Bloodtest Results - 11.5 years mild CR

[drewab]

Hi All,

I thought I would share my blood test results after 11.5 years of mild CR and feeling incredibly vibrant and energetic. The only two changes I've noticed are that my ferritin is low (albeit just a little) for the first time ever and my thyroid appeared to be considerably more active than normal. My test choices are limited by what can be ordered and covered by the Canadian medical system for a healthy individual without paying out of pocket. Sometimes they seem comfortable to order more, sometimes less... Just though I'd share for anyone interested. I tend to be very consistent with my regime day after day, month after month, year after year. So I have found a sustainable way of living for me. 

Test	Result	Range	Flag
Vitamin B12	329 pmol/L	>=160 pmol/L
Triglycerides	0.58 mmol/L	0.00 - 1.70 mmol/L
Cholesterol, Total	3.45 mmol/L	mmol/L
HDL Cholesterol	1.17 mmol/L	mmol/L
Low Density Lipoprotein Cholesterol (Calculated)	2.02 mmol/L	0.00 - 3.40 mmol/L
Non High Density Lipoprotein Cholesterol	2.28 mmol/L	0.00 - 4.20 mmol/L
Prostate Specific Antigen (PSA), total	0.3 ug/L	<2.6 ug/L
Hemoglobin A1c	5.0 %	4.3 - 5.9 %
Glucose, Fasting	4.5 mmol/L	3.3 - 6.0 mmol/L
Ferritin	28 ug/L	30 - 500 ug/L	Low
Potassium	4.4 mmol/L	3.6 - 5.2 mmol/L
Sodium	140 mmol/L	135 - 145 mmol/L
Creatinine	79 umol/L	50 - 120 umol/L
eGFR (mL/min/1.73m2)	109	>59 mL/min/1.73m2
Alanine Aminotransferase (ALT)	19 U/L	<60 U/L
Auto WBC	3.7 10*9/L	4.0 - 11.0 10*9/L	Low
RBC	4.93 10*12/L	4.30 - 6.00 10*12/L
Hemoglobin	165 g/L	135 - 175 g/L
Hematocrit	0.46 L/L	0.40 - 0.52 L/L
MCV	94 fL	80 - 100 fL
MCHC	358 g/L	310 - 360 g/L
RDW	15.8 %	<16.0 %
Platelets	129 10*9/L	140 - 400 10*9/L	Low
Thyroid Stimulating Hormone (TSH), Progressive	0.92 mIU/L	0.20 - 6.50 mIU/L
C-Reactive Protein (CRP)	<0.5 mg/L	<8.0 mg/L

[mccoy]

I would say that the healthy CR regime is paying off.

[Saul]

Hi drewab!

Low WBC is normal for CR; also, for mem, low ferritin (which is a lot better than high ferritin)

  --  Saul

[mccoy]

Anyway, a vegan regime should cause no problems for iron intake, I remember when vegan I used to have 300% of RDI, of course absorption might not be optimal. I would just eat more spinach, sesame seeds and Fe-rich food.

Vegans say that relatively low amounts are better than relatively high amounts of Fe, but there is always the middle ground, I would not be happy with a value equal to the lower bound, just for safety I would aim at something higher. Also, relatively low ferritin AND relatively low WBC may be a warning, although preliminary, of a trend to be avoided.

Unless otherwise specified by credible CR authorities like Fontana or very few others

[Dean Pomerleau]

It is rare that I have the opportunity to say this, but Saul is correct. Low WBC and low ferritin are pretty common for CR folks. Both of mine have been at or below the bottom of the reference range for the last 20 years.

--Dean

[mccoy]

7 hours ago, Dean Pomerleau said:

It is rare that I have the opportunity to say this, but Saul is correct. Low WBC and low ferritin are pretty common for CR folks. Both of mine have been at or below the bottom of the reference range for the last 20 years.

--Dean

Dean, I stand gladly corrected since I consider you among the very few others credible CR authorities, but do we have a more than anecdotal reference on this issue?

[Dean Pomerleau]

3 hours ago, mccoy said:

Dean, I stand gladly corrected since I consider you among the very few others credible CR authorities, but do we have a more than anecdotal reference on this issue?

See this Fontana paper [1] for low WBC on CR without compromised immune response. Studies [2] and [3] are suggestive about the benefits of keeping ferritin near the bottom of the reference range.

--Dean

 

--------------------------

[1] Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans.

Published: 07/13/16

Full paper

Abstract

Calorie restriction (CR) inhibits inflammation and slows aging in many animal species, but in rodents housed in pathogen-free facilities, CR impairs immunity against certain pathogens. However, little is known about the effects of long-term moderate CR on immune function in humans. In this multi-center, randomized clinical trial to determine CR's effect on inflammation and cell-mediated immunity, 218 healthy non-obese adults (20-50 y), were assigned 25% CR (n=143) or an ad-libitum (AL) diet (n=75), and outcomes tested at baseline, 12, and 24 months of CR. CR induced a 10.4% weight loss over the 2-y period. Relative to AL group, CR reduced circulating inflammatory markers, including total WBC and lymphocyte counts, ICAM-1 and leptin. Serum CRP and TNF-α concentrations were about 40% and 50% lower in CR group, respectively. CR had no effect on the delayed-type hypersensitivity skin response or antibody response to vaccines, nor did it cause difference in clinically significant infections. In conclusion, long-term moderate CR without malnutrition induces a significant and persistent inhibition of inflammation without impairing key in vivo indicators of cell-mediated immunity. Given the established role of these pro-inflammatory molecules in the pathogenesis of multiple chronic diseases, these CR-induced adaptations suggest a shift toward a healthy phenotype.

------------------

[2] Clin Chem. 2014 Nov;60(11):1419-28. doi: 10.1373/clinchem.2014.229013. Epub 2014 Aug 25.

Total and cause-specific mortality by moderately and markedly increased ferritin concentrations: general population study and metaanalysis

Christina Ellervik 1, Jacob Louis Marott 2, Anne Tybjærg-Hansen 3, Peter Schnohr 2, Børge G Nordestgaard 4
Affiliations expand
PMID: 25156997 DOI: 10.1373/clinchem.2014.229013
Full text linksCite
Abstract
Background: Previous population-based studies of plasma ferritin concentration have not revealed a relationship with total mortality. We tested the possible association of increased ferritin concentrations with increased risk of total and cause-specific mortality in the general population.

Methods: We examined total and cause-specific mortality according to baseline plasma ferritin concentrations in a Danish population-based study (the Copenhagen City Heart Study) of 8988 individuals, 6364 of whom died (median follow-up 23 years). We also included a metaanalysis of total mortality comprising population-based studies according to ferritin quartiles or tertiles.

Results: Multifactorially adjusted hazard ratios (HRs) for total mortality for individuals with ferritin ≥200 vs <200 μg/L were 1.1 (95% CI 1.1-1.2; P = 0.0008) overall, 1.1 (1.0-1.2; P = 0.02) in men, and 1.2 (1.0-1.3; P = 0.03) in women. Stepwise increasing concentrations of ferritin were associated with a stepwise increased risk of premature death overall (log rank, P = 2 × 10(-22)), with median survival of 55 years at ferritin concentrations ≥600 μg/L, 72 years at 400-599 μg/L, 76 years at 200-399 μg/L, and 79 years at ferritin <200 μg/L. The corresponding HR for total overall mortality for ferritin ≥600 vs <200 μg/L was 1.5 (1.2-1.8; P = 0.00008). Corresponding adjusted HRs for ferritin ≥600 vs <200 μg/L were 1.6 (1.1-2.3; P = 0.01) for cancer mortality, 2.9 (1.7-5.0; P = 0.0001) for endocrinological mortality, and 1.5 (1.1-2.0; P = 0.01) for cardiovascular mortality. The metaanalysis random effects odds ratio for total mortality for ferritin upper vs reference quartile or tertile was 1.0 (0.9-1.1; P = 0.3) (P heterogeneity = 0.5).

Conclusions: Moderately to markedly increased ferritin concentrations represent a biological biomarker predictive of early death in a dose-dependent linear manner in the general population.

--------------------

[3] Clin Chem. 2018 Feb;64(2):374-385. doi: 10.1373/clinchem.2017.276055. Epub 2017 Oct 16.

Increased Plasma Ferritin Concentration and Low-Grade Inflammation-A Mendelian Randomization Study

Ingrid W Moen 1, Helle K M Bergholdt 1 2, Thomas Mandrup-Poulsen 1 3, Børge G Nordestgaard 1 4 5 6, Christina Ellervik 7 2 8 9
Affiliations expand
PMID: 29038157 DOI: 10.1373/clinchem.2017.276055

Abstract
Background: It is unknown why increased plasma ferritin concentration predicts all-cause mortality. As low-grade inflammation and increased plasma ferritin concentration are associated with all-cause mortality, we hypothesized that increased plasma ferritin concentration is genetically associated with low-grade inflammation.

Methods: We investigated whether increased plasma ferritin concentration is associated with low-grade inflammation [i.e., increased concentrations of C-reactive protein (CRP) and complement component 3 (C3)] in 62537 individuals from the Danish general population. We also applied a Mendelian randomization approach, using the hemochromatosis genotype C282Y/C282Y as an instrument for increased plasma ferritin concentration, to assess causality.

Results: For a doubling in plasma ferritin concentration, the odds ratio (95% CI) for CRP ≥2 vs <2 mg/L was 1.12 (1.09-1.16), with a corresponding genetic estimate for C282Y/C282Y of 1.03 (1.01-1.06). For a doubling in plasma ferritin concentration, odds ratio (95% CI) for complement C3 >1.04 vs ≤1.04 g/L was 1.28 (1.21-1.35), and the corresponding genetic estimate for C282Y/C282Y was 1.06 (1.03-1.12). Mediation analyses showed that 74% (95% CI, 24-123) of the association of C282Y/C282Y with risk of increased CRP and 56% (17%-96%) of the association of C282Y/C282Y with risk of increased complement C3 were mediated through plasma ferritin concentration.

Conclusions: Increased plasma ferritin concentration as a marker of increased iron concentration is associated observationally and genetically with low-grade inflammation, possibly indicating a causal relationship from increased ferritin to inflammation. However, as HFE may also play an immunological role indicating pleiotropy and as incomplete penetrance of C282Y/C282Y indicates buffering mechanisms, these weaknesses in the study design could bias the genetic estimates.

[Todd Allen]

On 9/20/2022 at 7:26 AM, Dean Pomerleau said:

Low WBC and low ferritin are pretty common for CR folks.

One more anecdotal data point.  After about 2 years of CR my WBC and ferritin both dropped to the bottom of their reference ranges.  After shifting from a plant heavy diet to mostly red meat but still fairly low in calories my ferritin has rebounded to 201 ug/L but WBC is unchanged.  

 

[mccoy]

Thanks to Dean for the articles.

I've just read Fontana's. One point seems to be clear, that CR lowers the markers of inflammation, without impairing immune response (which remains the same as AL even if WBC is in the lower percentiles of the distribution of the general population).

About WBC, it is not clear which is the optimum range. All right, too high a count is associated with inflammation and metabolic diseases and cancer, but too low is probably associated with impaired immune response. Which is the optimum range for the AL group, and which is for the CR subgroup? Maybe the former (but not the latter) is explained in the cited articles.

I was initially nonplussed because I mistook WBC for RBC, which worried me not a little.

Edited September 22, 2022 by mccoy

[mccoy]

By the way, this topic prompted me to consult my latest analyses.

WBC is slightly below the optimum range, with 3.9 units*10^3/uL (optium 4-10 according to the lab). Please note that my regime is one of dietary, but not caloric restriction.

Ferritin is 64 ng/ml, which is in the relatively low percentiles but above the lower normality threshold (30-350 for men).

I'll express my consideration in ferritin after having read the other articles cited by Dean.

Edited September 22, 2022 by mccoy

[Dean Pomerleau]

1 minute ago, mccoy said:

WBC is slightly below the optimum range, with 3.9 units*10^3/uL (optium 4-10 according to the lab)

Ferritin is 64 ng/ml, which is in the relatively low percentiles but above the lower normality threshold (30-350 for men).

Sounds like you are in our club Mccoy! 

--Dean 

[mccoy]

21 minutes ago, Dean Pomerleau said:

Sounds like you are in our club Mccoy! 

--Dean 

MMmmmm..., right, maybe dietary restriction in this aspect is similar to caloric restriction...

[mccoy]

I'm reading the first article linked by Dean on ferritin hazard. 

The range chosen as a HR=1 is <200 ug/L, so there is a wide enough 'safe' range from the lower thresholds indicated by the lab. HR values start to be dangerous with values = >600 ug/L, which are values higher than the usual upper bound of the normal range, also apparently men are less sensitive to the hazard of high ferritin.

 

[mccoy]

Continuing the above considerations. There is a pretty huge difference in median survival between the <200 subgroup and the = > 600 subgroup (79 versus 55 years)

 

[mccoy]

Last, the dose-response plots, I drew a red line in correspondence of 50 ug/L of ferritin, which sounds a representative value for the CR subgroup. THe confidence interval of the linear regression in the CV mortality plot is pretty wide (high uncertainty of HR values). The plot all say loudly that the lower, the better, but plausibly zero ferritin may not be optimal.

Edited September 22, 2022 by mccoy

[IgorF]

Maybe I am too sceptical on the WBC topic but there are things that are not really answered from the different data posted on these forums. Or maybe I missed it, never be sured 100%.

My thoughts on lower WBC is based on the following (maybe I am wrong off course, just a common sense of a non-medical person):

- the major contributors to the WBC count are lymphocytes and neutrophiles

- while both are fluctuating thus changing the total count and both are reflecting only a part of their total numbers from these two groups neutrophiles count is more dynamic and "elastic"

- neutrophil count can be raised very fast by producing new cells on signs of acute requirement, lymphocytes will rather migrate from their "places of socialization" thus also could raise WBC numbers but to a less degree (my own test - neutrophiles jump from normally less than 2 to 5+ on the third hepatitis B vaccine shot in 2 days, they are newly born, not relocated from settlements in organs)

- a person on long term CR has depleted stores for spare energy and matter to build new things, thus it is expected that things like cell counts will be on the lower normal part of the range

- sometimes it could be required to take into account the way lab range is defined - there are let's say "absolutized" normal (like data assessed from a lot of studies and took as a hard value of normal - e.g. with lipids novadays) and a "localized" range - labs have to calibrate them on the data of local healthy volunteers to establish their ranges; perhaps WBC count is the second one, so it is completely normal to be slightly less then lower range when CR is practised long - just math for energy and matter will limit the count (as a share of total) and doing CR is extending a bit such normal range in other words

 

And now getting back to the things that are questionable.

First of all - the signs of compromized immune function. I do not recoll any reliable biomarkers that could be used in a "forward way". There are known signs of something is bad but assessments of immune function is usually a set of special analyses I never seen here reported or in the CR-related articles/books.

When I did some combo tests on immunity (because of curiosity) they reported a lot of very special things related to the topic and different labs are doing it in a different manner. I spend a lot of time trying to decypher at least some part of the reports but it is very, very complicated thing, without an experienced immunologist it seems I will not be able to understand the things to the degree I wish.

Because of these analyses I would not trust the proxy markers like the absense of elevation of CRP or ferritine and so on, the absense of inflammation does not confirm the absense of impairment of the immune function, just the absense of accute inflamation markers. In other words - they will not predict what will happen if there will be a need to answer fast on something.

 

And here comes my biggest concern. Since the first line (actually one of it, but very important) of defense against both external intrusion and over commensals are neutrophiles for CR people I would take into account neutrophiles count on blood tests. My own were 2+ ths/l w/o CR (but no overeating as well) and with mild CR they are observed to be mostly in 1.1-1.9 range in 1.6-6 diapason of normal.

Why I am curious about it? Because of the following easy to face scenarios:

- accute situation happened, there is a need to have enough neutrophiles already available (at 0.5 ths/l absolute value a person is doomed to have neutropenia), being too low at the beginning is risky

- accute situation is tackled but the rate of dying neutrophiles os lower than the rate of new forming - a few days "window" for adaptive immune response is not covered, neutrophiles depletion happens earlier == commensals (or controlled dormant enemy) could attack the body or a secondary infection could happen after a primary

- a special case - neutrophiles are forming but are not functional

 

So that is IMHO it makes sense to always look on details regarding WBC and be very careful with assumption that low count in CR comes without immune function impairment, serious challenge can be much more risky for a CR-person than for non-CR.

 

Br,

Igor

 

 

Edited April 3 by IgorF

[BabaGanush]

If we are indifferent to the choice of diet and only analyze your biomarkers, it seems that some are not youthful or associated with minimal all-cause mortality risk:

• Auto WBC: 3.7 10*9/L
• MCV: 94 fL
• RDW: 15.8 %
• HDL Cholesterol: 1.17 mmol/L is equivalent to 45.2 mg/dL.

 

Have you taken a DunedinPace test to check your current rate of aging?

Edited May 26 by BabaGanush

[IgorF]

Few more cents on ferritin.

In many typical longevity-related texts iron is described as highly wanted by bacterias and because of this we have it stored in sophisticated "cages" where it is not available for them. At least I saw it a lot of time and almost never oxidative risk associated with iron was mentioned in the same texts. No idea why and if it was just me so unlucky to face many of such texts.

So, the other thing about iron and IMHO it is what really happens behind the associations data in most of the studies (they are done on people at lower bacterial risks par excellence and controlled for bacterial emergencies for obvious reasons) is its immense ability to create serious oxidative damage by so called Fenton reaction (or Fenton chemistry, since it seems more than just a reaction). The topic is a subject of a big part of a wonderful book by Nick Lane about oxigen and how it created our life and how this mode (probably) sets a "hard limit" on longevity (I think it is one of the best book on longevity topic despite it is not focused on life extension or "curing aging").

Author argues that even caged iron is sometimes still can initiate the oxidation damage chains and being curious about this I tried to find if we do have some interesting data that could be interpreted that way. Here is an example:

https://pubmed.ncbi.nlm.nih.gov/10656286/
 

Quote

 

Abstract

We measured 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in human leukocytes from healthy donors to evaluate oxidative DNA damage and its correlation with smoking, physical exercise, and alcohol consumption. A significant increase in oxidative DNA damage was induced by cigarette smoke, with the mean level of 8-OHdG being significantly higher in smokers (33.1 +/- 10.6 per 10(6) 2-deoxyguanosine (dG) [mean +/- SE], n = 16) compared with nonsmokers (15.3 +/- 1.8 per 10(6) dG, n = 31) and former smokers (17.8 +/- 1.5 per 10(6) dG, n = 9). The highest values were observed after smoking more than 10 cigarettes per day (41.8 +/- 17.1 per 10(6) dG, n = 9). A large interindividual variation in 8-OHdG levels was observed in all analyzed groups. We also observed a correlation between 8-OHdG levels and age in nonsmokers and former smokers. Neither frequency of physical exercise nor alcohol drinking significantly modified 8-OHdG levels in leukocytes.

 

8-OHdG could be a part of the other processes but seems still a useful marker for oxidative damage to dna. The article is available via scihub. It is interesting from the perspective of immediate dose-response perspective to one of the most known oxidative stress generators. This is rather to get familiar with this test, it is relatively widely available, I never did it before but I will perhaps have it in my toolset.

 

And getting back to ferritin. Here is a pair of ferritin status and 8-OHdG

 

OXIDATIVE DNA DAMAGE (8-HYDROXYDEOXYGUANOSINE) AND BODY
IRON STATUS: A STUDY ON 2507 HEALTHY PEOPLE
MASARU NAKANO,* YOSHIKAZU KAWANISHI,* SEIKA KAMOHARA,* YOSHIKO UCHIDA,* MAMI SHIOTA,*
YUKA INATOMI,* TOYONORI KOMORI,* KATSUMI MIYAZAWA,* KAZUMI GONDO,† and IKUHIRO YAMASAWA*
*Medicine and Health Sciences Institute, Tokyo Medical University, Tokyo, Japan; and †Analysis Center for Medical Science SRL
Inc., Tokyo, Japan
(Received 20 March 2003; Revised 9 June 2003; Accepted 27 June 2003)

 

Quote

 

Abstract

To clarify the relationship of oxidative stress and body iron status, we detected urinary 8-hydroxydeoxyguanosine (8-OHdG) as a biomarker of oxidative DNA damage, and measured serum ferritin and total iron-binding capacity (TIBC), both reflecting body iron store, on 2507 healthy people aged between 22 and 89 years (males, 1253; females, 1254). The urinary 8-OHdG excretion of males showed almost no change with age, but the excretion of premenopausal females was lower than that of males, whereas postmenopausal females excreted significantly more than males. The values of serum ferritin showed no remarkable change with age in males, but increased gradually in postmenopausal females without iron loss due to bleeding, although the males' values remained higher than those of females at all ages (p<.05). On the other hand, the values of TIBC remained within the narrow limits in males, regardless of age, whereas those of females always stayed at a higher level than the males (p<.05). Conclusively, urinary 8-OHdG correlated with serum ferritin positively and with TIBC inversely, which suggested that body iron status would control the generation of 8-OHdG in vivo. After all, the increase of urinary 8-OHdG excretion in postmenopausal females may be caused by the decrease of body iron loss.

 

 

 

(via scihub)

Offcourse there are other studies but this one is nice the way it presents the data - it is easy to understand the TIBC, women menopause, CRP and ferritin treated as inflammation markers and well, the suspicion of iron to be one of the things we do want to have at minimum minimorum levels despite its core role in our ability to live at all.

 

Br,

Igor

 

Edited June 20 by IgorF