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Is phosphorous deadly?

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I’m glad you brought this up Tom because when I saw nutrition datas 0% phosphorus I knew something was wrong. Phosphorus is endemic. Life forms plant and animals must have some. So 0% made no sense unless it eas processed out somehow which seemed unlikely. I was using solgar which as you show does not indicate phosphorus levels. So I searched and found a label for lewis labs yeast and indeed there is 26% phosphorous for a serving 3tbs which is 182 mg of phosphorus which is quite high as a per calorie basis higher then most foods I have checked(see previous posts). I ordered a can and I might use one tablespoon daily which would only be 60 mg or about 9%.



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Interesting. The brewer's yeast I used to take - Lewis Labs - it's shown as zero:




And now I take the Solgar brand, and phosphorus isn't shown at all, implying that there is zero of it in this brand also.




I'm not doubting that your brewer's yeast has the phosphorus you say, but maybe it depends on the brand?


There are "zeros" all over the place in food listings, especially for commerical foods and supplements: they generally only list what they're required to, and presumably went further in this case because it wouldn't look all that nutritious with just a the standard required stuff.


In any case, the current LL label indicates 26% DV phosphorus, and the LL entry in COM lists 260 mg/serving.

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  • 1 month later...
mikeccolella:  Al Pater recently posted:  Phosphate toxicity and tumorigenesis   Brown RB, Razzaque MS.   Biochim Biophys Acta. 2018 Apr 20.



A full text of that paper is available here:




It's definitely worth reading. 


Mccoy,  being an mTor specialist you might like the discussion of  high dietary  phosphate interacting with various pathways to activate mTOR  and  promote tumorigenesis.


Fig. 2. Cancer cells respond to growth factors through a signaling pathway in which phosphoinositide 3-kinase (PI3K) phosphorylates Akt (protein kinase B) [18]. Akt activates  mTOR kinase, which in turn can suppress apoptotic cell removal and induce cell proliferation [77]. High dietary phosphate was found to activate Akt phosphorylation, facilitating cap-dependent protein translation and increasing lung tumorigenesis in mice [78]. High dietary phosphate in mice also suppressed PTEN, a tumor suppressor phosphatase, and suppressed CTMP, a negative regulator of Akt activity [78].


There is also mention of a low phosphate ketogenic diet:


An analysis of the micronutrient content of a classic high-fat, low-carbohydrate ketogenic diet for children shows that the

diet is low in phosphate. For example, a sample ketogenic menu [72], modified in amounts for an adult, provides 2025cal a day with a 4:1

ratio of fat to non-fat grams and only 599mg of phosphate, which is below the adult RDI of 700mg.


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Saul:  IMO, the only wat to know if you're out of line (or in line) for some nutrient, is blood and urine work.  (Dietary intake only hints at that.)



The relationship between dietary phosphorus levels and serum phosphorus levels is quite complex, and it seems both measurements are important since, among other things,   excessive dietary phosphorus intake may be harmful even in the absence of high serum phosphorus concentrations.



High dietary phosphorus intake is associated with all-cause mortality: results from NHANES III

Alex R Chang et al.

Am J Clin Nutr. 2014 Feb; 99(2): 320–327.
PMCID: PMC3893724

PMID: 24225358


Excessive dietary phosphorus intake may be harmful even in the absence of high serum phosphorus concentrations.Serum phosphorus concentrations are tightly regulated by parathyroid hormone and fibroblast growth factor-23 (FGF-23), which is a hormone that increases urinary phosphorus excretion. Individuals with normal kidney function are largely able to maintain serum phosphorus in a physiologic range, even in the setting of high phosphorus consumption because increased phosphorus consumption leads to physiologic increases in parathyroid hormone and FGF-23 (810). Over the long term, high FGF-23 concentrations may stimulate left ventricular hypertrophy (11), and epidemiologic studies have linked high FGF-23 concentrations with heart failure (12), cardiovascular events, chronic kidney disease (CKD) progression, and mortality (7, 13).


In this nationally representative sample of healthy US adults with normal kidney function, we showed that high phosphorus consumption was associated with increased all-cause mortality. The relation between increasing absolute phosphorus intake and mortality appeared flat until a threshold of ∼1400 mg/d, which is an amount of phosphorus consumption that is twice the adult US RDA. A similar continuous relation was seen with increasing phosphorus density and mortality at amounts >0.35 mg/d, which corresponded to 700 mg/d in subjects who consumed a 2000-kcal diet. Findings were also robust by the subgroup of dietary quality. These findings may have important public health implications because more than one-third of Americans reported phosphorus consumption that exceeded 1400 mg/d.





Excessive dietary phosphorus could lead to death by increasing mean serum phosphorus concentrations throughout the course of the day (27), although there was no evidence of a mediation by serum phosphorus in our study. It is possible that repeated measurements of serum phosphorus are needed to accurately capture the effect of phosphorus intake. Previous investigators, by using repeated measurements of serum phosphorus, have shown that changes in phosphorus intake have little effect on random or fasting serum phosphorus concentrations but do result in changes in 24-h mean serum phosphorus concentrations (27, 28). Elevated serum phosphorus concentrations are associated with endothelial dysfunction, vascular calcification, and low-grade albuminuria (2932). In addition, changes in phosphorus intake are directly associated with changes in urinary albumin excretion (33).


Unfortunately, few data exist on long-term effects of restricting phosphorus intake. Previous randomized trials either have been of short duration (9, 34, 35), focused primarily on protein intake (36), or used phosphorus-binding medications, which may have independent effects on vascular calcification (37). In addition, phosphorus may have a role in regulating cell growth, proliferation (38), and protein translation (39). In a mouse model of skin carcinogenesis, elevated serum phosphorus concentrations promoted cell transformation and tumorigenesis (40), and epidemiologic studies have suggested a link between dietary (41) and serum phosphorus (42) with certain forms of cancer.


Alternatively, high phosphorus intake could lead to increased mortality by stimulating higher concentrations of FGF-23 (8, 9), which may lead to left ventricular hypertrophy (11), congestive heart failure, and mortality (7, 12, 13).


Dietary phosphorus intake and health

Jaime Uribarri Mona S Calvo

The American Journal of Clinical Nutrition, Volume 99, Issue 2, 1 February 2014



There are many potential mechanisms through which a high dietary phosphorus intake may induce disease with or without a measurable elevation within the normal range of fasting serum phosphate. The potential toxicity mechanism that has garnered the most attention is the disruption of the endocrine regulation of calcium and phosphorus. In both animal models and clinical studies, a high-phosphorus diet has been shown to induce parathyroid hormone (PTH) and/or fibroblast growth factor-23 (FGF-23) release from bone, both of which may have significant pathogenic cardiovascular effects, such as arterial calcification, endothelial dysfunction, and left ventricular hypertrophy (8).


The study by Chang et al (4) in this issue of the Journal is the first to show a direct relation between dietary phosphorus intake and all-cause mortality in healthy people who participated in a large national survey, NHANES III. Previously, dietary phosphorus intake was shown to be associated with biomarkers of cardiovascular outcome, such as left ventricular mass measured by cardiac MRI in healthy subjects from the Multi-Ethnic Study of Atherosclerosis and concentrations of FGF-23 among participants in the Health Professionals Follow-Up Study (3, 9).


In the study by Chang et al (4), the significant association found between total phosphorus intake or phosphorus density (mg/kcal) and all-cause mortality remained after adjusting for other lifestyle and demographic confounders. The strongest associations were found with phosphorus density, suggesting that expressing phosphorus intake as a function of caloric intake, another commonly underreported variable, compensated for its probable underestimation.




As described earlier, calcium intake and the calcium-to-phosphorus ratio of habitual diets may also have influenced the impact of phosphorus intake on hormones other than FGF-23, as discussed by Chang et al, namely PTH. PTH concentrations within the normal range have been shown to be significantly associated with all-cause mortality and specifically with arteriosclerosis in older people (10). PTH is acutely elevated in response to oral phosphate loading, persistently elevated in response to weeks of consuming grocery foods high in phosphate additives, and significantly higher in young women whose habitual diets had calcium-to-phosphorus ratios of <0.6 (5). In fact, by using the mean calcium and phosphorus intakes in each quartile to approximately calculate the dietary calcium-to-phosphorus mass ratio in the study by Chang et al, we noted a marked decrease in the ratio, from 0.92 at the lowest dietary phosphorus quartile to 0.47 at the highest intake quartile, suggesting that elevated PTH may also be involved.


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Hi Siberiac!


Here are the numbers for my renal (urinary) phosphorus,


7/23/14 10/12/14 4/2/14 4/14/16 5/23/16 12/7/16 12/23/16 6/9/17 11/13/17 5/14/18


3.8 3.7 3.7 3.3 2.9 3.7 5.1 3.7 3.6 4.1


(The table is a bit offset; the earliest date is 7/23/14, the most recent is 5/14/18. The standard range for renal phosphorus is 2.7 - 4.5 mg/dL. All but 1 one of these numbers is in that range. Most of these tests were fasting tests; but several of them weren't. (I've noticed that most of my tests -- bloodwork or urine -- seem to vary very little, whether taken with fasting or not.)


-- Saul

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Here are the figures for alkaline phosphate:


84 76 74 70 79 82 63 90 94 105


The standard range is 40 - 130 U/L.


Again, most of these tests were for fasting tests, but not all of them. The fasting tests were taken in the morning; the others at other times (usually the afternoon).

I'm too lazy to include the dates; but the earliest is 5/11/11, the last is 5/14/18.


-- Saul

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Here are my numbers for serum calcium (standard range is 8.6 - 10.2 mg/dL).


8.8 9.1 8.9 9.1 8.9 9.1 9.4 9.0 9.6 9.6


The earliest of these tests was on 10/29/15, the latest on 5/14/18. Again, all tests in the normal range; most (but not all) of these tests were done while fasting.


-- Saul

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I should note that I've been doing both bloodwork and urine work for a long time prior to the earliest of the above dates -- but that material isn't as easy to dig up (it's before the University of Rochester began making the convenient "MyChart" system available.)

The earlier numbers are similar to the recent ones.


-- Saul

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