Oxidized LDL

[jozzee]

My mom's oxidized LDL is 52. Doctor says this is, moderage risk.
Does anyone else ask for this test?

[ofonorow]

I have a bias against "oxidized LDL" because it seems to be an invention to justify the continued interest in lowering LDL through drugs. When it became clear the ordinary LDL was harmless, "they" began researching "oxidized" LDL. Taking antioxidants should be the standard treatment, so if you mom is taking enough vitamin C, I don't see why this would be an issue?

[Johnwen]

I second what Owen said!!
But order her some Lipo-GSH (Glutathione) while your waiting for it, pick up some Pills from the health food store. Say 500mg. 2x a day and have her STICK with the Pauling protocal also.
If she needs to lose some weight now would be a good time to start. There is a realationship between weight gain and oxLDL.

Here's a link to some info on GSH effects with oxLDL.

http://www.ncbi.nlm.nih.gov/pubmed/17588583

[Saw]

Has she had her homocysteine checked, according to Kilmer McCully high homocysteine plays a role in forming oxy-cholesterols.

Outside sources are powdered milk and powdered eggs. Both are found in almost every processed food out there.

[ofonorow]

Has she had her homocysteine checked, according to Kilmer McCully high homocysteine plays a role in forming oxy-cholesterols.

The Pauling/Rath unified theory of cardiovascular disease uses the fact that homocysteine is inversely related to vitamin C as evidence of their theory:

Beside lipoproteins, certain metabolic disorders, such asdiabetes and homocystinuria, are also associated with the development of CVD. Despite differences in the underlying pathomechanism, all these mechanisms share a common feature: they lead to a thickening of the vascular wall and thereby can counteract the increased permeability in ascorbate deficiency. In addition to these genetic disorders, the evolutionary pressure from scurvy also favored certain metabolic countermeasures.

Homocystinuric angiopathy Homocystinuria is characterized by the accumulation of homocyst(e)ine and a variety of its metabolic derivatives in the plasma, the tissues and the urine as the result of decreased homocysteine catabolism.18 Elevated plasma concentrations of homocyst(e)ine and its derivatives damage the endothelial cells throughout the arterial and venous system. Thus homocystinuria is characterized by peripheral vascular disease and thromboembolism. These clinical manifestations have been estimated to occur in 30 per cent of the patients before the age of 20 and in 60 per cent of the patients before the age of 40.19

Ascorbate supplementation prevents homocystinuric angiopathy and other clinical complications of this disease by increasing the rate of homocysteine catabolism.20 Thus, ascorbate deficiency unmasks a variety of individual genetic predispositions that lead to CVD in different ways. These genetic disorders were conserved during evolution largely because of their association with mechanisms that lead to the thickening of the vascular wall. Moreover, since ascorbate deficiency is the underlying cause of these diseases, ascorbate supplementation is the universal therapy.

http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf

[pamojja]

The Pauling/Rath unified theory of cardiovascular disease uses the fact that homocysteine is inversely related to vitamin C as evidence of their theory:

I really wished I could confirm that evidence from my experience, but despite high dose vitamin C since more than 3 years my homocysteine misbehaves. Also Lp(a) went a bid down only to come up again. But I'll persist and prove the theory true, ultimately

No, seriously, even if it didn't lowered those numbers, there are enough directly felt health benefits for continuing taking vitamin C.

Though my recent attempt to have my plasma levels verified failed (lab was too unfamiliar with, despite instructing them, and failed to have it tested). However, with ox-LDL they succeeded, it came back at 66 with a normal range of 20 - 170. Glutathione peroxidase at 42.7 with a range of 27.5 - 73,6. Already increased selenium because of my hair analysis a year ago.


The interpretation from the lab (with the help of Google translator):


MEDICAL - SCIENTIFIC COMMENTS ON OXIDATIVE STRESS / DETOXIFICATION


Lipid peroxidation: initiation and progression of atherosclerotic changes need to be at least partly considered as chronic systemic inflammatory processes in the vessel wall. It involves penetration of LDL particles in the subendothelial layers of the blood vessels, followed by lipid peroxidation of LDL and absorption of this modified LDL in macrophages. This creates cholesterol-enriched foam cells. The oxidative changes affecting especially apolipoprotein B. This modified apo B is detected by the test for oxidized LDL cholesterol. It means those oxidatively modified LDL particles are measured, associated with an increased cardiovascular risk. The extent of the oxidative damage of LDL-cholesterol depends on the balance between the oxidative stress from the one side and the antioxidant protection potential on the other side.

The concentration of oxidized LDL cholesterol is in the normal range, so that there are no indications of increased oxidative modification of LDL cholesterol.


Glutathione peroxidase (GPX): GPX is one of the most important antioxidant enzymes in the detoxification of peroxides in living cells. The highly toxic hydrogen peroxide is converted under the influence of the enzyme glutathione peroxidase in a glutathione-dependent reaction into water. Lipid peroxides can also be detoxified in this way. Glutathione peroxidases contain in the catalytic center a L-selenocysteine, so that these enzymes are selenium-dependent. Glutathione peroxidases play an important role in tumor diseases, and possibly in tumor development.

Glutathione peroxidase shown here is settled in a normal range concentration, so a priori no diminished peroxide detoxification can be assumed.

[ofonorow]

I really wished I could confirm that evidence from my experience, but despite high dose vitamin C since more than 3 years my homocysteine misbehaves. Also Lp(a) went a bid down only to come up again. But I'll persist and prove the theory true, ultimately

Lets review. (Assume we have no idea how much vitamin C you now take).

What is your daily vitamin C intake?

Do you also take lysine/proline? If so, how much?

Was the Lp(a) measured, and what is it?

And I didn't see the homocystein number?

[Johnwen]

Owen and Pam

I got a question.
What are the goals/accomplishment were trying to achive here?
Are we crunching numbers or dealing with a specific problem I got a little lost reading the posts?
Good info/questions but not very specific!

[pamojja]

John,

the reason for testing is to see if there are associations between diet, supplements (also synergism and/or antagonism) and laboratory markers with my state of health (the later is sort of easy in my case with PAD: just have to measure the time I'm able to walk without a break). So if something becomes obvious I would be able to adjust.

For example, I've been perplexed that despite high vitamin C, niacin and a number of other lipid-modifying nutrients they just went up and down without obvious reason. Even paradoxically being lowest with my worst infection during the last 3 years, when lipids actually should be the highest.

A plausible explanation came from Masterjohn:

In that with non-fatty alcoholic fatty liver disease and an increased nutrient dense diet (especially in choline) an increased clearance of lipids from the liver into the bloodstream often results, and make numbers look worse at first, but actually contributes to its resolution.

Now I already had forgot about my 7 malarias a decade ago, and how it together with its pharmacological treatment had caused me liver pain, especially after the 7th (sonography confirmed a enlarged liver at that time).

So for verification, if this could be the case for me too, I plotted a graph of changes in percent from allegedly optimal values for the last 3 years, subsuming different areas (like combining all the liver enzyms, HDL, LDL and trigs together, etc..).

Though erratic testing gives little significance in many areas, liver enzymes (thick yellow line) and the basic lipids (thick gray line) both have been both most regular nevertheless.

If you take a look at this chart, though really hard to see meaningful associations at a first:

Changes in basic lipids till the beginning of 2011 were almost identically to those in liver enzymes (though not right from the very beginning, only after a high enough dose of niacin caused additional stress to my liver about the second half of 2009).

And interestingly the point where enzymes took a sudden different turn correlates exactly to the time my choline intake was relatively highest: about 500 mg/d, along with almost as much from diet.

Therefore I increased measures to improve liver heath.


Still too many open questions and not so apparent areas which very likely are involved just as well. Without such tracking I would not learn anything new. Of course I would prefer a practitioner with experience and knowledge too, without access this is the second best.

I'm aware that you don't give much value to lipid numbers, neither do I, really. I'm just inquiring what they could mean in relation to a particular state of health.

Till now can't deny a correlation (not necessarily causation between 'better' lipid numbers (including Lp(a), Apo B and A), Inflammation (homocystein, fibrinogen, hsCRP) and improved walking distance (without claudication) - which nevertheless could be different next year again. And I'll have learned something new.

Oven, the answers about my intake and numbers - probably much more than you wanted to know, you could find under different tabs of the same spreadsheet I linked to with the chart.

[Johnwen]

[pamojja]

[Johnwen]

I've been trying to get a hold of our ID Doc for his opion but I haven't been able to catch up to him yet. Here's what I surmized so far.

You have Stage 1 kidney disease which isn't all that bad! It's just a yellow flag! Possibily low water or stress when getting tested (Normal) will throw this off at this point I wouldn't worry about this.

You have all the indications of a chronic infection and thinking about it I would still get retested for malaria. Since it's been over 30 years since I've seen a case I did a little search for testing their using now and found they even have a stick test for it now. This is were you put a drop of blood on a stick tester and it gives you a Yes or no type responce within a time frame. Kind of like a prego test. According to the paper it's 98.7% accurate. My thoughts are that a person who has had malaria it would be a good annual check for it.
As far as getting rid of residual lukers the quinine based drugs are used the same as full blown infestation.
I'll post more as it becomes available.

[pamojja]

Thanks for the update.

You have Stage 1 kidney disease which isn't all that bad!

Well, if that is the case I worry rather earlier than later, from wikipedia:

The prognosis of patients with chronic kidney disease is guarded as epidemiological data has shown that all cause mortality (the overall death rate) increases as kidney function decreases.[16] The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5. [16][17][18]

Don't need one more factor contributing to..

I need this info to calculate kidney function from your other test results.

Therefore to be enabled to keep an eye on this, would be great if you let me know the formula which made you come to this conclusion. Because this would be the least obvious to me from my lab tests. Any additional test you could recommend? (cystatin-C, sonography..?)

You have all the indications of a chronic infection and thinking about it I would still get retested for malaria.

Well, as far as I know testing for malaria - though easy to verify with a single drop of blood under the microscope during an actual fit (at least in Africa they're really good at that) - wouldn't work if it's only dormant in the liver. By the way, with my 7nd and last malaria I used a double medication which was recommended at that time and place for getting rid of any dormant kind.

Also I feel unsure if this infection is really chronic, since usual inflammation markers have been quite low most of the time until recently. However, a dormant chronic infection would very well explain the abnormalities I regularly see with my blood counts.

Remembering my experience with searching unsuccessfully for an infection during my one week hospital stay about 6 years ago doesn't makes me particularly hopeful it would lead to anything today. Because if this is the case, then beside the malarias I really would have to test for a number of infectious diseases (of which nothing was really tracked down 6 years ago):

* Though not active, got some tubercles in my chest X-rays
* Bilharzia is an other one (unable to get verified, other than the ceasing of all symptoms with medication. As with 3 of my 7 malarias)
* Finally an infection of the spine occurring right after the last malaria, and interesting, right at the height of my main stenosis at the abdominal aorta. Which left inter-grown lubar vertebraes at that spot

[Johnwen]

Looked at about 6 different calcs. This one seems about this most accurate. DaVita is a big name in dialysis in the states they tend to be honest in their claims and products which is probably why they make the big$$$.

http://www.davita.com/gfr-calculator/index.cfm

[ofonorow]

Trying to figure out where this changed from LDL cholesterol to infectious disease? Will probably split