Fit and 40 Something

'A Fitness Social Network for Persons 40 and Over'

Never leave Home with out it!
ACID-ALKALINE BALANCE:
ROLE IN CHRONIC DISEASE AND DETOXIFICATION

The concept of acid-alkaline balance in the field of medicine is not novel or new – its been embraced and well-documented by several groups within the medical community. Naturopathic medicine has used the acid-alkaline balance as a theoretical model to explain the foundation of many chronic health conditions, and increasing tissue alkalinity is well established in modern medicine as a potent means of detoxification.

Combine this information with the fact that our modern diets are excessively acidic (take a quick look at the Table 1 on the first page – you’d have to eat 14 servings of vegetables to balance the acids out of a typical lunch or dinner) and you can see that we desperately need to share this information with our friends and family to improve, preserve, and protect the health of those we love.

Read this incredible peer-reviewed journal article and share it with as many people as you can. The more people who read this…the more people who will want to buy X2O and become a Xooma Member.

ACID-ALKALINE BALANCE: ROLE IN CHRONIC

DISEASE AND DETOXIFICATION

Deanna M. Minich, PhD, FACN, CNS; Jeffrey S. Bland, PhD, FACN

Deanna M. Minich, PhD, FACN, CNS, is the Director of

Information Integration and Innovation at Metagenics, Inc,

and a clinical nutritionist at the Functional Medicine

Research Center in Gig Harbor, Wash. Jeffrey S. Bland, PhD,

FACN, serves as the chief science offi cer of Metagenics, Inc,

and is president of the MetaProteomics Nutrigenomics

Research Center.

Several researchers have noted that the contemporary

Western diet has increased in net acid load relative to

diets of the ancestral pre-agricultural Homo sapiens.1-3

Quite possibly, this shift occurred because of the agricultural

revolution and the ubiquity of processed

grains and shelf-stable food products devoid of essential nutritional

components. In addition to this underlying foundational

change in diet, there is the overlay of various nutritional fads that

have risen and fallen over the past few decades. Most recently,

the latest diet trend has been an interest in high-protein foods

accompanied by a compensatory decrease in the phytochemical

load from fresh fruits and vegetables. Indeed, high-protein diets

increase net dietary acid load and acidify the urine pH.2-5

Conversely, diets high in fruits and vegetables have been proposed

to be associated with a greater degree of alkalinity.4,6

Remer and Manz calculated the potential renal acid loads of certain

food groups and reported that alkaline-forming foods were

primarily vegetable and fruits, whereas acid-forming foods were

derived from cheese, meat, fi sh, and grain products (Table 1).4

Over time, ingestion of a high dietary acid load can progress

to a chronic low-grade level of metabolic acidosis. The incidence

of low-grade acidosis resulting from our modern diet has

been well documented.1-3,6 A chronic acidic load can cause a

number of health conditions such as osteoporosis, kidney disease,

and muscle wasting.1,7 Sebastian et al articulates this cause

and effect relationship eloquently: “Increasing evidence . . . suggests

that such persisting, albeit low-grade, acidosis, and the

relentless operation of responding homeostatic mechanisms,

result in numerous injurious effects on the body including dissolution

to bone, muscle wasting, kidney stone formation, and

damage to the kidney.”1(p1308)

In order to maintain acid-alkaline balance throughout the

various body systems, one system may be required to support

another. For example, the bone matrix contains a substantial

alkaline reserve such as calcium and magnesium cations that are

released from the bone to balance an overly acidic dietary load in

the event of inadequate buffering capacity in the blood. However,

repeated borrowing of the body’s alkaline reserve in response to

a consistent increased (dietary) acid load can be potentially detrimental.

In humans, hypercalciuria and negative calcium balance

due to calcium effl ux from bone may lead to metabolic bone

disease and calcium nephrolithiasis.2,8,9 In the chapter titled

“Potassium” of its report Dietary Reference Intakes for Water,

Potassium, Sodium, Chloride, and Sulfate, the Institute of Medicine

Food and Nutrition Board states the following:

In the setting of an inadequate intake of bicarbonate

precursors, buffers in the bone matrix neutralize the

excess diet-derived acid, and in the process, bone

becomes demineralized. Excess diet-derived acid titrates

bone and leads to increased urinary calcium and

reduced urinary citrate excretion. The resultant adverse

clinical consequences are possibly increased bone

demineralization and increased risk of calciumcontaining

kidney stones.7(p187)

Conversely, dietary modification can positively influence

bone metabolism. A diet favoring neutralization of net endogenous

acid production increases calcium and phosphate retention,

reduces bone resorption markers, and increases markers of

bone formation in postmenopausal women.10 Furthermore, studies

have demonstrated a positive association between a high

intake of alkali-rich fruits and vegetables with preservation of

bone mineral density.6,11,12

PHYSIOLOGY OF ACID-ALKALINE BALANCE

From a physiological perspective, the body has compartmentalized

organ systems operating within specifi c pH ranges

(Table 2).13 The “potential of hydrogen,” or “pH,” is based on a

logarithmic scale, meaning that there is a 10-fold difference

between each number going from 1 to 14. The lower numbers

(1-6.99) represent the acid (or H+ donating) range, and the higher

numbers (7.01-14) represent the alkaline (or H+ accepting)

range. For the most part, body tissues remain within the neutral

pH of 7. Some body systems such as the blood (7.35-7.45) are

more tightly regulated than others (eg, urine pH ranges from 4.5-

8.0), and any extended disturbance in acid-alkaline balance may

upset cell functioning via its transport and signaling processes.14-

16 The human body has several means whereby it is able to regulate

acid-alkaline balance, including the following: (1) at the

cellular level via chemical reactions generating or consuming H+;

(2) in the blood with the assistance of bicarbonate, amino acids,

albumin, globulin, and hemoglobin; and (3) systemically through

the release of carbon dioxide from the lungs and hydrogen ions

from the kidney.17

CLINICAL DETERMINATION OF ACID-ALKALINE BALANCE

Although it is not common, blood pH levels can shift to the

side of excessive acidity or alkalinity, in which case several clinical

symptoms will appear. Acidosis can lead to symptoms of lethargy,

progressing to stupor and coma, while alkalosis can lead to

a host of nervous conditions such as cramps, muscle spasms, irritability,

and hyperexcitability. Clinical determination of a high

systemic acid load can be accomplished by a number of methods,

including a review of the diet diary for at least 3 to 7 days to

gauge the degree of processed food and animal protein intake

relative to fruit and vegetable consumption and a measurement

of urine pH using narrow-range indicator paper. Urine pH is a

good indicator of the net dietary acid load, as reported by Remer

and Manz, who observed an inverse relationship between the

two variables.4 The urine compartment appears to be well suited

for measuring the effect of acute and chronic factors. In our clinical

experience, we have noted that the urine pH responds to a

dietary intervention in as little as 2 hours. Additionally, the fact

that the urine pH range spans a greater continuum (4.5-8.0) indicates

that it has more potential to refl ect systemic pH changes.

From our testing, it was determined that due to the wide pH

range of the urine, it is important to take a fasting urine sample

and to control for water intake during the fasting period. Intraand

inter-individual variability can be further reduced if the

same person is determining the pH readings consistently.

URINARY ALKALINIZATION

The concept of acid-alkaline balance in the fi eld of medicine

is not entirely novel, as it has been embraced by several groups

within the medical community. Naturopathic medicine has used

the acid-alkaline balance as a theoretical model to explain the

foundation of many diseases. Allopathic medicine has examined

pH modulation in specifi c organ systems such as the kidney to

control the formation of stones and the elimination of toxins. For

example, urine alkalinization has been part of the medical protocol

for the management and prevention of uric acid stones.18,19

Another aspect of the acid-alkaline balance is its role in

detoxifi cation, via either the acute removal of a drug or poison

due to overdose or a nutritional protocol to support metabolic

detoxifi cation and decrease dietary toxins. Urinary pH alkalinization

is a method employed under acute medical settings for the

enhanced elimination of toxins in the event of a severe overdose.

Conversely, acidifi cation of urine also increases the elimination

of specifi c toxins, although to a seemingly lesser degree.20,21 The

method by which urine alkalinization works to enhance toxin

elimination is by the medically recognized process of “ion trapping,”

which is the ability to enhance urinary excretion of weak

acids in alkaline urine, preventing the reabsorption of xenobiotics

by renal tubules.22,23 Proudfoot et al published a position

paper on urine alkalinization, approved by the American

Academy of Clinical Toxicology, which describes the use of urine

alkalinization to ≥7.5 via intravenous sodium bicarbonate administration

for acute poisoning and toxicity.22 In this extensive

review, the effect of urine alkalinization on the excretion of various

pharmaceuticals and environmental toxins is elucidated.

This report states that “urine alkalinization increases the urine

elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid,

difl unisal, fl uoride, mecoprop, methotrexate, phenobarbital, and

salicylate.”22 The potential of urine alkalinization to enhance

toxin excretion is exemplifi ed by the work of Blank and Wolffram,

wherein they modulated urine pH in pigs with 2% dietary sodium

bicarbonate, changing the urine pH from 5.7 ア 0.2 to 8.3 ア 0.1,

and favorably impacted the excretion of ochratoxin A, a mycotoxin,

from 9.3 ア 1.9% to 22.2 ア 4.3% of the dose.24 Also, experimental

and clinical studies confi rm that urine alkalinization is

effective for salicylate poisoning.23,25,26 Garrettson and Geller

showed in humans that an increase in urine pH from 6.1 to 8.1

changed the renal clearance of salicylate from 0.08 ア 0.08 L/h to

1.41 ア 0.82 L/h.23

Therefore, if the rapid removal of toxins can be achieved to

a large extent with increasing urine pH 2 points on the pH scale

(which corresponds to a 100-fold decrease in H+ ions), it would

follow that smaller quantities of toxins may be removed on a prolonged

basis if there were a subtle increase of urine pH in the

alkaline direction. Due to the logarithmic pH scale, a small

change in urine pH could have a disproportionately large effect

on drug and xenobiotic clearance.22 The concept of “progressive”

versus rapid alkalinization of urine may be useful as an adjunct

for integrative health approaches employing metabolic detoxifi -

cation using specifi c (nutritional) protocols. Traditionally, functional

medicine has addressed detoxifi cation or the removal of

harmful endo- or exogenous substances, from the aspect of

upregulating hepatic phase I and phase II enzymes to enable the

chemical biotransformation of toxins into water-soluble metabolites

for excretion in the urine. With the added clinical procedure

of urine alkalinization, the removal of these compounds from the

body is accelerated. There are many dietary agents to assist in

progressive alkalinization. Foods that are high in potassium are

noteworthy (Table 3).27 One approach to clinically implementing

these strategies for metabolic detoxifi cation involves initiating

the patient on an elimination diet high in whole fruits and cruciferous

vegetables and low in animal protein. In addition to potassium,

cruciferous vegetables contain myriad phytochemicals,

such as indole-3-carbinol and sulforaphane, which are essential

for facilitating toxin biotransformation.28-30 Additionally, these

vegetables can favorably alkalize urine pH. In a pilot trial with 5

volunteers, we found that a 200 g serving of cooked broccoli, carrots,

and caulifl ower (with broccoli as the predominant vegetable)

resulted in an increase in urine alkalinization for up to 4

hours afterwards (baseline pH = 6.20 ± 0.51; after vegetables =

6.91 ± 0.45, P=.01). Thus, the simple instruction to alter diet to

include cruciferous vegetables can promote detoxification by

upregulating phase II enzymes and by alkalizing urine, resulting

in enhanced excretion of toxins.

Moreover, alkalinization during metabolic detoxification

may be particularly useful, as it is believed that cellular pH and

the blood buffering system shift to the acid side of ideal pH

reserve during detoxifi cation due to increased circulation of xenobiotics

and organic acids (eg, glucuronic acid). Furthermore,

organic cation transporters that are responsible for the transport

of xenobiotics in and out of the cell are pH-sensitive.31,32

ALKALIZING AGENTS

In addition to dietary changes, nutritional supplementation

for a short-term course of 3 to 4 weeks with select botanicals can

facilitate metabolic detoxifi cation. It would be appropriate to

include specifi c alkalizing agents, such as potassium, within this

nutritional regimen (Table 3). Unfortunately, the mainstream

American diet is poor in potassium, as it often lacks suffi cient

fruits and vegetables. The adequate intake (AI) established by

the Food and Nutrition Board of the Institute of Medicine for

potassium is 4.7 g daily,7 which is the same amount that is

encouraged by the Dietary Approaches to Stop Hypertension

(DASH) diet to maintain lower blood pressure levels, decrease

the effects of salt intake, decrease the risk of kidney stones, and

possibly reduce the incidence of bone loss. Current median

intakes of potassium in the United States are roughly 35% and

50% below the AI for men and women, respectively.7 African

Americans would particularly benefi t from increased potassium

intakes due to their relatively low potassium intakes and high

prevalence of elevated blood pressure and salt sensitivity.7 For the

healthy population, intake of potassium at levels higher than the

AI is not of particular high risk due to the ability of the kidney to

excrete excess amounts.7 However, potassium intakes should be

closely monitored for patients with acute or chronic renal failure

and pre-existing heart disease and for those on medications that

increase potassium reserves in the body, such as potassiumsparing

medications.7

Various potassium salts are available to alter urine pH.

Studies using sodium bicarbonate administration reveal little

effect on urinary calcium excretion in contrast to studies that

used potassium bicarbonate or potassium citrate supplementation

and found significant reductions.33,34 Potassium citrate, a

therapeutic regimen to prevent kidney stones, can effectively

alkalize urine. Doses of 4 to 8 g daily for 2 weeks in patients with

homozygous cystinuria have effectively alkalized urine.35

Additionally, there are a number of studies on the use of potassium

citrate to counteract bone resorption caused by chronic acidemia

of protein-rich diets.36-38

The effects of potassium depend on its accompanying

anion.7 Potassium chloride, commonly used in processed food

products, does not appear to have the same alkalizing ability as

potassium citrate.7 In a recent study, Jehle et al demonstrated

that potassium citrate was more effi cacious than potassium chloride

in increasing bone mineral density in postmenopausal

women with osteopenia.39 Furthermore, potassium chloride led

to decreased bone mineral density in the lumbar spine.

Potassium citrate supplementation in these subjects resulted in a

sustained and signifi cant reduction in urinary calcium excretion

and an increase in urinary citrate excretion, indicating that alkalinization

had occurred.39,40

Additionally, the citrate anion may be especially relevant for

detoxifi cation since it is an intermediate of the Krebs cycle and

can potentially play a role in energy production. As many clinicians

acknowledge from their experience, lack of energy is a common

side effect of the fi rst stages of metabolic detoxifi cation.

Therefore, eating foods that are high in citrate, such as certain

fruits and vegetables, may be benefi cial. It is also worth noting

that citrate is metabolized to bicarbonate in the body, thereby

further adding to the buffering potential.7

SUMMARY

In conclusion, the increasing dietary acid load in the contemporary

diet can lead to a disruption in acid-alkaline homeostasis

in various body compartments and eventually result in

chronic disease through repeated borrowing of the body’s alkaline

reserves. Adjustment of tissue alkalinity, particularly within

the kidney proximal tubules, can lead to the more effective excretion

of toxins from the body. Metabolic detoxifi cation using a

high vegetable diet in conjunction with supplementation of an

effective alkalizing compound, such as potassium citrate, may

shift the body’s reserves to become more alkaline.

Acknowledgments

Special thanks to those individuals who reviewed this manuscript, including Gary Darland,

PhD; Bhaskar Shenai, PhD; Robert Lerman, MD, PhD; and Barbara Schiltz, MS, RN, CN.

REFERENCES

1. Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr. Estimation of the

net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid

ancestors. Am J Clin Nutr. 2002;76(6):1308-1316.

2. Maurer M, Riesen W, Muser J, Hulter HN, Krapf R. Neutralization of Western diet

inhibits bone resorption independently of K intake and reduces cortisol secretion in

humans. Am J Physiol Renal Physiol. 2003;284(1):F32-40.

3. Frassetto LA, Todd KM, Morris RC Jr, Sebastian A. Estimation of net endogenous noncarbonic

acid production in humans from diet potassium and protein contents. Am J

Clin Nutr. 1998;68(3):576-583.

4. Remer T, Manz F. Potential renal acid load of foods and its infl uence on urine pH. J Am

Diet Assoc. 1995;95(7):791-797.

5. Reddy ST, Wang CY, Sakhaee K, Brinkley L, Pak CYC. Effect of low-carbohydrate highprotein

diets on acid-base balance, stone-forming propensity, and calcium metabolism.

Am J Kidney Dis. 2002;40(2):265-274.

6. Tucker KL, Hannan MT, Kiel DP. The acid-base hypothesis: diet and bone in the

Framingham Osteoporosis Study. Eur J Nutr. 2001;40(5):231-237.

7. Institute of Medicine of the National Academy of Sciences. Potassium. In: Dietary

Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC:

National Academies Press; 1994:186-268.

8. Green J, Kleeman CR. Role of bone in regulation of systemic acid-base balance. Kidney

Int. 1991;39:9-26.

9. Brenner RJ, Spring DB, Sebastian A, et al. Incidence of radiographically evident bone

disease, nephrocalcinosis and nephrolithiasis in various types of renal tubular acidosis.

N Engl J Med. 1982;307(4):217-221.

10. Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr. Improved mineral balance

and skeletal metabolism in postmenopausal women treated with potassium bicarbonate.

N Engl J Med. 1994;330(25):1776-1781.

11. Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP. Potassium, magnesium

and fruit and vegetable intakes are associated with greater bone mineral density

in elderly men and women. Am J Clin Nutr. 1999;69(4):727-736.

12. Sellmeyer DE, Stone, KL, Sebastian A, Cummings SR. A high ratio of dietary animal

to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal

women. Study of Osteoporotic Fractures Group. Am J Clin Nutr.

2001;73(1):118-122.

13. Lehninger AL. Biochemistry: The Molecular Basis of Cell Structure and Function. 2nd ed.

New York: Worth Publishers, Inc;1977.

14. Charoenphandhu N, Tudpor K, Pulsook N, Krishnamra N. Chronic metabolic acidosis

stimulated the transcellular and solvent drag-induced calcium transport in the duodenum

of female rats. Am J Physiol Gastrointest Liver Physiol. 2006;291(3):G446-455. Epub

2006 May 4.

15. Nijenhuis T, Renkema KY, Hoenderop JG, Bindels RJ. Acid-base status determines the

renal expression of Ca2+ and Mg2+ transport proteins. J Am Soc Nephrol.

2006;17(3):617-626.

16. Bailey JL, Zheng B, Hu Z, Price SR, Mitch WE. Chronic kidney disease causes defects in

signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt

pathway: implications for muscle atrophy. J Am Soc Nephrol. 2006;17(5):1388-1394.

17. Thomas L ed. Clinical Laboratory Diagnostics: Use and Assessment of Clinical Laboratory

Results. 1st ed. Frankfurt, Germany: TH-Books;1998.

18. Preminger GM, Harvey JA, Pak CY. Comparative effi cacy of “specifi c” potassium citrate

therapy versus conservative management in nephrolithiasis of mild to moderate

severity. J Urol. 1985;134(4):658-661.

19. Pak CY, Sakhaee K, Fuller CJ. Physiological and physiochemical correction and prevention

of calcium stone formation by potassium citrate therapy. Trans Assoc Am

Physicians. 1983;96:294-305.

20. Simpson GM, Khajawall AM. Urinary acidifiers in phencyclidine detoxification.

Hillside J Clin Psychiatry. 1983;5(2):161-168.

21. Nahata MC, Cummins BA, McLeod DC, Schondelmeyer SW, Butler R. Effect of urinary

acidifi ers on formaldehyde concentration and effi cacy with methenamine therapy. Eur

J Clin Pharmacol. 1982;22(3):281-284.

22. Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on urine alkalinization. J Toxicol

Clin Toxicol. 2004;42(1):1-26.

23. Garrettson LK, Geller RJ. Acid and alkaline diuresis: When are they of value in the

treatment of poisoning? Drug Saf. 1990;5(3):220-232.

24. Blank R, Wolffram S. Alkalinization of urinary pH accelerates renal excretion of ochratoxin

A in pigs. J Nutr. 2004;134(9):2355-2358.

25. Vree TB, Van Ewijk-Beneken Kolmer EW, Verwey-Van Wissen CP, Hekster YA. Effect of

urinary pH on the pharmacokinetics of salicylic acid, with its glycine and glucuronide

conjugates in human. Int J Clin Pharmacol Ther. 1994; 32(10):550-558.

26. Proudfoot AT, Krenzelok EP, Brent J, Vale JA. Does urine alkalinization increase salicylate

elimination? If so, why? Toxicol Rev. 2003;22(3):129-136.

27. USDA/ARS Nutrient Data Laboratory Food Database. Available at: http://www.nal.

usda.gov/fnic/foodcomp/search/. Accessed June 1, 2007.

28. Nho CW, Jeffery E. The synergistic upregulation of phase II detoxifi cation enzymes by

glucosinolate breakdown products in cruciferous vegetables. Toxicol Appl Pharmacol.

2001;174(2):146-152.

29. Steinkellner H, Rabot S, Freywald C, et al. Effects of cruciferous vegetables and their

constituents on drug metabolizing enzymes involved in the bioactivation of DNAreactive

dietary carcinogens. Mutat Res. 2001;480-481:285-297.

30. Fahey JW, Talalay P. Antioxidant enzymes of sulforaphane: a potent inducer of Phase II

detoxifi cation enzymes. Food Chem Toxicol. 1999;37(9-10):973-979.

31. Sweet DH, Pritchard JB. rOCT2 is a basolateral potential-driven carrier, not an organic

cation/proton exchanger. Am J Physiol. 1999;277 (6 Pt 2):F890-F898.

32. Fujita T, Urban TJ, Leabman MK, Fujita K, Giacomini KM. Transport of drugs in the

kidney by the human organic cation transporter, OCT2 and its genetic variants. J

Pharm Sci. 2006;95(1):25-36.

33. Lemann J Jr, Gray RW, Pleuss JA. Potassium bicarbonate, but not sodium bicarbonate,

reduces urinary calcium excretion and improves calcium balance in healthy mean.

Kidney Int. 1989;35(2):688-695.

34. Sakhaee K, Nicar M, Hill K, Pak CY. Contrasting effects of potassium citrate and sodium

citrate therapies on urinary chemistries and crystallization of stone-forming salts.

Kidney Int. 1983;24(3):348-352.

35. Fjellstedt E, Denneberg T, Jeppsson JO, Tiselius HG. A comparison of the effects of

potassium citrate and sodium bicarbonate in the alkalinization of urine in homozygous

cystinuria. Urol Res. 2001;29(5):295-302.

36. Marangella M, Di Stefano M, Casalis S, Berutti S, D’Amelio P, Isaia GC. Effects of

potassium citrate supplementation on bone metabolism. Calcif Tissue Int.

2004;74(4):330-335.

37. Sakhaee K, Maalouf NM, Abrams SA, Pak CY. Effects of potassium alkali and calcium

supplementation on bone turnover in postmenopausal women. J Clin Endocrinol

Metab. 2005;90(6):3528-3533.

38. Sellmeyer DE, Schloetter M, Sebastian A. Potassium citrate prevents increased urine

calcium excretion and bone resorption induced by a high sodium chloride diet. J Clin

Endocrinol Metab. 2002;87(5):2008-2012.

39. Jehle S, Zanetti A, Muser J, Hulter HN, Krapf R. Partial neutralization of the acidogenic

Western diet with potassium citrate increases bone mass in postmenopausal women

with osteopenia. J Am Soc Nephrol. 2006;17(11):3213-3222.

40. Trivedi B, Tannen RL. Effect of respiratory acidosis on

intracellular pH of the proximal

tubule. Am J Physiol. 1986; 250(6 Pt 2):F1039-1045.

Tags: +, +water, health, live

Share 

Add a Comment

You need to be a member of Fit and 40 Something to add comments!

Join this social network

About

Maureen Guest Maureen Guest created this social network on Ning.

Create your own social network!

Relaxation Therapy

Health, Fitness & Sports


Bodybuilding.com


Footlocker.com

HPL PureSport LLC

Need all day Energy? Runner

Foot Action (Footlocker)

Championcatalog.com


Native Remedies The Natural Choice





Wellness Tips

    follow me on Twitter

    Industry Directory

    Notes

    3-for-1 Health Deal

    Created by Maureen Guest Jan 16, 2009 at 3:42am. Last updated by Maureen Guest Jan 16.

    Few tips to look younger

    Created by Maureen Guest Oct 19, 2008 at 10:54pm. Last updated by Maureen Guest Oct. 20, 2008.

    7 Anti-Aging Super Foods

    Created by Maureen Guest Oct 5, 2008 at 4:19am. Last updated by Maureen Guest Oct. 5, 2008.

    Badge

    Loading…

    © 2009   Created by Maureen Guest on Ning.   Create Your Own Social Network

    Badges  |  Report an Issue  |  Privacy  |  Terms of Service