity and mortality among adult subjects. Random-effects models were used to determine the pooled effect sizes.

RESULTS:
Twenty-eight publications met our inclusion criteria and 25 studies provided quantitative data for meta-analysis. Results showed that individuals in the highest consumption category of, or with the highest serum concentration of, lycopene had significantly lower risk of stroke (hazard ratio (HR) 0.74, 0.62-0.89, p = 0.02; I2 = 32) and CVDs (HR 0.86, 0.77-0.95, p = 0.003; I2 = 0). In addition, individuals categorised in the highest serum concentration of lycopene also had significantly lower risk of mortality (HR 0.63, 0.49-0.81, p<0.001; I2 = 46). Lycopene was not significantly associated with myocardial infarction, while scarce evidence on the association of lycopene with atherosclerosis, congestive heart failure, or atrial fibrillation was evident. Evidence from three studies suggested that higher intakes of tomatowere associated with non-significantly lower stroke, CVDs and CHD.

CONCLUSIONS:
This comprehensive meta-analysis suggests that high-intakes or high-serum concentration of lycopene are associated with significant reductions in the risk of stroke (26%), mortality (37%) and CVDs (14%).

KEYWORDS:
cardiovascular disease; lycopene; meta-analysis; mortality; systematic review; tomato

PMID: 28799780

DOI: 10.1080/10408398.2017.1362630

 

[pamojja]

A short video explanation (10 min.) of the most important lab test target values by Dr. Davis at the bottom of this thread:

https://www.cureality.com/forum/topics.aspx?id=19859#reply-134596

 

[Gondwanaland]

https://www.ncbi.nlm.nih.gov/pubmed/28735349
Curr Atheroscler Rep. 2017 Sep;19(9):36. doi: 10.1007/s11883-017-0673-y.
Connecting the Dots Between Fatty Acids, Mitochondrial Function, and DNA Methylation in Atherosclerosis.

Abstract
PURPOSE OF REVIEW:
The quest for factors and mechanisms responsible for aberrant DNA methylation in human disease-including atherosclerosis-is a promising area of research. This review focuses on the role of fatty acids (FAs) as modulators of DNA methylation-in particular the role of mitochondrial beta-oxidation in FA-induced changes in DNA methylation during the progression of atherosclerosis.

RECENT FINDINGS:
Recent publications have advanced the knowledge in all areas touched by this review: the causal role of lipids in shaping the DNA methylome, the associations between chronic degenerative disease and mitochondrial function, the lipid composition of the atheroma, and the relevance of DNA hypermethylation in atherosclerosis. Evidence is beginning to emerge, linking the dynamics of FA type abundance, mitochondrial function, and DNA methylation in the atheroma and systemically. In particular, this review highlights mitochondrial beta-oxidation as an important regulator of DNA methylation in metabolic disease. Despite the many questions still unanswered, this area of research promises to identify mechanisms and molecular factors that establish a pathological gene expression pattern in atherosclerosis.