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Biology and the properties of water

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Cellular hydration state in health and disease

Professor Dieter Haussinger and colleagues have published data in the Lancet, one of the world's most prestigious medical journals, that correlates cell hydration to anabolic metabolism. The authors state that an increase in cell hydration acts as an anabolic proliferative signal, whereas cell shrinkage is catabolic and antiproliferative. The authors suggest that in a clinical setting physicians should pay more attention to body cell hydration.

The authors state that in liver, an increase in cell hydration (cell swelling) inhibits breakdown of glycogen, glucose, RNA, and protein and simultaneously stimulates synthesis of glycogen, RNA, DNA, and protein. An increase in cell hydration is anabolic. The authors note that an increase in cell hydration (cell volume) occurs under the influence of the hormone insulin. It is known that the multiple effects of insulin include the recruiting to the plasma membrane of glucose transporters, the stimulation of glycogen synthesis and the uptake of amino acids into muscle(1). The authors note that a decrease in cell hydration (cell volume) occurs under the influence of the hormone glucagon with a loss of potassium from cells. A decrease in cell hydration is catabolic.

Abstract in The Journal of Biological Chemistry

http://www.ncbi.nlm.nih.gov/pubmed/12033446

Abstract in paper in International Review of Cytology:

http://www.ncbi.nlm.nih.gov/pubmed/12696593

Abstract in Cellular Physiology and Biochemistry:

http://www.ncbi.nlm.nih.gov/pubmed/11125222

It is known that healthy kidneys can excrete more than 10 liters of water per day, well above any normal level of water intake(2). It is known also that the ingestion of water results in the entry of water into body cells. Water ingestion decreases plasma osmolality. When plasma osmolality is decreased, interstitial fluid osmolality is decreased which creates osmotic and hydrostatic pressure gradients across cell membranes favoring the entry of water into body cells(3). Body cells hydrate.  With few exceptions, the membranes of body cells are highly permeable to water.

The body responds to water ingestion by suppressing the release of antidiuretic hormone (ADH, vasopressin) from the posterior pituitary gland. The suppression of ADH release results in decreased water reabsorption from the collecting duct cells of the kidneys and the excretion of excess water. Peak diuresis is delayed for 90 to 120 minutes, the time necessary for the metabolism of previously circulating ADH(2).

Perhaps there is a level of daily water ingestion that modulates ADH release and decreases extracellular fluid osmolality sufficiently to allow the entry of water into body cells. The increase in cell hydration that results may act as an anabolic proliferative signal. The anabolism in body cells stimulated by body hydration may explain the results of several epidemiological studies. These studies show that the consumption of extra water per day may be associated with a decrease in fatal coronary heart disease(4) and colon cancer(5). Certainly, more studies appear to be warranted.

The authors state that cell shrinkage is catabolic. Cell shrinkage occurs when water exits body cells because extracellular fluid osmolality is increased and an osmotic gradient favors the transfer of water from cells to the extracellular fluid.

Extracellular fluid osmolality is increased with increased extracellular salt concentrations, with dehydration, with excess diuresis and with excess alcohol consumption. Although the increase in extracellular fluid osmolality due to excess alcohol consumption is physiologically complex, it is a fact nevertheless that alcohol per se can increase osmolality by its interference with hydrogen bonding between water molecules. Alcohol interference with hydrogen bonding between water molecules results in a decrease in water volume(6). Is the pathology observed with long term excess alcohol consumption partly a result of cell chronic dehydration and shrinkage?

Numerous epidemiological studies over the past 30 years have identified a correlation between alcohol consumption and cancer(7,8).  Does the alcohol dehydration of body cells affect the structure and function of hydrated biomolecules such as proteins and DNA?  Would the consumption of extra water promote the structure and function of DNA and help to prevent cancer?  There is evidence certainly that water consumption may decrease the risk of colon(5), bladder(9) and breast(10) cancers.

1. Metabolism at a Glance. Salway JG. Third Edition. 2004. Blackwell Publishing Ltd, Massachusetts. Pgs 108-119.

2. Clinical Physiology of Acid-Base and Electrolyte Disorders. Rose BD and Post TW. Fifth Edition. 2001. McGraw Hill, New York. Pgs 285-298.

3. Clinical Physiology of Acid-Base and Electrolyte Disorders. Rose BD and Post TW. Fifth Edition. 2001. McGraw Hill, New York. Pgs 241-257.

4. Chan J, et al. 2002. Water, Other Fluids and Fatal Coronary Heart Disease. Am J Epidemiol 155(9): 827-833.

5. Shannon J, et al. 1996. Relationship of Food Groups and Water Intake to Colon Cancer Risk.  Cancer Epidemiology, Biomarkers & Prevention 5: 495-502.

6. Dill KA and Bromberg S. Molecular Driving Forces, Statistical Thermodynamics in Chemistry and Biology. 2003. Garland Science, New York. Pgs 577-591.

7. Longnecker MP. 1994. Alcoholic beverage consumption in relation to risk of breast cancer:  meta-analysis and review.  Cancer Causes Control 1:  73-82.

8. Longnecker MP. 1995. Alcohol consumption and risk of cancer in humans:  an overview.  Alcohol 12(2): 87-96.

9. Michaud DS, et al. 1999. Fluid intake and the risk of bladder cancer in men.  N Engl J Med 340: 1390-1397.

10. Stookey JD, et al. 1997. Correspondence re: J. Shannon et al., Relationship of Food Groups and Water Intake to Colon Cancer Risk.  Cancer Epidemiol., Biomarkers & Prev., 5: 495-502. Cancer Epidemiol Biomarkers & Prev 6: 657-658.

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Link to PubMed

Abstract of publication in Lancet

http://www.ncbi.nlm.nih.gov/pubmed/ 8098459

Link to The Lancet - Journal article:  1993, 341(8856):  1330-32

http://www.sciencedirect.com/science/article/pii /0140673693908285

Häussinger D, Roth E, Lang F, Gerok W.

Lancet. 1993 May 22; 341(8856):1330-32

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