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Blood Panel: What to Test Annually?


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To make this a bit more useful, editing to include where I got a few cancer-related biomarkers I am including in my list.  Note that since I am a male, I am not including biomarkers for breast cancer, discussion of which can be found here:

https://www.americanmetaboliclaboratories.net/ca-profile.html
 

Edited by Ron Put
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Well, it appears that nobody here seems to have a good, comprehensive list.  The various threads on the subject are old and peppered with longwinded arguments, and thus not particularly helpful to someone looking for a quick guide.

I am posting what I came up with, mostly based on Ben Greenfield's list for males, plus additional items I believe might be useful to test as a baseline.

The list is personal and since I am a male, it does not include items specific to female health. Those looking for female-specific biomarkers to add should check out the links in the posts above.

Not every item would need to be tested every year, but I am satisfied with it, overall.  Note that I have omitted the more granular thyroid tests Greenfield suggests, other than TSH, mainly because I already have established a baseline for myself and because the basics are covered in most regular blood tests.  For many, this may be total overkill and a waste of money, but I personally am curious to know. 

So, for those interested, here is my list for this year.  If I missed anything significant, please chime in and I will update this post as necessary.

25-Hydroxy-Vitamin D

Adiponectin

Apolipoprotein A-1

Apolipoprotein B

CA 19-9

CEA

Cardio IQ Lipoprotein Fractionation, Ion Mobility

Complete Blood Count with Differential ( include RCDW calculation)

Complete Metabolic Panel

Copper

Cortisol

Cyanide (if you eat a lot of almonds, flax, etc.)

Dehydroepiandrosterone Sulfate

Estradiol

Erythrocyte Zinc Protoporphyrin

Ferritin, serum

Fibrinogen

Folate

Free Fatty Acids

Hemoglobin A1c

Homocysteine

High-sensitivity C-reactive protein

IGF-1 (Growth hormone surrogate)

IGF bonding protein 3

Iodine (if you don't use enriched salt)

Insulin

Iron, TIBC

Lipid Panel with Particle Size

Lipoprotein (a)

Lipoprotein-associated Phospholipase A2

Luteininzing Hormone

Methylmalonic Acid ( MMA)

Omega 3 Fatty Acids

PHI

PTH

RBC Magnesium

Selenium

SHBG (sex hormone binding globulin)

Testosterone + Free Testosterone

Thiamine

TSH

Uric Acid

Vitamin A

Vitamin B12

Edited by Ron Put
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1 hour ago, InquilineKea said:

why not just get 8-oxo-G testing?

I must admit, I had to look this one up :)  I am not sure that I see a commercial test being available, based on a rather casual search.

BTW, for those in my position of ignorance, this is the simplest explanation I found:

https://www.eurekalert.org/pub_releases/2006-08/giot-suc082306.php

Edited by Ron Put
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4 hours ago, TomBAvoider said:

What I would recommend, is that when you take the blood test, go ahead and take a urine test as well (at the same time) - pairing that data can give you a lot of insights, including much more comprehensive information about your kidneys and other organs.

It appears that the 8-oxo-G test is a urine test.  My doctor runs a standard one as part of the annual, but is there anything else that's a useful marker you would recommend?

 

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Thanks, Tom. Some of these, like Bilirubin, are already part of the general chemistry blood panel. Is there an additional benefit from getting the urine values as well?

Similarly, if the basic Albumin, Globulin and A/G ration values are normal, is there a benefit to the more detailed breakdown provided by the Protein Electrophoresis test (I might actually do it anyway to establish a baseline)?

BTW, any value from doing a Vitamin E test, if it seems I hit my daily RDI from food?

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The electrophoresis breaks it down in more detail with alpha1, alpha2 globulins, beta and gamma - for example, I discovered that my gamma globulins were at the lower end (still in range, just at the extreme low end) - which tells me that my immune system is producing fewer of these.

Why would I care? It is after all, still within the range - but it's the same question about bilirubin etc. it goes to why we take tests at all. It has less to do with measuring something in immediate response to a condition, but establishing a baseline. This is important, because it affects all your subsequent interventions. For example, I'm interested in rapamycin - but the trick with rapa is in dosage and timing protocol. The danger is that at a cetain dosage it can be immunosuppressant (and results in cancer rates going up), but at the same time a dose too low has little effect and very unfortunately the separation between the two is rather slim - so it's easy to either have it do nothing, or do too much.

How would you know if the dose you're taking is immunosuppresant? There is anectotal stuff from folks who take it for anti-aging puproses (f.ex. lip lesions - too much rapa), but it's way too imprecise. Now, if I already know my gamma globulin levels and now I take rapa, I can directly compare to see how that is affected. Since my alpha(1,2) and beta are smack in the middle of the range, but my gamma is at the extreme low end of the range, I could lay it down to rapa... except I have a baseline measurement to compare to. I can immediately see the effect of rapa. 

And so on for many of these tests the function of which is to establish a valuable baseline so you can evaluate future interventions (drugs, diet, exercise, lifestyle choices etc.). Otherwise, you are flying dark.

Vit. E test - again, nothing immediate, but it *might* be useful as a baseline for some future purpose. My philosophy is to gather as much data as I can, because while I may at present not know of any particular value to a test (as I'm not aware of in the case of Vit. E), what if some future intervention I'm interested in affects that value - it's good to have something to compare to. 

The more you know, the more you know.

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On 6/6/2020 at 2:59 PM, TomBAvoider said:

The electrophoresis breaks it down in more detail with alpha1, alpha2 globulins, beta and gamma - for example, I discovered that my gamma globulins were at the lower end (still in range, just at the extreme low end) - which tells me that my immune system is producing fewer of these.

.... The more you know, the more you know.

Thanks, Tom. I added it to the list above since my doctor agreed that it is a very useful test, even if he said I am an unlikely candidate for it.

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Different metabolic reactions have radicalized side products, often environmental impacts cause oxidative stress, as a result oxidative damage markers are widely spread in organism, their amounts usually grow with age as oxidative stress is one of the most studied phenomena being both a cause and a consequence of aging so discussed compounds fit properly on the role of aging biomarkers. Such compounds as 3-nitrotyrosine, 3-chlorotyrosine and o-tyrosine are strongly associated with protein damage in aging (Stadtman 2006). Malondialdehyde, 4-hydroxy-transhexenal, 4-hydroxy-trans-nonenal, 8-isoprostaglandin F2α and aldehydes C6–C12 are usually applied as biological markers of lipid oxidative damage during aging (Marcourakis et al. 2008). Such compounds as 8-hydroxy-2-deoxyguanosine and 8-hydroxyguanosine appear when DNAisdamaged under prooxidant treatment and oxidative stressor exposure, thus these residues may be used as indicators of agerelated oxidative damage (Rübe et al. 2011; Mecocci et al. 1993)

 

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Serum pentosidine correlates with a loss of muscle mass and can serve as a biomarker for sarcopenia237. However, is it just a marker? Some studies suggest that there might be a causative relationship, i.e. with aging in mice, muscle ECM hydroxyproline content increased twofold and advanced glycation end-product protein adducts increased threefold238

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High serum CML, a marker of the glycation process, was associated with a 2.3-fold increase in cardiovascular diseases (CVD) mortality in non-diabetic women275. In other study subjects with CML in the highest vs. lowest tertile had 84% increased risk of death from all causes and 111% increased risk of dying from CVD276. However, there are some conflicting reports: Finnish study reported an increase in CVD-mortality only for women277, and CARLA study reported no association between mortality and AGEs in serum278. This discrepancy could be explained by the fact that AGEs in serum are a variable biomarker and most of the studies measure it only once. This could be the source of variance between the studies. The more robust biomarker should reflect the accumulation of AGEs. On of such markers — skin autofluorescence — is significantly associated with both CVD-mortality (HR: 2.06; 95% CI 1.58–2.67) and all-cause mortality (HR: 1.91; 95% CI: 1.42–2.56)279. However, skin autofluorescence is not an ideal biomarker too: it is an indirect measure of crosslinking degree in the skin which introduces some error, but more importantly, it does not measure the most abundant AGE in the skin — glucosepane280,281⁠ — since glucosepane is not a fluorescent AGE. However, it is known that solubility of skin collagen decreases with age (r=0.809) and the fraction of glycated collagen in insoluble fraction increases with age(r=0.662)282. Moreover, the logarithm of the time required to digest 50% of the collagen increases linearly with age283. It is probable that collagen solubility could serve not only as a precise predictor of chronological age but also as a better predictor of mortality since it was demonstrated that mice with a mutation, that makes type I collagen resistant to collagenase cleavage, have accelerated aging with weight loss, reduced adiposity, kyphosis, osteoporosis, hypertension, and premature death284. This study also revealed a new potential mechanism of ECM-mediated cellular aging: upon collagenase-mediated cleavage, the triple helix unwinds to expose cryptic RGD sites that serve as ligands for ß3 integrins including αvß3 integrin, which has anti-apoptotic properties. Inhibiting αvß3 integrin signaling in smooth muscle cells mimicked the pro-senescence effect of collagenaseJournal

 

Edited by InquilineKea
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Erythrocyte zinc protoporphyrin is a simple test I think ought to be done as commonly as metabolic panels and CBCs.  An elevated level indicates an issue with heme formation which can stem from a diverse range of fairly common bad things such as iron deficiency, metals poisoning such as lead and vanadium,  and a variety of anemias and cancers.

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On 6/13/2020 at 6:44 AM, Todd Allen said:

Erythrocyte zinc protoporphyrin is a simple test I think ought to be done as commonly as metabolic panels and CBCs.  An elevated level indicates an issue with heme formation which can stem from a diverse range of fairly common bad things such as iron deficiency, metals poisoning such as lead and vanadium,  and a variety of anemias and cancers.

Thanks, Todd. I looked it up, it does look rather useful, so I added it to the list.

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  • 2 weeks later...
On 6/6/2020 at 2:59 PM, TomBAvoider said:

The electrophoresis breaks it down in more detail with alpha1, alpha2 globulins, beta and gamma

So, I got my results and now I've established more granular protein markers :)  All seem good, with gamma globulin at 1.4, which seems to be on the upper end (0.4 to 1.8 range) -- not sure if this is good, bad or irrelevant.

I have elevated amylase -- it has been always high since I started measuring a few years ago, fluctuating between just over 100 and close to 200. Lipase is always normal and I have no symptoms of pancreatic inflammation.  Weird.  I am wondering if it is because of the high carbs and fiber I consume, although I haven't seen anything mentioned in the literature. Does anyone else here have elevated amylase?

I tested CEA and it came up at 3.8, which is a bit high. I have been vaping fairly regularly for over two years (pot, to go to sleep) so I am cutting it out, as CEA is increased in smokers (an average of 4.5, as opposed to an average of 2.5 for non-smokers).  I also did a CA19-9 test and it came at 9 (<25 is considered healthy).  I guess these are useful to do periodically.  PSA is down to 0.38 from 0.51.

IGF-1 has dropped from 185 to 161. My cholesterol has dropped further down, to the high 130s with HDL in the 60s.  VLDL is at 6, triglycerides are down to 28 and HSCRP is at 0.02.  So, I am sticking to no extra virgin olive oil, except on rare occasions :)

Overall, I'd say that approximating moderate CR and intermittent fasting (16:8 on most days) is showing results, for me at least.

Edited by Ron Put
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Another note, which may be of interest to vegans and vegetarians: I had the Cleveland HeartLab OmegaCheck test done and the results were a bit surprising, to me.

The whole blood EPA+DPA+DHA value was 5.2, a bit below >5.5, the value above which they find the lowest risk of sudden cardiac death. 

This is despite the fact that I have been trying to maintain a roughly 2 to 1 ratio of Omega-6 to Omega-3, based on Cronometer data.  As I am vegetarian, thus the Omega-3 was provided primarily by a daily dose of flax.  According to Cronometer, my average daily intake of Omega-3 over the last year was 11.1g and Omega-6 was 16.5g.

My blood test results are:

Omega-3:
EPA: 1.4 (range 0.2-2.3)
DPA: 2.1 (range 0.8-1.8)
DHA: 1.7 (range 1.4-5.1)

Omega-6:
Arachidonic Acid: 11.7 (range 8.6-15.6)
Linoleic Acid: 31 (range18.6-29.5)

So, my DPA is higher than their range, which is good.  Linoleic Acid is also higher, I am not sure if it's good or bad.

The bottom line is, flax doesn't seem to do it for me in terms of EPA and DHA, so I have started taking 600 DPA and 300 EPA daily, in the form of algae oil supplement.

When I retest my amylase in about a month or so, I will probably redo the OmegaCheck and see if the algae oil helps (it should).

Edited by Ron Put
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P.S.  I did a quick search on linoleic acid and it appears that higher concentrations reduce inflammation, which seems to be supported by my rather low HSCRP value of 0.02.

Omega-6 fatty acids do not promote low-grade inflammation
 

The individual response may also be based in part on genes (I am T/T at rs174550, which jives with the theory):

Effects of linoleic acid on inflammatory response depend on genes

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  • 1 month later...

A quick question about  Mean Platelet Volume (MPV) values for those practicing CR and/or intermittent fasting:

If you have tested MPV, are your results on the high end?  Mine is just above the normal cutoff of 11.9. 

My optimistically biased guess is that autophagy is responsible for the presence of younger platelets, but I also see a few studies which suggest that it increases certain risks, although these are done in subjects with compromised health, such as pre-diabetics.

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6 minutes ago, Ron Put said:

autophagy is responsible for the presence of younger platelets...

Keep in mind:

"The average life span of circulating platelets is 8 to 9 days.   Life span of individual platelets is controlled by the internal apoptotic regulating pathway, which has a Bcl-xL timer. Old platelets are destroyed by phagocytosis in the spleen and liver."  (Wiki)

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Huh, Ron, that's very interesting - I just checked my numbers, and my latest test from the end of May, the MPV is "flagged" as being outside of the range, although the range is different from what your lab is showing. My lab is UCLA and the range is 9.3 - 13.0 fL 

The lab is:

Lab
RONALD REAGAN UCLA MC CLINICAL LABORATORY
757 Westwood Plaza
Los Angeles CA 90095
Tel: 310-267-8100
Lab Director: Alyssa Ziman, MD

and FWIW, they have had the same range for a very long time (looking through my records). Now, my last test came flagged as outside of range at 13.1 which is just outside of the upper limit of 13.0. However, looking through the years, it looks like I'm consistently at 13.0 (i.e. right at the upper limit), except for 2016, where I'm a LOT more outside of the range at 13.8.

Very interesting. I never paid much attention to this, so thanks for that, Ron. 

Edited by TomBAvoider
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