~  Truvia  ~   new  Low Calorie Sweetener (toxin)

Manufactured by Cargill  (in conjunction with Coca Cola )


This is a non-organic, manufactured and possibly a chemically processed product

originally starting with from Stevia leaves (the real thing). There is no

evidence, yet, that the finished product is healthy, or that it remains a

STEVIA-like product, with its original beneficial qualities intact.


NOTE:  As with SPLENDA...the firm said it was from sugar. Yet, after processing, it turned out that SPLENDA evolved ( was processed ) into a chlorocarbon, with a molecular structure closely resembling chlorine-based DDT, the banned pesticide.


SPLENDA being a chlorocarbon, contained chlorine and chlorine derivatives that the human body cannot metabolize. Whenever you see this aspect in processed food or sweeteners or additives, almost 99 % of the time, this means that the body expends vast amounts of energy trying to metabolize it, putting stress on the liver, pancreas, and other organs.


As you may know, the body does NOT metabolize chlorine very well, and therefore created long term health consequences associated with hepatomegaly (enlarged liver), increased size of thymus gland, kidney malfunctions, and a host of other pathologies leading into a diseased state. That is SPLENDA ...a chlorinated, processed molecule that more closely resembles DDT, than any sugar.


In addition to our previous experience with SPLENDA, Aspartame, and cyclamates, et al, problems always developed from their use. Some of these issues, like with aspartame,  were substantially (neuro)toxic.



Thus, this has led us to formulate and research several important questions and queries...


First: Erythritol, a sweetening agent contained in TRUVIA ® (and ZEROSE ®), is processed AND SYNTHESIZED from its original state. TRUVIA is processed with Erythritol and treated (Rebiana). This does not mean that the finished product resembles the original state from which it is manufactured. So, that’s a red flag.


Second: To date (Nov. 2008) Our investigation is currently involved with looking into the following issues:


a)     That this PROCESSED Rebiana or Stevia may not reflect the original starting product.


b)     Increased calcium loss, along with potassium, and phosphate (from what we discovered currently) may have a severe, long-term consequence on kidney function by causing or increasing renal lesions.


c)      Noted increases in urinary calcium, potassium, etc. reflects these constituents being released into the blood stream from moderate intake of Erythritol (PROCESSED REBIANA), and that this increase

accumulates in the kidneys, causing calcification and lesions. We found testing which showed weight changes in animal kidneys upon examination, with developing lesions.


d)     We are also finding data that “alludes” to the development of an enlarged cecum, a small pouch attached to the ascending large colon, near the ilio-cecal valve in the intestine. This seems to make sense due to the fact that unmetabolized and artificially processed additives may aggravate or instigate inflammation of the cecum. We have learned that most artificial products (chemicals, additives, flavor enhancers, coloring agents, etc) that are not capable of being metabolized have led to pathological health issues. This raises another red flag.


e)     With natural Stevia - Rebiana available on the market, why would anyone destroy this perfectly wholesome, safe natural sweetener by processing it, using chemicals and other additives in the finished production process ?


This question is may be answered three-fold = 1) It is being developed by a multi-national corporation with significant influence over the FDA ;  2) Profit motive, and,  3) the agenda to eventually provide another pharmaceutical requisite for a “precondition of illness” for further profit. 


It sounds sinister, because it is sinister, as these people, focused on profit, care less about our health or well-being. So, what we have included in this research, is MOTIVE....  We think these days, this has become an important aspect of planned investigative research, especially when it comes to the FDA or pharmaceutical firms.


Why process an already natural product ???


To process Stevia into Stevioside (powdered form) requires that the leaves are subject to a process of using nitrogen, water, and in some cases, methanol (like caffeine-free coffee) to create the powdered sweetener of Stevia.   So, Why not simply add natural Stevia to these products ? 


                                      Good question...and it deserves an answer.


This is where we are, so far.   We have a way to go yet.

We will keep this site updated as the information becomes available and is validated.


Currently, we recommend promoting and using natural Stevia. We found one firm, Stevita, Inc., from Dallas, Texas operated by a man (Oscar Rhodes)  with direct connections to Stevia-Pharma in southern Brazil, where it is naturally produced and packaged, retaining all its natural beneficial qualities.




Here are some of the PROBLEM and PATHOLOGICAL  studies we have found, so far...

Additional Supporting Documents, as found, below :



Manufacturing of Erythritol (from Industry)



Erythritol is the first polyol to be industrially manufactured by a fermentation process.


It would be good to know and understand this “fermentation process”, as the same thing can be said for hydrolized protein (neurotoxin) ??     We want to know if the "MAIZE or corn they are using is GMO ?       

                        More questions than answers  ...    ~ Arthur Evangelista,  Dir. of Operations


The starting material is a glucose-rich substrate (?) obtained by enzymatic hydrolisis from the natural raw material starch.  Glucose is then fermented by a yeast to yield erythritol. 


Erythritol is crystallised at over 99.5% purity from the filtered and concentrated fermentation broth.

A fermentation process using natural raw materials derived from maize was developed by Cargill, first on laboratory scale, then on a pilot industrial scale. Commercial production of purified, high quality erythritol - initially for the Japanese market - started in 1993.





Chronic Toxicity and Carcinogenicity Study of Erythritol in Rats

B. A. R. Linaa, M. H. M. Bos-Kuijpersa, H. P. Tila and A. Bär b, 1

a TNO Nutrition and Food Research Institute, P.O. Box 360, 3700 AJ, Zeist, The Netherlands

b Bioresco AG, Hauptstrasse 63, Postfach 406, 4102, Binningen, Switzerland

Received 29 July 1996. 

Available online 22 April 2002.


Abstract   comments by: Dr. E in BLUE

The potential toxicity and carcinogenicity of erythritol, a low-calorie sugar substitute, were examined in Wistar Crl:(WI) WU BR rats. Groups of 50 rats of each sex consumed diets with 0, 2, 5, or 10% erythritol, or 10% mannitol, for a period of 104–107 weeks. To each of these main groups, two satellite groups of 20 males each were attached for interim kills after 52 and 78 weeks of treatment. At start of the study, the rats were 5–6 weeks old.


The average intakes of erythritol in the 2, 5, and 10% groups were 0.9, 2.2, and 4.6 g/kg body wt/day for males and 1.0, 2.6, and 5.4 g/kg body wt/day for females, respectively. Mannitol intakes were 4.4 and 5.2 g/kg body wt/day in males and females, respectively. All treatments were well tolerated without diarrhea or other side effects. Body weights were significantly below control levels during most of the study in males of the 5% erythritol group and in males and females of the 10% erythritol and 10% mannitol groups. Survival of the animals was not adversely affected by the treatments. Hematological and clinicochemical examinations did not reveal noticeable changes which could be attributed to treatment.     What were they attributed to  ??


Analysis of urine samples collected during five 48-hr periods, from rats of the satellite groups in Weeks 26, 42, 50, and 78 and from rats of the main groups in Week 102, showed that about 60% of ingested erythritol was excreted unchanged.


The urine volumes (this refers to urinary output in general) increased with increasing dietary erythritol levels.


In line with previous observations on other polyols, erythritol and mannitol ingestion led to an increased excretion of urinary calcium and citrate. The urinary excretions of sodium, potassium, phosphate,N-acetylglucosaminidase (NAG), γ-glutamyltransferase (GGT), low-molecular-weight protein (LMP), and total protein (TP) were slightly elevated in the 10% erythritol group. (This means that these minerals and proteins are removed from bone, cellular tissues, plasma ?? ...and then released into the bloodstream due to direct consumption of Erythritol…and that these, subsequently, pass through the kidney, and are supposedly excreted.)


Diagram of the Structure of the Kidney


(Gross Anatomy of the Kidney)



Increased GGT and NAG excretions also were seen occasionally at the 5% dose. Significantly increased relative cecum weights were seen in rats of either sex in the 10% mannitol and, somewhat less pronounced, 10% erythritol groups. Some cecal enlargement also was seen in the 5% erythritol group. The relative weight of the kidneys was highest in the 10% erythritol group, the difference from controls reaching statistical significance at interim kills (males) and termination (females).


Except for more frequent pelvic nephrocalcinosis in female rats, of all erythritol dose groups, the histopathological examinations did not reveal any nonneoplastic, preneoplastic, or neoplastic changes that could be attributed to the ingestion of erythritol. (This statement may reflect the industry’s funding for these studies, as this appears to downplay the issues of nephrocalcinosis due to the high excretion rates of calcium, citrate, potassium, and phosphate).


 In male and female rats of the 10% mannitol group, pelvic nephrocalcinosis, which in females was associated occasionally with pelvic hyperplasia, was the only remarkable finding. The incidence and progression of nephrosis, which is commonly seen in aging rats of this strain, were not influenced by the treatments.


(Do you think they used aged rats on purpose, to cover up the renal calcification lesions ? ) Considering corporate testing these days, it is my belief that testing for renal nephrocalcinosis is most likely much worse than what is being explained here.


Until we have more information, I would suggest natural Stevia rather these processed or synthesized sweeteners (Truvia or Zerose), or anything else these "companies of disease" can synthetically formulate.


The reason these companies have not sought to legalize, STEVIA, is because they would not be able to patent it, and because the natural health industry would pose serious competition.

So, in order to protect their profits, these pharma-chemical companies decided to process their synthesized version of a sweetener (again), in order to reap their money, of course, at the expense of the public health.


In the absence of morphological alterations in the kidneys or other signs of nephrotoxicity, the increased excretions of NAG, GGT, LMP, and TP are regarded as innocuous, functional sequelae of the renal elimination of erythritol.    This does not make any sense. This, being "innocuous", is a lie. The increase, per above, is pathological in nature.


In conclusion, the toxicological profile of erythritol in rats resembles that of other polyols in several respects. Except for nephrocalcinosis, which is commonly seen in polyol-fed rats, no other treatment-related, morphological changes were observed in the kidneys. Evidence for a tumor-inducing or tumor-promoting effect of erythritol was not seen. (Was it looked for ??)


You can see how this industry funded or "watered-down" study downplays the ominous facts to kidney pathogenesis.  At least  they mentioned the problems...albeit, sugar-coated.








The Concentrations and Ratio of Dietary Calcium and Phosphorus Influence Development of Nephrocalcinosis in Female Rats1

Kevin A. Cockell2, Mary R. L’Abbé and Bartholomeus Belonje

Nutrition Research Division, Food Directorate, Health Products and Food Branch, Health Canada, 2203C Banting Research Centre, Ottawa, ON, Canada K1A 0L2


Nephrocalcinosis (NC) in female rats can complicate the interpretation of nutritional or toxicological studies involving the kidney. Recent reformulations of standardized rodent diets such as AIN-93G and NTP-2000 sought to optimize the dietary Ca:P ratio, an important etiologic factor in NC.


The effect of increasing intakes of Ca and P together at their optimal molar ratio has not been systematically studied. Weanling female and male Sprague-Dawley rats were fed modified AIN-93G diets containing Ca and P at AIN-93G diet concentrations (5 g Ca + 3 g P/kg diet), with multiples of Ca and P at the same ratio (1.5x = 7.5 g Ca + 4.5 g P, 2.5x = 12.5 g Ca + 7.5 g P, 4.0x = 20.0 g Ca + 12.0 g P/kg diet), or Ca and P at concentrations found in the AIN-76A diet (5 g Ca + 5 g P/kg diet), for 16 wk.


Incidence and severity of NC and kidney Ca concentration in female rats increased with dietary Ca and P, although not to levels in female rats fed at the AIN-76A Ca:P ratio. Male rats showed limited evidence of kidney Ca accumulation or NC. The concentrations of dietary Ca and P, as well as the ratio of these two elements, affected development of NC in female rats.

KEY WORDS: • dietary calcium • dietary phosphorus • nephrocalcinosis • female rats



NOTE:  ERYTHRITOL causes leeching or osmotic removal of dietary or bioavailable systemic calcium, phosphorus, and other constituents to be released into the bloodstream. This increases potential for nephrocalcinosis, plus, a reduction of system, cellular, or biologically available calcium.


It is possible that enlargement of the cecum (at the ilio-cecal valve proximity) is due to irritation of this release of constituents, or is a reflection of UNKNOWN irritants attached to erythritol from processing, ingestion, or other interaction from cellular metabolism. ALSO, any food, which is attempted to be metabolized by the liver, such as chlorinated compounds, may place undo strain on liver, as it does with kidney function, and possibly other unknown implications (at this time).   ~ Arthur M. Evangelista





Subchronic Oral Toxicity Studies with Erythritol in Mice and Rats


H. P. Tila, C. F. Kupera, H. E. Falkeb and A. Bär b, 1

a TNO Nutrition and Food Research Institute, P.O. Box 360, 3700 AJ, Zeist, The Netherlands

b Board for the Authorization of Pesticides (CTB), P.O. Box 217, 6700 AE, Wageningen, The Netherlands

Bioresco AG, Hauptstrasse 63, Postfach 406, 4102, Binningen, Switzerland

Received 29 July 1996. 

Available online 22 April 2002.



Erythritol is a sugar alcohol (polyol) with potential applications as a low-calorie, bulk sweetener. Ingested erythritol is efficiently absorbed and excreted unchanged via the urine since it is not metabolized systemically by the animal or human body.


Erythritol was administered to four groups of 10 male and 10 female Swiss CD-1 mice and four groups of 15 male Wistar Crl:(WI) WU BR rats at dietary levels of 0, 5, 10, or 20% for 90 days. A fifth group of rats received a diet containing 20% erythritol on a time-restricted basis (6 hr/day), and a sixth group received a diet containing 20% mannitol for comparison. There were no treatment-related mortalities in either mice or rats. Soft stools and occasional diarrhea were observed in rats fed diets with 20% erythritol or mannitol but not in mice.


Body weights were slightly yet significantly reduced in rats fed 20% erythritol or mannitol and in male mice of the 20% dose group. Erythritol intake in the high-dose group was approximately 12 g/kg body wt in rats and 44 and 45 g/kg body wt in male and female mice, respectively.


Hematological and clinicochemical examinations of blood and plasma did not reveal any treatment-related effects. Urine output increased with increasing erythritol dose. In male and female mice of the 20% erythritol group, the creatinine-normalized urinary excretion of protein, K-glutamyltransferase (GGT), and electrolytes (Na+, K+, Ca2+, Pi, citrate) was significantly increased while urinaryN-acetylglucosaminidase (NAG) remained unchanged.


At the 10% level, significantly increased urinary protein (both sexes) and GGT (males only) excretion were seen. In rats, the creatinine-normalized urinary excretion of GGT, NAG, and some electrolytes (Na+, K+, and Ca2+) was increased in some erythritol groups but a clear dose–response relationship was evident only for calcium.


On termination of the study, cecal enlargement was seen in rats of the 10 and 20% dose groups and in mice of the 20% dose group.


Increased relative and absolute kidney weights were observed in both sexes of mice in the 20% erythritol group, in male mice of the 5 and 10% groups, and in rats of the 10 and 20% erythritol groups.

Histopathological examination did not reveal any treatment-related abnormalities in either mice or rats.


In conclusion, the ingestion of erythritol for 90 days at dietary levels of up to 20% did not produce signs of toxicity in mice or rats. In particular, the morphological integrity of the kidneys was not adversely affected by the treatment in either species. The increases in urinary excretion of protein, GGT, NAG, and electrolytes were considered to result from extensive osmotic diuresis and a potential overload of the renal excretory system at the high dose levels employed.



I have seen this "sidestepping" of issues with other industry funded results...It seems that Truvia and Erythritol based sweeteners are more toxic than what is being casually revealed here. 




            Two-Generation Reproduction Study of

                             Erythritol in Rats


D. H. Waalkens-Berendsena, A. E. Smits-van Prooijea, M. V. M. Wijnandsa and A. Bär b, 1

a TNO-Nutrition and Food Research Institute, P.O. Box 360, 3700 AJ, Zeist, The Netherlands

b Bioresco AG, Hauptstrasse 63, 4102, Binningen, Switzerland

Received 29 July 1996. 

Available online 22 April 2002.



Erythritol was fed at dietary concentrations of 0, 2.5, 5, or 10% to Crl:(WI) WU BR rats of both sexes through two successive generations (F0and F1). Twenty-four rats of each sex were mated in each group.



For each generation one litter was reared until the pups were 21 days old. In the 10% erythritol group, food consumption among F0-males and -females was initially significantly reduced until the animals adapted to the erythritol diet during the first week of the study. Thereafter, food intake was higher than in controls.


A consistently increased food intake also was seen in F1-males and -females of this dose group. This effect was considered* to result from the caloric dilution of the food by erythritol, which has a low physiological energy value.     * They do not know, or will not tell us, but for a scientific study, this is very vague, wouldn't you say  ??


We are investigating other reasons why Erythritol causes overeating (and eventual obesity ?? )


 The lower body weight and weight gain of the F0-animals of the 10% erythritol group were attributed to the initially reduced food consumption and occurrence of transient diarrhea until the animals had adapted to the erythritol intake.


In the F1-animals of the 10% erythritol group, which were adapted to the treatment from weaning, the rate of body weight gain did not differ from controls.


The F1-males and -females of this dose group did, however, have a reduced body weight from weaning, which was attributed to a reduced energy intake among the corresponding F0-dams during Weeks 2 and 3 of lactation. This effect was not seen in the F2-generation. It is concluded that under the conditions of this experiment, the intake of erythritol had no adverse effect on fertility and reproductive performance of parent rats or on the development of their progeny.


Gross necropsy and microscopic examination of the parenteral reproductive organs also did not reveal treatment-related changes.


The wording of this report sounds “fictitious”.  This issue of calcium loss and increased appetite could lead to overeating and obesity, along with decalcification / demineralization of the body. This can have serious health consequences and requires further investigation.





Cargill launches erythritol product line under  Zerose™  brand name

New Zerose™ web site helps consumers understand erythritol’s benefits

MINNEAPOLIS – Cargill has branded its erythritol product line under a new name, Zerose™ erythritol, that clearly conveys to food manufacturers and consumers that the all-natural sweetener contains zero sugar, zero calories*, zero aftertaste and zero artificial ingredients. The brand launch includes the introduction of a new consumer education web site, www.zerosesweetener.com, designed to answer questions about erythritol and explain its benefits as a natural sugar alternative.

Formerly known as Eridex™ erythritol, Zerose™ erythritol is a bulk sweetener that tastes and functions like sugar in beverages, dairy products and confections that appeal to consumers who want to manage their weight or sugar levels or sugar intake. Like sugar, it reduces water activity in a food product, provides volume and provides the freeze point depression needed in many frozen treats.

Zerose™ erythritol tastes 60 to 70 percent as sweet as sugar, so people can reduce their sugar intake without sacrificing taste. The ingredient also is non-glycemic and non-insulemic, making it a useful sugar alternative for people on diabetic diets. In addition, Zerose™ erythritol is noncariogenic (does not promote tooth decay) and is endorsed by Toothfriendly International.**

Cargill’s application and manufacturing expertise

Cargill is in a unique position with more than a decade of experience in the use and manufacture of erythritol. “We recognized the benefits of erythritol in the 1980s and began building the manufacturing, food safety and application database that led to the eventual U.S. and EU approval and commercialization of the ingredient,” said Kathy Fortmann, polyols and dextrose global business director, Cargill Sweetness Solutions. Cargill has an extensive patent portfolio through its own patent estate and through the licensing of other intellectual property.

Zerose™ erythritol is easy for food and beverage manufacturers to use because it comes in an easy-to-ship powder form, has heat and pH stability and freeze-point depression, and gives finished products the same volume that sugar does in baked goods.

Zerose™ erythritol is unique, natural and organic

Erythritol exists naturally at low levels in many fruits and at higher levels in naturally fermented foods such as soy sauce, cheese, wine and beer. Zerose™ erythritol is produced by growing a natural culture that converts sugars and other nutrients into erythritol. This process is similar to the way yogurt is made from milk.

It is then filtered, crystallized and dried, resulting in a final product that is greater than 99 percent pure. Zerose™ erythritol is natural; the ingredient also is available in a U.S. Department of Agriculture (USDA) certified organic grade (certified by QAI International).

For more information about Cargill’s sweetness products, visit www.cargillsweetness.com.

*Zero calorie determination is based on scientific studies cited in a petition submitted to the U.S. Food and Drug Administration.

Above information provided by your local chemcial and processed food company.



The Concentrations and Ratio of Dietary Calcium and Phosphorus Influence Development of Nephrocalcinosis in Female Rats1  

Kevin A. Cockell2, Mary R. L’Abbé and Bartholomeus Belonje

Nutrition Research Division, Food Directorate, Health Products and Food Branch, Health Canada, 2203C Banting Research Centre, Ottawa, ON, Canada K1A 0L2


This reflects  issues of calcium and mineral loss during ingestion of Erythritol  ~ Dr. E

The rats were fed the test diets for 16 wk, with feed consumption and body weight gain measured weekly. Rats were maintained in accordance with the guidelines of the Canadian Council on Animal Care, in stainless steel wire-bottomed cages in a temperature- and humidity-controlled room with a 12-h light:dark cycle. The experiment protocol was approved by the institutional Animal Care Committee of the Health Products and Food Branch of Health Canada.

Tissue sampling and histopathology.

Rats were killed by exsanguination under isoflurane anesthesia. Kidneys were dissected out and cut in half (left kidney cut longitudinally, right kidney cut transversely). One half of each was preserved in formalin for subsequent processing and paraffin embedding following routine methods for histopathology. Adjacent 5-µm sections were cut and stained with hematoxylin and eosin (H&E) or by the von Kossa technique (10 ).

Black granular precipitates on von Kossa–stained sections were manually counted and a histochemical score was assigned according to the number of granules found in one transverse plus one longitudinal kidney section per rat. A score of 0 was given for no granules found in the sections, + for 1–25 granules, ++ for 26–75 granules, +++ for 76–150 granules and ++++ for >150 granules in the sections. The other half of each kidney was frozen at -80°C for subsequent mineral analyses.

Mineral analyses.

Samples of tissues and diets were dry ashed at 450°C using concentrated nitric acid as an oxidizing agent before analysis for Ca by flame atomic absorption spectrometry (Perkin-Elmer 5100PC, Perkin-Elmer, Norwalk, CT) (11 ) and P by a colorimetric method (12 ). Analytical standards were prepared from certified single-element stock solutions (SPEX Chemical, Metuchen, NJ). These analytical methods have been checked in multilaboratory quality control studies (13 ) and analysis of NBS Bovine Liver (1577 or 1577a, National Institute of Standards and Technology, Gaithersburg, MD) gave results within 5% of certified values.

Statistical analyses.

Growth results were analyzed by ANOVA followed by Scheffé’s test for difference of means (comparing Ca + P concentration effects, diets AIN93, 1.5x, 2.5x and 4.0x) or t test for independent samples (comparing Ca:P ratio effects, AIN93 vs. AIN76 diets), using P < 0.05 as the threshold of significance. Kidney Ca+  results were analyzed by nonparametric methods (Kruskal-Wallis ANOVA followed by Dunn’s multiple comparison or Mann-Whitney U test) due to profound heterogeneity of variances, which could not be overcome by standard transformation procedures. For Kruskal-Wallis ANOVA and Mann-Whitney U test, P < 0.05 was used as the threshold of significance. For Dunn’s multiple comparison, which was performed only where Kruskal-Wallis ANOVA achieved significance, a threshold of = 0.15 was used, yielding an experiment-wise error rate threshold for significance of 0.0125 (14 ). The association between kidney Ca or P concentration and histological score was investigated using the Spearman Rank Order correlation. Statistical analyses were conducted using Statistica for Windows, version 5.1 (StatSoft, Tulsa, OK). Results are presented as mean ± SD, with ranges also specified for kidney Ca concentrations.


The Ca and P concentrations of the test diets were (dry weight basis): diet AIN93, 5.4 ± 0.3 g Ca and 3.9 ± 0.3 g P/kg diet, molar ratio 1.07; diet 1.5
x, 7.9 ± 0.3 g Ca and 5.4 ± 0.3 g P/kg diet, molar ratio 1.12; diet 2.5x, 12.9 ± 0.2 g Ca and 8.7 ± 0.3 g P/kg diet, molar ratio 1.14; diet 4.0x, 20.3 ± 0.3 g Ca and 13.4 ± 0.2 g P/kg diet, molar ratio 1.17; diet AIN76, 5.3 ± 0.2 g Ca and 6.2 ± 0.3 g P/kg diet, molar ratio 0.66. No significant differences in body weight gain or feed efficiency were found as a result of the dietary treatments used (results not shown).

Kidney Ca+ concentration in the group of weanling rats killed at the outset of the study was 7.53 ± 0.40 µmol/g dry kidney (range 6.90–8.18) for female rats and 7.05 ± 0.30 µmol/g dry kidney (range 6.65–7.50) for male rats. All weanling rats killed at the outset of the study had histochemical scores of zero, indicating no evidence of black precipitates on von Kossa–stained kidney sections.

Male rats showed almost no histochemical evidence of NC with any of the diets and had less kidney Ca accumulation than female rats (Table 2 ). In female rats, increased kidney Ca concentration and incidence of histochemically determined NC was found after 16 wk of feeding increasing amounts of dietary Ca and P at the optimal molar ratio (comparing diets AIN93 through 4.0x, Table 2 ), although more extensive Ca accumulation and more severe NC resulted from imbalance in dietary Ca and P intakes (comparing diet AIN93 and AIN76;Table 2 and

Fig. 1 ).                                    16 Wks. is a relatively short study...perhaps too short  !

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Table 2. Kidney calcium concentration, kidney calcium score and range of histochemical score for female and male Sprague-Dawley rats fed modified AIN-93G diets differing in calcium and phosphorus content for 16 wk1


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Figure 1. Histological appearance of kidneys from female Sprague-Dawley rats fed diets differing in Ca and P concentrations for 16 wk (see text for details). Section from outer capsule (at left) to inner stripe of outer medulla (at right); von Kossa stain; original X75. Ca deposits appear as large black granules against a lighter background. (A) Diet AIN93, 5 g Ca + 3 g P/kg diet, Ca: P molar ratio 1.07 by analysis. (B) Diet 4.0x, 20 g Ca + 12 g P/kg diet, Ca: P molar ratio 1.17 by analysis. (C) Diet AIN76, 5 g Ca + 5 g P/kg diet, Ca: P molar ratio 0.66 by analysis.

These results were supported in a categorical examination of kidney Ca+ concentration, namely, the kidney calcium score (Table 2)
. For categorization of kidney calcium score in our laboratory, the "normal" level for rats is 7.50 ± 0.63 µmol Ca/g dry kidney (mean ± SD) based on historical data from several studies. This value is similar to the analyzed value for female rats killed at the outset of the present study. With increasing dietary Ca and P concentrations, a higher proportion of female rats had "elevated" kidney calcium score (>2 SD above "normal") and 1 of 8 female rats fed diet 4.0x had a kidney calcium score indicative of Nephrocalcinosis (NC), >10 times the normal level (i.e., Ca concentration >75 µmol/g dry kidney). Kidney P concentration was significantly increased only in female rats fed diet AIN76 in comparison to AIN93 (445 ± 80 vs. 351 ± 11 µmol P/g dry kidney, respectively).


The location of mineral precipitation in kidney sections, shown by von Kossa staining, was similar with elevated concentrations of Ca and P at the optimal ratio (e.g., diet 4.0x, Fig. 1 B) to that seen with Ca:P imbalance (diet AIN76, Fig. 1 C) although the degree of precipitation was generally more severe in the latter group.


Most of the female rats fed diet AIN93 had no histochemical evidence of mineral precipitation after 16 wk of feeding (Fig. 1 A). There was considerable variation among rats within a treatment group in the extent of kidney Ca+ accumulation and the severity of Nephrocalcinosis (NC)    (Table 2) .


Even with diet 2.5x, there were some female rats with kidney Ca concentrations in the normal range and no histochemical evidence of NC. With diet 4.0x, all female rats showed elevated kidney Ca+, although the range of responses was still very large. Higher incidence and severity of NC was seen with the suboptimal dietary Ca:P molar ratio (diet AIN76) than when these elements were present at 4 times the normal concentrations but "optimally" balanced (diet 4.0x) (Fig. 1 and Table 2 ).   This  statement  means that an imbalance of Calcium to Phosphorus accelerates Nephrocalcinosis (NC)....    ~ Dr. E


There was a significant positive association between kidney histochemical score and kidney Ca concentration in female rats (Fig. 2 ) which yielded a Spearman Rank Order correlation coefficient r = 0.87 (P < 0.00001, n = 40). A similar positive association between kidney histochemical score and kidney P concentration in female rats (data not shown) yielded a Spearman Rank Order correlation coefficient r = 0.65 (P < 0.00001, n = 40).

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Figure 2. Relationship of histochemical score with kidney calcium concentration in female Sprague-Dawley rats fed diets containing different concentrations of Ca and P for 16 wk (see text for details). Values are means ± SD, n = 8, 15, 8, 5, 4 for histochemical scores of 0, +, ++, +++ and ++++, respectively. Histochemical score is based on the number of granules seen in 1 transverse and 1 longitudinal kidney section (von Kossa stain): 0 = 0 granules seen, + = 1–25, ++ = 26–75, +++ = 76–150, ++++ = >150 granules. Spearman Rank Order correlation coefficient for the relationship of histochemical score with kidney calcium r = 0.87 (P < 0.00001).



The present study focused on the effects of elevating dietary Ca and P concentrations together while maintaining the optimal ratio of these two elements. Hoek et al. (15
) examined the effect of increasing dietary Ca and P concentrations, comparing 0.25% Ca + 0.20% P or 0.25% Ca + 0.4% P to diets containing twice the content of each (0.5% Ca + 0.4% P or 0.5% Ca + 0.8% P, respectively). In both cases, the diets with the higher Ca + P content yielded more severe NC. Low incidence and severity of NC was found using a diet containing 0.75% Ca + 0.4% P (15 ), which is similar in Ca and P composition to our diet 1.5x.


This refers to blood values of dietary calcium, and its over-release  into the bloodstream, from various chemicals, diets, and other intakes or releases. Calcium may affect muscle contractility, blood vessel constriction or dilation and blood pressure, blood pressure affects kidney function, and / or other calcium-associated biological or physiological activities.



It has been suggested that the Ca:P molar ratio must be >1 to prevent kidney calcification in female rats (16 ). Although this was achieved in our AIN93 through 4.0x diets, the higher concentrations of Ca and P intake at the recommended ratio still produced NC. Studies described by Reeves et al. (16 ) indicated that a Ca:P molar ratio of 0.97 (5 g Ca + 4 g P/kg diet) did not completely eliminate kidney calcification in female rats, although normal kidney Ca concentrations were found in female rats fed a purified diet with a Ca:P molar ratio of 1.3 for 16 wk.

The present finding of slightly elevated kidney Ca in one of eight female rats fed diet AIN93 suggests that a Ca:P molar ratio of 1.07 does not completely prevent Ca accumulation in kidneys. Earlier work in our laboratory indicated that even with a diet formulated according to AIN-93G specifications, with an analyzed Ca:P molar ratio of 1.31, some female rats had elevated kidney Ca after 16 wk of feeding, and one of eight female rats had a kidney Ca concentration consistent with Nephrocalcinosis (NC) (5 ). It is important to note that kidney Ca concentration in female rats in the present study varied widely within a treatment group, as did the severity of histochemically assessed NC. Similar results have been reported by others (2 ,5 ,15 ).

The typical histological appearance of diet-induced NC shows calcification primarily in the corticomedullary junction region (1 ) and this was the pattern seen in the present study. The von Kossa histochemical procedure detects principally phosphate and carbonate ions, which are the counterions with which Ca is commonly associated in normal and pathologically calcified tissues, rather than being specific for Ca (10 ).

Others have demonstrated that the kidney precipitates found in rats fed diets varying in Ca and/or P content, such as ours, are typically composed of calcium and phosphate (17 ,18 ). The significant association between histochemical score and kidney Ca concentration using the Spearman rank correlation indicates the robustness of this histological grading scheme. A similar correlation was shown previously in rats fed diets varying in Ca and P content (15 ,19 ,20 ) and in human renal biopsy specimens (21 ). A similar association between histochemical score and kidney P concentration has also been reported (15 ). Together, these associations support the identification of the kidney concretions found in female rats in the present study as calcium phosphate.

NC in female rats can complicate the interpretation of toxicity studies (22 –24 ). This problem has been noted in cereal-based diets as well as semipurified diets, and has led the National Toxicology Program to reformulate their standard cereal-based diet to conform to the AIN recommendation regarding Ca:P molar ratio (25 ). Because rats are one of the standard laboratory animal species used in toxicity testing for regulatory purposes (26 ), NC in rats can have widespread implications for human safety and risk assessment activities. Researchers should be cognizant of Ca and particularly P concentrations and adjust mineral mixes accordingly when substituting different protein sources in modified AIN-93G diets.

Although the reformulation leading to the AIN-93G diet was largely successful in reducing the incidence and severity of nephrocalcinosis in female rats, it must be remembered that the absolute concentrations of dietary Ca and P, and not just their ratio, influence the development of nephrocalcinosis in female rats.


1 Publication no. 562 of the Bureau of Nutritional Sciences. Portions of this work were presented in poster form at the 43rd Annual Meeting of the Canadian Federation of Biological Societies, Ottawa, Canada, June 22–24, 2000 [Cockell, K. A., L’Abbé, M. R. & Belonje, B. (2000) Dietary calcium and phosphorus levels and not just their ratio, influence development of nephrocalcinosis in female rats. Abstract T156].

3 Abbreviations used: AIN93, modified AIN-93G diet containing Ca and P at the concentrations specified in the AIN-93G formulation; 1.5x, 2.5x and 4.0x, diets containing Ca and P at 1.5, 2.5 and 4.0 times, respectively, the concentrations in the AIN-93G diet; AIN76, modified AIN-93G diet containing Ca and P at the concentrations specified in the AIN-76A formulation; H&E, hematoxylin and eosin stain; NC nephrocalcinosis.

Manuscript received 6 September 2001. Initial review completed 28 September 2001. Revision accepted 27 November 2001.


 NEW INFORMATION    Dec. 9, 2008


So, these guys ( Coke Cola ) are in bed with Cargill, Inc. to produce what ?...

…another synthesized and processed sweetener they claim to be natural ?


They tell you its from a natural source called, Stevia.  Yet, like the chlorocarbon, SPLENDATruvia is processed and synthesized  into an artificially produced, chemically processed, lo-cal sweetener that is toxic and illness-producingunlike the safe, natural, and the original source from which “TRUVIA is reportedly manufactured.


One problem, is that Coke nor Cargill ( nor any chemical - biotech company) can patent the original, natural, and safe source sweetener, Stevia, not to mention the strong competition from the natural health foods' industry.


Trusting Coke and Cargill to come up with a toxic-free or chemical-free sweetener, is like trusting “Baby Face Nelson” (or the government) with your IRA & bank accounts !! 

So much for corrupt NAFTA  ...                  ~ comment by: Dr. E


Coke & Pepsi poisons in more trouble,

the ULTIMATUM from BIG Business:

India threatened by business interests:

Sell Coke and Pepsi, or your economy will suffer

Found on  http://www.naturalnews.com/019946.html

(NaturalNews) After a Center for Science and Environment study found 24 times the acceptable level of pesticides in soda sold in India, a few state governments acted quickly to ban the big name soft drinks -- Coca-Cola and PepsiCo -- but the country's top business groups warned Thursday that the move could hurt India's economy.


Both the Confederation of Indian Industry and the Federation of Indian Chambers of Commerce and Industry say that decisions to ban Coca-Cola and PepsiCo products from schools, colleges and hospitals run by the government are likely to hurt the country's broader economy, slowing the investment climate. Representatives reported being particularly disturbed by the total ban on the soft drink brands by the Southern state of Kerala, where both companies run plants.

"Government actions have to be driven by rule of law and in the overall public interest," said R. Seshasayee, president of Confederation of Indian Industry, who noted that the standards used by CSE were part of a government "proposal" that has not yet passed into Indian law. "We are concerned that the apparently arbitrary decisions have been taken ... without going through the due process of law."

Both Seshasayee and FICCI President Saroj K. Poddar assert that the states should have followed up the CSE study with their own tests, and then sent notice to Coca-Cola and PepsiCo, in keeping with proper procedures.

"It is amazing to observe the legal and regulatory contortions these pro-business Indian politicians will go through to keep selling pesticide-laden products to their own people," remarked Mike Adams, a consumer health advocate and critic of the marketing practices of soft drink companies. "And claiming that the banning of soft drinks containing unsafe chemicals would be harmful to India's economy is preposterous. Why do they not consider the potential of harm to India's people and their health?"

While India-based Coca-Cola and PepsiCo officials have declined to comment to the media on the issue, Kari Bjorhus, a U.S.-based spokesperson for Coca-Cola, said they were "disappointed that the (Kerala) government would make a decision like that based on inaccurate information."

"Our products are perfectly safe ( and  government and big business never lie ) and there is no reason to take them away from consumers," she said.

India has brought similar charges against both Coca-Cola and PepsiCo before; three years ago, a CSE study caused allegations (proof) of excessive pesticides to be leveled at the companies, and their sales suffered. A few months later, the sales figures recovered (forced and strong-arm economic tactics via NAFTA ??   ~ Dr. E )

"For three years we have looked very hard at this and engaged the best scientific minds in the world," said Dick Detwiler, a spokesman for PepsiCo's international division in New York. "All of the data and all of the science point to the fact our products in India are absolutely safe, just as they are elsewhere in the world."  Like Aspartame, Splenda, DDT, Agent Orange, Teflon, Mercury, or Fluoride, etc... ?

This is a small comfort for Indian parents, many of whom think the ban is a great idea. ( Dr. E says, "It is a terrific idea by which to keep children, and the entire population healthier and illness-free !" )

"It is a good decision," said Molly Kurian, a housewife in Kerala's capital, Cochin. "My children have been addicts of Pepsi and Coke. Now I can teach them how to drink water."

"In my opinion," added Adams, "even without the presence of pesticides, these beverage products are harmful enough on their own to ban their sale in schools and government institutions. The link between sugary beverages and diabetes or obesity is well established in the scientific literature."

 Information: The main ingredient in dark cola soda is, PHOSPHORIC ACID. It is a high corrosive. Thus, a Coke or Pepsi will "eat the paint off your car". When consumed, it causes an acidic environment, causing damage to enzyme activity, and paves the way for disease, which requires an acidic environment to thrive...


Caffeine is also added to these drinks to cause a caffeine addiction, just like heavy coffee drinkers... and this is targeted toward children !!  This is both malfeasant and morally reprehensible.



Educate yourself.    Ask the right questions,     Do your "homework",    Be discerning,  

Be objective,  and "connect the dots".   You will live longer and healthier.  ~  Dr. E




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