Tracking Deep Sleep-Can It Be Improved?

Deep sleep, the stage of sleep also known as “slow wave sleep” declines during aging. Based on a meta-analysis of 65 studies representing 3,577 subjects (aged 5 years to 102 years; Ohayon et al. 2004), slow wave sleep, expressed as a percentage of total sleep time decreases during aging from 25% in childhood to less than 10% in adults older than 65 years:Screen Shot 2019-02-16 at 5.14.10 PM.png Continue reading “Tracking Deep Sleep-Can It Be Improved?”

100 Days Of Dietary Data

I’ve posted individual dietary days as an example of what and how much I eat ( However, a few days of examples may not represent the whole dietary picture. To address this, below is my average nutrient intake for the past 100 days (from October 24, 2018-Feb 5 2019):

100 days of nutrition.png

Notice that my average values for many of these variables (i.e. potassium, selenium, Vitamin C, Vitamin K, etc.) are way above the RDA. For more info on that, I have several blog posts that explain the “why” behind that. Where am I getting those nutrients from? Shown below are 100-day averages for my food intake, ranked in order from most consumed (in grams, or ounces, if it’s a drink) to least:

100 days of foods.png

During the past 100 days, my top 5 foods in terms of daily intake include carrots, strawberries, red peppers, watermelon, and cauliflower. Scroll through the list to see how much I average on a daily basis for each food!


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Resting heart rate: What’s optimal?

One of the goals of my exercise program is to reduce my resting heart rate (RHR). A stronger heart beats less times per minute, but pumps more blood per beat. In contrast, a weaker heart beats more times per minute, but less blood per beat.

Is there an optimal level for RHR? Based on a meta-analysis of 59 studies that included 1,810,695 subjects, RHR values < 50 beats per minute (bpm) are associated with maximally reduced risk of death from all causes. Conversely, RHR values > 50 bpm are associated with a higher mortality risk (Aune et al. 2017):

Screen Shot 2019-02-02 at 10.48.29 AM

What’s my resting heart rate? Shown below is that data, tracked by WHOOP since August. Note that my RHR wasn’t significantly different from August until October, ranging from 51-53 bpm (average, 51.7). However, because I was tracking my RHR, I noticed that I was overtraining, leading to very high HRs, lower heart rate variability, and less deep sleep (topics for another post!) the day(s) after exercise. So early in November, I changed my exercise routine. As a result, from November until the end of January, my average RHR (49.7 bpm) has been significantly less (p-value =1E-10), and based on January’s average RHR, I’m trending closer to 47 bpm! Also note that * = significantly different when compared with August.


What did I change in my exercise program? Since I’ve been in Boston (~9 years), I’ve walked 15-20 miles per week: it’s 1.1 miles to and from work, plus at least an hour of walking on Saturdays and Sundays. That’s a constant that hasn’t changed. In contrast, I split my 3-day weight training routine, which totaled ~5-6 hours/week into 3-5 days at less than an hour each session, and at a lower intensity with more reps. My strength is still as good as it was before, and as a result, my recovery HRs aren’t as high, thereby leading to a lower average RHR over time,. I’ve been training like that consistently for the past 30 years, but it took wearing a fitness tracker to change it!



Aune D, Sen A, ó’Hartaigh B, Janszky I, Romundstad PR, Tonstad S, Vatten LJ. Resting heart rate and the risk of cardiovascular diseasetotal cancer, and all-cause mortality – A systematic review and dose-response meta-analysis of prospective studiesNutr Metab Cardiovasc Dis. 2017 Jun;27(6):504-517.


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Dietary Cholesterol Vs. Plasma Cholesterol: My n=1 Data

With use of a food scale,  I’ve been tracking my daily macro- and micronutrient intake every day since April 2015. In addition, I have 15 blood test measurements during that period, and accordingly, I’m able to examine correlations between my dietary intake with my circulating biomarkers. In this post, I’ll address the question, is my dietary cholesterol intake significantly correlated with plasma levels of cholesterol?

1. Plasma levels of total cholesterol vs. dietary cholesterol:


In the plot we see a borderline significant (p = 0.06), moderate correlation (r = 0.5) between my plasma total cholesterol with my dietary cholesterol intake. However, note that total cholesterol is comprised of “good” and “bad” parts, with HDL as the “good”, and with non-HDL cholesterol, including LDL and VLDL, as the “bad”. What does that data look like?

2. Plasma levels of non-HDL (LDL+VLDL) cholesterol vs. dietary cholesterol:


In the plot we see a highly significant (p = 0.006), strong correlation (= 0.67) between my non-HDL cholesterol levels with my dietary cholesterol intake. It’s not possible to show causation via correlation, but this data suggests that my dietary cholesterol intake may be driving increased levels of non-HDL cholesterol.

3. Plasma levels of HDL cholesterol vs. dietary cholesterol:


In the plot, first note that in contrast with the positive correlations between total and non-HDL cholesterol with my dietary cholesterol intake, the correlation between HDL with my dietary cholesterol intake is negative (i.e., going in the opposite direction; r = 0.51), and borderline significant (p = 0.054).

Cumulatively, it looks like my dietary cholesterol intake may be related to increased “bad” cholesterol and decreased “good” cholesterol. As a limitation of this approach, although I’ve shown blood test data for 15 measurements (which is a decent sample size), I only have 4 measurements with an average daily cholesterol intake around 200 mg or greater. In the near future, I expect to average 200 mg of daily cholesterol (or more) per day, so let’s see if these correlations hold up!


If you’re interested, please have a look at my book!


Serum Albumin Decreases During Aging: Can Diet Help?

Levels of serum albumin peak at about 20 years old (~4.6 g/dL for males, ~4.4 g/dL for females), then decrease during aging, as shown for the 1,079,193 adults of Weaving et al. (2016):

Screen Shot 2018-07-04 at 1.19.29 PM.png

Similar age-related decreases for serum albumin albumin have also been reported in smaller studies: Gom et al. 2007 (62,854 subjects); Dong et al. 2010 (2,364 subjects); Le Couteur et al. 2010 (1,673 subjects); Dong et al. 2012 (1,489 subjects).

Why is it important that serum levels of albumin decrease during aging? Reduced levels of albumin are associated with an increased risk of death from all causes. For example, in the 1,704,566 adults of Fulks et al. 2010, serum albumin levels > 4.4 g/dL and 4.5 g/dL for females and males, respectively, were associated with maximally reduced risk of death from all causes, regardless of age (younger than 50y, 50-69y, or 70y+):

albumin mort.png

The association between reduced levels of serum albumin with an increased risk of death from all causes have also been found in smaller studies. In a ~9 year study of 7,735 men (age range, 40-59y), when serum albumin was less than 4 g/dL, the mortality rate was 23/1000/per year, compared with 4/1000/per year for subjects with values greater than 4.8 g/dL (Phillips et al. 1989):

albumin 3 mort

Similarly, in older adults (average age, ~80y, 672 subjects), serum albumin levels  greater than 4.5 g/dL (equivalent to 45 g/L) were associated with significantly reduced all-cause mortality risk, when compared with compared with < 4.1 g/dL (equivalent to 41 g/L, Takata et al. 2010):

albumin 2 mort

Decreased levels of serum albumin (less than 4 g/dL) being associated with an increased all-cause mortality risk was also identified in a 12-year study of 287 older adults (average age, ~75y, Sahyoun et al. 1996).

Can the age-related decrease in serum albumin be minimized, or prevented? Shown below is my data for serum albumin since 2005, when I was 32y:


First, note the period from when I was 32y until 40y. No age-related decrease! My average albumin value over 7 measurements was 4.74 g/dL. Unfortunately, I didn’t track my dietary info during that time.

Also note the period from 43y to 45y. First, my albumin levels are significantly higher than the first period, 4.92 g/dL (p=0.027)! Second, again note the absence of an age-related decrease. Based on the data of Weaving et al. (2016), my albumin levels should be around 4.4 g/dL, but I’ve got them going in the opposite direction! How have I been able to do that?

Since April 2015, with use of a food scale, I’ve been tracking my daily dietary intake, including macro and micronutrients (54 variables). For each orange data point in the second period, I have an average dietary intake for each of the 54 variables that I can use to correlate with serum albumin. Based on that data, I can make an educated guess at what could potentially increase, or decrease it.

Of the 54 dietary variables that I track, only 3 were significantly correlated with albumin: positive associations for alpha-carotene (r = 0.66, p = 0.027), beta-carotene (r = 0.75, p =0.007), and a negative association for Vitamin K (r = -0.64, p = 0.03). Shown below is the strongest correlation of the three, beta-carotene, vs. serum albumin.

bcarot alb.png

The majority of my alpha and beta-carotene intake comes from carrots, with a smaller amount coming from butternut squash. Interestingly, beta-cryptoxanthin, a Vitamin A metabolite that is abundant in butternut squash, was not significantly associated with serum albumin. Butternut squash is also a good source of alpha- and beta-carotene, so if  butternut squash was driving the correlation between the carotenes with albumin, I’d expect beta-crypoxanthin to also be significantly associated with it. However, since it’s not, carrots are the most likely source driving the association. Also note that the my average intake of Vitamin K is dramatically higher (1410 mcg; range, 1080-2203 mcg) than the RDA or AI, which are ~100-120 mcg/day. The negative association between my Vitamin K intake with albumin suggests that I should keep it closer to 1100 mcg/day to potentially keep my albumin levels high.


If you’re interested, please have a look at my book!



Dong MH, Bettencourt R, Barrett-Connor E, Loomba R. Alanine aminotransferase decreases with age: the Rancho Bernardo Study. PLoS One. 2010 Dec 8;5(12):e14254.

Dong MH, Bettencourt R, Brenner DA, Barrett-Connor E, Loomba R. Serum levels of alanine aminotransferase decrease with age in longitudinal analysis. Clin Gastroenterol Hepatol. 2012 Mar;10(3):285-90.e1.

Gom I, Fukushima H, Shiraki M, Miwa Y, Ando T, Takai K, Moriwaki H. Relationship between serum albumin level and aging in community-dwelling self-supported elderly population. J Nutr Sci Vitaminol (Tokyo). 2007 Feb;53(1):37-42.

Dong MH, Bettencourt R, Barrett-Connor E, Loomba R. Alanine aminotransferase decreases with age: the Rancho Bernardo Study. PLoS One. 2010 Dec 8;5(12):e14254.

Fulks M, Stout RL, Dolan VF. Albumin and all-cause mortality risk in insurance applicants. J Insur Med. 2010;42(1):11-7.

Le Couteur DG, Blyth FM, Creasey HM, Handelsman DJ, Naganathan V, Sambrook PN, Seibel MJ, Waite LM, Cumming RG. The association of alanine transaminase with aging, frailty, and mortality. J Gerontol A Biol Sci Med Sci. 2010 Jul;65(7):712-7.

Phillips A, Shaper AG, Whincup PH. Association between serum albumin and mortality from cardiovascular disease, cancer, and other causes. Lancet. 1989 Dec 16;2(8677):1434-6.

Sahyoun NR, Jacques PF, Dallal G, Russell RM. Use of albumin as a predictor of mortality in community dwelling and institutionalized elderly populationsJ Clin Epidemiol. 1996 Sep;49(9):981-8.

Takata Y, Ansai T, Soh I, Awano S, Sonoki K, Akifusa S, Kagiyama S, Hamasaki T, Torisu T, Yoshida A, Nakamichi I, Takehara T. Serum albumin levels as an independent predictor of 4-year mortality in a community-dwelling 80-year-old population. Aging Clin Exp Res. 2010 Feb;22(1):31-5.

Weaving G, Batstone GF, Jones RG. Age and sex variation in serum albumin concentration: an observational study. Ann Clin Biochem. 2016 Jan;53(Pt 1):106-11.

Reducing Homocysteine? Updates.

In an earlier post I wrote about the association between elevated circulating levels of homocysteine with an increased risk of death from all causes ( I started to post updates in that link, but I’ve decided to move them to here.

As of 6/2018, I now have tracked dietary data (I weigh all my food and record the values in that corresponds to 7 homocysteine measurements:

12/5/2017: Despite 42 days of 800 micrograms of supplemental folic acid, bringing my average daily folate intake to 2026 micrograms/day, my plasma homocysteine was essentially unchanged at 11.7 uMoL, when compared with my baseline value of 11.8 uMol.What’s next on the list to reduce it? Trimethylglycine, also known as betaine. I’m a proponent of using diet as a first strategy,  and to increase my dietary betaine levels, I’ll eat beets and quinoa, bringing my daily betaine levels to ~500 mg/day. Let’s see how it turns out on my next blood test!

1/2/2018: ~500 mg/day of betaine from beets and quinoa did absolutely nothing to my homecysteine levels. In fact, it got worse (15.3 uMoL)! To test the hypothesis that it wasn’t enough betaine, next I tried 4 grams/day of betaine (also known as trimethylglycine, TMG).

2/20/18: Supplemental TMG did absolutely nothing in terms of reducing my homocysteine to values below baseline! Also note that there is evidence that TMG increases blood lipids, including LDL and triglycerides (TG; Olthof et al. 2005), and that’s exactly what it did to me. My average LDL and TG values since 2015 (11 measurements) are 77 and 50 mg/dL, respectively. On TMG, these values increased to 92 and 72 mg/dL, respectively, making them my highest values over 11 individual blood tests (with the exception of 1 day with an LDL of 93 mg/dL). Next, I tried a stack that included 50 mg of B6, 1000 mcg of B12, and 400 mcg of methylfolate, as supplementation with these B-vitamins has been shown to lower homocystine (Lewerin et al. 2003).

3/20/18: Finally, some progress! My homocysteine levels were reduced during the B-vitamin supplementation period. I’ve written it like that because I’m not sure if it was the B-vitamins that caused it. For example, in the image below, we see the correlation between my dietary B6 intake with homocysteine. The trendline is down, which I would expect if B6 supplementation actually is playing a role in reducing my homocysteine levels. However, note that the correlation between my dietary B6 levels with homocysteine is not very strong (= .48), resulting in a moderate R2 of 0.23 (similar data was obtained for B12 and folate). With 5 blood test measurements corresponding to 5 dietary periods, if B6 is playing a role, I would expect a stronger correlation. Nonetheless, with more data, the correlation may strengthen, so stay tuned for that!


5/14/2018: I changed B6-B12-methylfolate supplements so that I’d only have to take pills from 1 bottle instead of from 3. That supplement, however, had 1.5 mg of B6 instead of the 50 mg that was in my original supplement. Less B6 didn’t result in a higher homocysteine value-in fact, it went down (slightly), from 10.8 to 10.6. If an increased amount of B6 was causing lower levels of homocysteine, I would’ve expected higher, not (barely) lower homocysteine levels. This suggests that maybe my B6 intake has nothing to do with my homocysteine levels.

6/4/2018: Despite no changes to my supplements, my homocysteine came down a little more, to 10.2. Interestingly, the correlation (r) between homocysteine with my total dietary (diet + supplements) intake of B6, B12, and methylfolate is 0.39, 0.68, 0.29, respectively. The correlation between my B12 intake with homocysteine looks moderately strong, whereas the correlations for B6 and folate are weak. Based on this data, it’s possible I had a mild B12 deficiency that was causing elevated homocysteine. Note that my average B12 intake, without supplements is ~8 mcg/day, which is more than 3-fold higher than the RDA.

In looking at the association between my dietary data with homocysteine, a stronger correlation (r = 0.91; R2 = 0.83) has emerged…for my protein intake! In other words, a higher protein intake is more strongly correlated with lower homocysteine than B12:


7/11/2018: To explore the strong association between my protein intake with homocysteine, I increased my protein intake from an average value of 104 g/day for the period that preceded my June measurement (5/15/2018 – 6/4/2018) to 136 g/day for the period up to my 7/11/2018 measurement (6/5/2018 – 7/10/2018). The result? Lower homocysteine, to 8.2 uMol/L! Interestingly, the correlation between my dietary protein intake with homocysteine remained strong (r = 0.86, R2 = 0.73, n = 7 measurements).

What about my B6, methyl-B12, methyl-folate stack? I’m still taking it, although it looks like methyl-B12 may be the only factor that is associated with my homocysteine levels. In support of that, the correlation between each with homocysteine is = 0.02, 0.73, 0.36, respectively.

Because I now have my homocysteine < 9 umol/L, it may be time to optimize other variables (in addition to the metabolic panel and CBC). Stay tuned!


If you’re interested, please have a look at my book:



Lewerin C, Nilsson-Ehle H, Matousek M, Lindstedt G, Steen B. Reduction of plasma homocysteine and serum methylmalonate concentrations in apparently healthy elderly subjects after treatment with folic acid, vitamin B12 and vitamin B6: a randomised trial.vEur J Clin Nutr. 2003 Nov;57(11):1426-36.

Olthof MR, van Vliet T, Verhoef P, Zock PL, Katan MB. Effect of homocysteine-lowering nutrients on blood lipids: results from four randomised, placebo-controlled studies in healthy humans. PLoS Med. 2005 May;2(5):e135.

Homocysteine and All-Cause Mortality Risk

On a recent blood test, my plasma level of homocysteine (Hcy) was 11.9 uMol. Is that optimal minimizing disease risk and maximizing longevity? Let’s have a look at the literature.

A 2017 meta-analysis of 11 studies including 27,737 participants showed an increased risk of death from all causes (“all-cause mortality”; ACM) as circulating levels of homocysteine increase (Fan et al. 2017):

hcy acm.png

When looking at meta-analyses, it’s important to examine each of the individual studies. Here are the data for the 11 included studies:

  • Kark et al. 1999: 1,788 older adults, average age 65y, followed for 9-11 years. Compared with values less than 8.5 uMol, subjects with elevated homocysteine (> 14.7) had a 2-fold higher risk of death from all causes.
  • Bostom et al. 1999: 1,933older adults, verage age, 70y, median follow-up, 10y. Subjects with values > 14.3 uMol had 2-fold ACM risk, when compared with < 14.3.
  • Hoogeveen et al. 2000: 811 older adults (average age, 65y), 5 yr follow-up. Non- diabetics had a 34% increased ACM risk (p=0.08), but diabetics had 2.5-fold increased ACM risk after a 5-yr follow-up.
  • Vollset et al. 2001: 4,766 older adults (age range, 65-67y at study entry), median 4 yr follow-up. Compared with 5.1-8.9 uMol, values greater than 12 were significantly associated with a 2.4-4.5 increased ACM risk.
  • Acevedo et al. 2003. 3,427 subjects, average age 56y, ~3yr follow-up. ACM risk lowest for < 9.4 uMol, compared with > 14.4.
  • González et al. 2007: 215 older adults (average age, 75y), median 4 yr follow-up. Compared with < 8.7 uMol, values > 16.7 had 2.3-fold increased ACM risk.
  • Dangour et al. 2008: 853 older adults (average age, 79y), ~7.6y follow-up. Homocysteins > 19.4 uMol associated with ~2-fold higher ACM risk, when compared with < 9.8.
  • Xiu et al. 2012: 1,412 older adults (average age, ~75y), up to 10 year follow-up. 1.8-fold higher ACM risk comparing those with >14.5 uMol with < 9.3.
  • Waśkiewicz et al. 2012: 7,165 middle aged adults, ~5yr follow- up. 1.8-fold increased ACM risk for subjects with homocysteine > 10.5 uMol(average age, 52y) when compared with < 8.2 (avg age, 40y).
  • Wong et al. 2013: 4,248 older men, average age ~77y, ~5yr follow-up. 1.5-fold increased ACM risk for homocysteine values > 15 uMol.
  • Swart et al. 2012: 1,117 older adults (average age, 75y), up to a 7yr follow-up. In 543 men, homocysteine was not associated with ACM risk. In 574 women, 1.7 to 1.9-fold higher ACM risk when comparing  > 12.7 and >15.6 vs < 10.3 uMol.

Not included in their analysis:

  • Petersen et al. 2016: 670 subjects, average age 65y, average follow-up 14.5y. Subjects with homocysteine values ≥ 10.8 μmol/l  had a significant higher incidence of all-cause mortality:

hcy 2

In sum, the evidence appears consistent across these 12 studies that elevated homocysteine is associated with an increased risk of death from all causes. Based on the Fan et al. (2016) meta-analysis, lower appears better, with values < 5 uMol associated with maximally reduced ACM risk. Also based on that data, my ACM risk is ~1.5-fold increased!

To see how dietary changes and supplements have impacted my homocysteine levels, see this link:

If you’re interested, please have a look at my book:



Bostom AG, Silbershatz H, Rosenberg IH, Selhub J, D’Agostino RB, Wolf PA, Jacques PF, Wilson PW. Nonfasting plasma total homocysteine levels and all-cause and cardiovascular disease mortality in elderly Framingham men and women. Arch Intern Med. 1999 May 24;159(10):1077-80.

Dangour AD, Breeze E, Clarke R, Shetty PS, Uauy R, Fletcher AE. Plasma homocysteine, but not folate or vitamin B-12, predicts mortalityin older people in the United Kingdom. J Nutr. 2008 Jun;138(6):1121-8.

Fan R, Zhang A, Zhong F. Association between Homocysteine Levels and All-cause Mortality: A Dose-Response Meta-Analysis of Prospective Studies. Sci Rep. 2017 Jul 6;7(1):4769.

González S, Huerta JM, Fernández S, Patterson AM, Lasheras C. Homocysteine increases the risk of mortality in elderly individuals. Br J Nutr. 2007 Jun;97(6):1138-43.

Hoogeveen EK, Kostense PJ, Jakobs C, Dekker JM, Nijpels G, Heine RJ, Bouter LM, Stehouwer CD. Hyperhomocysteinemia increases risk of death, especially in type 2 diabetes : 5-year follow-up of the Hoorn Study. Circulation. 2000 Apr 4;101(13):1506-11.

Kark JD, Selhub J, Adler B, Gofin J, Abramson JH, Friedman G, Rosenberg IH. Nonfasting plasma total homocysteine level and mortality in middle-aged and elderly men and women in Jerusalem. Ann Intern Med. 1999 Sep 7;131(5):321-30.

Petersen JF, Larsen BS, Sabbah M, Nielsen OW, Kumarathurai P, Sajadieh A. Long-term prognostic significance of homocysteine in middle-aged and elderly. Biomarkers. 2016 Sep;21(6):490-6.

Swart KM, van Schoor NM, Blom HJ, Smulders YM, Lips P. Homocysteine and the risk of nursing home admission and mortality in older persons. Eur J Clin Nutr. 2012 Feb;66(2):188-95.

Waśkiewicz A, Sygnowska E, Broda G. Homocysteine concentration and the risk of death in the adult Polish population. Kardiol Pol. 2012;70(9):897-902.

Wong YY, Almeida OP, McCaul KA, Yeap BB, Hankey GJ, Flicker L. Homocysteine, frailty, and all-cause mortality in older men: the health in men study. J Gerontol A Biol Sci Med Sci. 2013 May;68(5):590-8.

Vollset SE, Refsum H, Tverdal A, Nygård O, Nordrehaug JE, Tell GS, Ueland PM. Plasma total homocysteine and cardiovascular and noncardiovascular mortality: the Hordaland Homocysteine Study. Am J Clin Nutr. 2001 Jul;74(1):130-6.


Platelets and All-Cause Mortality Risk

Have you had a blood test and aren’t sure what values for platelets may be optimal for health? The reference range is 150-400 platelets per nanoliter (*10^9/L). Within that range, what’s optimal?

In a study of 21,635 adults older than 35y (average age wasn’t reported) with a 7.6-year follow-up, platelets between 230-270 was associated with maximally reduced risk of death from all causes (Bonaccio et al. 2016):

platets acm

In a study of 21, 252 adults (average age 53y) with an average follow-up of 3.5y, values ~250 were associated with maximally reduced risk of death from all causes Vinholt et al. (2017) :

plat2 acm

What about in older adults? In a study of 159, 746 postmenopausal women (average age, 63y) with a 16-year follow up, maximally reduced risk of death from all causes was associated with platelet values between 200-256 (Kabat et al. 2017).

In a study of 36, 262 older adults (average age, 71y) with an 11-year follow-up, platelet values ~250 were associated with maximally reduced risk for all-cause mortality. Interestingly, even at platelet values ~250, mortality risk was highest for non-Hispanic whites, when compared with non-Hispanic blacks and Hispanics (Msaouel et al. 2014):

plat ethnicity

In 5,766 older adults (average age, 73y) that were followed for 12-15 years, values higher than 200-300 had an increased risk of death from all causes (van der Bom et al 2009). Risk for values between 100-199 was not different when compared against 200-299, but there was a non-significant trend towards increased risk (1.05, 95% CI: 0.97, 1.14).

In 131,308 older adults (~73y) with a 6-yr follow-up, maximally reduced risk of death from all causes was associated with values between 200-300, whereas risk significantly increased below and above that range, respectively Tsai et al. (2015):

plat eld

In sum, the data suggests that platelet values ~250 may be optimal for heath, with 200-300 as the “optimal range” within the 150-400 reference range. What are your values?


If you’re interested, please have a look at my book!



Bonaccio M, Di Castelnuovo A, Costanzo S, De Curtis A, Donati MB, Cerletti C, de Gaetano G, Iacoviello L; MOLI-SANI Investigators. Age-sex-specific ranges of platelet count and all-cause mortality: prospective findings from the MOLI-SANI study. Blood. 2016 Mar 24;127(12):1614-6.

Kabat GC, Kim MY, Verma AK, Manson JE, Lin J, Lessin L, Wassertheil-Smoller S, Rohan TE. Platelet count and total and cause-specific mortality in the Women’sHealth InitiativeAnn Epidemiol. 2017 Apr;27(4):274-280.

Msaouel P, Lam AP, Gundabolu K, Chrysofakis G, Yu Y, Mantzaris I, Friedman E, Verma A. Abnormal platelet count is an independent predictor of mortality in the elderly and is influenced by ethnicityHaematologica. 2014 May;99(5):930-6.

Tsai MT, Chen YT, Lin CH, Huang TP, Tarng DC; Taiwan Geriatric Kidney Disease Research Group. U-shaped mortality curve associated with platelet count among older people: a community-based cohort study. Blood. 2015 Sep 24;126(13):1633-5.

van der Bom JG, Heckbert SR, Lumley T, Holmes CE, Cushman M, Folsom AR, Rosendaal FR, Psaty BM. Platelet count and the risk for thrombosis and death in the elderlyJ Thromb Haemost. 2009 Mar;7(3):399-405.

Vinholt PJ, Hvas AM, Frederiksen H, Bathum L, Jørgensen MK, Nybo M. Thromb Res.Platelet count is associated with cardiovascular disease, cancer and mortality: A population-based cohort study. 2016 Dec;148:136-142.