Sep 13, 2013
Green Tea and the Kidneys
Apr 12, 2013
Green Tea and Neurodegenerative Diseases
Feb 06, 2013
The Benefits of Green Tea and Exercise
Dec 03, 2012
Gluten-free diet: is this the right solution to a healthier life?
Oct 17, 2012
Effects of Green Tea on Cholesterol
Jul 24, 2012
Food Additives and Preservatives
Jul 24, 2012
How Green Tea Affects Blood Pressure
Jun 06, 2012
Green Tea & Our Blood
Oct 12, 2011
Anomalous And Unique Properties of Water
Jun 07, 2011
Formaldehyde: An Unwelcome Guest
Apr 01, 2011
Health Benefit of Green Tea - Obesity and Green Tea
Mar 31, 2011
Mar 30, 2011
Recent Trends in Obesity-related Research in Medicine
Mar 25, 2011
Health Effects of the Japanese Nuclear Accident
Mar 23, 2011
Chronic Constipation - The Causes, Symptoms, and Treatment
Sep 13, 2013
Green Tea and the Kidneys
By HCLI Staff

How does green tea affect the kidneys? Recent animal studies have highlighted some interesting results. As many people know, one of the most important functions of the kidneys is to remove wastes from the bloodstream. These wastes include excess water and nutrients, as well as the byproducts of cellular processes and substances taken up by the body through the digestive system, skin, and lungs. However, there are some circumstances when kidney functioning may be impaired. A few of these circumstances include kidney disease that results from having diabetes (diabetic nephropathy), kidney stones, low blood supply to the organs (ischemia), and blood coagulation or clotting(thrombosis). A plethora of new animal studies now show that green tea may have the potential to improve these conditions. It might also help maintain the function of our kidneys in spite of these serious health problems.

Diabetes mellitus is a serious condition that affects an increasing number of people. This condition can lead to kidney disease, or nephropathy.[1] When diabetes mellitus progresses to kidney disease, there is damage to the kidneys and their ability to function. Research published in the British Journal of Nutrition investigated rats with diabetic nephropathy that were fed a concentration of 16% green tea as their only drinking source for 12 weeks. These animals experienced a number of benefits. They showed lower levels of nitrogen in their blood, as well as the waste products creatinine and malondialdehyde.[2] These waste products must be filtered out of the bloodstream by the kidneys. In addition, less glucose and protein were found in the rats' urine, showing that there was an improvement in their kidney function.[2] This research clearly shows that green tea helps the kidney function in rats with diabetes and raises interesting questions for humans.

Kidney stones are painful and disrupt the functioning of the kidney. Oxalate is a compound that promotes the growth of kidney stones (also called "calcium oxalate stones"). It also kills the tubular epithelial cells which line the inside of the kidneys.[3] As a result of damage to these cells, crystals of calcium oxalate stick more easily to them , making it more likely that a kidney stone will develop.[4] A study published in the Journal of Endourology looked at the cells lining rat kidneys and the effects of EGCG (a compound in green tea). Rats given EGCG experienced remarkable benefits from it. The compound prevented free radical production by oxalate and also cut down on the number of crystals formed in their kidneys.[4] Since EGCG is the main component in green tea, green tea is involved in preventing kidney stone formation.[4] Researchers from the Institute of Biophysics noted that green tea itself contains many polyphenols with antioxidant properties, which means it can help control the damage caused by free radicals.[5]

Renal ischemia is a serious condition where the kidneys do not get enough oxygen for a certain period of time. A lack of oxygen leads to inflammation and damage in the kidneys once blood and oxygen are reintroduced; this is referred to as a reperfusion injury. Renal Ischemia/ Reperfusion (I/R) cause many problems in the kidneys. Some of these problems include a lower glomerular filtration rate, which refers to how much blood is being moved through the tiny filters in your kidneys. The blood flow through the kidneys is important because it takes out the waste product creatinine. Another serious problem that comes from not getting enough oxygen is damage and the eventual death of tissue in the kidneys.[6]

A 2006 study published in Transplantation Proceedings examined rats with renal I/R. The researchers found that three indicators of kidney function---blood urea nitrogen levels (BUN), serum creatinine (sCr), and creatinine clearance (CrCl) levels--- improved in rats that were given EGCG (10 mg/kg) after renal I/R injury.[6] In addition, the rats given EGCG also had lower tissue death in their kidneys, as well as increased regeneration of these tissues after the damage. This research highlights the beneficial effects of EGCG: it limited damage to the kidneys, promoted tissue regeneration, and maintained the function of the kidneys.[6]

Scientists at the Nestlé Research Center in Switzerland examined diabetic rats and the formation of blood clots (thrombosis).[7] Blood clots impair kidney function by causing the kidney tissue to die. Research published in the Asia Pacific Journal of Clinical Nutrition showed that green tea given to rats helped to restore the proper balance of chemicals that prevents the formation of blood clots.[8] This study highlights the antithrombotic effect of green tea in rats with diabetes. Isn't it possible that green tea may also benefit other vascular conditions such as hypertension and atherosclerosis?

These animal studies highlight some interesting effects green tea has on bodily systems. All of these studies examined serious issues related to diabetes (like tissue death, kidney stones, low oxygen levels, and blood clots). What may be the benefits of green tea in regards to healthy kidneys? As research into the influence that green tea has on the kidneys continues, our understanding of the role that green tea plays on the day-to-day functioning of the kidneys will only improve.


1. Selby Jv, F.-S.S.C.N.J.M.K.P.P.S.S.S.J., The natural history and epidemiology of diabetic nephropathy: Implications for prevention and control. JAMA, 1990. 263(14): p. 1954-1960.

2. Renno, W.M., et al., Effect of green tea on kidney tubules of diabetic rats. British Journal of Nutrition, 2008. 100(03): p. 652-659 M3 - 10.1017/S0007114508911533.

3. Hackett, R.L., P.N. Shevock, and S.R. Khan, Madin-Darby canine kidney cells are injured by exposure to oxalate and to calcium oxalate crystals. Urological Research, 1994. 22(4): p. 197-203.

4. Byong Chang Jeong, B.S.K., Jung In Kim, and Hyeon Hoe Kim, Effects of Green Tea on Urinary Stone Formation: An in Vivo and in Vitro Study. Journal of Endourology, 2006. 20(5): p. 356-361.

5. Guo, Q., et al., Studies on protective mechanisms of four components of green tea polyphenols against lipid peroxidation in synaptosomes. Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 1996. 1304(3): p. 210-222.

6. Jang, Y.H., et al., Polyphenol (-)-Epigallocatechin Gallate Protection from Ischemia/Reperfusion-Induced Renal Injury in Normotensive and Hypertensive Rats. Transplantation proceedings, 2006. 38(7): p. 2190-2194.

7. Crespy, V. and G. Williamson, A Review of the Health Effects of Green Tea Catechins in In Vivo Animal Models. The Journal of Nutrition, 2004. 134(12): p. 3431S-3440S.

8. Rhee, S.-J., M.-J. Kim, and O.-G. Kwag, Effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in streptozotocin-induced diabetic rats. Asia Pacific Journal of Clinical Nutrition, 2002. 11(3): p. 232-236.
Apr 12, 2013
Green Tea and Neurodegenerative Diseases
By Justin H. Joe, Ph.D. & H. S. Jeon, Ph.D.

With the prolonging of the lifespan in humans, many age-related diseases are becoming more of a problem. While there have been numerous studies on neurodegenerative diseases, studies on the effects of green tea on neurodegenerative diseases have only fairly recently been undertaken. Current research shows that because green tea has natural and potent anti-oxidative properties, drinking green tea regularly can have neuro-protective effects.[1]

Neurodegenerative diseases are disorders that affect the neurons in the brain. These diseases are not curable and progressively get worse as the nerve cells degenerate or die over time. This can cause huge problems in mental functioning.[2] This loss of mental function/ cognitive function and behavioral abilities is called dementia.[3] Commonly known diseases that fall under dementia include Alzheimer's disease, Parkinson's disease, and vascular dementia. Alzheimer's disease and vascular dementia are considered primary types/causes of dementia. Alzheimer's disease can also be considered a vascular disorder (disorder involving the interruption of blood flow to the brain).[1]

Furthermore, before an individual is diagnosed with a full blown dementia, there can be a transitional state between cognitive decline due to normal aging and mild neurodegenerative diseases. This is called MCI or mild cognitive impairment. It is characterized by deficits in memory performance despite normal cognitive functionSMCs or subjective memory complaints are indicative of cognition related mental problems and are acknowledged as initial criteria of mild cognitive impairments. In other words, subjective memory complaints are important in the diagnosis of mild cognitive impairments. The early diagnosis and treatment of subjective memory complaints is important because individuals with subjective memory complaints are considered to be at higher risk for dementia.[4]

A major characterization of the neuropathy of aging and neurodegenerative diseases is oxidative stress. Oxidative stress is a condition of cellular pro-oxidant-antioxidant disturbance that favors the pro-oxidant state.[1] Oxidative stress plays an important role in the development of many neurodegenerative diseases and plays a large role in the cognitive decline in the early stages of these diseases.[5]

Green tea itself has very potent anti-oxidative properties. Flavonoids are natural antioxidant substances present in dietary sources such as fruits and vegetables, and from plant derived drinks such as pomegranate, raspberry, and blueberry juice, red wine, and tea. The largest group of flavonoids present in green tea is that of natural antioxidant polyphenolic catechins. The major green tea catechins include EC, EGC, ECG, and EGCG. All four green tea catechins have been shown to be powerful antioxidants, EGCG being the most active of the green tea catechins. Green tea catechins can protect and rescue brain neurons against many types of exogenous damage; and it can modulate several signal transduction pathways, cell survival/ death genes, and mitochondrial function. All this contributes to the normal growth and development of neurons.[5]

Another benefit of green tea is that it can improve cognitive ability in individuals at risk for dementia. A study published in 2011 demonstrates that LGNC-07, an ingredient that contains both green tea extract and L-Theanine, improves memory and attention in individuals with mild cognitive impairment. This study took 91 individuals with mild cognitive impairments who scored between 21 and 26 on the MMSE-K, and divided them into a treatment group (45 individuals took a total of 1,680mg of LGNC-07) and a placebo group (46 individuals were given maltodextrin and lactose for 16 weeks). The MMSE-K is a neuropsychological test that is designed to measure various cognitive functions such as memory, orientation, language, attention, and concentration. The test is used to assess patients with moderate to severe Alzheimer's disease. The results of this study showed that LGNC-07 improves cognitive function (increased memory and attention) in individuals with mild cognitive impairment whose MMSE-K score was between 21 and 23. Through the use of an EEG, it was also found that LGNC-07 increased theta activity during active mental states.[4]

Finally, an animal study on rats shows that green tea polyphenols improved cognitive deficits caused by chronic cerebral hypoperfusion (similar to vascular cognitive impairment in people). The study used 10-week-old Wistar rats and surgery was performed on these rats to induce hypoperfusion. For the next 4-8 weeks, the rats were fed either a saline treatment or different dosages of green tea polyphenols. Results of the study showed that the rats given 400 mg/kg per day had better spatial learning and memory than the rats given the saline treatment. Through this study, it is seen that green tea polyphenols scavenge free radicals, enhance antioxidant capabilities, and reduce lipid peroxidation and oxidative DNA damage after chronic cerebral hypoperfusion, which may underlie cognitive function improvement.[1]

In conclusion, although green tea cannot outright cure and stop the symptoms of neurodegenerative diseases, there is much hope in using green tea as treatment for the prevention of such diseases and to perhaps slow down their progression. Regular consumption of green tea over long periods of time has numerous benefits that may aid neurodegenerative diseases such as combating oxidative stress, improving memory and cognition in individuals with MCI, and potentially improving spatial learning and memory in individuals with vascular dementia.



1.Xu, Yan, Jun-jian Zhang, Li Xiong, Lei Zhang, Dong Sun, and Hui Liu. "Green Tea Polyphenols Inhibit Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion via Modulating Oxidative Stress." Journal of Nutritional Biochemistry 21, (2010): 741-748). Doi: 10.3233/JAD-2011-101803.
2. JPND Research. "What Is Neurodegenerative Disease?" Accessed March 18, 2012.
3. NIH-NIA. "About Alzheimer's Disease: Other Dementias." Accessed March 18, 2012.
4. Park, Sang-Ki, In-Chul jung, Won Kyung Lee, Young Sun Lee, Hyoung Kook Park, Hyo Jin Go, Kiseong Kim, Nam Kyoo Lim, Jin Tae Hong, Sun Yung Ly, and Seok Seon Rho. "A Combination of Green Tea Extract and L-Theanine Improves Memory and Attention in Subjects with Mild Cognitive Impairment: A Double-Blind Placebo-Controlled Study." J Med Food 14, no. 4(2011): 334-343. Doi: 10.1089/jmf.2009.1374.
5. Mandel, Silvia A., Tamar Amit, Orly Weinreb, and Moussa B.H. Youdim. "Understanding the Broad Spectrum Neuroprotective Action profile of Green Tea Polyphenols in Aging and Neurodegenerative Diseases." Journal of Alzheimer's Disease 25, (2011): 187-208. Doi: 10.3233/JAD-2011-101803
Feb 06, 2013
The Benefits of Green Tea and Exercise

By Justin H. Joe, Ph.D. & H.S. Jeon, Ph.D.

Exercise and green tea are considered beneficial to our daily health. However, the combined effect of consuming green tea and exercising is not as widely known. Current research elucidates the benefits of green tea consumption in combination with exercise in both humans and mice. These benefits include improved endurance, weight loss, and resting metabolism, as well as a reduction in the oxidative stress related to exercise.

One prominent finding concerning the connection between green tea and exercise indicates that green tea enhances the body's metabolism and adipose tissue oxidation when consumed concurrently with moderate to intense exercise over a period of a several weeks.[1,2] A human study in Japan that included moderate-intensity exercise (endurance training) over the span of 10 weeks found that the group receiving Green Tea Extract (GTE) had a decrease in whole-body fat in comparison to the group receiving a placebo.[1] Another investigation involving overweight individuals confirms the enhancing effect of green tea on exercise.[2] 102 overweight adults were randomly assigned either GTE catechins or a placebo and made to exercise with moderate intensity over a 12-week period. The group that received the green tea supplement had a larger decrease in abdominal fat compared to the control group.[2] These studies show that, in overweight women and men, a higher concentration of green tea catechin consumption led to an increased loss in body weight and fat when combined with exercise.

According to a study on green tea and exercise, GTE usage has resulted in a 1.4 fold increase in the fat oxidation of individuals who do not perform any exercise.[3] However, it should be noted that a combination of exercise (EX) and GTE consumption led to significant fat oxidation when compared to GTE consumption alone or exercise alone.[3]

Studies using mice have also shown a relationship between green tea consumption, fat usage, and endurance. Mice provided with 0.2% and 0.5% GTE were able to run 21% and 30% longer, respectively, than the mice without GTE.[4] The mice that received the extract were also shown to have experienced an 'anti-obesity effect' in comparison to the control mice.[4] In this particular study, it is interesting to note that caffeine was shown to have a synergistic effect with the tea catechins in promoting fat oxidation and energy usage.[4] The benefits of GTE also extend to the improvement of physical conditions. A recent study showed that in mice with a condition that simulates physical decline, the mice that were given GTE had improved endurance compared to the mice without the extract, possibly due to the increased fat utilization in place of carbohydrates.[5] Although the anatomy, physiology, and biochemical pathways in mice and humans differ, this research certainly raises interesting questions about individuals pursuing activities that require physical endurance.

Finally, green tea has properties that counteract the muscular damage and oxidative stress related to exercise. In a study that involved 35 untrained healthy men who went through strength training, the individuals who received 640 mg of GTE daily showed reduced oxidative stress after a 4 week period, as well as a trend towards reduced muscle damage when compared to the individuals who took the placebo.[6] The differences between the two groups were diminished after an 8 week period, which may be related to the adjustments that the body naturally makes to adapt to strength training.[6] Therefore, green tea may be useful for those who are beginning enter intensive physical training for the first time.

Along with the intake of green tea and copious amounts of fluids, proper exercise is important to ensure that blood is able to perfuse throughout the body and mediate an efficient exchange of nutrients and waste from the cells. Exercise not only balances weight and builds muscle, but it also facilitates blood flow in the body. Exercises like stretching help blood reach the extremities and regions of the body to which the heart has to work harder to send blood.

In conclusion, whether individuals are beginning intense physical training, exercising moderately over a long period of time, or hoping to increase their endurance, numerous trials involving humans and animals have shown the benefits of combining green tea consumption with exercise. More human trials are needed to help fully understand the role of green tea in the increase in fat oxidation and weight reduction.


1. Ichinose, T. et al. Effect of endurance training supplemented with green tea extract on substrate metabolism during exercise in humans. Scandinavian Journal of Medicine & Science in Sports 21, 598-605, doi:10.1111/j.1600-0838.2009.01077.x (2011).

2. Maki, K. C. et al. Green Tea Catechin Consumption Enhances Exercise-Induced Abdominal Fat Loss in Overweight and Obese Adults 1 , 2. The Journal of Nutrition, 1-7, doi:10.3945/jn.108.098293.Materials (2009).

3. Ota, N. et al. Effects of Combination of Regular Exercise and Tea Catechins Intake on Energy Expenditure in Humans. J Health Sci 51, 233-236, doi:10.1248/jhs.51.233 (2005).

4. Murase, T., Haramizu, S., Shimotoyodome, A., Tokimitsu, I. & Hase, T. Green tea extract improves running endurance in mice by stimulating lipid utilization during exercise. American journal of physiology. Regulatory, integrative and comparative physiology 290, R1550-1556, doi:10.1152/ajpregu.00752.2005 (2006).

5. Murase, T., Haramizu, S., Ota, N. & Hase, T. Tea catechin ingestion combined with habitual exercise suppresses the aging-associated decline in physical performance in senescence-accelerated mice. American journal of physiology. Regulatory, integrative and comparative physiology 295, R281-289, doi:10.1152/ajpregu.00880.2007 (2008).

6. Jówko, E. et al. Green tea extract supplementation gives protection against exercise-induced oxidative damage in healthy men. Nutrition research (New York, N.Y.) 31, 813-821, doi:10.1016/j.nutres.2011.09.020 (2011).


Dec 03, 2012
Gluten-free diet: is this the right solution to a healthier life?

By H.S. Jeon, Ph.D.

Today, we tend to see more products that are labeled "Gluten-free." Some of us consider them as healthier options, but not all of us know exactly what gluten is and what it means to our diet. There are several facts that should help us understand the meanings of food labels regarding gluten when we are out grocery shopping.

Gluten is categorized under several different types of food additives, such as dough conditioner, nutrient, stabilizer, texturizer, and thickener. Gluten is the composite of gliadin and a glutelin that make up about 80% of the protein in wheat. It is found in various grass-related grains as a combined form of starch with the water-soluble protein albumen. In simple terms, it is a protein compound found in wheat, barley, rye, and other grains.

The main effects of gluten when added to foods are the sticky and chewy texture and retained structure. The easiest example to illustrate what gluten does is in breadmaking; the shape of bread rises during the baking process, and it stays in the same shape while having a chewy texture. Generally, if the flour contains more refined gluten, the gluten forms more strands and cross-links during the baking process and produces products that are chewier. Thus, certain products, such as pizza and bagels, offer chewier textures than, say, pastry products by using more refined gluten. This type of bread flour is called hard wheat while pastries with lower gluten are made from soft wheat. Other common foods that contain gluten are cookies, candy, gum, fried foods, dairy, and some condiments such as soy sauce, ketchup, and mustard [1,2].

It seems gluten is quite commonly found in our daily foods. Why then do some food products avoid gluten and emphasize being "Gluten-free" in their labeling? The issue was raised when celiac disease came into public attention. Celiac disease is a digestive disease. People who suffer from it are intolerant to gluten. When they eat foods that contain gluten, their immune system reacts and attacks the small intestine. Eventually, the lining of the intestine becomes so damaged that it cannot absorb any nutrients from food. According to the National Institute of Health (NIH), about 1 percent of the United States population has celiac disease [3]. For other countries like Germany, Italy, Spain, and Brazil, less than 0.2% suffers from celiac disease. On the other hand, Mexico seems to have the highest percentage of the population with celiac disease (2.6%) [4]. It is thought that some people who do not necessarily have celiac disease might be still intolerable to gluten. As such awareness grew, people with either celiac disease or gluten intolerance began to seek alternative options to protect their diet, and as a result many food manufacturers began to produce and offer "gluten-free" foods.

However, gluten-free foods are not clearly explained to the public. In the United States, FDA is still under the process of establishing the legal definition of "gluten-free." [5] Two main methods to produce gluten-free foods can be considered. The first method is by choosing ingredients that give similar effects but do not have gluten, such as maize, potatoes, and rice. The other method is using special treatment to remove the gluten compound from wheat. One of the common methods to remove gluten is to separate it from flour. First, kneading flour yields a dough, and applying certain agitation forces to the dough forces gluten to coagulate and separate from the starch. However, it is almost impossible to remove all wheat gluten with the existing methods, and many manufacturers are still confused on how much gluten can remain and still be considered "gluten-free." Currently, the only international standard, called Codex Alimentarius, provides a general standard, allowing the label "gluten-free" for products with less than 200 ppm of gluten [1].

The trend of today's society seems to take the awareness of celiac disease further into a form of paranoiac concern of a specific protein compound found in wheat. Many related articles claim that there is even a spectrum of gluten intolerance, with celiac disease on one end, and suggests that every one of us may fall on that spectrum. However, there is no current medical diagnosis available that could prove such a claim [6]. Before limiting our dietary options, we should question whether we are too quickly judging a compound that is not yet entirely proven to be harmful. In other words, instead of limiting ourselves to follow one single diet, we consider our everyday diet and lifestyle as a whole to find the true answer to a healthier life. After all, it is up to us to control our own body, and not the other way around.


  1. Winter, Ruth. A Consumer's Dictionary of Food Additives. New York: Three Rivers Press, 2009.
  2. Minich, Deanna M. An A-Z Guide to Food Additives. San Francisco: Conari Press, 2009.
  3. National Institutes of Health (NIH): National Digestive Information Clearing House. "Celiac Disease". Last updated January 27, 2008.
  4. Tack, Greetje. "The Spectrum of Celiac Disease: Epidemiology, Clinical Aspects and Treatment." Nature Reviews Gastroenterology & Hepatology 7 (2010): 204-213
  5. Food and Drug Administration (FDA): Department of Health and Human Services. "Gluten Allergy Labeling." Last updated April 26, 2012.
  6. Storrs, Carina. "Will a Gluten-free Diet Improve Your Health?" CNN, April 12, 2011.
Oct 17, 2012
Effects of Green Tea on Cholesterol
By Moa Park, PharmD

High cholesterol is one of the major health concerns affecting many people worldwide. According to the World Health Organization, about 39% of the world's population has high cholesterol. 1

Cholesterol is one of the substances essential in maintaining the normal functions of the body, including the structuring of cells and production of hormones. High cholesterol, however, can lead to increased risk of heart disease and stroke.2 Current high cholesterol treatments primarily target Low Density Lipoprotein (LDL), which is often referred to as the "bad cholesterol." LDL is known as "bad" because it carries cholesterol from the liver to body cells and often causes plaque buildup in the arteries.2 Many clinical trials show an increased risk of heart disease when there is a raised level of LDL, making LDL the primary target of therapy.3

Green tea contains potent antioxidants known as catechins, and its beneficial effects on cholesterol have been suggested by many epidemiological studies, clinical trials, and animal experiments. Lower levels in both total cholesterol and LDL were observed with consumption of green tea in many population studies.4 The cholesterol-lowering effects of green tea have been suggested to be mediated by reduced absorption of cholesterol from the small intestine and its production by the liver.5, 6 Through several animal experiments, catechins in green tea, especially Epigallocatechin gallate (EGCG) - the most abundant catechins - have been shown to interfere with intestinal absorption of cholesterol and production of LDL by the liver enzymes. 5-7

In addition to the cholesterol-lowering effects, some studies suggest catechins in green tea may also prevent plaque formation by LDL. 7 Although the exact process of plaque formation in the arteries is unknown, one of the proposed mechanisms involves LDL oxidation in the artery walls.7, 8 LDL deposited in the blood vessels can react with free radicals and become oxidized.

Oxidized LDL causes direct damages and initiates an inflammation process involving the surrounding vessel walls, resulting in the buildup of more cholesterol as well as other substances including cell debris to the injured site of the blood vessel. Then, over time, this "plaque buildup" causes narrowing and hardening of the vessels, and, depending on its severity and the tissues involved, it can cause a heart attack or stroke.8 Green tea catechins were shown to reduce LDL oxidation in several animal experiments, and these results suggest that catechins might play a significant role in reducing plaque formation. 7, 9

Current research suggests that green tea and its catechins may have beneficial effects on cholesterol, further reducing the risk of cardiovascular disease. More studies are still needed, however, to determine the clinical implications of these findings and to better understand their physiological effects on the human body.



1. World Health Organization. Raised Cholesterol. Retrieved from

2. National Heart Lung and Blood Institute. What is Cholesterol? Retrieved from

3. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III). JAMA 2001; 285:2486-2497.

4. Zheng XX., Xu YL., Li SH et al. Green tea intake lowers fasting serum total and LDL cholesterol in adults: a meta-analysis of 14 randomized controlled trials. Am J Clin Nutr 2011; 94(2): 601-10.

5. Koo SI., Noh SK. Green Tea as Inhibitor of the Intestinal Absorption of Lipids: Potential Mechanism for its Lipid-Lowering Effect. J Nutr Biochem2007; 18(3): 179-183.

6. Bursill CA., Abbey M., Roach PD. A green tea extract lowers plasma cholesterol by inhibiting cholesterol synthesis and upregulating the LDL receptor in the cholesterol-fed rabbit. Atheroscloerosis 2007; 193: 86-93.

7. Velayutham P, Babu A, Liu D. Green tea catechins and cardiovascular health: An update. Curr Med Chem 2008; 15(18): 1840-1850.

8. American Heart Association. Atherosclerosis. Retrieved from

9. Inami S., Takano M., Yamamoto M et el. Tea catechins consumption reduces circulating oxidized low-density lipoprotein. Int Heart J 2007; 48(6): 725-732.
Jul 24, 2012
Food Additives and Preservatives
By H.S. Jeon, Ph.D.

Food Additives

Food additives refer to any substances that are added to change food in some way before it is consumed. Additives include preservatives for extending shelf life, flavoring and coloring for improving taste and appearance, and nutritional supplements such as vitamins and minerals. The contaminants from manufacturing, storing and packaging processes are also considered as indirect food additives.1-6

It has been reported that 90% of an average meal of an American family is prepared from processed foods, which are very likely to contain additives.4 While most of these food additives are approved for human consumption in America, it is strongly recommended to prepare our meals from whole foods to avoid any possible threats to our health by researchers and consumers.

Natural food additives, such as salt, sugar and vinegar and natural spices are also considered as food additives. However, the main concerns of using food additives are mostly related to chemical substances and artificial ingredients. Many studies have shown possible impact on human health of the continuous consumption of food with such additives. Common food additives include:

  • Monosodium glutamate (MSG) for enhancing flavor

  • Artificial sweeteners such as aspartame, saccharine, and sodium cyclamate

  • Preservatives in oily or fatty foods such as BHA, BHT, and sodium benzoate

  • Preservatives in fruit juices such as benzoic acid

  • Sulfites for stopping fermentation of beer, wine, and packaged vegetables

  • Nitrates and nitrites in hot dogs and other meat products for color retention

  • Antibiotics given to food producing animals

  • Food stabilizers and emulsifiers such as lecithin, gelatins, corn starch, waxes, gums, and propylene glycol

  • A number of different coloring agents such as annatto, cochineal, and betanin

  • Anti-foaming agent for reducing the formation of foam in the industrial process of liquids

Additives Commonly Found in Our Daily Meals: Preservatives

The names in the list above may sound complicated and far from our daily life encounters. However, in fact, they are the most frequently used ingredients found in the processed foods we buy at the market. For example, cereals we eat every morning contain certain preservatives called BHA and BHT (Figure 1). These chemicals are usually added to prevent oxidation of fats and oils in food. Oxygen tends to react with BHA and BHT before oxidizing fats, which in turn keeps the food from going rancid.

Although the United States Food and Drug Administration (FDA) has approved BHA and BHT along with about 3,000 food additives for consumption, they have been shown to cause a number of health problems.4, 5 Some studies claim that synthetic preservatives worsen Attention Deficit Disorder (ADD) and Attention Deficit Hyperactivity Disorder (ADHD) symptoms in those affected.3 Other studies also show that certain persons may have more difficulty with digesting and metabolizing the compounds of BHA and BHT, which results in behavioral changes and other health problems.7

Additionally, most fruit juices that are often marketed to parents of young children contain additives, including preservatives, artificial sweeteners and colorings. A study reports that preservatives such as sodium benzoates may cause increased hyperactivity in 3-year-old and 8/9-year-old children.3 the increase of the hyperactivity was about 50% greater for those children who regularly drank fruit juices with additives than those who drank juice without additives.8

The function of preservatives often falls into three different categories: prevention of bacterial or fungal growth, prevention of oxidation, and prevention of natural ripening of fruits and vegetables. According to the FDA, consumption of food that is manufactured with preservatives is almost inevitable.9 Recently, food irradiation has become more common in order to preserve meat and dairy products. In the process, due to potential microbes existing in the food, food is exposed to high-energy radiation to kill microorganisms, bacteria, viruses, and insects. However, the labeling for irradiation is not required. Similarly, many of these modern synthetic preservatives are often labeled as ingredients for "freshness" while their true meanings and dangers are concealed from consumers.

The Safety of Food Additives

Food additives approved by the FDA are considered to be safe for human consumption, and many processed food manufacturers claim that there is no solid evidence to show direct association between food additives and human health. However, the U.S. government has claimed that safety aspects of food additives are not fully known10:

"any substance the intended use of which results or may reasonably be expected to result, directly or indirectly, in its becoming a component or otherwise affecting the characteristics of any food.... Such substance is not generally recognized, among experts qualified by scientific training and experience to evaluate its safety, as having been adequately shown through scientific procedures ... to be safe under the conditions of its intended use...."

While both sides of the opinions are uncertain about the safety of the consumption, the safety of the food additives and preservatives should be carefully examined once more before eating them.

In addition to the previously mentioned health problems of consuming modern synthetic preservatives, other food and color additives have been linked with allergic reactions, cancer, asthma, and birth defects.11 For example, sulfites used to prevent discoloration are shown to cause allergic reactions, according to the FDA. Once a person develops sulfite allergies, it can potentially lead to fatal respiratory distress.12

Alternative Solutions

Once we decide to avoid these unknown dangers, an alternative can be whole foods. Whole foods, unlike processed food, do not contain any additional ingredients including natural ingredients such as salt; therefore, they do not contain any of the modern synthetic additives such as preservatives and colorings. However, there are many other synthetic inputs such as pesticides and growth hormones that are not categorized as "food additives." These chemical residues, for instance, are also found in whole foods, and they may put our health at risk.

The safest and healthiest way of eating food is to eat organic food. Organic foods do not necessarily mean whole foods; it is food that is produced without the use of any synthetic pesticides, chemical fertilizers, genetically modified organisms (GMO) and food additives.13 Due to the regulations of certifying organic food in the United States, we can worry less from the concerns of the unnatural and chemical substances that may lead to health risks and problems.

In order to pursue a Hemato-Centric Life, we must consider once more, before we consume foods of unknown sources, that they may possess potential threats to the health of our body and blood.


  1. Dalton, Louisa. "Food Preservatives." Chemical and Engineering News vol.80 no.45 (2002):40.

  2. Food Additives and Ingredients Association and the Chemical Industry Education Centre. "Using Preservatives." Accessed 3 February, 2012.

  3. McCann, Donna, Angelina Barrett, Alison Cooper, Debbie Crumpler, Lindy Dalen, Kate Grimshaw, Elizabeth Kitchin, Kris Lok, Lucy Porteous, Emily Prince, Edmund Sonuga-Barke, John O Warner, and Jim Stevenson. "Food Additives and Hyperactive Behaviour in 3-year-old and 8/9-year-old Children in the Community: A Randomised, Double-blinded, Placebo-controlled Trial." The Lancet vol.370 no.9598 (2007): 1560-7.

  4. Schlosser, Eric. Fast Food Nation: The Dark Side of the All-American Meal. New York: Perennial, 2002.

  5. U.S. Food and Drug Administration. "EAFUS: A Food Additive Database." Accessed June, 2006.

  6. U.S. Food and Drug Administration/Center for Food Safety and Applied Nutrition. "The List of Indirect Additives Used in Food Contact Substances." Accessed 13 September, 2006.

  7. Raloff, Janet. "Carcinogens in the Diet." Science News Online, February 19, 2005.

  8. Hollingham, Richard. "Common Food Additive Doubles Kids' Hyperactivity." Discover Magazine. January 15, 2008.

  9. Foulke, Judith E. "A Fresh Look at Food Preservatives." FDA Consumer. October 1993. Accessed 3 August, 2006.

  10. "U.S. Congress, Federal Food, Drug, and Cosmetic Act." 21 U.S.C. 301, chapter 2, paragraphs (s). (Includes all amendments through December 31, 2004.)

  11. U.S. Food and Drug Administration/International Food Information Council. "Food Ingredients and Colors." November, 2004; Revised April 2010.

  12. Papazian, Ruth. "Sulfites: Safe for Most, Dangerous for Some." FDA Consumer December, 1996. Accessed 28 July, 2006.

  13. Allen, Gary J. and Ken Albala. The Business of Food: Encyclopedia of the Food and Drink Industries. Westport: Greenwood Press, 2007.

Jul 24, 2012
How Green Tea Affects Blood Pressure
By Solha Park, PharmD and Moa Park, PharmD

Among the major risk factors of developing cardiovascular diseases such as heart attack, heart failure and stroke, high blood pressure is most closely and consistently related to the development of cardiovascular disease requiring immediate treatment with medications and lifestyle modifications.1 While there are many ways to control high blood pressure, regular consumption of green tea has been shown to have a positive relationship with lowering blood pressure when combined with healthy diet and regular exercise.2-5

High blood pressure is a chronic medical condition that can lead to many serious health problems including cardiovascular diseases and kidney disease. Persistent high blood pressure may damage other parts of body such as blood vessels and eyes. While it does not have any symptoms, these long-term complications usually take several years to develop. Fortunately, high blood pressure can be detected easily through a regular medical checkup and can be controlled with lifestyle modification and medications.6

Blood pressure is measured as two different pressure types: systolic and diastolic blood pressure. Systolic blood pressure refers to the measurement of blood pressure when the heart pumps out the blood, and diastolic blood pressure refers to the pressure in between two heartbeats. The systolic numbers are often written above or before the diastolic numbers and are higher. The following table shows different stages from normal blood pressure to stage 1 and 2 high blood pressure. The level of the patient's high blood pressure determines what kind of treatment one may need.6


Systolic (mmHg)

Diastolic (mmHg)


Less than 120

Less than 80


Between 120 - 139

Between 80 - 89

High Blood Pressure (stage 1)

Between 140 - 159

Between 90 - 99

High Blood Pressure (stage 2)

160 or Higher

100 or Higher

Important risk factors of high blood pressure are age, gender, family history, and lifestyle including lack of physical activity, obesity, diets high in sodium (from salt), and some medications.1,6 About one out of three adults in the United States develop high blood pressure.6 Older people are more likely to develop high blood pressure, and men tend to develop high blood pressure earlier than women at the age of 55 and older. High blood pressure can also be hereditary.6

How is blood pressure regulated? Blood pressure is regularly maintained by various chemicals in our bodies that send signals to several layers in blood vessels, such as elastic fibers, smooth muscles and connective tissues. Angiotensin, a powerful constrictor of the blood vessels, is an endogenous hormone (a hormone made in human body). Upon activation, it signals stress hormones to be released, constricting the blood vessels by tightening the smooth muscles surrounding the vessels, and causing the kidneys to reduce fluid loss.7 As a result, blood volume increases and blood vessels become narrower raising the blood pressure. On the other hand, nitric oxide, a dilator, is a gaseous chemical in our bodies involved in lowering blood pressure. When it is released into blood vessels, it relaxes the smooth muscles and dilates the vessels which keep blood vessels open as shown in the above figure.7,8 By doing so, nitric oxide decreases the pressure in blood vessels and allows for increased blood flow.

According to recent animal studies on green tea and high blood pressure, catechins in green tea have been shown to affect the activities of angiotensin and nitric oxide. EGCG in green tea has been shown to interfere with the activation process of angiotensin and consequently cause a decrease in blood pressure. EGCG has also been shown to promote biological production of nitric oxide.9-11

Moreover, drinking green tea has been associated with lowering blood pressure in many population studies. Catechins, the major chemicals found in green tea, have been shown to be an antioxidant. The antioxidant effect of catechins in green tea can reduce damages to the blood vessels caused by free radicals and help preserve normal blood vessel function over time.12

As the beneficial health effects of green tea are constantly being studied, it would be advisable to encourage the habitual consumption of green tea, especially for those at risk of developing high blood pressure or already suffering from the condition. Although a single food item should not be expected to have a significant impact on one's health, regular consumption of green tea combined with an improved lifestyle, such as regular physical exercise and healthy diet, may have a great impact on maintaining normal blood circulation and better health.


  1. Chobanian, A.V., G.L. Bakris, H.R. Black, W.C. Cushman, L.A .Green, J.L. Izzo Jr., D.W. Jones, B.J. Materson, S. Oparil, J.T. Wright Jr., and E.J. Roccella. "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report." JAMA vol.289 no.19 (2003): 2560-72.

  2. Chacko, Sabu M., Priya T. Thambi, Ramadasan Kuttan, and Ikuo Nishigaki. "Beneficial Effects of Green Tea: A Literature Review." Chinese Medicine vol.5 no.13 (2010). doi: 10.1186/1749-8546-5-13

  3. Hodgson, Jonathan M., Ian B. Puddey, Valerie Burke, Lawrence Beilin, and Nerissa Jordan. "Effects On Blood Pressure of Drinking Green and Black Tea." Journal of Hypertension vol.17 no. 4 (1999): 457-463.

  4. Kuriyama, S., T. Shimazu, K. Ohmori, N. Kikuchi, N. Nakaya, Y. Nishino, Y. Tsubono, and I. Tsuji. "Green Tea Consumption and Mortality Due to Cardiovascular Disease, Cancer, and All Causes in Japan: The Ohsaki study." Journal of American Medical Association vol.296 no.10 (2006): 1255-65.

  5. Wolfram, Sven. "Effects of Green Tea and EGCG on Cardiovascular and Metabolic Health." Journal of American College of Nutrition, vol.26 no.4 (2007):373S-388S.(1)(1)

  6. American Heart Organization. (2012).

  7. Persson, Ingrid A.L., Martin Josefsson, Karin Persson, and Rolf G. G. Andersson. "Tea Flavanols Inhibit Angiotensin-Converting Enzyme Activity and Increase Nitric Oxide Production in Human Endothelial Cells." Journal of Pharmacy Pharmacology vol.58 no.8 (2010): 1138-1144.

  8. Velayutham, Pon, Anandh Babu, and Dongmin Liu. "Green Tea Catechins and Cardiovascular Health: An Update." Curr Med Chem vol.15 no.18 (2009): 1840-1850.

  9. Persson, I.A., K. Persson, S. Hagg, and R.G. Andersson. "Effects of Green Tea, Black Tea and Rooibos Tea on Angiotensin-Converting Enzyme and Nitric Oxide in Healthy Volunteers." Public Health Nutrition vol.13 no.5 (2010).

  10. Papparella, I., G. Ceolotto, D. Montemurro, M. Antonello, S. Garbisa, G. Rossi and A. Semplicini. "Green Tea Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Rats by Modulating Reactive Oxygen Species Production and the Src/Epidermal Growth Factor Receptor/Akt Signaling Pathway." The Journal of Nutrition vol.138 no.9 (2008): 1596-601.

  11. Ryu, H.H., H. L. Kim, J. H. Chung, B. R. Lee, T. H. Kim and B. C. Shin. "Renoprotective Effects of Green Tea Extract on Renin-Angiotensin-Aldosterone System In Chronic Cyclosporine-Treated Rats." Nephrol Dial Transplant vol.24 no.4 (2011): 1188-93.

  12. Gramza, A., J. Korczak and M. Rudzinska. "Tea Extracts as Free Radical Scavengers." Polish Journal of Environmental Studies vol.14 no.6 (2005): 861-867.

Jun 06, 2012
Green Tea & Our Blood

1. About Blood

Components of Blood

  • Blood takes up 1/12th of body weight (about 8%). In other words, an average male weighing 70 kg (150 lbs.) carries about 6 kg (13 lbs.) of blood. In volume, an average person carries about 5L (1.3 gallons) of blood.

  • People are most familiar with the three major cells in blood: red blood cells, white blood cell and platelets. Each component plays a significant role in the human body, but one must understand that the other half of blood (55%) is composed of plasma.

  • 92% of plasma is made up of water mixed with a number of important substances and nutrients such as hormones, immunoglobulins, lipoproteins, mineral ions, and gases. Plasma is responsible for carrying these substances with other blood cells to different parts of the body

Blood and Our Body Organ

  • The most important task of blood is circulation. While each component of the blood has its own role, the role of the blood itself is to circulate through out the body as it carries various components to proper locations of the body. The lungs work to provide oxygen to blood, the liver works to remove toxic materials from the blood, the kidneys filter blood to remove toxins in the blood, and the organs of the digestive system work to provide nutrients to the blood.

Did you know?

  • Each kidney filters about 67 L (17.5 gallons) of blood per hour

  • The heart pumps about 300 L (80 gal) of blood per hour

  • Blood travels about 800 km (500 miles) in an hour

  • 2L (0.5 gal) of blood loss will cause immediate death


2. Antioxidant Effect of Green Tea

  • Green tea has abundant compounds that benefit our health. Notable compounds include catechins, theanine, vitamins, essential oil, minerals and caffeine. Catechins (tea polyphenols) act as antioxidants by scavenging reactive oxygen species (ROS) in the blood. This protects cells and plasma constituents against oxidative damage to blood.

  • Research has shown that green tea can help prevent the peroxidation of lipids and the rupturing of red blood cells. These studies examined the antioxidants in the blood, the evidence of lipid peroxidation, and changes in the membrane of red blood cells caused by oxidation in order to see how green tea might affect the oxidation of blood plasma and red blood cells. Lipid peroxidation occurs when oxidation in the blood steals away electrons from the lipids in red blood cell membranes, weakening them. Drinking green tea was found to reduce this process of lipid peroxidation. This may be the result of green tea boosting the antioxidant defense system. By blocking lipid peroxidation, the catechins in green tea can prevent red blood cell membranes from being damaged by oxidation and keep red blood cells healthy and strong.

  • Green tea can also reduce the oxidation of low-density lipoprotein, or LDL. The oxidation of LDL particles can cause the formation of atherosclerotic lesions, which is the thickening of artery walls caused by the accumulation of fatty materials under the blood vessel wall. This can increase the risk of cardiovascular diseases such as strokes and heart attacks. LDL particles that oxidize inside the wall of the artery can begin a cycle of cell damage and inflammation. This worsens the atherosclerotic lesions, further chocking off the blood vessel. Studies have shown that antioxidants in green tea can bind with the oxygenated molecules in blood, which prevents them from reacting with the LDL. This prevents the oxidation of LDL, thereby reducing the possibility of damage to blood vessels.


3. Green Tea and Cardiovascular Diseases


  • Although cholesterol is one of the essential substances necessary for the normal function of a human body, excessive level of cholesterol, or more precisely, excessive level of LDL may have a severe impact on blood vessels and eventually on human health.

  • Green tea has been shown to be beneficial by lowering blood choleterol levels, including total cholesterol and further decrease of LDL levels.


  • Diabetes is a condition of having too much sugar in blood, which may be due to a lack of insulin or problems with insulin sensitivity. It is considered as one of the major causes that can impact human health.

  • Lack of physical activity and obesity are the biggest causes of diabetes in that they may lead to insulin resistance and an eventual lack of insulin production in the long run.

  • Many studies show that drinking green tea increases the sensitivity of insulin, which means our bodies can recognize insulin better. In addition, drinking green tea has been shown to lower glucose production in the liver and decrease glucose absorption in the intestines. All of these effects can reduce the risk of diabetes and obesity.

High Blood Pressure

  • High blood pressure, which may be due to excessive levels of cholesterol and sugar and other related factors, is considered as one of the major risk factors of developing cardiovascular diseases such as a heart attack and stroke.

  • Long-term untreated high blood pressure may damage blood vessels and eventually damage organs such as the kidney, stomach and intestines.

  • A lifestyle of regular green tea consumption has been associated with lowering blood pressure. Catechins in green tea have been shown to dilate and relax the blood vessels, which can lower blood pressure. Antioxidants in green tea may reduce free radical damage to blood vessels and help maintain the normal function of blood vessels.

4. Glossary

Antioxidant a molecule that prevents other molecules from being oxidized
Atherosclerosis a condition where arterial walls become thickened due to fat accumulation such as cholesterol
Catechin a natural antioxidant compound primarily found in tea, categorized under polyphenols
Cholesterol an organic chemical substance classified as a steroid of fats
Diabetes a chronic medical condition referring to a high level of sugar in blood. Symptoms include blurry vision, excessive thirst, fatigue, frequent urination, hunger and weight loss.
Endothelial the innermost wall of a blood vessel
Glucose a type of sugar in blood used for energy
HDL High-Density Lipoprotein. The "good" cholesterol that removes the "bad" cholesterol
Hemolysis the breakdown of red blood cells, literally meaning "blood (hemo-) releasing (-lysis)" in Greek.
High blood pressure a chronic medical condition referring to an elevated blood pressure in the arteries at or above 140/90 mmHg. There are often no visible symptoms.
Insulin hormone produced by the pancreas. It is a type of signal for cells to take in sugar from blood to generate energy.
LDL Low-Density Lipoprotein. The "bad" cholesterol that causes the hardening and narrowing of blood vessels
Lesion any form of damage in the tissue of an organism. E.g., oxidative lesion means damage caused by oxidation.
Lipoprotein a particle that allows lipids (fats) to move around the body in the blood by binding to specific proteins
Obesity a medical condition referring to excessive body fat that may lead to many health problems
Oxidation a chemical reaction that produces free radicals, which will start chain reactions and eventually cause damage or death to the cell
Plasma a fluid in the blood that contains and transports water, proteins, sugar, nutrients, and other essential substances to different parts of the body
Platelet a type of blood cell that forms "blood clots" to prevent and stop bleeding
Reactive Oxygen Species (ROS) highly reactive molecules containing oxygen that may cause significant damage to cell structures; they are also known as free radicals.
Red blood cell a type of blood cell that carries and delivers oxygen to each cell in the body
White blood cell a type of blood cell that fights against infections in the body



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Oct 12, 2011
Anomalous And Unique Properties of Water
By H.S. Jeon, Ph.D
Mount Kisco, NY

Water is so simple, so beautiful, and so unique!

It is such a simple and small molecule, but it has very unique as well as anomalous chemical and physical properties. The chemical structure of a single water molecule is shown in Fig. 1. Two hydrogen atoms bound to one oxygen atom to form a 'V' shape with the hydrogen atoms at an angle of 104.5Ã. The hydrogen atoms have positive charges, and the oxygen atom on the opposite side has two negative charges. The net interaction between the covalent bond and the attracting and repulsion charges produces the 'V' shape of the molecule.

Fig. 1. Shape of A Single Water Molecule (Ball-and-Stick Model).

Think of how much water is important in our daily lives. Different people have different percentages of their bodies made up of water. Babies have the most, being born at about 78%. In adult men, about 60% of their bodies are composed of water whereas old men have less than 50% due to the loose of water as getting older. However, fat tissue does not have as much water as lean tissue. In adult women, fat makes up more of the body than men, so they have about 55% of their bodies made of water. [1] About 90% of our blood is water, which helps blood circulate, transport waste, and control body temperature due to the low viscosity and high heat capacity of water. Each day we need about 2-3 liters of water in order to sustain our health.

Looking at water, you might think that it's the simplest thing around. Water is a simple chemical substance with a molecular formula H2O: a water molecule has two hydrogen atoms covalently bonded to a single oxygen atom. Water appears in nature in all three common states of matter, such as gas, solid and liquid. Pure water is colorless, odorless, and tasteless. But it's not at all simple-in particular, when water molecules are together. Also it is vital for all life on Earth. Where there is water there is life, and where water is scarce, life is scared! There is a saying, "You spend money like water!" It can have two different meanings to the people who live in different environments. It means "waste of money" in Korea due to plenty of water whereas "conserve money" in Israel due to lack of water.

What are the physical and chemical properties of water that make it so unique and necessary for living things? There are many anomalous and unique properties that water should not have according to what we presently know about chemistry and physics. These characteristics strongly point to water as a simple but mysterious molecule. Therefore, finding and understanding the hidden properties of water give us very interesting subjects.

1. Maximum Density

Density change is not constant as temperature changes. With decreasing temperature water density increases and reaches its maximum at 40C, and then begins to decrease after crossing the critical point of 40C. Moreover the density of crystallized ice water is decreased, meaning that volume of water is expanded as water freezes to ice. Due to the higher density of liquid water than that of ice, ice floats on water surface although ice is solid. This causes an inversion and mixing of water bodies on Earth. It takes surface oxygen down to the bottom and raises bottom toxic gases to the surface to be neutralized and exhausted. Water is not supposed to be most dense as a liquid at 4o C. All other liquids are most dense when they reach the freezing or solid state. Because of this unusual property, we have circulation of water in lakes or oceans in temperate climates.

Floating ice on water acts as a shielding layer that protects the heat loss of water and the decrease in water temperature. If ice density was larger than that of water, ice would sink to the bottom of lakes, and the lakes in the temperate and arctic climates would be frozen from the bottom up. Thus, living creatures under water can be survived from cold as well as food shortage.

Without water circulation oxygenated surface water would not go to the bottom of lakes to enable life to exist at the bottom so that organic sediments could be biodegraded, bottom toxic gases brought up to the surface and removed, and fish to spawn and feed on bottom-feeding insects. Without this circulation, there would be no life in our lakes. This circulation is replaced by hurricanes, typhoons, monsoons, and torrential rain in the sub-tropic and tropic zones, where the temperature changes are small.

2. Ultrahigh Melting and Boiling Points

Water has an unusually high melting temperature of 00C instead of -1000C although its molecular weight (MW = 18 g/mole) is smallest among solvents. Its boiling temperature is 1000C, instead of about -800C. Graphs of adjacent molecules in the Periodic Table of Elements show a straight-line relationship of melting and boiling points far below 00C. With using this method, we can thus estimate the theoretical melting and boiling points of water. According to water's neighboring molecules in the Periodic Table of Elements, ice should melt somewhere around

-1000C instead of 00C, and should boil at about -800C instead of 1000C. If melting and boiling points were far below 00C all water would be in the gaseous state and there would be no life on earth!

3. Freeze Point for Water Under Pressure

3.1 Freeze Point Increase

Normally, water becomes ice at 00C and 1atm. It is, however, possible for water to become ice at 200C or for ice to become water at -200C at different pressure conditions. W hen you squeeze ice you lower its freezing temperature slightly so that it melts more easily. This behavior in which pressure can induce melting is extremely unusual. Almost every other material in nature becomes more difficult to melt as you squeeze it. That's because most materials expand during melting and have to do work against the pressure. Added pressure makes it harder for them to melt and you can even make them freeze by squeezing them. But ice shrinks during melting because ice is less dense than water. Rather than keeping ice from melting, pressure can actually liquefy ice, even below its normal melting temperature.

A related question is "Would it be possible to pass a thin wire through an ice cube without breaking the ice cube?" The answer is "possible". Here is an example. A piece of thin wire with a heavy weight on each side secured to the wire is put on the ice cube. Over a period of time the wire would cut through the ice and the ice would refreeze again where it had passed through. Finally the wire would completely pass through the ice. The freeze point of ice under the wire would be reduced as below zero due to the pressure of the wire causing the wire to cut through the ice and then refreeze. It means that the wire is actually passing through the thin water layer due to the melting of ice with a condition that is below the freeze point. Unlike nearly every other substance we know, water takes up more volume in its solid state than in its liquid state. When you put ice under pressure, you decrease the volume available to it, and it cannot remain as a solid. This application of pressure subsequently lowers the freeze point since the crystalline structure of the water is distorted or crushed.

Another example is how ice skates work, although the exact mechanism is somewhat disputed. If you apply pressure on the surface of ice, it melts. This is how ice skates work - the pressure of the blade causes a tiny bit of ice to be melted, allowing the blade to slide smoothly over it. While pressure-induced melting has long been used to explain the lubrication with a thin layer of water film between ice and skate blades in many texts, that explanation appears to be not good enough or incorrect.

We estimate an upper bound to the temperature change of ~0.1ÃC by using the Clausius-Clapeyron equation [2], with a skater's weight of 100kg and a surface area of two skate blades (2LW = 300 mm2),

?Tm = T0 (?P*?v)/(Hm),

where ?Tm = the change in the melting temperature to the absolute melting, T0

?v = change in specific volume from ice to water (~10-4 m3/kg)

Hm = Heat of melting of ice (= 3.34x103 J/kg) [3]

?P = pressure change (N/m2)

So, if this were the only cause of the slipperiness, ice-skating would be possible only at temperatures just a few degrees below freezing. From observation, it is possible to ice skate on ice at much lower temperatures than this. It is, thus, necessary to have another chemical or physical phenomenon to explain this melting phenomenon in skating. We can think of frictional heat from interface between ice and blades. Frictional heating due to the movement of the skate contributes to the melting of ice and generates a thin liquid layer of water.

Ice's huge melting heat (334,000 J/kg) is what keeps an interface or mixture of water and ice at 0 ÃC. As long as both water and ice are contacting together at the interface, they are in the process of either melting or freezing. Any heat you add to the interface goes into melting more ice, not into raising its temperature. Any heat you remove from the interface comes from freezing more water, not from lowering its temperature. With ice floating in your drink, it will remain at 0 ÃC, even in the hottest or coldest weather. After the blade passes the thin layer of liquid refreezes as pressure and temperature return to normal states.

On the other hand, it is easy to explain that why the surface of ice is at least a little slippery. At the surface of ice, water molecules are only hydrogen bonded to their neighbors on one side. Consequently, their energy is not as low as in bulk ice. At equilibrium they must have higher entropy in the air-ice interface than bulk ice. So ice must have a thin water layer on the surface, whose thickness would be expected to increase at temperatures close to the melting of ice. Such melting is particularly easy at the interface between ice and air, where the crystalline structure is incomplete and disordered. Because they lack a full complement of neighbors, the outermost water molecules are relatively mobile and already have a liquid-like character.

When heated by sliding friction, this layer melts entirely and acts as a lubricant to make ice extremely smooth. Since the layer is so thin, very little heat is needed to melt it and a tiny bit of frictional heating is all it takes to get something sliding along the ice. The thickness of a thin water layer between ice and blade can be controlled by given temperature and frictional heating. At warmer temperatures, the water layer is thicker and melts more easily when heated by friction. That's why ice is most slippery when the temperature is close to freezing and the surface is "wet". When the temperature is extremely cold, ice has a "dry" surface and is very difficult to slide solid objects on that surface. For example, if you hold an ice cube in your hand on a very cold winter day, it will stick quickly and strongly to your hand.

3.2 Freeze Point Decrease

In 1956, Buswell and Rodebush pointed out two very interesting natural phenomena about water freezing at above a normal freezing point [6]. One of them is that freezing water is sometimes found in a natural gas pipe at 200 C. Natural gas (mostly methane) is a non-electrolyte, which has, thus, a very limited solubility in water. Water is an excellent solvent due to its polarity, high dielectric constant and small size, particularly for polar and ionic compounds and salts.

They explained that some solubility is even possible not due to the attraction force between water and natural gas but due to the lack of attraction force. We can thus understand this unusual freezing by studying the solubility of methane in water. When methane is mixed with water, the reaction generates unexpectedly high heat despite the fact that methane has nearly no interactions with water and thus has a little solubility in it. Mixing of methane in water exerts ten times the heat than that of methane in hexane, which is a very good solvent for methane. It was discovered that the unusual heat generated from the water molecules forms a "cage" around a methane molecule. When methane molecules, which are relatively larger than water molecules, are dissolved in water, they push out many water molecules that break out the hydrogen bonding and reduce the other interaction forces between water molecules. This causes the reduction of strong internal forces of water molecules and an increase of freezing point of water. Water thus freezes at the interface between methane and water.

The other unique phenomenon is corn, which sometimes freezes at 40C. This can also be explained using the same physical chemistry principles as explained in the freezing water in methane gas as previously noted. The same phenomenon can occur between water and protein molecules. All protein molecules are much larger than water molecules and majority of them have non-polar or non-ionic groups of atoms like in methane. Therefore, water molecules can also form aggregates on the surface of protein molecules, and tend to be crystallized on the surface of protein molecules. The corn is thus damaged due to the expansion of water when it freezes to ice at 40C.

4. Very High Heat Capacity

Water has a very high heat capacity (or specific heat) compared to other materials. This means that it is more difficult to raise the temperature of water compared to other substances. Heat capacity is the amount of heat in calories required to raise the temperature of 1g of material 1 0C to raise its temperature.

For example, the heat capacity of water is 1.0cal/g0C while the heat capacity for ice is only 0.5cal/g 0C.

If water is frozen, its specific heat reduced by half, so ice tends to warm easily. If it is liquid, it tends to be more difficult to raise the temperature. Due to the very high differences in the heat capacity of water, ice, and steam, water tends to remain near the most desirable temperature for life on Earth regardless of drastic changes in atmospheric temperatures. The anomalously high heat capacity of water and the right quantity of water stabilize the Earth's temperature.

4.1 Strange Climates in the Deserts


In a desert region, air temperature drops quickly after sunset and remains much lower than that of daytime. The temperature differences between day and night in desert regions are much bigger than those at a typical area with common humidity. It is all due to the very high heat capacity of water than that of dry sand. At night, water releases the heat absorbed during daytime as the air temperature falls after sunset, whereas dry sand doesn't hold enough heat to release at night because of its much lower hear capacity. Deserts without humid air, plants, and lakes also exhibit very cold temperatures at night. That is the reason why deserts are much colder at night than during daytime. Due to the same reason, hydraulic power plants with large water dams also experience significant temperature change at wintertime.

4.2 Freezing Speed of Hot or Cold Water

In very cold winter days when the temperature falls below 10 0C, we can observe water freezing on glass on contact, such as when we throw water on a car windshield. The question here is "Which water will freeze first: hot or cold?" Surprisingly, the answer is hot water! Why? Because hot water evaporates faster than cold water, thus losing its energy and reaching its freezing point more quickly. It is again due to the different specific heats of water: latent heat (1cal/g 0C), heat of vaporization (540cal/g), and heat of melting (80cal/g).

For example, we need 75cal for heating one gram of water at 250C to 1000C, 540cal for heating one gram of water at 1000C to 1000C steam, and 80cal for heating one gram of ice at 00C to water at 00C. Therefore, 180cal must be released in order to turn one gram of 1000C water into ice. It indicates that the rate of evaporation is proportional to the decreasing of water temperature.

The same phenomenon is at work when we sweat to reduce skin temperature, by utilizing the properties of water as sweat evaporates on our skin. Heat capacities of various materials are given in Table 1 [5,7].

5. Very High Surface Tension

Surface tension is the property of the surface of a liquid that allows it to resist external force. This force gives liquid droplets their perfect spherical shape to minimize surface area if its surface tension is bigger. For example, a water droplet has a more perfect spherical shape than that of oil in the air because the surface tension of water (73 dyn/cm) is higher than that of acetone (24 dyn/cm) at room temperature [4]. Another example is the ability of some insects (e.g. water striders) to sit and run on the water surface. This property is caused by the cohesion of like molecules, and is responsible for many of the behaviors of liquids. Surface tension has the dimension of force per unit length, or of energy per unit area. Surface tension of water is very large and 2-4 times larger than that of most organic liquids.

The amount of force required to break apart pure water is enormous. The force of the resistance against this force is called tension or tensile strength. The theoretically calculated value of tensile strength is 95,000kg in order to break a pure water cylinder with a diameter of 1 inch and without any structural defects [8]. But there is no such perfect water in the real world. All normal waters in this world have structural defects and impurities, such as ions (H+, OH-), minerals (Mg, K, Na), and also isotopes (H2, H3, O17, O18). The experimental value of the tensile strength, 454 kg/in2 was obtained in a laboratory setting using the best quality of water [8]. This value can be comparable to some other materials: concrete (~174 kg/in2), glass (~2,130 kg/in2), ASTM A36 steel (~25,800 kg/in2), Diamond (~170,600 kg/in2) [7].

Why Does Water Have Such Anomalous and Unique Properties?

We reviewed some of the unique properties of water, many of which are the result of the "hydrogen bond" between water molecules. The polarity of water allows it to bind with other molecules, including another water molecule. Water molecules form the hydrogen bonds between hydrogen and oxygen molecules, giving shape to water as a liquid at normal conditions. Each single water molecule can form hydrogen bonds with four other water molecules in a tetrahedral arrangement. Although these bonds are weak compared to "covalent bond" they lead to many other unique properties. The V-shape of the water molecule is also important because it allows for other configurations of water to be formed (see Fig. 1).

These anomalous properties also give water the ability to transport minerals and waste products in water bodies, plants and animals. It gives water the ability to hold oxygen for animal life, and carbon dioxide for plant life. The unique dipole moment of water establishes the enormous extent of permanent-polarized bonding, and the angle between chemical bonds. These determine the water's ability to create the multitude of necessary molecules involved in every life process. For example [9], intra-molecular hydrogen bonding between hydrogen atoms and oxygen atoms enables molecules to fold into proteins having specific three-dimensional shapes essential for biological activity. If the angle between hydrogen atoms in the water molecule was not 104.50, there would be no complex life-giving molecules, and no life on Earth.



  1. Jeffrey Utz, Allegheny University (May 15, 2000),

  2. Çengel, Yunus A.; Boles, Michael A. (1998). "Thermodynamics - An Engineering Approach", 3rd ed., Boston, MA.: McGraw-Hill. ISBN 0-07-011927-9.

  3. Lide, D. R., ed (2005). CRC Handbook of Chemistry and Physics (86th ed.). Boca Raton (FL): CRC Press. ISBN 0-8493-0486-5.

  4. Yaws, Carl L., '"Handbook of Thermodynamic and Physical Properties of Chemical Compounds", Publisher: Knovel, Electronic ISBN: 978-1-59124-444-8 (Feb 1, 2003).

  5. Laider, Keith, J. (1993). The World of Physical Chemistry. Oxford University Press. ISBN 0-19-855919-4.

  6. A.M. Bushwell and W.H. Rodebush, Scientific American, April 1956.

  7. Wikipedia (Oct. 2011).

  8. Kenneth S. Davis and John A. Day, "Water: The Mirror of Science: Science study series", Anchor Book, 1st ed. (1961).

  9. Intelligent Design Theory, "Ch.14. Unique Properties of Water (2011)",


Table. 1. Heat Capacities of Various Materials (Unit: cal/g0C) [5,7].


Material Heat capacity Material Heat capacity
Water 1.00 Lead 0.04
Ice 0.50 Mercury 0.03
Steam 0.47 Nitrogen 0.25
Alcohol 0.55 Oxygen 0.22
Aluminum 0.22 Silver 0.06
Glass 0.12 Sand 0.19
Gold 0.03 Soil (wet) 0.35
Hydrogen 3.41 Turpentine 0.41
Iron 0.11 Wood 0.42

Jun 07, 2011
Formaldehyde: An Unwelcome Guest
By HCLI Staff

Formaldehyde is one of the most commonly known indoor pollutants. Less familiar might be that natural processes in the atmosphere may contribute up to 90 percent of the total formaldehyde in our environment[1]. As seen in its simple molecular formula H2-C=O (or CH2O, or HCHO, or H2CO) formaldehyde is made of carbon, hydrogen and oxygen, constituting the most basic form of aldehyde, called methanal by its systematic name. Numerous natural and anthropogenic sources contribute to the ubiquitous occurrence of this volatile organic compound (VOC). Even interstellar formaldehyde is widely spread. It was the first polyatomic organic molecule detected in the interstellar medium (ISM), the gas and dust that exist in open space between the stars.[2]

General Properties, Exposure and Impact

At room temperature, formaldehyde is a flammable, colorless gas with a pungent, irritating odor which can be smelled if present in higher concentrations[3], and then should be an alarming indicator for potential health threats. In the environment formaldehyde is broken down within a few hours either by sunlight (photodegradation) or by bacteria inhabiting soil or water (biodegradation)[4]. Within the body it is metabolized and secreted quickly[5]. However, even though it does not accumulate, neither in the environment nor in the body, due to its universal and ongoing distribution Formaldehyde remains to be present permanently, and it depends on its level of air concentration and on individual disposition whether it impairs a person's well-being.

The exposed body absorbs Formaldehyde easily and mainly through the respiratory tracts and to some extends through the gastrointestinal tracts, i.e. by inhalation and ingestion. For the general population dermal contact, occurring as route of exposure when skin comes into contact with liquids containing formaldehyde, seems to play a minor role, if any.[6]

The normal level of Formaldehyde both outside and inside is less than 0.03 ppm (parts per million parts of air). Usually much lower concentrations are found in rural areas and higher ones in urban areas, and compared to ambient air much higher ratios are found in indoor air[7]. At levels above 0.1 ppm formaldehyde can cause watery eyes, burning sensations in the eyes, nose and throat, nausea, coughing, chest tightness, wheezing, skin rashes, and allergic reactions[8]. Levels of formaldehyde much higher than 0.1 ppm have been found inside some buildings. Factors such as air temperature, humidity, insufficient ventilation, and of course the presence of sources emitting formaldehyde contribute to higher concentrations potentially dangerous. Exposure response among humans varies greatly. Some people may be much more sensitive than others, who seem to have no reaction to the same level.

Occupational exposure

Besides general exposure a large number of people are potentially exposed to higher doses of formaldehyde at their workplace[9]. Workers in factories using formaldehyde-based resins may be exposed to high air concentrations and may also face dermal exposure to liquid forms of formaldehyde. Other groups at higher risk include: dentists, doctors, pathologists, nurses, embalmers, teachers and students who handle preserved specimens in laboratories, veterinarians, and workers in the clothing industry or in furniture factories. [10]

Main Sources


Formaldehyde is an intermediate in the oxidation of methane and other organic compounds (methane cycle). As byproduct of combustion processes on both small and large scale, naturally and manmade, formaldehyde occurs virtually everywhere; e.g. in cells of all organic life forms including humans, in fuel driven engines, in the troposphere, or interstellar. Due to its major role as basic building-block molecule for a wide range of products of today's society, formaldehyde is widely spread in manufacture lines and is emitted by building material and consumer products. Especially inside buildings human activities and manmade products are dominating sources of higher formaldehyde air concentrations. Although ambient air may hold 90% of all formaldehyde, mean open air concentrations are significantly lower because here formaldehyde scatters throughout a much larger space.

Natural Sources

Formaldehyde derives as precursor from many natural processes and further decomposes into carbon monoxide and dioxide, hydrogen and water. Forest and bush fires release large amounts of formaldehyde. The oxidation of hydrocarbons in the troposphere caused by sunlight generates formaldehyde. Terpenes and isoprene produced and emitted by plants, per example, react with hydroxyl radicals leading to formaldehyde. As endogenous chemical emerging by metabolic processes formaldehyde occurs in minute amounts in nearly all forms of life.

Anthropogenic Sources

Manufacture and road traffic

Besides production facilities, where formaldehyde is either produced or technologically applied, the by far largest primary anthropogenic source are exhaust emissions of fuel driven vehicles. Both formaldehyde production processes[11] and automotive traffic are growing worldwide year by year. While critical concentrations of formaldehyde in and around industrial facilities are restricted locally, formaldehyde emission caused by on-road traffic is widely spread around the world. Since highest densities of road traffic take place in areas of high densities of population, the highest levels of on-road automotive releases are found where most people live. Since transportation never stops, decomposed Formaldehyde is replaced continuously, and obviously levels of exposure in densely populated areas remain comparatively high.

Indoor air at higher levels

Naturally the quality of indoor air cannot be better than the quality of ambient air surrounding building enclosures. In fact, additional sources of formaldehyde and limited airflow generally elevate indoor levels of air concentration. Studies in various countries have shown that indoor air contains substantially more Formaldehyde than outdoor air.

Indoor combustion processes

Unwanted combustion spills from boiler or water heaters (gas or oil), from wood stoves and fireplaces (wood), or from other fuel burning devices. Other combustion processes, such as certain cooking activities[12], in some cases tobacco consumption[13], or candle and incense burning, may add to indoor formaldehyde contamination.


The off-gassing from building materials (e.g. pressed wood, carpets, adhesives), which is most relevant in new or lately renovated spaces, and the off-gassing from a wide range of consumer products often dominate indoor sources of formaldehyde.

Example: particle boards

New built-in or mobile furniture made of particleboard are known for emitting comparatively high doses of formaldehyde. Kitchen cabinetry is one of the classical cases. The newer those products are the more formaldehyde they release. The first weeks, in some cases up to a year or longer, special attention must be paid to them and frequent ventilation of rooms where they are placed is necessary[14]. In extreme cases, when particleboard with high formaldehyde ratios[15] has been installed, formaldehyde air contamination can last for years and a complete and permanent removal could be the only way of eliminating the problem.

Mobile homes

The manufacturing process of travel trailers and mobile homes, a major housing facility in the US[16], involves the use of particularly large quantities of formaldehyde catalyzed resins needed for the production and assembly of particle board, fiberboard, plywood, surface coating, and foam insulation. Consequently, in many trailers, besides other pollutants, dangerous levels of formaldehyde fumes are detected[17].

Example: contaminated FEMA trailer

One recent prominent example of alarming formaldehyde levels in residential indoor air is the FEMA trailer incident. A large number of trailers and mobile homesprovided by the US Federal Emergency Management Agency (FEMA) for the housing of displaced victims of the hurricanes Katrina and Rita[18] have been found contaminated by formaldehyde in an unusually high average level of 0.77 ppm[19], and with many levels higher than this average, even more than two years after manufacturing[20]. After a number of occupants complained about respiratory distress such as asthma, sinus infections and bronchitis, nosebleeds, skin rashes, burning eyes, and persistent headaches, random samples of 519 travel trailers and mobile homes were tested between December 2007 and January 2008. Formaldehyde catalyzed resins of composite wood and plywood panels are believed to be the primary source of the massive formaldehyde emission in FEMA's temporary housing units.

Sadly but not surprisingly, the manufacturer who distributed those trailers to FEMA knew about their hazardous formaldehyde levels, yet for the sake of "good" business ignored them.[21] Even though lawsuits have been filed against FEMA in this case, and despite FEMA's promise it would work aggressively to relocate all residents of the temporary housing as soon as possible, a similar but smaller case occurred when again FEMA provided trailers for people displaced by the Iowa floods of June and July 2008[22].

Wide range of products contain Formaldehyde

According to the American Chemistry Council, "every day, people benefit from products that contain formaldehyde. This chemical is a critical, commercially valuable, and basic building block in our modern society. . Products derived from formaldehyde have an extremely broad role in the economy and provide many benefits to the public. In many instances . few compounds can replace it as a raw material without reducing performance and making the final product more expensive." [23]

Indeed, formaldehyde is not only ubiquitous in nature but also appears in countless products. The items listed below may contain and release formaldehyde or formaldehyde derivates[24]. Doses for one type of product can vary from zero or insignificantly low to rarely alarmingly high[25]. However, regardless how low the input of a single source might be, in worst case scenarios an unfavorable mix of primary and secondary sources can build up to an unwanted overall load of exposure. In general, BFGC recommends the examination of goods concerning potentially harmful substances before purchasing.

  • Formaldehyde is used in resins, largely needed for the manufacturing of pressed wood products, such as furniture, cabinets and building material made from particleboard, medium density fiberboard, and plywood.

  • Formaldehyde is an essential intermediate in the production process of many industrial chemical compounds, which in turn are used for manufacturing a great variety of raw and final products, such as polyurethane and polyester plastics, synthetic resin coating, synthetic lubricating oils, plasticizers, surface coatings, explosives, detergents, soft and rigid foams, and adhesives.

  • The polymerization of formaldehyde leads to polyacetal plastic components found in automobiles, in airplanes, and in electronic equipment, such as audio, video or computer devices.

  • Formaldehyde is the basis for products, such as dyes, tanning agents, precursors of dispersion and plastics, extraction agents, crop protection agents, animal feed, perfumes, vitamins, flavorings and drugs.[26]

  • As preserving and disinfecting agent formaldehyde is directly used in human and veterinary drugs including vaccines, for disinfecting hospitals, for preserving and embalming biological specimens and cadaver, and in dentistry.

  • Furthermore it is used as antimicrobial agent in cosmetics, such as soap, shampoo, hair preparation, shaving cream, deodorant, lipsticks, lotion, make-up, toothpaste, mouthwash and breath fresheners, and nail polish and hardener.[27]

  • As anti-corrosion agent formaldehyde is part of mirror finishing and electro-plating, of the electro-deposition of printed circuits, and of some photographic film developing processes.[28]

  • In the textile industry formaldehyde is used in crease-resistant finishes and in preservatives against fungal and other microbial decay, and against insects.

  • The paper industry applies formaldehyde in special treatments and coatings for some products, such as paper towels, paper money, and other special papers or cardboards.

  • In agriculture formaldehyde is applied as part of selected pesticides, in some fertilizers, as preservative for fodder, as a disinfectant, and in fumigation of products such as grain.

  • Although in small amounts, besides its natural occurrence in some food items, formaldehyde can be added to final fresh and preserved food products as well.[29]

  • Besides the above-mentioned commercial products and sanitary articles, here are some further popular consumer goods known for possibly or certainly containing formaldehyde: paint, lacquers, varnishes, wallpaper, cardboard and paper products, carpeting, durable press fabrics such as some curtains, sheets and certain clothing, fabric softeners, dishwashing liquids, shoe-care agents, fur and leather products, carpet cleaners, glues, adhesives, cigarettes, garden fertilizers, ink, decorative laminates.

Regulation of Formaldehyde


In many countries the use of formaldehyde is regulated. Often different agencies define different values for acceptable exposure limits for different purposes. In the US, for example, the EPA[30] has determined the exposure to formaldehyde in drinking water not expected to cause any adverse effects in a child at concentrations of 10 mg/L for 1 day or 5 mg/L for 10 days; the EPA has also set the general possible life time exposure not expected to cause any adverse effects to 1 ppm; The OSHA[31] has set the occupational exposure limit to an average of 0.75 ppm for 8-hour workdays and 40-hour workweeks; and the HUD[32] has set standard emission levels in manufactured housing at less than 0.2 ppm for Plywood and 0.3 ppm for particle board in order to provide a maximum ambient level of 0.4 ppm in manufactured housing.

In many cases existing surveys or studies do not cover the complete range of situations a defined exposure limit is set up for. This often applies to both the quality and the quantity of data. Information gained by animal experiments cannot be extrapolated to humans straight-line. Another problem might be posed by data collected not recently enough to be projected directly to current circumstances. And finally, different models of interpretation applied to the same pool of data can lead to different results. All this explains the sometimes wide range of numbers for the very same type of exposure limit recommended by the various institutions.

Government agencies that must consider a set of frequently contradicting viewpoints - ranging from health protection of individuals and the general public up to the competitiveness of companies, complete industrial sectors, and even the economy of a country as a whole - may conclude guidelines for exposure limits in a different way compared to a team of independent scientists devoted to the prevention of any possible health risk.

History of formaldehyde regulation

Frequently the knowledge backing up assumptions is incomplete or inaccurate or influenced by subjective prejudices. Newly acquired data could lead to revised insights. The history of the evaluation of health effects of formaldehyde is one of the many examples illustrating how science slowly finds increasing evidence for harmful long-term implications of doses lower than previously thought. Since commercial formaldehyde production began in 1889, great numbers of people have been exposed to it unregulated for more than 80 years. The increasing number of complains in the 1970s and 1980s about health problems caused by consumer products in homes containing fairly huge amounts of formaldehyde prompted health administrations to release various guidelines which not always, however, have been translated into legislation. At that time concerns that Formaldehyde could cause cancer arose when studies showed high levels of exposure, 6 - 15 ppm, induces nasal cancer in laboratory rats. Nevertheless, as these extreme exposure levels are not found in human environments, for the next two decades epidemiological studies failed to provide enough evidence for a potential carcinogenic risk to humans, and formaldehyde was classified first 1987 by the US EPA, and later 1995 by the ICAR[33] as "probably carcinogenic to humans" (Group 2A). In 2004, sufficient epidemiological evidence of nasopharyngeal cancer caused among formaldehyde-exposed workers[34] has led the ICAR to finally reclassify formaldehyde as "carcinogenic to humans" (Group 1). A link between occupational formaldehyde exposure and the development of myeloid leukemia documented in recent studies[35] seems to back up the reclassification.

This judgment promoted by the WHO is, however, controversial and has not yet caused action among national health agencies.[36] A recognition of formaldehyde as carcinogenic agent on governmental level would have sweeping consequences - in the EU, per example, according to existing legislation up to a severely restricted consumer exposure and a higher risk management at workplaces handling formaldehyde.

Current legal regulation on formaldehyde is limited to most urgent aspects of its use. For occupational formaldehyde exposure, 1987 OSHA reduced the permitted limit for 8-hour workdays from 3 ppm to 1 ppm, and amended this value again 1992 down to 0.75 ppm. In the field of consumer products a bill was passed in US congress 2010, to be in effect by January, 2013, restricting formaldehyde emission from plywood, particle board and medium density fiberboard to a maximum of 0.09 ppm.[37] In the EU generally the maximum concentration of formaldehyde allowed in finished products is 0.2% and any product holding a concentration of more than 0.05% has to be labeled with a warning that the product contains formaldehyde.


Generally, it is widely agreed that formaldehyde occurs in doses well below levels critical for human health. Higher air concentrations are found at workplaces related to the production or application of formaldehyde. The major exposure route for formaldehyde is inhalation from indoor sources. Considering the average time people spend inside, as well as the higher levels of indoor air concentration due to emitting building materials and consumer products, indoor exposure to formaldehyde contributes up to 98% to the average overall exposure. In some indoor locations concentration levels approach limits associated with signs of eye and respiratory tract sensory irritation.

Factors affecting formaldehyde emission

  • Indoor formaldehyde air concentrations vary according to following circumstances[38]:

  • The age of the building or the time passed since remodeling - since released formaldehyde degrades quickly, usually older buildings contain less formaldehyde.

  • The air exchange rate - the more indoor spaces are ventilated the less formaldehyde vapor can build up in them.

  • Air temperature and relative humidity - the higher both parameters are the more formaldehyde might be released as resins and other formaldehyde binding compounds are breaking off.

  • The season - because outdoor climate influences indoor temperature and humidity, in colder seasons windows are kept close, indoor heating devices can raise levels of formaldehyde, and lower outside temperatures lead to the fall out of condensation water inside. In warmer regions indoor formaldehyde levels are generally lower.

What can be done?

While it seems impossible to completely avoid exposure to materials and products releasing formaldehyde, the following measures can help reducing the level of formaldehyde air contamination around you:

  • First and most effective of all: Increase the air exchange rate of enclosed rooms, including vehicles, by opening doors and windows, and in rooms with no direct wall openings to the outside operate automated air exhausters. This advice does not only relate to formaldehyde emission but generally to improving indoor air quality.

  • Avoid unnecessarily high room temperatures and reduce indoor humidity.

  • Particle wood products made with formaldehyde resins are often a significant source of formaldehyde in homes. If you cannot avoid buying or using such products, as in cabinetry, furniture or flooring, look for certified eco-labels, such as the Blue Angel[39] in Germany, or the Green Seal in the US. Here certain ANSI[40] grades stamped on panels specify lower formaldehyde emission levels. So called "exterior-grade" pressed wood contains less formaldehyde.[41]

  • Choose furniture or cabinets containing a higher percentage of laminated or coated pressed wood panels with sealed edges. They generally emit less formaldehyde than openly exposed wood panels.

  • Before buying any consumer product check for harmful substances - not only for formaldehyde, of course.

  • Do not use unvented or insufficiently vented indoor heaters.

  • Strictly limit or completely avoid the use of formaldehyde containing cleaning and disinfecting supplies.

  • Avoid cosmetics containing formaldehyde. Amounts of 0.05% and higher must be labeled.

  • Do not smoke. The smoke of one cigarette can release up to 0.3 mg formaldehyde.

  • Wash durable-press fabrics before use.



[1] WHO, 2002, Concise International Chemical Assessment Document: Formaldehyde

[2] Snyder et al., 1970, Microwave Detection of Interstellar Formaldehyde: "Interstellar formaldehyde (H2CO) has been detected in absorption against numerous galactic and extragalactic radio sources by means of the 111-110 ground-state rotational transition at 4830 MHz. The absorbing regions often correspond in velocity with 18-cm OH features. H2CO is the first organic polyatomic molecule ever detected in the interstellar medium and its widespread distribution indicates that processes of interstellar chemical evolution may be much more complex than previously assumed."

[3] Most people recognize Formaldehyde in the air at a level of about 0.25 ppm (0.3 mg/m3). (DISU Mailbox Datenblatt Formaldehyde, DISU, Germany, 2007)

[4] Source: US Agency for Toxic Substances and Disease Registry (ATSDR), Toxicological Profile for Formaldehyde (1999); Lu et al (2010)

[5] The half life of inhaled Formaldehyde in the body is 10-15 minutes. A small part of it might be built into endogenous substances. (DISU Mailbox Datenblatt Formaldehyde, DISU, Germany, 2007)

[6] Environment Canada, 2001, Priority substances list assessment report, formaldehyde: "Available data on effects following ingestion or dermal exposure to formaldehyde are limited."

[7] Examples of formaldehyde concentrations: 0.0002 - 0.006 ppm in rural and suburban outdoor air, 0.0015 - 0.047 ppm in urban outdoor air, 0.020 - 4 ppm in indoor air (ATSDR, Public Health Statement Formaldehyde, 2008)

[8] US Consumer Product Safety Commission (CPSC), An Update on Formaldehyde, 1997 Revision

[9] No recent statistics are available. In a study by Kauppinen et al., 2000, CAREX, 2003, approximate numbers of workers exposed to formaldehyde above background levels (0.1 ppm) in the European Union 1990-93 in major industry sectors have been estimated. All industries combined presented a total of 971,000 people. For the US the National Institute for Occupational Safety and Health (NIOSH) survey (National Occupational Exposure Survey (NOES) 1981-1983) has statistically estimated that 1,329,322 workers (441,902 of them female) are potentially exposed to formaldehyde. The NOES Survey does not include farm workers.

[10] ATSDR, Public Health Statement Formaldehyde, 2008

[11] The USA, Western Europe, China and Japan produce and consume the largest quantities of 37% formaldehyde solution, the most typical commercial formaldehyde raw product.

[12] "Data from several studies indicate that various cooking activities may contribute to the elevated levels of formaldehyde sometimes present in indoor air (Health Canada, 2000). In recent work from the USA, the emission rate of formaldehyde from meat charbroiling over a natural gas-fired grill in a commercial facility was higher (i.e., 1.38 g/kg of meat cooked) than emission rates of all other VOCs measured except for ethylene (Schauer et al., 1999)." (CICADS, 2002, Formaldehyde)

[13] Cigarettes contain remarkable loads of Formaldehyde. "A range of mainstream smoke emission factors from 73.8 to 283.8 Ãg/cigarette was reported for 26 US brands, which included non-filter, filter, and menthol cigarettes of various lengths (Miyake & Shibamoto, 1995) " Nevertheless "ETS (environmental tobacco smoke) does not increase concentrations of formaldehyde in indoor air, expect in areas with high rates of smoking and minimal rates of ventilation (Godish, 1989; Guerin et al. 1992)." (CICADS, 2002, Formaldehyde)

[14] According to a US Environmental Protection Agency (EPA) study a new home measured 0.076 ppm formaldehyde when brand new and 0.045 ppm after 30 days.

[15] In the US, per example, recent legislation, to be in effect by January 2013, is going to limit the emission of formaldehyde from composite wood products to a maximum of 0.09 ppm. In the past, however, composite wood of much higher emission has been used, and there is no guarantee such material is still occasionally deployed.

[16] Approximately 8 million US citizens live in trailers and mobile homes.

[17] In addition to off-gassing building materials further typical sources of formaldehyde in trailers are insufficient air circulation of HVAC units and indoor emissions of gas burning cooking devices during times and seasons of restricted air ventilation.

[18] Hurricane Katrina of the historic 2005 Atlantic hurricane season was the costliest natural disaster, as well as one of the five deadliest hurricanes, in the history of the United States. August 29 Katrina hit the Gulf coast from central Florida to Texas. New Orleans, southeast Louisiana, and the coastal areas of Mississippi were affected most severely. Hurricane Rita hit again the Gulf cost of Texas and Louisiana just four weeks later, September 23, and was the fourth-most intense Atlantic hurricane and the most intense tropical cyclone in the Gulf of Mexico ever recorded. Some 143,000 trailers were used as emergency housing units following the two storms.

[19] Normal levels of formaldehyde are 0.1 to 0.2 ppm

[20] US CDC: Interim Findings on Formaldehyde Levels in FEMA-Supplied Travel Trailers, Park Models, and Mobile Homes from the Centers for Disease Control and Prevention, February 29, 2008. FEMA started to supply trailers 2006.

[21] "In July 2008, officials for Gulf Stream Coach, Forest River, Keystone RV, and Pilgrim International testified before the House Oversight and Government Reform Committee. They admitted that they knew the FEMA trailers they made for the hurricane victims contained unsafe levels of formaldehyde." (Source: Product Liability Law Blog, December 9, 2009, in: Thousands of FEMA Trailer Claims Filed by Victims of Hurricane Katrina and Rita)

[22] Rep. Bruce Braley, 2008 press releases: "Washington, DC - Rep. Bruce Braley (D-Iowa) released the following statement today after reports that unsafe levels of formaldehyde have been detected in temporary FEMA housing in Iowa: "It is disturbing and unacceptable that temporary housing provided by the agency responsible for helping people in times of emergency could be making them ill," Braley said. "Iowans affected by this year's unprecedented floods and tornadoes should be able to have confidence that FEMA will be helpful to them during this difficult time, not harmful to their health. ."

[23] American Chemistry Council, Inc. at, retrieved March 2011

[24] Taken partly from IARC monographs, volume 88, 2006;

[25] In developed countries under normal circumstances nowadays critical doses of formaldehyde in residential and other buildings not engaged in formaldehyde processing are rare and do not last long enough in order to impose verifiable health risks. In older buildings, constructed before formaldehyde has been regulated, formaldehyde from once highly contaminated building material has most likely degenerated by now. In those buildings semi volatile pollutants (e.g. PAH) remain more of a problem today. However, the recent FEMA trailer incident described above indicates potential risks of hazardous indoor formaldehyde exposure cannot be ruled out.

[26] WHO, 1989; Reuss et al., 2003

[27] Cosmetic Ingredient Review Expert Panel, 1984; Reuss et al., 2003

[28] Reuss et al., 2003

[29] Besides naturally low levels in some food (e.g. fruits), formaldehyde in fertilizers, fumigants, or preservatives may add additional exposure. "The Food and Drug Administration (2003) in the USA identifies formaldehyde: as a secondary direct food additive that is permitted in food for human consumption; for use as a preservative in defoaming agents; as an indirect food additive for use only as a component of adhesives; as an indirect food additive for use only as paper and paperboard components; as an indirect food additive for use only as a preservative in textile and textile fiber polymers; as an indirect food additive for use as an adjuvant in animal glue; and, under specified conditions, as an animal drug and in the manufacture of animal feeds." (IARC monographs, volume 88, 2004)

[30] EPA: Environmental Protection Agency

[31] OSHA: Occupational Safety and Health Administration

[32] HUD: Department of Housing and Urban Development

[33] IARC: International Agency for Research on Cancer, WHO

[34] 1994 follow-up of the National Cancer Institute (NCI) cohort study of formaldehyde-exposed workers (Hauptmann et al., 2003; 2004)

[35] Zhang et al., 2010, Formaldehyde and Leukemia: Epidemiology, Potential Mechanisms, and Implications for Risk Assessment; Zhang et al., 2008, Formaldehyde exposure and leukemia: A new meta-analysis and potential mechanisms

[36] Up to now the WHO itself did not issue the substantiation of her reclassification in 2004, yet.

[37] US Congress, Formaldehyde Standards for Composite Wood Products Act, 2010

[38] According to: WHO guidelines for indoor air quality: selected pollutants, 2010

[39] The Blue Angel (Blauer Engel) certificate, introduced in Germany 1978, was the first environmental label worldwide.

[40] ANSI: American National Standards Institute

[41] Exterior-grade pressed wood is made with phenol resins instead of urea resins, and therefore emits less formaldehyde.

Apr 01, 2011
Health Benefit of Green Tea - Obesity and Green Tea
By John E. Jernstad
Mount Kisco, NY


Few issues capture both medical and public attention as obesity. Widely associated with various illnesses as well as higher mortality, obesity may account for as many as 15 to 20% of deaths resulting from coronary heart disease and a whopping 65 to 75% of new cases of type 2 diabetes [1], and is blamed as a major culprit for myriad other disorders, respiratory illnesses, and even some types of cancer. In 2008, 66%, or fully two-thirds, of the United States population, was found to be overweight with approximately 31% of American adults being obese. In the same year 32% of children were overweight with 17% children between the ages two and 19 being obese [2].

The most fundamental principle of weight loss is simple: eat less, move more. However, a growing body of research indicates that green tea can be a powerful ally in boosting the metabolic process to give you an extra boost in your daily regimen of healthy eating and moderate exercise, as well as a lifestyle choice that can help you prevent and suppress weight gain.

Green Tea

First cultivated in China over 4,000 years ago, Green tea has long been used in all over Asia both as a beverage as well as a method of traditional medicine to aid in everything from controlling bleeding and helping heal wounds to regulating body temperature and blood sugar, helping with digestion, and focusing the mind and body. Clinical research continues to shed more light on these and heretofore unknown heath and medical benefits of green tea.

How does green tea help with weight loss?

A large number of studies and clinical trials are shedding light on green tea's ability to increase your body's metabolism and specifically prevent the buildup of blood sugar and body fat. Green tea speeds up the burning of "brown fat", a type of fat whose primary function is to generate body heat in humans by drawing calories from normal ("white") fat to burn it. Green tea also sends glucose, the sugar from foods that is absorbed into your bloodstreams, to muscles to be used for generating energy rather than to fat tissue. Green tea also reduces the action of fat-digesting enzymes to reduce the amount of fat the body uses from the food you eat. The active ingredients in green tea have also been found to lower the body's production of fatty acids, blood fat and cholesterol.

Growing body of evidence for green tea as obesity fighter

A study in 2005 showed that the daily consumption of green tea over a period of 12 weeks led to a significant reduction in body weight as well as waist size and body fat accumulation [3]. A group drank a bottle of green tea containing 690mg of catechins, while another "control group" drank tea containing only a small amount of catechins (far less than normally found in a cup). At the end of 12 weeks, the group that took the larger amount showed significant decreases in body weight, BMI, waist circumference, body fat mass, and fat found under the skin. A larger study in 2007 involving 240 volunteers confirmed the results of the earlier study [4]. Another study in 2009 involving 132 overweight or obese women over a period of 12 weeks showed a marked reduction in abdominal fat in the group that consumed green tea [5].

Another study in 2000 showed that a green tea extract could increase around-the-clock metabolism ("energy expenditure") and fat breakdown thanks to its caffeine and catechin polyphenol content. Under strictly controlled circumstances, three groups of volunteers were given tea extracts and caffeine, just caffeine, and a placebo containing no active ingredients, respectively. The results showed clearly that those who took the green tea extract saw a marked increase in their metabolism, while the group that only had caffeine didn't show the same increase in daily energy expenditure [6].

What about the caffeine?

Many people worry about increasing their caffeine intake by drinking several cups of green tea each day. Caffeine, a much-maligned substance, does in fact have several invigorating effects that fight sleepiness, speed up heart rate, increase alertness, and improve athletic performance. Of course, moderation is the key-excessive caffeine can make you nervous, irritate, unable to fall asleep, and cause dizziness and headaches in some people. Everyone's different, but most doctors recommend limiting caffeine to less than 200 to 250mg per day. Fortunately, green tea contains about 20mg of caffeine per cup, about half that of black tea (around 40mg) and a fraction of that found in drip coffee (a whopping 90 to 150mg) [7]. In addition, the tannin and L-theanine found in green tea work together to decrease the effect of caffeine on the body while providing a host of other positive benefits.

Why choose green tea?

Walk into any health food store and you'll be greeted with rows upon rows of supplements and nutrition aids that all seem so promising. So why should you choose green tea as part of your healthy lifestyle?

Green tea and its component substances have a positive effect on human health and metabolism, and it's all natural. Green tea is not invasive, and doesn't change the normal metabolic pathways of the human body or attempt to add or subtract anything that doesn't belong there. Polyphenols, a large group of substances which includes flavonoids such as the catechins found in abundance in green tea, are present all over nature in a wide variety of plants and plant-derived food including berries, olive oil, chocolate and coca, coffee, pomegranates, fruits and fruit drinks, and numerous other vegetables. In addition, organic green tea is widely available, reducing the dangers of pesticide exposure that can be amplified by the nature of the tea-brewing process, when chemicals can leech into the water while the tea leaves (which are directly exposed to pesticides during cultivation) are immersed in hot water.

With rising awareness of the greater dangers of obesity and more people turning to healthful lifestyles and sensible food habits to lose weight and keep healthy, green tea that is rich in beneficial substances can be a powerful ally in combating obesity and maintaining a healthy body composition. Drinking green tea, combined with healthful eating habits and exercise, is a sustainable and natural lifestyle choice for anyone seeking to become and stay fit and healthy.


1. Kopelman, P.G., I.D. Caterson, and W.H. Dietz, Clinical obesity in adults and children. 3rd ed2010, Chichester, West Sussex ; Hoboken, NJ: Wiley-Blackwell. x, 502 p.
2. Flegal, K.M., et al., Prevalence and trends in obesity among US adults, 1999-2008. JAMA : the journal of the American Medical Association, 2010. 303(3): p. 235-41.
3. Nagao, T., et al., Ingestion of a tea rich in catechins leads to a reduction in body fat and malondialdehyde-modified LDL in men. The American journal of clinical nutrition, 2005. 81(1): p. 122-9.
4. Nagao, T., T. Hase, and I. Tokimitsu, A green tea extract high in catechins reduces body fat and cardiovascular risks in humans. Obesity, 2007. 15(6): p. 1473-83.
5. Maki, K.C., et al., Green tea catechin consumption enhances exercise-induced abdominal fat loss in overweight and obese adults. The Journal of nutrition, 2009. 139(2): p. 264-70.
6. Dulloo, A.G., et al., Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. The American journal of clinical nutrition, 1999. 70(6): p. 1040-5.
7. Chin, J.M., et al., Caffeine content of brewed teas. Journal of analytical toxicology, 2008. 32(8): p. 702-4.
Mar 31, 2011
By Kevin D. Ham, M.D.
Vancouver, BC, Canada

We breathe, drink and eat in order to provide the necessary nutrients to build and maintain the cells of our bodies, but we must also remove any metabolic waste products produced by the cells and any substances that are either harmful to the body or no longer of any use to the body.

We excrete these waste products by breathing, sweating, urination and defecation.

Breathing facilitates the removal of metabolic by-products, such as carbon dioxide, from the blood through constant breathing. Breathing can also eliminate volatile toxicants such as ethanol or pesticidal fumigants as well as volatile metabolites including acetone and carbon dioxide.

There are about 2.6 million sweat glands that regulate body temperature via sweating. While sweat consists mostly of the plasma of blood, apocrine sweat from our armpit and genital areas also contain proteins and fatty acids. While sweat is odorless, the bacteria present on the hair and skin metabolize the proteins and fatty acids present in apocrine sweat and unpleasant odors can be produced. Some of this sweat can be absorbed by clothing or reabsorbed back into the blood via the skin if not washed regularly.

The kidneys are primarily organs of excretion and elimination by the kidney accounts for most by-products of normal body metabolism. They also are the primary organs for excretion of polar drugs and metabolites, such as pesticides and drugs. The kidneys remove urea from protein metabolism, creatinine from muscle metabolism, uric acid from nucleic acids, bilirubin from red blood cells and broken down products of hormones. One liter of blood flows into the kidney every minute and from that, one milliliter of urine is produced every minute.

The liver produces bile, which aids in the digestion of fats in the small intestine. Excess bile is stored in the gall bladder. It consists of bile salts and bile pigment, which come from the breakdown of red blood cells, cholesterol and lecithin. It emulsifies fats, making them easier to digest. Bile is also important in the elimination of toxins, heavy metals, drugs, and other harmful chemicals. These are delivered to the small intestine and removed in the feces. Some of these can be reabsorbed through the enterohepatic cycle back into the blood from the small and large intestine.

Undigested food enters our colon, which is about 1.5 meters in length. However, it takes about 8-12 hours for this stool to pass through our colon to our rectum. During this time, up to ten liters of gas is produced in our colon daily. Less than 1 liter exits as flatus. So where does this gas go? Where does this gas come from?

The quadrillion bacteria in our colon feast on the undigested food and multiply, producing metabolic waste products, such as acids, enzymes and gases. Most of this gas is absorbed into the blood and transported to the liver, which detoxifies most of it.

A rising epidemic of constipation, due to a diet of processed foods, not enough fiber, lack of physical activity, compounds to the problem of keeping in waste, as well as potential pressure effects in the abdomen, when such wastes should be excreted from the body regularly.

Timely, regular, frequent elimination of metabolic waste products and harmful chemicals should be removed from our bodies and help keep the blood clean and free of such burden.
Mar 30, 2011
Recent Trends in Obesity-related Research in Medicine
By Dr. In-ae Lee
Düsseldorf, Germany

Obesity is a phenomenon becoming more prevalent around the world that has reached epidemic proportions in Westernized cultures, and the diseases associated with it (including insulin resistance, type II diabetes mellitus, hepatic steatosis, and atherosclerotic cardiovascular diseases) have become major public health problems [1].

Obesity-related research has been conducted on multiple levels, from molecular to socio-environmental, showing that obesity results from the interaction of cellular factors with social factors. Potential biological drivers of obesity include neurobiological mechanisms, epigenetic gene-environment interactions and gut microbiota [2].

Neurohormonal Controls

A complex interplay of neurotransmitters, hormones and metabolites regulates food intake in the brain. Metabolic-sensing neurons respond to signals of energy intake, demand, or storage, including circulating glucose, leptin, insulin, ghrelin, adrenal steroids, polypeptide YY, fatty acids, ketone, lactate, vagal nerve afferents and intrinsic neurotransmitters [3]. In response, hypothalamic neurons release neurotransmitters that activate either catabolic or anabolic processes. For most humans, however, the feedback signals against excess food intake are not sufficient enough to maintain normal body weight when they have easy access to palatable, calorie-dense food[3].

When provided a diet high in calories, animals, prone to obesity, rapidly increase fat stores [4]. Furthermore, when obese rats lose weight they mount the neurohormonal drive to increase intake and decrease energy expenditure, effectively defending obesity [5, 6]. After weight loss, average resting energy expenditure of obese people is markedly and persistently reduced [7]. These factors are blamed for the weight regain that occurs in approximately 80-90% of obese people who have lost weight [7, 8].

Behavioral animal studies have shown that when a palatable and calorie-dense diet is provided, rats eat far beyond limits of homeostasis and develop extreme levels of obesity even among rats predisposed to leanness [9]. The more palatable the diet, the higher the degree of obesity and the longer it is sustained [9].

The stimuli that augment the drive to obtain foods, the so-called "reward properties of food", are mediated through receptors that also mediate addiction. Metabolic signals modify the sensing thresholds for food-seeking behavior and reward signals [10]. Chronic stress enhances the reward value of foods [11]. Subconscious drives for intake are cortically integrated into learned motivational cues that can drive intake well beyond subcortical demands of energy needs [12].

Neurohormonal mechanisms

Studies have found that shorter sleep times in childhood were significantly associated with increased body mass index [13, 14]. Experimental studies of sleep deprivation show increased hunger and appetite associated with neurohormonal mechanisms that promote food intake. Debate remains about the strength of the evidence that poor sleep causes obesity, as interventions to decrease obesity by increasing sleep have yet to be reported [15].

Distracting stimuli, such as television viewing while eating, strongly increase intake [16]. In a controlled experiment, viewing children's food advertisements caused children to eat much larger portions of snack foods compared to children who watched nonfood advertisements, and the effect was significantly larger on obese children than on normal-weight children. These advertisements associate fast-food restaurants or sweetened cereals with fun and happiness, seeking to influence the emotional response to foods, and successfully alter the perceived reward value of foods [17, 18].


The term epigenetics refers to cellular mechanisms that affect gene expression without changing DNA sequence [19]. Epigenetic markings can be inherited and modified throughout the lifespan [20]. Some changes in gene expression persist even across generations [21]. Several animal studies illustrate epigenetic influences on obesity.

The Agouty mouse is a well-described model of epigenetically-controlled obesity. Obesity is developed due to inadequate methylation of the obese allele [21]. Maternal ingestion of bisphenol A, a chemical used in plastic, decreased methylation of the obese allele in the offspring [22]. This decrease in methylation did not occur when a methyl donor, such as folic acid or vitamin B12, was added to the diet containing bisphenol A [22].

Rats whose mothers do not eat enough protein during pregnancy have decreased methylation and have increased insulin resistance, dyslipidemia and hypertension. Giving mothers folic acid supplements prevented the hypomethylation and normalized the gene expression in offspring [23].

Two rare human obesity syndromes, Prader-Willi and Beckwith-Wiedemann, can result from inappropriate methylation of imprinted genes [21].

A recent study of adults who were exposed to well-defined poor nutrition in utero, caused by the Dutch famine of 1944 -1945, showed that adults who were exposed to poor nutrition early in gestational development had an increased prevalence of glucose intolerance, dyslipidemia, early coronary heart disease, and obesity compared with unaffected siblings [24, 25]. This study is reportedly the first to provide empirical support for the hypothesis that environmental exposures can cause epigenetic changes in humans.

If epigenetic modifications that increase risk for obesity occur widely in humans, the implications for public health interventions could be substantial. At present, however, direct evidence in humans is sparse [1].

Gut Microbiota

Microbiological research indicates that the pathogenesis of obesity may be influenced by our endogenous gastrointestinal microbiota. These microbes metabolize otherwise indigestible components of the diet, and the products of microbial metabolism affect the amount of energy absorbed [26].

Two groups of beneficial bacteria are dominant in the human gut - the Bacteroidetes and the Firmicutes. Obese rodents and humans have a significantly lower percentage of Bacteroidetes in their gut microbiome, and an increase in Firmicutes bacteria, compared to their lean counterparts. Weight loss, on a low-calorie diet by obese individuals, corrected this disproportion [26].

Germ-free mice showed a dramatic increase in body fat within 10-14 days after colonization with bacteria from the distal gut of mice that were raised conventionally despite an associated decrease in food consumption [27].

Further studies were conducted using obese mice with homozygotous mutation in the leptin gene (ob/ob) as well their lean littermates (+/+). In the ob/ob mouse model increased food consumption due to genetic leptin deficiency was found to be the primary cause for obesity in these mice.

Comparative metagenomic analysis showed that the percentage of Bacteroidetes in ob/ob mice was lower by 50%, whereas that of Firmicutes was higher by a corresponding degree. These differences were not attributable to differences in food consumption. Analogous differences have been observed in the distal gut microbiota of lean versus obese humans [26]. This result revealed a correlation between host genotype and the gene content of the microbiome.

To determine if microbial community gene content is a potential contributing factor to obesity, lean (+/+) and obese (ob/ob) caecal bacteria were transplanted into germ-free wild-type mouse recipients. Ob/ob recipient microbiota had a significantly higher percentage of Firmicutes, and significantly less energy remaining in their faeces relative to their lean littermates, showing again that the microbiome associated with obesity is more efficient at harvesting dietary energy [26]. Most importantly, mice colonized with an ob/ob microbiota exhibited a significantly greater percentage increase in body fat over two weeks than mice colonized with lean (+/+) microbiota, corresponding to a difference of 2% of total calories consumed [26]. While this may not seem significant, the alteration in efficiency of energy harvest from the diet, produced by changes in gut microbial ecology, does seem to be great to contribute to obesity, given that small changes in energy balance over the course of a year can result in significant changes in body weight.

These results highlight a potentially relevant connection between gut microbial function and endogenous molecular pathways controlling energy balance, with potential therapeutic implications in the future. However, the exact properties in the obese gut that tip the balance towards the Firmicutes are still unclear.

A recent case-control study found that gut flora in infancy predicted overweight later in childhood [28]. On average, overweight children had lower numbers of the genus Bifidobacterium spp. and higher numbers of Staphylococcus aureus in their stools during infancy.

Studies of lean and obese adult twin pairs found a core group of functional genes across participants regardless of bacterial species type. In addition to this "core microbiome", the microbiomes of obese twins contained more genes involved in carbohydrate, lipid and amino acid metabolism [29].

These studies show the potential benefits of cross-disciplinary approaches for establishing key concepts of obesity intervention or prevention.


1. Tschop, M.H., P. Hugenholtz, and C.L. Karp, Getting to the core of the gut microbiome. Nat Biotechnol, 2009. 27(4): p. 344-6.
2. Haemer, M.A., T.T. Huang, and S.R. Daniels, The effect of neurohormonal factors, epigenetic factors, and gut microbiota on risk of obesity. Prev Chronic Dis, 2009. 6(3): p. A96.
3. Berthoud, H.R. and C. Morrison, The brain, appetite, and obesity. Annu Rev Psychol, 2008. 59: p. 55-92.
4. Levin, B.E., Why some of us get fat and what we can do about it. J Physiol, 2007. 583(Pt 2): p. 425-30.
5. Levin, B.E. and A.A. Dunn-Meynell, Defense of body weight against chronic caloric restriction in obesity-prone and -resistant rats. Am J Physiol Regul Integr Comp Physiol, 2000. 278(1): p. R231-7.
6. Levin, B.E. and R.E. Keesey, Defense of differing body weight set points in diet-induced obese and resistant rats. Am J Physiol, 1998. 274(2 Pt 2): p. R412-9.
7. Astrup, A., et al., Meta-analysis of resting metabolic rate in formerly obese subjects. Am J Clin Nutr, 1999. 69(6): p. 1117-22.
8. Wing, R.R. and J.O. Hill, Successful weight loss maintenance. Annu Rev Nutr, 2001. 21: p. 323-41.
9. Levin, B.E. and A.A. Dunn-Meynell, Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity. Am J Physiol Regul Integr Comp Physiol, 2002. 282(1): p. R46-54.
10. Zheng, H. and H.R. Berthoud, Neural systems controlling the drive to eat: mind versus metabolism. Physiology (Bethesda), 2008. 23: p. 75-83.
11. Adam, T.C. and E.S. Epel, Stress, eating and the reward system. Physiol Behav, 2007. 91(4): p. 449-58.
12. Berthoud, H.R., Multiple neural systems controlling food intake and body weight. Neurosci Biobehav Rev, 2002. 26(4): p. 393-428.
13. Taveras, E.M., et al., Short sleep duration in infancy and risk of childhood overweight. Arch Pediatr Adolesc Med, 2008. 162(4): p. 305-11.
14. Landhuis, C.E., et al., Childhood sleep time and long-term risk for obesity: a 32-year prospective birth cohort study. Pediatrics, 2008. 122(5): p. 955-60.
15. Marshall, N.S., N. Glozier, and R.R. Grunstein, Is sleep duration related to obesity? A critical review of the epidemiological evidence. Sleep Med Rev, 2008. 12(4): p. 289-98.
16. Blass, E.M., et al., On the road to obesity: Television viewing increases intake of high-density foods. Physiol Behav, 2006. 88(4-5): p. 597-604.
17. McClure, S.M., et al., Neural correlates of behavioral preference for culturally familiar drinks. Neuron, 2004. 44(2): p. 379-87.
18. Connor, S.M., Food-related advertising on preschool television: building brand recognition in young viewers. Pediatrics, 2006. 118(4): p. 1478-85.
19. Ubeda, F. and J.F. Wilkins, Imprinted genes and human disease: an evolutionary perspective. Adv Exp Med Biol, 2008. 626: p. 101-15.
20. Waterland, R.A. and K.B. Michels, Epigenetic epidemiology of the developmental origins hypothesis. Annu Rev Nutr, 2007. 27: p. 363-88.
21. Jirtle, R.L. and M.K. Skinner, Environmental epigenomics and disease susceptibility. Nat Rev Genet, 2007. 8(4): p. 253-62.
21. Dolinoy, D.C., D. Huang, and R.L. Jirtle, Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A, 2007. 104(32): p. 13056-61.
23. Lillycrop, K.A., et al., Dietary protein restriction of pregnant rats induces and folic acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring. J Nutr, 2005. 135(6): p. 1382-6.
24. Roseboom, T., S. de Rooij, and R. Painter, The Dutch famine and its long-term consequences for adult health. Early Hum Dev, 2006. 82(8): p. 485-91.
25. Ravelli, G.P., Z.A. Stein, and M.W. Susser, Obesity in young men after famine exposure in utero and early infancy. N Engl J Med, 1976. 295(7): p. 349-53.
26. Turnbaugh, P.J., et al., An obesity-associated gut microbiome with increased capacity for energy harvest. Nature, 2006. 444(7122): p. 1027-31.
27. Backhed, F., et al., The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A, 2004. 101(44): p. 15718-23.
28. Kalliomaki, M., et al., Early differences in fecal microbiota composition in children may predict overweight. Am J Clin Nutr, 2008. 87(3): p. 534-8.
29. Turnbaugh, P.J., et al., A core gut microbiome in obese and lean twins. Nature, 2009. 457(7228): p. 480-4.
Mar 25, 2011
Health Effects of the Japanese Nuclear Accident
By Justin H. Joe, Ph.D.
Mount Kisco, NY

The news from Japan of the recent nuclear crisis induced by a record breaking earthquake of magnitude of 9.0 on the Richter scale and subsequent tsunami struck fear into the hearts of people in Japan as well as the citizens of surrounding nations such as China and Korea. Common perception associates radiation exposure, and more specifically radioactivity, with cancer and other untreatable and long-lasting illnesses. Much of the perceived as well as real danger association with radiation can be attributed to its invisible and undetectable nature [1, 2]. This article examines the potential health effects of radionuclides of iodine-131 and cesium-137, which are believed to have been released in the accident in Japan and other similar accidents in the past [3, 4], as well as several ways to minimize long-term biological effects to people living in potentially affected areas.

Radioactivity of nuclides can be defined as the process of spontaneous transformation of the nucleus, generally with the emission of alpha or beta particles often accompanied by gamma rays [1]. The process is referred to as decay or the disintegration of an atom. Different types of radiations are capable of displacing electrons from atoms in bio-molecules, thereby producing ions. High doses of ionizing radiation may produce severe skin or tissue damage. Because approximately 70% of the human body is composed of water, water molecules (H2O) are naturally the most common building block of organic tissue. Ionization of water usually results in the formation of a hydroxyl radical (OH) or hydrogen peroxide (H2O2). These molecules can attack a biomolecule or a cell, and destroy it [2].

From a public health standpoint, however, the long-term health hazard of radionuclides, e.g. iodine-131 and cesium-137, from nuclear disasters lies in their ability to enter the body. This is the reason radioisotopes emitting alpha and low energy beta radiation are fundamentally harmless outside the body, but they can produce radiation damage to the target organs when taken into the body. Their biological behavior in their target organs is governed by their chemical properties, and their radioactive properties allow them to irradiate tissues in which they are localized. For example, cesium-137 is considered potassium equivalent and is expected to behave like potassium. Thus potassium abundance affects physical absorption and distribution of cesium-137 when the elements are chemically analogous [5].

The two main means of exposure to the nuclides are inhalation and ingestion. Soluble particles, which are inhaled, are absorbed quickly from the lung and delivered in the body depending on their chemical properties [6]. Insoluble particles are deposited on the bronchial mucosa and carried out of the lung by ciliary action. Finally they are swallowed. Sufficiently insoluble radionuclides are accumulated in the alveoli, small chambers of air in the lung. Such particles can be slowly repositioned to the pulmonary lymph nodes. Ingested or swallowed particles after inhalation can be absorbed from the gut and distributed to the target organ in the body.

There are three important isotopes that present significant health hazards when inhaled or ingested, which are iodine-131, and cesium-137 and strontium-90; these are cancer hazards for the thyroid gland and bone, respectively [7]. Fortunately iodine-131, which is collected in the thyroid, decays relatively quickly with a half-life of 8 days. Moreover, its bioeffect can be diminished quickly during food-chain transport. On the other hand, cesium-137 and strontium-90 with half-lives of 30 years and 28 years, respectively, can remain far longer in the body unless metabolized or driven out before localizing in different body parts including bones [2, 8].

There are several ways to minimize harmful exposure to these radioactive particles. First, only fall-out radionuclides such as iodine-131 and cesium-137 from nuclear disasters can stick to a person's skin. They can be washed off if not inhaled or ingested. If someone unintentionally walks through fall-out rain, he/she should breath through a wet handkerchief or gas mask, if available, to prevent dust inhalation [2]. Second, potentially contaminated foods and water should be avoided to prevent any ingestion of these radionuclides. Third, certain drugs can mitigate the effects of internal contamination. These include potassium iodide to protect against thyroid accumulation of iodine-131 and Prussian blue to help remove the effects of radioactive poisoning from cesium-137 [9].

While estimated internal and external radiation doses from iodine-131 and cesium-137 around Fukushima were above the public dose limit (1 mSv/y) established by the Nuclear Regulatory Commission [10], radiation exposure potency still exists in neighboring countries. Environmental monitoring in Fukushima as well as surrounding regions and countries and other long-term follow-up measures could further ensure radiation safety and reduce unnecessary exposure. In addition, populations residing in affected areas should be monitored for any occurrence of health issues.


1. Clements, B.W., Nuclear and Radiological Disasters, in Disasters and Public Health 2009, Butterworth-Heinemann: Boston. p. 211-236.
2. Eerkens, J.W., Safety Considerations in Nuclear Operations, in The Nuclear Imperative2010, Springer Netherlands. p. 135-156.
3. Jaworowski, Z., OBSERVATIONS ON THE CHERNOBYL DISASTER AND LNT. Dose-Response, 2010. 8(2): p. 148-171.
4. Romanenko, A., et al., Urinary bladder carcinogenesis induced by chronic exposure to persistent low-dose ionizing radiation after Chernobyl accident. Carcinogenesis, 2009. 30(11): p. 1821-1831.
5. Taira, Y., et al., Current Concentration of Artificial Radionuclides and Estimated Radiation Doses from Cs-137 around the Chernobyl Nuclear Power Plant, the Semipalatinsk Nuclear Testing Site, and in Nagasaki. Journal of radiation research, 2011. 52(1): p. 88-95.
6. Albert, R.E., Ionizing Radiation. Patty's Toxicology2001: John Wiley &Sons, Inc.
7. Hafemeister, D., Nuclear Pollution, in Physics of Societal Issues 2007, Springer New York. p. 163-196.
8. Lestaevel, P., et al., Neuro-inflammatory response in rats chronically exposed to (137)Cesium. Neurotoxicology, 2008. 29(2): p. 343-348.
9. Hammond, J.S. and J. Lipoti, Radiological Agents and Terror Medicine, in Essentials of Terror Medicine, S.C. Shapira, J.S. Hammond, and L.A. Cole, Editors. 2009, Springer New York. p. 241-253.
10. Cember, H. and T.E. Johnson, Ionizing Radiation. Patty's Industrial Hygiene 2011: John Wiley & Sons, Inc.
Mar 23, 2011
Chronic Constipation - The Causes, Symptoms, and Treatment
By Dr. Namhyun Kim
General Surgery
European Society of Hemato-Centric Medicine
Düsseldorf, Germany

Constipation is the most common digestive complaint in the United States according to survey data [19]. Chronic constipation is a common condition that affects up to 27% of the population [1] and is twice as common in women than in men [2]. More than four million Americans have frequent constipation, accounting for 2.5 million physician visits a year. Constipation-related healthcare costs total $6.9 billion in the U.S. each year [20], with another $725 million spent on laxative products [21].


Constipation is a symptom with many causes. The two primary causes are obstructed defecation (organic) and colonic slow transit (functional). The distinction between organic and functional types of chronic constipation has no practical relevance in the treatment of patients.

  • Primary: Primary or functional constipation are on-going symptoms that last more than six months that do not have any underlying cause such as medication side effects or a medical condition.

  • Diet: Constipation can be caused or exacerbated by a low-fiber diet, low liquid intake, or dieting.

  • Medication: Constipation is a side effect of several types of medication.

  • Metabolic and muscular: Metabolic and endocrine problems which may lead to constipation include hypercalcemia, hypothyroidism, diabetes mellitus, cystic fibrosis and celiac disease. Constipation is also common in individuals with muscular and myotonic dystrophy.

  • Structural and functional abnormalities:

    - Structural causes: spinal cord lesions, Parkinson, colon cancer, anal fissures, proctitis and pelvic floor dysfunction.
    - Functional (neurological) causes: anismus, descending perineum syndrome and Hirschsprung's disease.


The term "constipation" refers to a constellation of symptoms. The "Rome III criteria" are a useful set of diagnostic criteria for constipation. At least two of the following symptoms are required to have been present for at least three of the past six months:

  • Straining at stool at least 25% of the time

  • Hard stools at least 25% of the time

  • A feeling of incomplete evacuation at least 25% of the time

  • A feeling of anal blockage at least 25% of the time

  • Manual maneuvers for rectal emptying at least 25% of the time

  • Two stools or less per week

Diagnostic evaluation

It is important to be diligent in examining the patient's history, as many patients often do not report certain symptoms spontaneously. Apart from history-taking, diagnostic testing can be kept to a bare minimum for the vast majority of patients.

A digital rectal examination is part of the basic physical work-up, particularly when the symptoms point to a possible functional disturbance of the rectum. Large amounts of stool in the colon usually can be visualized by a simple X-ray examination of the abdomen; the more stool that is visualized, the more severe the constipation.

Colonoscopy is indicated only if an organic disease of the colon is suspected, or if the procedure is scheduled to be performed as part of cancer screening. It is not an essential element of the diagnostic evaluation of chronic constipation. Laboratory studies, too, are superfluous in most cases.

The next step is high-dose trial therapy with bacterially non-degradable dietary fiber, for a period of about two weeks. The most suitable substances for this purpose are wheat bran and psyllium preparations. Bran is less expensive, but also less well tolerated [3]. If a trial of non-degradable fiber results in adequate improvement of the symptoms, then no further diagnostic assessment is needed [4].

Measurement of the transit time mainly serves to objectify the patient's symptoms, as subjective reports of low stool frequency are often not very accurate. If the transit time is normal, for example, then this will effectively disprove a patient's claim of having had "practically no bowel movements at all for a week".

Colonic transit studies are simple X-ray studies that determine how long it takes for food to travel through the intestines. For transit studies, individuals swallow capsules for one or more days. Inside the capsules are many small pieces of plastic that can be seen on X-rays. The gelatin capsules dissolve and release the plastic pieces into the small intestine. The pieces of plastic then travel (as would digesting food) through the small intestine and into the colon. After 5 or 7 days, an X-ray of the abdomen is taken and the pieces of plastic in the different parts of the colon are counted. From this count, it is possible to determine if and where there is a delay in the colon. In non-constipated individuals, all of the plastic pieces are eliminated in the stool and none remain in the colon. When pieces are spread throughout the colon, it suggests that the muscles or nerves throughout the colon are not working, which is typical of colonic inertia. When pieces accumulate in the rectum, it suggests pelvic floor dysfunction.


Basic Treatment

Chronic constipation often impairs the patient's quality of life [5]. Patient education is important. Dietary fiber is worth trying, but it is not a magic bullet and some patients cannot tolerate it. If trial therapy with dietary fiber is successful and well tolerated, it is reasonable to recommend a high-fiber diet with whole wheat products. Fruit and vegetables are relatively ineffective, because most of the dietary fiber they contain is degraded by bacteria [6].


1. Water-binding laxatives

Some osmotic salts, such as Carlsbad salt, are found in natural sources and have been used to treat constipation for years. However, long-term use can be problematic due to their disagreeable taste.

In recent years, polyethylene glycol (macrogol), which has long been used to cleanse the bowel in preparation for diagnostic and therapeutic procedures, has been found to be effective for the long-term treatment of constipation [7].

The sugar alcohol sorbite and the disaccharide lactulose are also often used to treat constipation. They produce a considerable degree of bloating, however, and are not very effective if the colonic transit time is prolonged [7, 8].

2. Stimulating laxatives

The generic term "stimulating laxatives" includes the anthraquinones as well as the diphenylmethanes bisacodyl and sodium picosulfate. These agents have a dual mechanism of action. They inhibit fluid resorption from the small and large intestines and induce fluid secretion in dose-dependent fashion; they also have a marked prokinetic effect. The latter may cause cramp-like abdominal pain. These medications take effect 6 to 12 hours after they are consumed, causing one to three bowel movements [9].

Anthraquinones are naturally present in the form of glycosides. These compounds cannot be resorbed from the small intestine and thus have no effect on it. The pharmacologically active rhein canthrones arise only in the colon as the result of bacterial degradation of the drug.

The synthetic laxative bisacodyl is converted into the active substance BHPM (bis-[p-hydroxyphenyl]-pyridyl-2-methane) by hydrolases of the colonic mucosa. Because an effect on the small intestine is not wanted, this medication is given only in tablet form, and not in liquid form. An elegant alternative is to administer the sulphate ester of bisacodyl, i.e., sodium picosulfate [9]. This substance is enzymatically activated by hydrolases only after it is degraded by bacteria in the colon. It can thus be given in drop form and can be more finely dosed.


Because chronic constipation is usually a hypomotile disorder, it would seem logical to attempt to treat it with purely prokinetic agents. In accordance with our current state of knowledge, the main purely prokinetic agents coming into consideration are 5-hydroxytryptamine4 (5-HT4) agonists. In this class of medications, cisapride, prucalopride, and tegaserod have been well studied in randomized, controlled trials and have been found to be moderately effective against chronic constipation [1].

In recent years, the nonselective serotonin 5-HT4 receptor agonist tegaserod and the chloride-channel activator lubiprostone have been used in the United States to treat chronic constipation [10, 11].

Prucalopride, a dihydrobenzofurancarboxamide derivative, is a selective, high-affinity 5-HT4 receptor agonist, which accounts for its enterokinetic effects [12, 13]. Prucalopride increases colonic motility and transit [14-18].

The mechanism whereby Prucalopride relieves constipation is interesting and is related to its effects on the intestinal serotonin, a chemical that controls contractions of intestinal muscles. The contractions of the intestinal muscles control transit of digesting food through the intestine. More contractions speed transit while fewer contractions slow transit. In constipated patients, contractions are fewer.

Serotonin is a chemical manufactured in the intestine that is released and then binds to muscle cells. Depending on which receptor it binds to on the muscle, serotonin can either promote or prevent contractions. Prucalopride alters colonic motility patterns via serotonin 5-HT4 receptor stimulation: it stimulates colonic mass movements, which provide the main propulsive force for defecation. The increased contraction speed the transit of digesting food and reduces constipation.


Enemas (transanal irrigation) can be used to provide a form of mechanical stimulation. There are many different types of enemas. By distending the rectum, all enemas stimulate the colon to contract and eliminate stool.


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