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Alright then. This sounds like another opportunity for citizen science!


Here is a CR MCV & MCH Survey to poll folks on their MCV & MCH levels.


Please take a minute to fill out the very brief poll so we can see how people's MCV & MCH levels compare with "normal".


P.S. I'm going to start a thread that contains a link to all the polls, and their results.



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While we are on the topic of apparently-aberrant blood results, it might be a good idea to note the following:


Sometimes it is not fully appreciated how all these blood numbers interrelate.


For example, to take my numbers:  I have rather high hemoglobin; 2% above the top hematocrit; exactly middle of the range RBC; 4% above the top MCV; 3% above the top MCH; and below the middle MCHC, respectively:


165 // 0.50 // 4.95 // 101 // 33 // 331.


It may seem confusing but it shouldn't be, because it isn't:


Taking my data:


Mean corpuscular hemoglobin is, of course, mean corpuscular volume multiplied by mean corpuscular hemoglobin concentration:


MCV x MCHC = MCH, in my case the data are:


101 (4% above the top) x 331 (appreciably BELOW the middle of the range) = 33 (which, with the decimal point shifted three places, is my number for MCH, above the top of the range only because of high MCV)


Then, total hemoglobin is mean corpuscular hemoglobin multiplied by number of red cells:


MCH x RBC = Total Hemoglobin, in my case:


33.431 (from the calculation above) x 4.95 (right in the middle of the range) = 165 (my number for total hemoglobin - towards the higher end, but again, only because my MCV is high.)


Next:  Hematocrit equals number of red cells in a litre multiplied by the average red cell volume:


RBC x MCV = hematocrit.  So, using my numbers:


4.95 x 101 = 0.500 (which is my number, after another decimal shift, which is 2% above the top end of the range, but once again, only because MCV is high.  My RBC is right smack in the middle.  Although it is possible modest dehydration may have been a small factor also?)


So, high MCV will cause other numbers to be high.  Superficially, it may appear that I have three numbers that are out of range (in my case all on the high side).  But in reality the only number that is truly out of range is the size of my red cells, because it is that only which causes the others to be high.






"The unverified conventional wisdom is almost invariably mistaken."

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Wow Rodney,


Thanks a bunch. I had no idea about the way these various tests of red blood parameters related to each other. Your explanation was very clear and helpful. My bloodwork seems to show I am same boat as you - my elevated MCV (mean red blood cell volume) combined with my middle-of-reference-range MCHC (mean red blood cell hemoglobin concentration) results in an elevated amount of hemoglobin per red blood cell (MCH). But despite the fact that each of my red blood cell has a lot of hemoglobin, I have relatively few red blood cells (my RBC is below the bottom end of the reference range), so the total amount of hemoglobin per unit volume in my blood is low. 


I wonder if the elevated size of the red blood cells (MCV) may be driven by the need for each red blood cell to carry more oxygen since I, and perhaps other CR practitioners, have relatively few of them (low RBC count), just like we have lower WBC count. And perhaps low RBC count is driven by the general tendency of CR to dial back on anabolic processes and/or dial up catabolic processes (like apoptosis of defective cells). In other words, maybe we don't make as many red blood cells in our bone marrow and/or we cull red blood cells that aren't functioning properly.


I'm surprised there hasn't been more study of the impact of CR on red blood cell parameters. Like Michael, I did quite a bit of Pubmed searching and was disappointed at how little research exists on the topic.




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Hi Dean:


Too much booze is also a cause of high MCV.  When my Toronto GP sheepishly (a little shy!) asked about my alcohol consumption I replied:  "Insufficent".  She asked for a more specific answer, so I said:  "Appreciably less than two glasses of wine a day."  That satisfied her it was not C2H5OH that explained my aberrant MCV.


I don't know about other people's data.  Might it be that your below-the-low-end RBC, compared with my middle of the range, might be because I am only moderately CRed while you are rather strictly CRed?  (A survey might find out!)  If so, then perhaps 'RBC-relative-to-reference-range' might be the definitive measure of degree of CRedness?






"The unverified conventional wisdom is almost invariably mistaken."

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CR & MCV / MCH Survey Results


A few days, and a few posts ago, I set up a survey to see if CR practitioners MCV and MCH levels are generally elevated, as a couple of us have observed. We only got 4 responses  :(xyz , three of them from long-term CR practitioners (> 10 years) and they were unanimous. All four report their MCV as above the high end of the reference range, and having gone up since starting CR. All four report MCH as above the reference range (3/4) or high-normal (1/4), and having gone up (3/4) or stayed the same (1/4) since starting CR. The full results are included below.


While the data is obviously very limited, it adds some credence to the theory at high MCV (i.e. big red blood cells) is a biomarker of CR. Its funny we haven't seen more scientific investigation of this, but perhaps that's what citizen science is for - to identify new and interesting hypotheses worthy of further, more controlled, study.


If anyone reading this hasn't taken the short survey, I encourage you to do so, in hopes of firming up this hypothesis.






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  • 3 weeks later...

Dean, you're becoming famous among my hematology team! I just had another appointment to review my recent blood work (the values I had done myself, posted earlier in this thread, and some new ones done last week, which show little change -- but they also tested testosterone, which is 15 nmol/L, a bit below the middle of the ref. range (too high for CR...); and haptoglobin, which is now completely normal.)


We looked at your results online, and it was very useful. (But they wondered: "Why didn't his doctor order a haptoglobin test? How else would they know whether it's hemolytic anemia?")


The puzzle about iron supplementation is that iron-deficiency anemia by itself wouldn't normally produce larger red blood cells. It should be the opposite. But I relayed your experience with iron supplementation and they said "Go for it, and see how you feel!"


So, I'm going for it. I grabbed the only reasonable option I saw on a health food store shelf: Solgar Gentle Iron.


Still a lot more experimentation to do, but this is a simple measure that might really help.


Do you recall how long it took after starting the iron for you to start feel a change?



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I'm glad you and your doctors have come around, and you've giving iron supplements a try. 



Do you recall how long it took after starting the iron for you to start feel a change?


From this post earlier in this thread, I wrote:


Subjectively, my symptoms of anemia (generalized fatigue, windedness after climbing stairs, pale gums) improved markedly after a couple weeks of intensive iron supplementation (e.g. Niferex-150 3x per day) post anemia diagnosis. Note that on 5/10/13, three weeks after the second anemia diagnosis and commencement of iron supplements, the footnote (#11) indicates that my anemia symptoms had improved considerably, but my hemoglobin and ferritin were still low.


So hopefully it won't be too long until you may see some improvement. Two things to note. First, several of my doctors over the years, including the hematologist I saw for my anemia, were quite explicit about recommending Niferex-150 to correct my anemia. Niferex-150 is a prescription, but Amazon sells equivalents, Second, at 3x per day, that was quite a large dose of iron I was taking, but it did the trick, and did it quickly.



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Dean, sorry -- you go to the trouble of putting a bunch of useful info online and I don't even make use of it (fully)! (Although I made use of a lot of it sitting with the hematologist and his med students.) Right, then, a couple weeks or so. But man, you were taking a lot of iron. The Solgar bottle says take one capsule/day (25 20 mg. iron (1), as bisglycinate chelate). That's obviously not very much. I'm still puzzled by why someone without microcytopenia (indeed, like me and many on CR, with the opposite) would benefit so much from iron. Iron is generally contraindicated with hemolytic anemia, but, as I understand it, this is because iron stores are generally not reduced in hemolytic anemia (1). For you and me, iron stores are low, but not freakishly low, so supplementing is worthwhile treatment shot in the dark. It obviously worked with you! But it's puzzling that a lot of your red blood cell-related test results don't change much as your symptoms are improving (though your iron status obviously changed!)




(1) 2015-12-20; 04:00 EST: I had copied the amount from Solgar's US website, but the version they sell in Europe has only 20 mg.

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25mg iron per day is not very much if you are trying to correct for anemia (or an anemia-like condition). I'm not convinced you'll see a marked improvement only taking that much.


I'm taking one of these per day, with 65mg iron, to keep my hemoglobin and ferritin from falling below the low end of the reference range - although I do donate blood every 3 months, so that may be keeping my iron on the low side.



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I've reviewed your data, and done more research, and realize the only potential harm from upping my dosage for a couple weeks is GI side-effects, so I'm going to start with three 25 mg capsules/day, then go up to four or possibly five -- but only for two weeks, then retest iron levels.



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Dean, I'll definitely keep everyone posted -- in part because I'll probably have more questions.


One question now, actually: did you have any GI problems with iron supplements? I've been reading about how common problems can be, but, so far, I've experienced nothing.


What I'm doing:


- Wake, have coffee. 1 hour later: 1 capsule 20 mg iron, as bisglycinate chelate (1).

- Mid- to late-afternoon: 2nd capsule

- Bedtime: 3rd capsule.


And as I said I'm going to increase that. I mean, you were taking a lot more iron than that, at least at the beginning! (Not sure how the different forms equate precisely, though -- Solgar claims its form is highly absorbable, and I'm trying to take them away from meals and coffee.) To match your initial dose -- if the respective claimed equiv. elemental iron amounts can be equated -- I'd have to take over 20 of the Solgar capsules.




(1) [A] I had written 25 mg but in Europe the Solgar variant sold and the one I'm using has 20 mg. Solgar claims the bisglycinate chelate isn't irritating to the gut, which is, as noted, consistent with my so far limited experience.

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No I've never had any gastrointestinal problems with iron. But I seem to have an iron stomach [...].


Pun perhaps intended!


I also have an iron stomach, but ... "paper" -- whatever the opposite of iron in this context would be -- intestines. I think I'll stick with the three pills for today and tomorrow, then ratchet up.


No black stools either (which I've read is a common side-effect, a benign one, apparently -- unless the stools are also tarry).



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Al Pater posted a study [1] showing that elevated (>= 95.8 fL) Mean Corpuscular Volume (MCV) is associated with about a 40-50% increase in overall cancer rate in men and women, and 3.5x (!!!) increase in liver cancer in men in a population of of 40+ year-old non-anemic Korean adults followed for an average of 8 years, after adjusting for age, BMI, diabetes, hypertension, smoking status, regular drinking, regular exercise, hemoglobin, hematocrit, RDW, GFR and HBsAg status.


Hopefully this is a one of those situations where a biomarker means something different in the general population than in CR practitioners. In the full text (via sci-hub.io) study authors' suggest the mechanistic explanation for their finding may be poor lifestyle leading to long-term oxidative stress resulting in deformed red blood cells and elevated MCV:


Oxidative stress is considered as a critical pathophysiological
mechanism in various diseases, including
cancer [8]. In this study, subjects in the highest quartile
MCV levels were more likely to be older, current smokers,
regular heavy drinkers and HBsAg [a marker of hepatitis
B infection] carriers who might have sustained oxidative stress.
Because red blood cell is
considered to be closely related with whole body antioxidant
capacity [9], the association between increased MCV
and increased total and cancer mortality in our study can
be explained by the long-term oxidative stress. Reduced
deformability of red blood cell due to oxidative stress
influences blood flow in microcirculation and impairs
oxygen supply to the tissue [10, 11]. The change of flow
behavior and oxygen supply might contribute to the association
between total deaths and higher MCV levels.
Poor nutrition and systemic inflammation is another possible explanation the authors suggest:
Second, nutritional imbalance and the systemic
inflammatory response might be another explanation for
the relationship between elevated MCV and all-cause and
cancer mortality. In this study, total cholesterol, albumin
levels and BMI, which reflect the nutritional status, and
the proportion of subjects with a better PNI score
decreased with increasing MCV quartiles. Underweight
subjects are more likely to suffer from occasional protein / energy
malnutrition and cytokine-mediated inflammation
[12]. Systemic inflammatory response produced by
repetitive simultaneous chronic exposure to smoking,
heavy drinking and viral infection is also correlated with
an increase in resting energy expenditure, loss of lean
body mass, and decreased performance and survival, particularly
in lean subjects [13]. PNI and NLR, which are the
markers of nutritional decline and inflammation, were
survival predictors in this population. 


So hopefully those of us CR folks who have high MCV don't need to worry, but given the alarming 3.5x increase in liver cancer rate in men with high MCV in this study, I think I'm going to continue to supplement with milk thistle just in case, based on its safety and apparent effectiveness for treatment / prevention of liver-related damage and cancer [2-5].





[1] Mean corpuscular volume levels and all-cause and liver cancer mortality.
Yoon HJ, Kim K, Nam YS, Yun JM, Park M.
Clin Chem Lab Med. 2015 Dec 2. pii: /j/cclm.ahead-of-print/cclm-2015-0786/cclm-2015-0786.xml. doi: 10.1515/cclm-2015-0786. [Epub ahead of print]
PMID: 26630695



An elevated mean corpuscular volume (MCV) is associated with aging, nutrition, alcohol abuse and more, and it is known as a survival predictor in chronically ill patients. The aim of this study was to investigate the association between MCV levels and mortality from all-causes, cancer and site-specific cancer in a non-anemic healthy population.


A total of 36,260 participants aged 40 years or older who underwent routine check-ups at Seoul National University Hospital Health Promotion Center between 1995 and 2008 were followed-up for mortality until December 31, 2008, retrospectively.


During an average follow-up of 8.0 years, 1107 deaths including 547 cancer deaths were observed. The adjusted hazard ratios (aHRs) of the subjects with the highest quartile of MCV =/>95.8 fL in men and MCV =/>94.2 fL in women for all-cause and cancer mortality were 1.44 [95% confidence interval (CI), 1.15-1.80] and 1.51 (95% CI, 1.10-2.07) for men and 1.55 (95% CI, 1.08-2.22) and 1.25 (95% CI, 0.74-2.11) for women, respectively, compared with those in the reference group (90.5 fL</=MC <93.0 fL in men and 89.2 fL</=MCV<91.6 fL in women). Elevated MCV level was related to an increased risk of liver cancer mortality in men (aHR, 3.55; 95% CI, 1.75-7.21).


This study suggests that the elevated MCV level in non-anemic cancer-free individuals was associated with increased all-cause mortality in both men and women, and with cancer mortality, in particular liver cancer mortality in men. Future prospective studies are required to consolidate our findings.



[2] Phytother Res. 2010 Oct;24(10):1423-32. doi: 10.1002/ptr.3207.

Milk thistle in liver diseases: past, present, future.

Abenavoli L(1), Capasso R, Milic N, Capasso F.

Author information:
(1)Department of Experimental and Clinical Medicine, University Magna Graecia,
Catanzaro, Italy. l.abenavoli@unicz.it

Silybum marianum or milk thistle (MT) is the most well-researched plant in the
treatment of liver disease. The active complex of MT is a lipophilic extract from
the seeds of the plant and is composed of three isomer flavonolignans (silybin,
silydianin, and silychristin) collectively known as silymarin. Silybin is a
component with the greatest degree of biological activity and makes up 50% to 70%
of silymarin. Silymarin is found in the entire plant but it is concentrated in
the fruit and seeds. Silymarin acts as an antioxidant by reducing free radical
production and lipid peroxidation, has antifibrotic activity and may act as a
toxin blockade agent by inhibiting binding of toxins to the hepatocyte cell
membrane receptors. In animals, silymarin reduces liver injury caused by
acetaminophen, carbon tetrachloride, radiation, iron overload, phenylhydrazine,
alcohol, cold ischaemia and Amanita phalloides. Silymarin has been used to treat
alcoholic liver disease, acute and chronic viral hepatitis and toxin-induced
liver diseases.

Copyright © 2010 John Wiley & Sons, Ltd.

PMID: 20564545



[3] Altern Med Rev. 2005 Sep;10(3):193-203.

A review of the bioavailability and clinical efficacy of milk thistle phytosome:
a silybin-phosphatidylcholine complex (Siliphos).

Kidd P(1), Head K.

Author information:
(1)University of California, Berkeley, USA. dockidd@dockidd.com

Certain of the water-soluble flavonoid molecules can be converted into
lipid-compatible molecular complexes, aptly called phytosomes. Phytosomes are
better able to transition from a hydrophilic environment into the lipid-friendly
environment of the outer cell membrane, and from there into the cell, finally
reaching the blood. The fruit of the milk thistle plant (Silybum marianum, Family
Asteraceae) contains flavonoids that are proven liver protectants. The
standardized extract known as silymarin contains three flavonoids of the flavonol
subclass. Silybin predominates, followed by silydianin and silychristin. Although
silybin is the most potent of the flavonoids in milk thistle, similar to other
flavonoids it is not well-absorbed. Silybin-phosphatidylcholine complexed as a
phytosome provides significant liver protection and enhanced bioavailability over
conventional silymarin.

PMID: 16164374



[4] Am J Gastroenterol. 1998 Feb;93(2):139-43.

Milk thistle (Silybum marianum) for the therapy of liver disease.

Flora K(1), Hahn M, Rosen H, Benner K.

Author information:
(1)Division of Gastroenterology, Oregon Health Sciences University, Portland
97201-3098, USA.

Comment in
Am J Gastroenterol. 1999 Feb;94(2):545-6.

Silymarin, derived from the milk thistle plant, Silybum marianum, has been used
for centuries as a natural remedy for diseases of the liver and biliary tract. As
interest in alternative therapy has emerged in the United States,
gastroenterologists have encountered increasing numbers of patients taking
silymarin with little understanding of its purported properties. Silymarin and
its active constituent, silybin, have been reported to work as antioxidants
scavenging free radicals and inhibiting lipid peroxidation. Studies also suggest
that they protect against genomic injury, increase hepatocyte protein synthesis,
decrease the activity of tumor promoters, stabilize mast cells, chelate iron, and
slow calcium metabolism. In this article we review silymarin's history,
pharmacology, and properties, and the clinical trials pertaining to patients with
acute and chronic liver disease.

PMID: 9468229



[5] Integr Cancer Ther. 2007 Jun;6(2):146-57.

Review of clinical trials evaluating safety and efficacy of milk thistle (Silybum
marianum [L.] Gaertn.).

Tamayo C(1), Diamond S.

Author information:
(1)Research and Development at Flora Inc, Bethesda, MD 20817, USA.

Milk thistle extracts have been used as traditional herbal remedies for almost
2000 years. The extracts are still widely used to protect the liver against
toxins and to control chronic liver diseases. Recent experimental and clinical
studies suggest that milk thistle extracts also have anticancer, antidiabetic,
and cardioprotective effects. This article reviews clinical trials of milk
thistle conducted in the past 5 years including pharmacokinetic and toxicity
studies, herb-drug interactions, and other safety issues. Several trials have
studied the effects of milk thistle for patients with liver diseases, cancer,
hepatitis C, HIV, diabetes, and hypercholesterolemia. Promising results have been
reported in the protective effect of milk thistle in certain types of cancer, and
ongoing trials will provide more evidence about this effect. In addition, new
established doses and improvement on the quality and standardization of this herb
will provide the much-awaited evidence about the efficacy of milk thistle in the
treatment of liver diseases. Milk thistle extracts are known to be safe and well
tolerated, and toxic or adverse effects observed in the reviewed clinical trials
seem to be minimal. The future of milk thistle research is promising, and
high-quality randomized clinical trials on milk thistle versus placebo may be
needed to further demonstrate the safety and efficacy of this herb.

PMID: 17548793

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Thanks, Dean, and thanks to Al! Interesting, but I think the hope you note here --


Hopefully this is a one of those situations where a biomarker means something different in the general population than in CR practitioners.


-- is almost certainly entirely reasonable. We are different creatures.


(Comments on your latest bloodwork coming after my next hematol. appt., where I'm going to ask about them!)




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Comments on your latest bloodwork coming after my next hematol. appt., where I'm going to ask about them!


That would be great. I look forward to hearing what your team has to say about both my numbers and yours, now that you've been supplementing with iron for a little while. Any subjective progress to report on your anemia symptoms?


FYI, I just got a followup call from my GP, who looked at my bloodwork and is concerned with what appears to him to be macrocytic anemia, as a result of my low iron, ferritin, WBC, RBC and elevated MCV/MCH. He's recommending that I bump up my iron supplementation from 65mg/day to double that, 130mg/day, which seems excessive even to me, especially since I'm not suffering any symptoms of anemia, which I know all too well from my two previous bouts of anemia. He says it's safe (for me at least) to take in that much iron, but I'm reluctant.


So I'll be curious what your team (presumably much more knowledgeable than my GP) suggests for you, and for me!



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I had a phone consultation last week, and we decided to hold off on the iron, and go back on a fairly high dose of sulfasalazine, just to be certain that wasn't causing the problem (we didn't really test that hypothesis well in Oct.-Nov.). I'll be having blood drawn weekly for the next 4-6 weeks, THEN I'll go back on iron.


I still have an appt. next week though, and I'll be asking some general questions about CR, you, and pancytopenia. One thing I brought up again in the phone call was the importance of testing haptoglobin (and while you're at it lactate dehydrogenase). My doctor says that's the only way to know whether the red blood cells are being destroyed (instead of not being manufactured quickly enough).


Looking at various hematology-related CR papers on PubMed, I see surprisingly little on the mechanism of red blood cell changes via CR. The dissertation Michael found was helpful, but that seems to be about it on the subject.



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I had a phone consultation last week, and we decided to hold off on the iron, and go back on a fairly high dose of sulfasalazine, just to be certain that wasn't causing the problem (we didn't really test that hypothesis well in Oct.-Nov.). I'll be having blood drawn weekly for the next 4-6 weeks, THEN I'll go back on iron.


That sounds to me like a rather bizarre and likely futile strategy for getting to the bottom of your problem. In this post from mid-november, you report finally being off sulfasalazine. If you're still feeling crappy with subjective and objective signs of anemia after being off sulfasalazine for a month and a half, doesn't that strongly suggest it is not the cause of your troubles?


One thing I brought up again in the phone call was the importance of testing haptoglobin (and while you're at it lactate dehydrogenase). My doctor says that's the only way to know whether the red blood cells are being destroyed (instead of not being manufactured quickly enough).


That is a good idea - I've contacted my GP to see if he agrees and will prescribe those tests (along with Reticulocyte Count).


I see surprisingly little on the mechanism of red blood cell changes via CR.


Agreed. I swear I posted sometime in the past about evidence of slower turnover of red and/or white blood cells as a result of CR. But for the life of me I can't find the post. I suspect it was to the old email list, which remain unavailable  :(xyz .



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Dean, no, see my previously posted blood values: the anemia was objectively gone (though borderline), and subjectively there was some improvement, but still not nearly enough! (1) The whole thing is complicated by the fact that I have to sort of "game the system" a bit: play along with my doctors' sleuthing, even though I'm actually pretty convinced the cause of my pancytopenia (to a degree beyond that caused, predictably and non-pathologically, by CR), is more likely one of the following, in (sharply, after the heavy metal poisoning) increasing order of likeliness, than sulfasalazine:


- heavy metal poisoning

- autoimmunity

- (mild) chronic post-infectious fatigue and immune dysfunction syndrome (≈ CFS, CFIDS,ME)

- mild, chronic, viral infection (possibly a redescription of the above)



I swear I posted sometime in the past about evidence of slower turnover of red and/or white blood cells as a result of CR. But for the life of me I can't find the post. I suspect it was to the old email list, which remain unavailable   :(xyz .


The haptoglobin and reticulocyte counts will nail that phenomenon pretty unambiguously. My haptoglobin went from barely measurable to normal towards the end of November. But something very weird: for a long time I had low haptoglobin AND low retic. count. That was worrying because it seemed like I was in aplastic crisis. But normal haptoglobin and low retic. count along with mild anemia might just be a healthy CR state: low production of red blood cells ('cause we don't need a lot of 'em!).



The key research question -- which maybe Luigi or someone knows the answer to?? -- is whether borderline anemia in CR is a result of increased destruction of red blood cells, or decreased production of them.





(1) The good values were confirmed on 2015-12-15, but then had worsened appreciably six days later!

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The questions about what CR does re anemia in a species that was shown to benefit from CR in increased lifespan, seem to be addressed in the below papers.


Influence of lifetime food restriction on physiological variables in Labrador retriever dogs.
Lawler DF, Ballam JM, Meadows R, Larson BT, Li Q, Stowe HD, Kealy RD.
Exp Gerontol. 2007 Mar;42(3):204-14. Epub 2006 Nov 14.
PMID: 17107768
Effects of lifetime food restriction on erythrocytes and numerous clinical chemistry, thyroid, parathyroid, and acid-base variables are reported from a paired-feeding study of 25% diet restriction in dogs. The 48 dogs were paired by gender and weaning weight within litter, and 1 dog in each pair was fed 25% less than its pair mate, from age 8 weeks until death. Erythrocyte and serum biochemistry profiles were evaluated by annual sampling intervals and longitudinally. Erythrocyte variables were slightly higher among control-fed dogs, a possible reflection of the need to support both higher body fat mass and lean mass that uses energy less efficiently. Among serum biochemistry variables, glucose and triglyceride were lower among diet-restricted dogs, while creatinine was slightly higher in the absence of renal disease or failure, over the life spans of the dogs. Glucose outcomes reflect improved glucose tolerance that has been demonstrated with diet restriction protocols in several species, while triglyceride data may reflect the difference in total body fat cells between feeding groups. Creatinine outcomes may reflect lean mass responses to diet restriction or more efficient function of the intracellular proteasome. Serum triiodothyronine levels were lower among diet-restricted dogs. Other clinical chemistry and thyroid variables, parathyroid variables, and acid-base variables were not strongly influenced by diet restriction but revealed age-related effects.
Influence of lifetime food restriction on causes, time, and predictors of death in dogs.
Lawler DF, Evans RH, Larson BT, Spitznagel EL, Ellersieck MR, Kealy RD.
J Am Vet Med Assoc. 2005 Jan 15;226(2):225-31.
PMID: 15706972
To describe effects of lifetime food restriction on causes of death and the association between body-mass characteristics and time of death in dogs.
Paired-feeding study.
48 dogs from 7 litters.
Dogs were paired, and 1 dog in each pair was fed 25% less food than its pair mate from 8 weeks of age until death. Numerous morphometric and physiologic measures were obtained at various intervals throughout life. Associations of feeding group to time and causes of death were evaluated, along with important associated factors such as body composition components and insulin-glucose responses.
Median life span was significantly longer for the group that was fed 25% less food, whereas causes of death were generally similar between the 2 feeding groups. High body-fat mass and declining lean mass significantly predicted death 1 year prior to death, and lean body composition was associated with metabolic responses that appeared to be integrally involved in health and longevity.
Results were similar to results of diet restriction studies in rodents and primates, reflecting delayed death from species- and strain-specific intrinsic causes. Clinicians should be aware that unplanned body mass changes during mid- and later life of dogs may indicate the need for thorough clinical evaluation.
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  • 4 weeks later...



Over on this thread, you told newcomer Drew that you've had to back off CR as a result of low leukocytes (i.e. low White Blood Cell (WBC) count):


Yet I couldn't push it further because other biomarkers were getting too low (leukocytes) -- what we call "discordant biomarkers".


As best as I can tell from the long stream of posts in this thread, you're worried about a WBC count of 2.1 (RR 3.5 - 8.8), (or more recently, 2.7) saying in this post:


Has anyone on CR ever had white blood cell counts as low as mine (see below)?


The answer is yes, that value is not all that low for a CRer. My latest WBC (see here for data) last month was 2.2 (RR 4.0 - 10.5). And several other people (e.g. Rodney) have chimed in that theirs is 2.3. I know Al Pater's have been down in this neighborhood (or lower) as well. So you're not that unusual in this regard. 


Moreover, in that same post to Drew you note that for testosterone (T):


I think low T via CR shouldn't be regarded as a health problem; if anything, it's more likely the opposite.


You express a similar sentiment even more explicitly here.


So why the double standard? In other words, for testosterone (where there is some evidence that low values may be detrimental regardless of the cause, which I'm about to post on - stay tuned) you give a low value a pass (suggesting instead that it's probably beneficial to have low T if it's a result of CR), but as for low WBC count as a result of CR, you express concern and report having to back off CR in an (only partially successful) attempt to bring it up.


So I'm wondering - are you questioning the idea that low WBC via CR is harmless, or are you concerned that you personally have a low WBC for other (potentially frightening) reasons, which CR is exacerbating?


If it's the former, do you have evidence that CR-induced low WBC count is likely to be harmful, given the reduced rate of colds and flus reported by CR folks (especially long-term practitioners) in our recent survey on the topic, despite reporting low WBC counts? Also, if it is the former, you should consider the recent Fontana paper (PMID: 25500208), on improved immune response in anorexics despite low WBC count, discussed here.


If it's the latter, why potentially scare off Drew and other CR newbies by not qualifying your concern about low WBC count for CRers with your special personal circumstances?


Just wondering...


Also, it has been 3 weeks since you said you were going to visit your doctor to talk about your unusual bloodwork (and about mine!). Any update to report on that visit, or the weekly blood tests you mentioned you were going to be conducting?



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Dean, a simple misunderstanding. I wrote:



Yet I couldn't push it further because other biomarkers were getting [my emphasis] too low (leukocytes) -- what we call "discordant biomarkers". 

I doubt 2.5 or even 2.2 is too low for most people in the absence of symptoms, but my concern was partly what would happen if my levels dropped even lower.
About my tests and my hematologist: the tests are continuing (I can't see the results until I see the doc, though -- arg!), but my hematologist has been ill (possibly with something serious, though I hope not). He's out until early March. Sigh.... But I sent him links to a few of Luigi's papers, and he's got the link to your data, and I will certainly ask him about it when I see him, which, I'm told, will be no later than March 9.
And about testosterone: Just when I was starting to think my low T (actually it's not so low now because I've gained weight as part of my pancytopenia experiment) was not a worry, you're going to pop my bubble!! :)
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Thanks Zeta. I understand, although I'm skeptical about your concern regarding going too low in the WBC department via CR.


Sorry to hear about your doctor's illness. Hopefully it is not serious. Let us know when you get a chance to see him.


And about testosterone: Just when I was starting to think my low T (actually it's not so low now because I've gained weight as part of my pancytopenia experiment) was not a worry, you're going to pop my bubble!! :)


Yes - sorry to be the bearer of potentially bad tidings. For anyone reading this in the future, here is the post about the potentially troubling new study I was referring to, on the newly renamed thread "Low Testosterone via CR - Good or Bad?". 



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