Jump to content

All my lab results/blood tests here (Alex K. Chen)


Recommended Posts

https://www.rapamycin.news/t/grimage2-and-its-dnam-based-proteins-packyrs-logcrp-loga1c-adrenomedullin-adm-beta-2-microglobulim-b2m-cystatin-c-gdf-15-leptin-pai-1-and-tissue-inhibitor-metalloproteinases-1-timp-1-blood-tests/7378/3?u=alexkchen

My values:

DNAmadm DNAmB2M DNAmCystatin_C DNAmGDF_15 DNAmleptin DNAmlog.A1C DNAmlog.CRP DNAmPACKYRS DNAmpai_1 DNAmTIMP_1
256.2984699 791294.7258 416886.0024 96.58857561 4333.618852 1.731211957 -0.5672573947 -3.988701324 17683.9436 26111.63214

my DNAmCystatin_C is > 4 SDs below the dataset, but the dataset is also GrimAge2 so it only includes older people…

I have reasonably low PAI1, which is not too correlated with age. This is good, and also shows that even if I have an ASD, I don’t phenotypically match with ALL attributes matched in ALL papers about ASDs (understandably, b/c I know my case is peculiar). Ruling out high PAI-1 is a weight off my shoulders.

DNAmlog.A1c.. average is 1.73769.. Mine is 1.73121. SD is 0.032. .. Ugh.. it's not that different.. 0.00648. My A1C is always 4.8 but people have commented that my BG spikes are "thicker" than other people's, and my spikes tend to be worse from eating an equivalent amount of food => this means I have to eat less fruit and more acarbose-receptive meals. I'm so jealous of people who can eat fruit without much of a glucose spike (and there are LOTS of people like that) - even if my inflammation is hella-low, I need way more time than other people (I need 1.8 more years for another person's year [roughly]) and cannot afford to have high glycation.

Edited by InquilineKea
Link to comment
Share on other sites

  • 1 month later...

iollo-report.xlsx

I got my iollo results back. They.. seem.. generally pleasing? [only on what the report mentioned]... I have no vegetarian-related deficiencies (tho I supplemented with taurine the day *before* the test [aka I need to do it regularly]) and even my cortisol is not that high (I have high neuroticism)...

But only in terms of the report-related metabolites. Homocysteine is higher than ideal and a massive bitch to reduce... (vegetarians/vegans tend to have much higher levels, so I should jack up my creatine)

Also I have to look at what the carnosine concentrations here mean..

methionine sulfoxide/methionine ratio (0.111111) might not be optimal, but there's just no way to tell rn...

my methionine is 15.3 (only slightly smaller than mike's). my methionine sulfoxide is 1.7 [mike's is 0.79]. my ratio is 0.1111111... Mike Lustgarten has a ratio of 0.05... I have an unusually high level of methonine sulfoxide/methionine...
Quote

Uniquely, the methionine sulfoxide reductase (Msr) group of enzymes act with thioredoxin to catalyze the enzymatic reduction and repair of oxidized methionine residues.[5] Moreover, levels of methionine sulfoxide reductase A (MsrA) decline in aging tissues in mice and in association with age-related disease in humans

Quote

Although fRMsr reduces free Met-R-SO, this enzyme is only present in unicellular organisms, and thus mammals are unable to reduce this compound

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311537/

https://pubmed.ncbi.nlm.nih.gov/17922679/ says MsrB in mammals... (need to find more)

cystine/cysteine ratio (0.00194) [Mike Lustgarten is 0.06].

So I have one level of oxidative stress that's higher than that of a healthy adult older than me, and one level that's lower. Methionine sulfoxide is a reversible modification [it's unclear if Met-R-SO is reversible], but increases in it may still be an issue... Could be related to hypofunction in Methionine sulfoxide reductases (which may contain a selenium component)

https://pubmed.ncbi.nlm.nih.gov/17922679/

Taurine is 114.42. From the curve below, it is not the most youthful. Iollo says its normal, but iollo is incomplete... Mike Lustgarten has 173.1... I was vegan for the week before the test (and I'm vegan most of the time), so this entire explains it, so I need to supplement more heavily, damnit, I hate taking taurine pills b/c they're so bulky.

Kynurenine-to-Tryptophan ratio. Your value is 20.75 nM/μM, which is in the optimal range. [Mike Lustgarten is 23]. However, these levels could still be as low as 15.... [and in older people...]

Dehydroepiandrosterone sulfate. Your value is 3.08 µM, which is slightly elevated compared to the optimal range. This puts you in the monitor only range, meaning that your values are trending towards levels considered outside of the optimal range.

Look at Mike Lustgarten's (his is 3.5 and he says it's very low..) THE TESTS ARE DIFFERENT EVEN IF THE UNITS ARE UMOL...

This is the main issue:

Quote

 

Hydroxybutyrylcarnitine. Your value is 4.85 points, which is elevated compared to the optimal range. This puts you in the pay attention range, meaning that your values are considered outside of the optimal range.

Your Hydroxybutyrylcarnitine levels are out of range. This marker is involved in the metabolism of short-chain fatty acids, which are crucial for energy production. Abnormal levels may indicate an issue with short-chain fatty acid oxidation. Given your reported low energy levels, it's possible that your body is having trouble metabolizing these fatty acids for energy. However, this is just one possible explanation and it's recommended that you speak with your healthcare provider for a more accurate assessment.

 

Quote

Malonylcarnitine is a metabolite that accumulates with specific disruption of fatty-acid oxidation caused by the impaired entry of long-chain acylcarnitine esters into the mitochondria and failure of the mitochondrial respiratory chain at complex 11 and malonyl-CoA decarboxylase (EC 4.1.1.9) deficiency (OMIM: 248360 ). Malonylcarnitine has also been found to accumulate in some newborns with medium-chain acyl-CoA dehydrogenase (EC 1.3.99.3) deficiency (OMIM: 201450 ). (PMID:11558490 , 15303003 , 12651823 ).

Quote

 

Malonyl-CoA and Fatty Acid Metabolism

Malonyl-CoA plays a pivotal role in energy metabolism. As the substrate for fatty acid synthase, the cytosolic concentration of malonyl-CoA determines maximum rates of de novo fatty acid synthesis. As an inhibitor of carnitine palmitoyltransferase, malonyl-CoA controls the rate of fatty acid entry into the mitochondria, and hence is a key determinant of the rate of fatty acid oxidation. Thus, conditions that lead to high levels of malonyl-CoA (e.g., high carbohydrate intakes) suppress fatty acid entry into the mitochondria and increase their flux to triglycerides. On the other hand, conditions that result in low cellular concentrations of malonyl-CoA favor fatty acid oxidation because the inhibition of carnitine palmitoyltransferase is released. The synthesis of malonyl-CoA is catalyzed by the biotin-containing enzyme, acetyl-CoA carboxylase. Acetyl-CoA carboxylase exists as two isoforms: a liver or type I and a muscle or type II. The two isoforms are distributed in the cell in a manner that results in an intracellular compartmentalization of malonyl-CoA (i.e., malonyl-CoA produced by acetyl-CoA carboxylase type I is the substrate for fatty acid synthase, while malonyl-CoA generated by the type II enzyme governs fatty acid entry into the mitochondria via regulation of carnitine palmitoyltranserfase). Like pyruvate dehydrogenase, the catalytic activity, and hence the production of malonyl-CoA, by both acetyl-CoA carboxylase isoforms is regulated by phosphorylation and dephosphorylation of the protein. Acetyl-CoA carboxylase I and II are substrates for AMP-activated protein kinase (AMPK) and cyclic AMP-dependent protein kinase (PKA). AMPK activity is enhanced by leptin and adiponectin, two hormones that stimulate fatty acid oxidation and inhibit fatty acid biosynthesis. The dephosphorylation of acetyl-CoA carboxylase is carried out by protein phosphatase 1 and 2, and phosphatase activity appears to be stimulated under conditions where glucose flux through glycolysis is high. In addition to its rate of production by acetyl-CoA carboxylase, the concentration of malonyl-CoA is also dependent upon its rate of decarboxylation by malonyl-CoA decarboxylase. Malonyl-CoA decarboxylase is also a substrate for AMPK, and its phosphorylation leads to an increase in decarboxylation activity and a loss of malonyl-CoA. Thus, AMPK activation governs fatty acid partitioning between triglyceride synthesis and oxidation by coordinately inhibiting malonyl-CoA synthesis and stimulating its degradation. In addition to having its activity acutely regulated via phosphorylation and dephosphorylation, the amount of hepatic acetyl-CoA carboxylase, like other lipogenic enzymes, increases and decreases in concentration depending upon nutritional conditions, dietary composition, and hormonal milieu. For example, the hepatic abundance of acetyl-CoA carboxylase is low during fasting and diabetes, but is greatly induced by refeeding glucose or administering insulin. On the other hand, muscle type II acetyl-CoA carboxylase is not an adaptive enzyme. Thus, its production of malonyl-CoA is solely dependent upon the phosphorylation state of acetyl-CoA carboxylase type II. In addition to playing a key role in the partitioning of fatty acids between storage and oxidation, malonyl-CoA may also be a central metabolite in appetite regulation. Thus, even though net fatty acid synthesis by humans is relatively small, the fatty acid biosynthetic pathway plays an instrumental role in human lipid metabolism. Since excessive cellular triglyceride production and accumulation is causatively linked to the development of insulin resistance and type II diabetes, factors regulating the fatty acid biosynthetic pathway will also exert a direct influence on the development of diabetes.

 

Acyl groups are interchangeable between CoA and carnitine after conversion with CPT1/CPT2 [carnitine acyltransferase] enzymes

But this was more than ideal...

 

Quote

 

What was measured in your blood?

Symmetric dimethylarginine. Your value is 0.32 µM, which is in the optimal range.

Reference ranges: Optimal: less than 0.36 µM
Monitor only: 0.36 to 0.4 µM
Pay attention: higher than 0.4 µM

What is it?

SDMA is a byproduct of proteins breaking down in your body and is passed out by your kidneys. Studies have demonstrated that SDMA in blood reflects kidney function better than the commonly used eGFR measurement. High blood levels of SDMA have been shown to be an early sign of kidney damage.

 

THIS IS WHAT I AM MOST CONCERNED ABOUT

https://www.degruyter.com/document/doi/10.1515/CCLM.2005.199/html

Asymmetric dimethylarginine, homocysteine and renal function – is there a relation?

Edited by InquilineKea
Link to comment
Share on other sites

methionine sulfoxide seems like a more worrisome adduct than cystine... The results of this are still unclear...

 

 

Quote

 

3.11 Unusual conditions and chronic or excessive exposure to ROS/RES may lead to modification of residues other than cysteine

 

3.11.1 Reaction of residues other than cysteine with ROS

 

3.11.1.1 Reaction of methionine with ROS

Methionine can be oxidized relatively efficiently.(516) Unlike cysteine and acetyl cysteine, the oxidation of methionine (although slow) by peroxide is pH independent (10−2 M−1s−1) and can in fact dominate glutathione and acetyl cysteine oxidation (by >10 fold) below pH 4. However, by pH 6, glutathione is 4–5 fold faster in terms of peroxide reaction than methionine, likely due to partial formation of the GSH thiolate. This indicates that in acidic organelles, methionine could be the most relevant signaling target, if signaling occurs in such regions. Interestingly, peroxymonocarbonate [formed from reaction of bicarbonate with peroxide, a process that occurs with a rate constant of 10−2 M−1s−1(517)] oxidizes methionine much faster than peroxide oxidizes methionine (0.5 M−1s−1).(518) Of course, peroxymonocarbonate is a better oxidant of cysteine, although the rate acceleration may be less significant than for methionine (around about 20-fold for protein tyrosine phosphatase and only two-fold for papain).(519) Reduction of sulfoxides is much more difficult than sulfenic acids; for instance, the second-order rate constant for the reaction of glutathione with DMSO is 0.00005 M−1s−1.(520) Thus methionine-S-oxide requires enzymatic reduction. Methionine S-oxide is chiral due to the increasing difference in s-p orbital energies as one proceeds down a group of the periodic table,(521) shutting down of the “umbrella inversion” effect in Period-3 elements. Reduction of the R and S forms of methionine-S-oxide is carried out by two separate enzymes.(522) Given the differences in rates of chemical oxidation of cysteine and methionine as well as the shorter half-lives of sulfenic acids relative to methionine-S-oxides, it is very likely that these two modifications fulfill very different roles in cells. As was noted above, HOCl can oxidize methionine with similar efficiency to cysteine. It is believed that HOCl generated from myeloperoxidase may be involved in modification of several proteins,(523) including inhibition of cholesterol export by ABCA1.(524)

 

 

Link to comment
Share on other sites

https://docs.google.com/document/d/e/2PACX-1vQzDipCcOrvJGt2UnORgGleW8gmhdZQLOSmiCsfRSZkHj67mjNhC2-QXs2bI0ayFfgRfKjKsEoSZjXX/pub

Issues with asymmetric dimethylarginine, symmetric dimethylarginine. This could all be due to my high vegetable consumption (as seen below) so maybe not a huge worry..

Screenshot 2023-07-10 at 16.53.31.png

Screenshot 2023-07-10 at 16.53.48.png

Screenshot 2023-07-10 at 16.53.54.png

Screenshot 2023-07-10 at 16.54.29.png

 

Quote

Plasma ADMA, symmetric dimethylarginine (SDMA), and l-arginine levels were measured by high-performance liquid chromatography. Median tea and coffee consumption was 2 cups/d, while vegetable and fruit intake was 152 (120-179)g/d and 120 (108-134)g/d, respectively. Median plasma ADMA, SDMA and arginine were 0.47 (0.43-0.53)μmol/L, 0.59 (0.54-0.66)μmol/L and 86 (68-101)μmol/L, respectively. ADMA correlated inversely with tea (r = -0.70, P < .0001) and vegetable consumption (r = -0.50, P < .0001) even after adjustment for age, sex, body mass index, smoking status, and potential dietary and biochemical parameters. No association between ADMA and fruit consumption was found. ADMA correlated positively with coffee intake (r = 0.37, P < .0001), although these associations were less potent after adjustment for dietary factors. Higher tea and vegetable intake is associated with lower plasma ADMA levels in healthy middle-aged subjects

Quote

Another mechanism has been suggested for the benefits associated to a vegetarian diet. A study including renal transplant patients showed that a soy protein-based diet for 5 weeks improved endothelial function, mediated by an increase in the L- arginine/asymmetric dimethyl arginine (ADMA) ratio, independently of change in lipid profile, oxidative stress, or isoflavones20 .

https://pubmed.ncbi.nlm.nih.gov/23438481/

Quote

exogenous presence of methylarginines, like that in fruits and vegetables, has never been described so far. Here, we report the finding that methylarginines are ubiquitous in vegetables which represent an important part of human daily diet. Some of these vegetables contain discrete amounts of ADMA, SDMA, and NMMA. Specifically, among the vegetables examined, soybean, rye, sweet pepper, broad bean, and potato contain the highest ADMA and NMMA mean levels. Our results establish that the three methylarginines, in addition to being produced endogenously, can also be taken daily through the diet in conspicuous amounts

tomatoes are high in them - this might be sufficient to explain it. My tested creatinine (59) was lower than it ever was (I'm low muscle mass, but it being lower than ever says *something*)

Edited by InquilineKea
Link to comment
Share on other sites

On 7/10/2023 at 5:12 PM, InquilineKea said:

Plasma ADMA, symmetric dimethylarginine (SDMA)

From what I understand, this is still considered to be a BS test, especially in humans, at least according to Mayo as I remember. I would ignore it until there is better evidence.

They market SDMA heavily for vets primarily, and even there it's more likely to be BS, and it has not been independently validated to the best of my knowledge.

I just did a quick search and even in cats it's all over the place:
 

https://pubmed.ncbi.nlm.nih.gov/32228261/

Results: Mean ± SD measured GFR was 1.58 ± 0.39 mL/min/kg, and the calculated reference interval was 0.84 to 2.37 mL/min/kg. There were significant negative correlations between GFR and serum creatinine concentration (r = -0.499), BUN concentration (r = -0.592), and age (r = -0.463). Serum SDMA concentration was not significantly correlated with GFR (r = 0.385), BUN concentration (r = -0.281), or serum creatinine concentration (r = 0.165). 

Link to comment
Share on other sites

  • 3 months later...

at redmond home now, a few papers to photograph (still looking for echocardiography) but not much

More on my health history: I once got hives in 8th grade (after DDT vaccination), I also remember I got laryngitis in middle school. At UW, I had enough colds that I needed a neilmed sinus rinse (but I have not needed one in a very long time). I have last had cold-like symptoms in late 2017, and have not been sick since then (or, really, sick anywhere in between 2014 and now). I got sleep apnea surgery in 2021, which was surprisingly painless despite being warned (no need for opioids).

i know I got flu and chicken pox and strep throat (maybe in 2nd/3rdgrade) and other common childhood illnesses in the far past. Parents told me this

My main persisting health issue has been chronic neck/back pain. I did enough PT to make it "65% treated" [enough that neck pain one day does not carry into the next day, and I don't need massages anymore like I used to]

The only other "health issues" I had were accidental drug overdoses. Let's just say that you learn not to overdose the same drug twice...

Edited by InquilineKea
Link to comment
Share on other sites

EKG from 2010 (though I was RUNNING on the way to EKG so ventricular rate artificially increased [and this also decreased pre-corrected QT interval)

Lab tests - OTHER PLEASE COMMENT

 

Results

New

VENTRICULAR RATE

View trends
BPM
Value
107
Your value is 107 BPM

ATRIAL RATE

View trends
BPM
Value
107
Your value is 107 BPM

P-R INTERVAL

View trends
ms
Value
140
Your value is 140 ms

QRS DURATION

View trends
ms
Value
92
Your value is 92 ms

Q-T INTERVAL

View trends
ms
Value
314
Your value is 314 ms

QTC CALCULATION(BEZET)

View trends
ms
Value
419
Your value is 419 ms

P AXIS

View trends
degrees
Value
79
Your value is 79 degrees

R AXIS

View trends
degrees
Value
90
Your value is 90 degrees

T AXIS

View trends
degrees
Value
77
Your value is 77 degrees

DIAGNOSIS LINE

View trends
Value
***age and gender specific ECG analysis*** Sinus tachycardia Rightward axis ST elevation, consider early repolarization Abnormal ECG When compared with ECG of 17-APR-2006 18:32, QRS axis Shifted right
Edited by InquilineKea
Link to comment
Share on other sites

Estradiol: 10 pg/ml (very long ago)

My teenage homocysteine was 8. Then 8.5 in 2020. Then 9.2 in 2023... This is the only biomarker (other than LDL) with a concerning trend, but it's not a huge one.

SOMATOMEDIN C was 200ng/ml in 2011

https://www.rapamycin.news/t/igf-1-inhibitors-and-lifespan-extension/2220/21

RDW

Date Value Normal Range
Apr 21, 2014
12
12
8 to 18.5 8 - 18.5
Dec 28, 2007
11.9
11.9
8 to 14.8 8 - 14.8
Sep 23, 2006
11.3
11.3
8 to 14.8 8 - 14.8
Aug 3, 2006
11.5
11.5
8 to 14.8 8 - 14.8

Testosterone:

Date Value Normal Range
Apr 21, 2014
680 NG/DL
680NG/DL
220 to 800 NG/DL220 - 800 NG/DL
Jun 21, 2011
587 NG/DL
587NG/DL
220 to 800 NG/DL220 - 800 NG/DL
Dec 28, 2007
410 NG/DL
410NG/DL
220 to 800 NG/DL220 - 800 NG/DL
Edited by InquilineKea
Link to comment
Share on other sites

  • 1 month later...
  • Alex K Chen changed the title to All my lab results/blood tests here (Alex K. Chen)
Posted (edited)

Just realized.. My RDW went down A LOT in 3 days last year.. this could have been bc I was overdosing on B12 for a period of time then..

Also my DunedinPACE might vary a lot bc I binged on A LOT of nuts in the days prior to my test.. now that Ezekiel bread and keto culture bread is safe for me, I have much lower need to binge on them.. this might also take my LDL cholesterol down too

Edited by InquilineKea
Link to comment
Share on other sites

  • 3 weeks later...

SDMA:

From his show notes (#257😞 “Peter’s concern is mostly cardiovascular because there is good evidence that homocysteine impairs clearance of two molecules (SDMA and ADMA [symmetric and asymmetric dimethylarginine]) that impair nitric oxide synthase

==

I do have cystatin C of 59 which is ultralow

Link to comment
Share on other sites

  • 3 weeks later...
Posted (edited)

Blood tests today. The turnaround was WITHIN A FEW HOURS/almost INSTANT...

Ugh hemoglobin a1c of 5.1 despite flozins half the time, and loads of beans, tomatoes, acarbose (but most of it was hibose up to around 2 weeks ago)... I mean I did go on several bread binges just to try it out. There were a couple of blueberry binges but overall fruit consumption is less

I'm going to try more semaglutide over the next month bc that's the best longevity low self control agent. Atomic habits, make it a habit to habitually eat less. Semaglutide simplifies life, it does not make you need to take more drugs like what you would need to do if you took rapa 

BP is 103/72 though I had loads of arugula and beets lately. I don't need to complicate my life with BP beds even if some increase lifespan in men..

Homocysteine 9, I did take more betaine but I lapsed for a while... Lapsed with creatine.. Slightly less

LDL 138, how the fuck is this possible, I've been low fat for a while, fuck. BOTH canagliflozin and rapa increase LDL, FYI.. I later posted on rapamycin.news, did a deep investigation, found cheap bempedoic acid from india..

T3 is just 48 which is low (maybe this is semaglutide acting on me at last)

AST 27... unusually high.

==

I was really freaked out for a while b/c LDL 138, so I asked doctor if he can as for Lp(a) blood tests. I'm taking a break from rapamycin to see if the numbers go down after (easy to take a break when u have flozins and semaglutide).

Semaglutide makes me eat most of my food towards a single point in the day, but I stil sometimes supplement with beans after...

==

Replacing MUFAs with carbs did NOT decrease my LDL..

I have opportunity to take estriol and estrogen...

Edited by Alex K Chen
Link to comment
Share on other sites

Posted (edited)

Growth Hormone: 0.2 (barely low)

IGF-1: 167 ng/L [well within normal, damnit]. Still, below from 200 ng/mL when I joined the forum.

Ref range https://www.ncbi.nlm.nih.gov/books/NBK279163/

i did eat like 4 cubes of tofu on the days prior to the test, but also did semaglutide so I was eating lower than usual calories

lead undetectable (when ur importing indian meds, it's impt to periodically test)

Edited by Alex K Chen
Link to comment
Share on other sites

In 2019, I got an unnecessary CT scan...

Quote

 

A DLP (Dose-Length Product) of 1840.95 mGy-cm is considered a relatively high radiation dose for a CT scan. To put this value into perspective, here are some general guidelines:

The average DLP for a standard head CT scan is around 800-1200 mGy-cm.
The average DLP for a standard chest CT scan is around 300-600 mGy-cm.
The average DLP for a standard abdominal CT scan is around 500-1000 mGy-cm.
A DLP of 1840.95 mGy-cm is higher than the typical range for most common CT scans. However, it's important to note that the radiation dose for a CT scan can vary significantly depending on the specific protocol, the patient's size, and the clinical indication for the scan.

To estimate the effective dose (in mSv) from the DLP, you can use a conversion factor that depends on the body region being scanned. For example:

Head: 0.0021 mSv/(mGy-cm)
Neck: 0.0059 mSv/(mGy-cm)
Chest: 0.014 mSv/(mGy-cm)
Abdomen: 0.015 mSv/(mGy-cm)
Pelvis: 0.015 mSv/(mGy-cm)
Using these conversion factors, a DLP of 1840.95 mGy-cm would correspond to an effective dose of approximately:

3.9 mSv for a head scan
10.9 mSv for a neck scan
25.8 mSv for a chest scan
27.6 mSv for an abdominal scan
27.6 mSv for a pelvic scan
These effective doses are relatively high compared to the typical annual background radiation exposure, which is around 3 mSv. However, the benefits of a clinically indicated CT scan often outweigh the potential risks associated with radiation exposure. Doctors and radiologists always weigh the benefits against the risks when deciding to perform a CT scan.

 

 

Link to comment
Share on other sites

Join the conversation

You can post now and register later. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...