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All my lab results here (Alex K. Chen)

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Posted (edited)


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
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Posted (edited)


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...

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


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://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)


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:



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.



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 deficiency (OMIM: 248360 ). Malonylcarnitine has also been found to accumulate in some newborns with medium-chain acyl-CoA dehydrogenase (EC deficiency (OMIM: 201450 ). (PMID:11558490 , 15303003 , 12651823 ).



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...




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.




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

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





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 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)



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Posted (edited)


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



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


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 .



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
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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:


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). 

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