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June 2009 - Volume 7, Issue 5
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From the Editor
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Original Contributon and Clinical Investigation

Emotional Status of Primary Health Care Physicians in Saudi Arabia
Khalid S. Al-Gelban, Yahia M. Al-Khaldi, Hasan S. Al-Amri, Ossama A. Mostafa

Carbonated Beverages and Urinary Calcium Excretion
Tayfoor Jalil Mahmoud
Persistent Khat Chewing Habit During Pregnancy May Affect Neonatal Birth Weight
Dr. Abdelrahman H. Al Harazi, Dr. Kaima A Frass
Chest Pain in Women
Mazen Ahmad Asayreh
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Medicine and Society
Ante-Natal Care Service Uptake in Slum Areas of Dhaka City
Md Aminul Haque, Amir Mohammad Sayem, Dr. Nilufar Yeasmin Nili
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International Health Affairs
Increasing Incidence of Suicidal Poisoning in the Turmoil Affected Kashmir Valley - a Threatening Situation
G. Hassan, Waseem Qureshi, Kadri S.M., G.Q. Khan, D.C. Kundal, Qureshi K.A., Manish Kak, Manzoor Ahmad, H. Arshid, Maajid, Nazir A. Khan
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Clinical Research and Methods
Risk of Fetal Lloss Due to Chorionic Villous Sampling in Iran
Farzad Mehrnaz
Maternal and Umbilical Cord Blood Lead Levels and pregnancy outcomes: A Hospital Based Enquiry
Asma A. Al- Jawad, Zina W. A. Al-Mola, Raghad A. Al- Jomard
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June 2009 - Volume 7, Issue 5
Carbonated Beverages and Urinary Calcium Excretion
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Tayfoor Jalil Mahmoud
Ph.D. / Medical Biochemistry/ Dept. of Medical Biochemistry/ Hawler Medical University/ Erbil/ Iraq

ABSTRACT

Background and objectives: Intake of carbonated beverages has been associated with increased urinary calcium excretion and fracture risk in observational studies.
The aim of the present study was to assess the short-term effects of carbonated beverages on total urinary calcium excretion in normal young males in Erbil city.

Materials and methods: Eighteen randomly selected male volunteers of 24.05 years age were given each 500 ml of Coca Cola® / day for six successive days. Their pre and post- Coca Cola consumption urine samples were collected and analyzed for calcium excretion levels.
Total urinary calcium was estimated by an enzymatic colorimetric method.

Results: A significant increase (P < 0.05) in urinary calcium level was observed in subjects consuming Coca Cola.

Conclusions: The excess calciuria is confined to normal males who are habitual consumers of Coca Cola. These findings suggest that excess consumption of carbonated beverages in general, and mainly Coca Cola, which mostly replaced milk, must be discouraged in order to prevent bone resorption and hence early osteoporosis.

Key words: Hypercalciuria, Carbonated beverages, Colas, Caffeine, Calcium, Phosphorous.



INTRODUCTION

Inadequate calcium intake is a serious public health concern, since this mineral is involved with numerous metabolic processes including bone remodeling (bone turnover), vascular function, muscular contraction and others. Moreover, the literature suggests that adequate calcium intake may reduce the risk of obesity, insulin resistance syndrome and certain chronic diseases of aging such as hypertension, some forms of cancer and osteoporosis(1).

Carbonated beverages (soft drinks) are beverages that do not contain alcohol and usually contain phosphoric acid, caffeine, sugar or aspartame or saccharin, caramel coloring, carbon dioxide and are commonly known as soda, soda pop, pop, tonic, fizzy drinks, minerals, colas, coke, flavored water, sparkling water, iced tea, lemonade, squash and fruit punch.

Carbonated beverages are junk food - sugary drinks that are high in calories, but supply no nutrient (empty calories). A 12-ounce Cola contains the equivalent of 10 teaspoons of sugar and 150 calories. Soft drinks are prepared by pumping carbon dioxide, which is a waste product of metabolism that is exhaled. So why should we want to further add a waste product to our bodies?
Carbonated beverages also contain large amounts of carbonic acid, hence the term carbonated beverages. This carbonic acid causes the body to deplete the bones of calcium, to remain alkaline(2).

Frequent consumption of carbonated beverages has been associated with reduced bone mass, or increased fracture risk, both later in life and in children and adolescents, obesity, diabetes, tooth decay, nutritional deficiencies, heart disease, kidney stones, and other health problems(3).
In most reports, Colas were more strongly associated than were other carbonated beverages. Several investigators suggested that the factor or factors responsible for this association may be the increase in phosphorous intake, or the net acid load of those beverages that use phosphoric acid as the acidulant or the caffeine of those beverages that are caffeinated(4).

For most of these factors, the effect is usually attributed to increased total urinary calcium loss, and the biochemical explanation is that parathyroid hormone (PTH) primarily controls calcium levels in our blood. When the brain senses low calcium to phosphorous ratios (normally = 1.5-2/1), it triggers the release of PTH, which acts in a complex manner on three major body parts (intestines, bones, and kidneys) to restore or increase calcium levels. PTH causes calcium release from bone as it causes osteoclasts to increase in size, and number, leading to enhanced osteoclast activity and bone resorption (bone loss)(5).

The issue is especially important today because calcium intakes in our region fall far short of current recommendations (1000-1300 mg/day). Per capita, carbonated beverage consumption has risen dramatically, and has replaced milk in the diet of most Iraqi - Kurdistan region children, adolescents and adults and carbonated sodas are now the preferred beverage of young individuals. This increase in consumption of soft drink is not a surprise because soft drink manufacturers have spent billions of dollars in advertising to attract more consumers and to increase consumption of their products. Accordingly, and because of the interest among nutritionists and dietitians as to the possible effects of carbonated beverages, we undertook the present study.

We investigated the acute effect of Coca Cola on urinary calcium loss by young subjects, who were habitual users of such beverages.

 

MATERIALS AND METHODS

Subjects
This study was carried out during the period: March to June 2008 at the Department of medical biochemistry,College of medicine, Hawler Medical university, Erbil, Iraq.

The present investigation was conducted on 18 randomly selected young male volunteers who were on usual dietary intakes of foods and nutrients and divided into two groups:

Group I (pre-carbonated beverage consumption group = control group): included 18 apparently healthy male volunteers, their mean age was 24.05 years and the range of age was 19-30 years.

None of this group had clinical or biochemical evidence of any type of diseases, none were taking carbonated beverages and medications containing calcium and vitamin D six days before the test, and informed consent was obtained from each individual.

Group II (post-carbonated beverage consumption group = case group): Included the same 18 subjects of group 1. Each individual of this group had drank about 500 ml of Coca Cola / day for six successive days.The Coca Cola was purchased from a public market and is a popular brand that is available worldwide .

The details concerning the two groups are elucidated in Table (1).

Table 1 Number and age of the studied groups.
Groups Number of subjects Age (years)
Mean ±S.E.M      Range
Group I 18 24. 05 ± 0. 20         19—30
Group II 18 24. 05 ± 0. 20         19—30

Samples
Pre- and post- Coca Cola consumption 24 hour urine samples were collected from the two groups for estimation of total urinary calcium levels.

Methods
Total urinary calcium was estimated by an enzymatic colorimetric method described by Tietz N.W.(6), using commercial kits (BIOLABO SA, France). The principle of this method was explained by Morehead and Briggs(7), and depends on the reaction of O-Cresol Phtalein Complexone (CPC) with calcium in an alkaline medium to form a dark-red colored complex, the intensity of which is measured at 570 nm and proportional to the amount of total calcium in the urine samples.

Statistical analysis
The statistical evaluation of the results (mean, standard deviation (S.D.), and standard error of mean (S.E.M.) were calculated using the sSPSS system version 15}. The different variables were compared to each other; simple correlations were tested with the unpaired 't' test. Only (P<0.05) is regarded as significant (8).


RESULTS

Group I (control group): The mean ± S.E.D. level of urinary calcium was 144.74±2.58 mg / dl, and the range of variation was 41.64-239.07 mg / dl, table (2).
Group ? (case group): The mean ± S.E.D. level of urinary calcium was 189.36±5.33 mg/dl, and the range of variation was 83.78-376.00 mg / dl, Table 2.

Table 2 Biochemical Parameters of the Studied Groups.
Biochemical Parameters Group  I
Mean ±S.E.             Range
Group II
Mean ±S.E.           Range
Statistical  value
Total Urinary Calcium mg/dl 144.74 ±2.58     41.64 - 239.07 189.36 ±5.33    83.78 - 376 P < 0. 05

Figure 1. Total urinary calcium excretion (mg / dl) of the studied groups.

 

DISCUSSION

The previous studies carried out on the same aspect, were mostly on children, adolescents and female subjects(4,9), whereas we have seen the acute effects of Coca Cola on young male subjects.

The most apparent detail in our data is the significant rise (P < 0.05) in total urinary calcium excretion after consumption of Coca Cola. This most likely means that carbonated beverages as a whole have a significant intrinsic effect on calcium economy. However even a small excess urinary excretion, if cumulative and not offset by additional calcium absorption would inevitably lead to hypocalcemia, hypercalciuria and bone loss(4)

Massey LK and Wise KJ(10) conducted a study on the effect of caffeine, a constituent of carbonated beverages and reported a rise in urinary calcium excretion.
Published data by Robert P Heaney and Karen Rafferty(4) revealed that phosphoric acid contents of carbonated beverages would lower blood calcium by 0.09 mmol (3.6 mg) and increase its urinary excretion.

Our results are consistent with that of Michelle AO Kinney(11), who reported that drinking Cola beverages, which contain phosphoric acid and often caffeine, may increase calciuria, and cause fragility of bones in children and adolescents, through interaction with the bone mineral content.

Wyshak G(3) also conducted a study on the effect of carbonated beverage consumption on teenage girls and showed an increase in urinary calcium excretion and increased risk of bone fracture in active girls who drank Colas; conversely, there was no increased urinary calcium excretion and no risk of fractures in those whodrank non-Colas.

Phosphoric acid is associated with altered calcium homeostasis and development of hypocalcaemia. Consumption of approximately 0.6 or more cans or bottles of Cola beverages per day, is a risk factor for the development of hypocalcaemia in children 14 years of age or younger. Similarly, the consumption of one or more bottles of Cola beverage per day is associated with hypocalcaemia in postmenopausal women(3).

Garcia Contreras et al(12) showed that rats that drank Cola beverages developed hypocalcaemia and lower femoral mineral density compared with control rats that drank water.
Caffeine is also present in most Cola beverages, recognized as a mild diuretic, with short-term increase in urinary calcium excretion, and may affect bone health.

Ohta et al.(13) showed that caffeine intake affected the content and crystallite size of bone minerals and that the femur of rats fed caffeine tended to be weaker compared with controls.
Michael Murray and Joseph Pizzorno(14) reported that soft drinks have long been suspected of leading to lower calcium levels and higher phosphate levels in the blood.

When phosphate levels are high and calcium levels are low, calcium is pulled out of the bones. The phosphate content of soft drinks like Coca Cola and Pepsi Cola is very high, and they contain virtually no minerals, vitamins, proteins, fibers, or other essential nutrients .Most soft drinks contain food additives such as food coloring, artificial flavoring, emulsifiers and preservatives. Carbonated beverages may also displace other healthier choices in people's diet, such as water, milk and natural fruit juices.

The same authors added that of the 57 children who had low calcium levels, 38 (66.7%) drank more than four bottles (12-16 ounces per bottle) of soft drinks per week.

These results, more than support the contention that soft drink consumption leads to lower calcium levels in children. This situation ultimately leads to poor bone mineralization.

In another study conducted by Marion Nestle(15), it was found that soft drinks are the single greatest source of caffeine in children's diet; A 12-ounce can of Cola contains about 45 mg, but the amounts in more potent soft drinks can exceed 100 mg, a level approaching that found in coffee.

Moreover Mette Kristesen et al.(16) carried out a study on the effects of Cola on urinary calcium excretion, and showed that over a 10 day period, high intake of Cola (2.5 liters / day) caused an increase in urinary calcium excretion in young men.

Grace Wyshak et al(17) conducted a study to evaluate the effects of non-alcoholic carbonated beverage consumption on bone fractures among 2,622 women, former college athletes, and found a statistically significant association between nonalcoholic carbonated beverage consumption and bone fracture.

Tero H et al.(18) conducted a study on the effects of carbonated beverages and the risk of kidney stones among male smokers and found that the incidence of kidney stones could be decreased by limiting soft drink consumption.

Saldana Tina M et al.(19) carried out also a study on the relationship between carbonated beverage consumption and kidney disease and reported that Cola consumption may increase the risk of chronic kidney disease.

Ogor R et al(20) conducted a study to determine bone mineral density changes caused by consumption of Cola drinks and the associated factors, and reported that Cola consumption had a statistically significant decrease in (BMD) bone mineral density (approximately 20% lower) compared to the control rats. They found also non significant decrease in serum calcium. Moreover they revealed evidence of renal damage in the Cola-fed rats.

Finally Katherine L Tucker et al(21), conducted a study using data from > 2,500 men and pre- and post-menopausal women and found also that intake of Cola, but not of other carbonated beverages, is associated with low bone mineral density in older women.


CONCLUSION

The results of the present study, confirm previous findings that high consumption of Carbonated beverages induce calciuria and suggest that the habitual and excessive consumption of soft drinks must be discouraged and replaced by milk and natural fruit juices, in order to avoid the negative calcium balance seen in carbonated beverage drinkers, which may cause bone resorption and osteoporosis in later life.



REFERENCES

  1. Maureen L Storey, Richard A Forshee and Patricia A Anderson. Association of adequate intake of calcium with diet, beverage consumption, and demographic characteristics among children and adolescents. Journal of American College of Nutrition 2004; 23 (1): 18-33.
  2. Petriodou E, Karpathios T, Dessypriss N, et al. The role of dairy products and non-alcoholic beverages in bone fracture among school children. Scan. J. Soc. Med. 1997; 25: 119-125.
  3. Wyshak G Teen-aged girls, carbonated beverages consumption and bone fracture. Arch. Pediatr. Adolesc. Med. 2000; 154: 610-613.
  4. Robert P Heaney and Karen Rafferty Carbonated beverages and urinary calcium excretion. Am. J. Clin. Nutr. 2001; 74: 343-347.
  5. Barger-Lux MJ, and Heaney RP Caffeine and the calcium economy revisited. Osteoporosis Int. 1995; 5: 97-102
  6. N.W.Tietz Text book of clinical biochemistry, 3rd ed. C.A. Burtis, E.R. Ashwood, W.B. Saunders 1999: 1395-1406, 1435-1439.
  7. Morehead WR and Briggs HG Clin Chem. 1974; 20: 1458-1460.
  8. Noursis MJ SPSS for windows. SPSS Advanced statistic release 1996 ; 7.5 SPSS Inc. Chicag.
  9. Khan SA, Qureshi H, Karira KA, et al. The effects of soft drinks on normal healthy women, Medical Channel 2004; 10 (4): 11-13.
  10. Massey LK and Wise KJ, The effect of dietary caffeine on urinary excretion of calcium, magnesium, sodium and potassium in healthy females, Nutr. Res. 1984; 4: 43-50.
  11. Michelle AO Kinney. Does consumption of cola beverages causes bone fracture in children?, Mayo Clin. Proc. 2002; 77: 360-365.
  12. Garcia- Contreras F, Pantiagua R, Avila Diaz M et al. Cola beverage consumption induces bone mineralization reduction in ovariectomized rats, Arch. Med. Res. 2000; 31: 360-365.
  13. Ohta M , Cheuk G , Thomas KA et al. Effects of caffeine on the bone of aged, ovariectomized rats. Ann. Nutr. Metab. 1999; 43: 52-59.
  14. Michael Murray and Joseph Pizzorno, The health hazards of drinking coca-cola and other soft drinks. http: // www.newstarget.com
  15. Marion Nestle Food politics: How the food industry influences nutrition
    http : // www.newstarget.com
  16. Mette K, Marlene J, Jane K, Marianne H, and Christian M, Short effects on bone turnover of replacing milk with cola beverages: a 10 days interventional study in young men, J. Osteoporosis Internat. 2005 ; 16 (12): 1803-1808.
  17. Grace Wyshak , Rose E Frisch , Tenley E Albright , Nile L Albright , Isaac Schiff and Jelia Witschi. Non alcoholic carbonated beverage consumption and bone fractures among women former college athletes. Journal of Epidemiology 2005 ; 7 (1): 91-99.
  18. Tero H , Pirjo P , Mikko V , Demetrius A , and Jarmo V, Nutrient intake and use of beverages and the risk of kidney stones among male smokers, Am J. Epidemiol. 1999;150 (2): 187-194.
  19. Saldana Tina M, Basso Olga, Darden Rebecca and Sandler Dale P. Carbonated beverages and chronic kidney disease. Epidemiology 2007; 18 (4): 501-506.
  20. Ogor R et al. Bone density and consumption of Cola beverages Basic and Clinical Pharmacology and Toxicology 2007; 100: 334-338.
  21. Katherine L Tucker et al. Colas, but not other carbonated beverages, are associated with low bone density in older women: The Framingham Osteoporosis Study. American Journal of Clinical Nutrition 2006;84:936-942.
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