🍂 Bringing Spicy Back - Use code PSM25 to get 25% off Pumpkin Spice Mocca🍂
X Energy Sports Organic Beauty
Mocca Shots High Energy Gummies Mocca Shots Sample Pack
Energon Qube Power Up Performance Gummies Energon Qube Recover Performance Gummies
Functional Fruit Multivitamin Fruit Bits Functional Fruit Prenatal Multivitamin
Seattle Beauty Multivitamin for Skin, Hair, and Nails Seattle Beauty Mixed Berry Antioxidant

The investigation into the holistic effect of the gut microbiome on the human body has been continuously expanding in the past 10 years. We are rapidly discovering that the vast communities of bacteria that live in our gut are actually playing roles in everything from Multiple Sclerosis to depression. Two additional studies have now found connections between the gut microbiome and Alzheimer’s disease.

Researchers from the University of Wisconsin compared the gut microbiome of 25 human subjects with Alzheimer’s disease to 25 cognitively healthy human subjects.  DNA sequencing was used to take the ‘snapshot’ of gut bacterial composition during the study. The researchers found that individuals with dementia had decreased microbial richness and diversity in their gut microbiome compared to people without a diagnosis of dementia.   The researchers were able to identify broad taxonomical changes in gut bacterial composition, as well as changes in abundance of a number of bacterial groups, some of which were more abundant in people with dementia due to Alzheimer’s disease and some of which were less abundant.

The results of this study support a previous study by the researchers from the University of Chicago in 2016, which suggested that gut bacteria plays a role in the accumulation of amyloid plaques, a buildup of proteins characteristic of a number of diseases including Alzheimer’s, diabetes and Huntington’s disease. Specifically, the U Chicago study showed that the prolonged shifts in gut microbial composition and diversity induced by long-term antibiotic treatment regime decreases amyloid plaque deposition.

These findings suggested that the gut microbiota community diversity can impact amyloidosis hence progression of Alzheimer’s. Keeping a healthy gut microbiota might be an additional tool to delay the progression of the disease.

Thanks for reading.

Dr. Connie Wan

Journal References:

  1. Nicholas M. Vogt,Robert L. Kerby,Kimberly A. Dill-McFarland, Sandra J. Harding, Andrew P. Merluzzi, Sterling C. Johnson, Cynthia M. Carlsson, Sanjay Asthana, Henrik Zetterberg, Kaj Blennow, Barbara B. Bendlin, Federico E. Rey, Gut microbiome alterations in Alzheimer’s disease Scientific Reports 7, Article number: 13537(2017); doi:10.1038/s41598-017-13601-y
  2. Myles R. Minter,Can Zhang,Vanessa Leone, Daina L. Ringus, Xiaoqiong Zhang, Paul Oyler-Castrillo, Mark W. Musch, Fan Liao, Joseph F. Ward, David M. Holtzman, Eugene B. Chang, Rudolph E. Tanzi, Sangram S. Sisodia, Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of Alzheimer’s disease, Scientific Reports 6, Article number: 30028 (2016); doi:10.1038/srep30028

Colorectal cancer is one of the most common cancers. In the US, colorectal cancer is the third most common cancer among both men and women, with an estimated 371 cases diagnosed each day. The World Cancer Research Fund estimates that 47% of US colorectal cancer cases could be prevented each year through healthy lifestyle changes.

To understand the correlation between diet/lifestyle and incidence of colorectal cancer, scientists from the Harvard TH Chan School of Public Health evaluated the scientific research worldwide on how diet, weight and physical activity affect colorectal cancer risk. They analyzed 99 studies, including data on 29 million people, of whom over a quarter of a million were diagnosed with colorectal cancer.

The Harvard scientists found that eating whole grains daily, such as brown rice or whole-wheat bread, reduces colorectal cancer risk, with the more you eat the lower the risk. The report concluded that eating approximately three servings (90 grams) of whole grains daily reduces the risk of colorectal cancer by 17%. This adds to previous evidence showing that foods containing fiber decreases the risk of this cancer.

The report also found links between the consumption of fish and foods containing vitamin C with the lowered risk of colorectal cancer. Oranges, strawberries and spinach are all foods high in vitamin C. There is limited evidence correlating higher intake of non-starchy vegetables and fruit with lower risk of the cancer.

On the other hand, the study found that hot dogs, bacon and other processed meats consumed regularly increase the risk of the cancer. Other factors found to increase colorectal cancer include:

  • Eating high amounts of red meat (above 500 grams cooked weight a week), such as beef or pork
  • Being overweight or obese
  • Consuming two or more daily alcoholic drinks (30 grams of alcohol), such as wine or beer

For physical activity, people who are more physically active have a lower risk of colon cancer compared to those who do very little physical activity. Here, the decreased risk was apparent for colon and not rectal cancer.

This report demonstrates there is a lot people can do to dramatically lower their risk of colorectal cancer. Factors such as maintaining a lean body weight, proper exercise, limiting red and processed meat and eating more whole grains and fiber would lower risk substantially. Moreover, limiting alcohol to at most two drinks per day and avoidance or cessation of smoking also lower risk.

When it comes to cancer there are no guarantees, but it’s clear now there are choices you can make and steps you can take to lower your risk of colorectal and other cancers.

Thanks for reading.

Dr. Connie Wan

Journal reference: American Institute for Cancer Research. “Whole grains decrease colorectal cancer risk, processed meats increase the risk: Report analyzing the global research finds hot dogs and other processed meats increase risk of colorectal cancer, eating more whole grains and being physically active lowers risk.” ScienceDaily, 7 September 2017. <www.sciencedaily.com/releases/2017/09/170907093623.htm>.

I traveled extensively in the past few weeks.  Usually, when traveling, I try to take time to relax through yoga and meditation and control my stress level.  However, in this round of trips, I became negligent in keeping up with my exercise routine.  And, this morning, two pimples popped up on my chin.  This is not the first time that I observed the direct link between my stress level and skin condition.  I’ve also seen the same phenomena with my teenage son—whenever he is under stress (believe me, it’s pretty often for a 14-year old), his eczema would flare up.  So, is there a link between our mind and our skin condition?  A quick google scholar seems to suggest yes.

The skin has long been recognized as an organ system that responds to emotional stress and to psychological influences with both short- and long-lasting effects. See, for example, Dunbar F: Emotions and Bodily Changes: A Survey of Literature on Psychosomatic Interrelationships 1910-1953. 4th edition. New York, Columbia, 1954, 594-631; and Selye H: The Physiology and Pathology of Exposure to Stress. Montreal, Acta Inc., 1950, 726-741.   Studies have shown that the skin is a prominent target of key stress hormones, such as corticotropin-releasing hormone, ACTH, cortisol, catecholamines, prolactin, substance P, and nerve growth factor.  Several of these stress hormones are known to activate sebum secretion, expand pore size and cause inflammation in skin.

In a British studied published in 1994, the role of stressful life events in the progress of various skin conditions was studied retrospectively in patients who presented with either psoriasis, urticaria, acne, alopecia and non-atopic eczema, malignant melanoma, fungal infection, basal cell carcinoma and melanocytic naevi. When patients in the three groups were matched for age, those with psoriasis were more likely to report that the experience of stress pre-dated the onset and exacerbations of their condition than patients with other skin diseases. For the psoriasis patients the most common types of life events were family upsets (such as bereavements), and work or school demands, but chronic difficulties were also common. The results support the notion that stress is likely to be associated with skin problems. See AL’ABADIE, M.S., KENT, G.G. and GAWKRODGER, D.J. (1994), The relationship between stress and the onset and exacerbation of psoriasis and other skin conditions. British Journal of Dermatology, 130: 199–203.

The stress induced skin condition can be modulated by relaxation treatments.  Case reports have described positive responses with hypnosis, thermal biofeedback, meditation coupled with imagery, and psychotherapy, and some investigators.  See, for example, Frankel FH, Misch RC: Hypnosis in a case of long-standing psoriasis in a person with character problems. Int J Clin Exp Hypn 21:121-129, 1973; Goodman M: An hypothesis explaining the successful treatment of psoriasis with thermal biofeedback: A case report. Biofeed Self Regul 19(4):347-352, 1994; Tsushima WT: Current psychological treatments for stress-related skin disorders. Cutis 42(5): 402-404, 1988; Kantor SD: Stress and psoriasis. Cutis 46:321-322, 1990; Winchell SA, Watts RA: Relaxation therapies in the treatment of psoriasis and possible pathophysiologic mechanisms. J Am Acad Dermatol 18:101-104, 1988; Zachariae R, Oster H, Bjerring P, Kragballe, K: Effects of psychologic intervention on psoriasis: A preliminary report. J Am Acad Dermatol 34:1008-1015, 1996; and Keinan G, Segl A, Gal U, Brenner S: Stress management for psoriasis patients: The effectiveness of biofeedback and relaxation techniques. Stress Med 11:235-241, 1995.

In one such report, a group of researchers from UMass Medical School studied the influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis.   In the study, thirty-seven patients with psoriasis were randomly assigned to one of two conditions: a mindfulness meditation-based stress reduction intervention guided by audiotaped instructions during light treatments, or a control condition consisting of the light treatments alone with no taped instructions. Four sequential indicators of skin status were monitored during the study: a First Response Point, a Turning Point, a Halfway Point, and a Clearing Point.  The results suggest that the rate of skin clearing in patients with moderate to severe psoriasis can be accelerated when subjects engage in an audiotape-guided, meditative stress reduction exercise.  The psychological outcome data, taken as a whole, suggest that the tape intervention resulted in reduced distress and increased well-being. See, Kabat-Zinn, Jon et al. Psychosomatic Medicine, 60 (5), 625-632, 1998.

Therefore, psychological wellbeing is essential for keeping a healthy and beautiful skin.  Stress shows not only through deepened wrinkles around your eyes and forehead but also through pimples and acne.   Your mind does affect your skin condition—be happy and be beautiful.

Thanks for reading.

Dr. Connie Wan

In the previous post, we learned about the brain-gut-skin theory proposed by two dermatologists, John Stokes and Donald Pillsbury, in 1930s.  Here is the gist of the theory: stress produces stress hormones, which leads to low acid production in your stomach, which leads to the changes in your gut microbiota population, which leads to local and systemic inflammation, which leads to skin breakouts.

Here are some evidences that support the brain-gut-skin theory:

Brain-gut connection

Several months before Stokes and Pillsbury completed their theory on the “emotional linkage” between the brain, gut and skin, a study published in the Journal of Mental Sciences reported low stool levels of L. acidophilus in 53 patients with a variety of mental health disorders  (Shera G, J Mental Sci 1930, 76:56-65)

The research has confirmed that low stomach acid production is a significant risk factor for small intestinal bacterial over growth (SIBO).   In 1993, Toskes reported that the excessive small intestinal bacteria compete for nutrients, produce toxic metabolites, and cause direct injury to enterocytes in the small intestine (Toskes PP, Adv Intem Med1993, 38:387-407).   In 2010, just as Stokes and Pillsbury had proposed, a research showed that excess bacteria in SIBO caused increased intestinal permeability and that antimicrobial treatment of SIBO helped to restore the normal intestinal barrier (Lauritano EC et. al. Scand J Gastroenterol 2010, 45:1131-2)

In the mean time, SIBO has been reported to be prevalent in functional syndromes such as fibromyalgia and chronic fatigue syndrome.  In 2005, Wang et al. reported that psychological stress stagnates normal small intestinal transit time, encourages overgrowth of bacteria, and compromises the intestinal barrier (Wang SX et al., World J Gastroenerol 2005, 11:2016-21).  Also, two separate studies observed the strong association between SIBO and depression and anxiety and that the eradication of SIBO improves emotional symptoms (Addolorato G. et al., Int J Clin Pract 2008, 62:1063-9; Pimentel M., et al., Gastroenterology 2000, 118:A414).

A series of experimental and human studies spanning from 2003 to 2008 has shown that a variety of psychological and physiological stressors – confinement, extremes of temperature, crowding, acoustic, academic examination – can impair normal intestinal microflora (Logan AC et al., Med Hypotheses 2005, 64:533-8; Logan AC et al., Med Hypotheses2003, 60:915-23; and Knowles SR et al., Biol Psychol 2008, 77:132-7).  Most notable in these studies are the stress-induced reductions in Lactobacillus and Bifidobacteria species.

Gut-skin Connection

Although the frequency of SIBO in acne vulgaris has not yet been investigated, a recent report indicates that SIBO is 10 times more prevalent in those with acne rosacea vs. healthy controls. Correction of SIBO leads to marked clinical improvement in patients with rosacea (Parodi A. et al., Clin Gastroenterol Hepatol 2008, 6:759-64).

As for intestinal permeability in acne vulgaris, there have been hints that the intestinal lining may be compromised.  As early as in 1916, Strickler et al. observed that approximately 66% of the 57 patients with acne showed positive reactivity to stool-isolated coliforms, this compared to none of the control patients without active skin disease (Strickler A. et al., J. Cutaneous Dis 1916, 34:166-78).  In 1983, a study involving 40 acne patients showed both the presence of, and high reactivity to, lipopolysaccharide (LPS) endotoxins in the blood.  In this study, none of the matched healthy controls reacted to the E. coli lipopolysaccharide endotoxin (E. coli LPS), while 65% of the acne patients had a positive reaction (Juhlin L., et al., Acta Derm Venereol 1983, 63:538-40). The inference of these results is that circulating endotoxins derived from gut microbes is a common feature of acne vulgaris and that intestinal permeability is an issue for acne patients.

In summary, up to date researches seem to show that patients with distress or anxiety and patients suffering from skin diseases tend to have a gut microbiota population low in “good” bacteria; the researches further show that an impaired gut microbiota causes an increase in gut permeability, which allows the leaking of E. coli endotoxin into the blood, and that the E. coli endotoxin in blood is a common presence in the acne patients.  The modern research is still ongoing providing more clues about Stokes and Pillsbury’s Brain-gut-skin theory.  Based on what have been reported so far, the theory is standing solid.

Thanks for reading!

Dr. Connie Wan

Gut microbiota is the name given today to the microbe population living in our intestine. Our gut microbiota contains tens of trillions of microorganisms, including at least 1000 different species of known bacteria with more than 3 million genes (150 times more than human genes). Microbiota can, in total, weigh up to 2 kg. One third of our gut microbiota is common to most people, while two thirds are specific to each one of us. Extensive researches have shown that the gut microbiota, often developed at a very young age, can have a big impact on person’s health all life.  Previous studies have shown links between human gut bacteria and increased risk of a wide variety of diseases including diabetes, autism, heart disease, and even some forms of cancer. A study published in the Genome Medicine reported that people’s genes may have an influence over some of the intestinal bacteria that cause Crohn’s disease and ulcerative colitis.

Crohn’s disease is a chronic disease that causes inflammation of the digestive or gastrointestinal tract. Although it can involve any area of the GI tract from the mouth to the anus, it most commonly affects the small intestine and colon. Ulcerative colitis is a chronic disease of the large intestine that causes inflammation and ulceration of the colon’s innermost lining. Collectively know as inflammatory bowel disease (IBD), these conditions affect millions of people today.

The study, carried out by the researchers from the University of Minnesota, Harvard, MIT, University of Toronto and University Medical Center Groningen, is one of the largest international studies of its kind. The researchers examined three independent cohorts of a total of 474 adults with IBD who live in Boston, Mass. (USA); Toronto, Ontario (Canada); and Groningen (Netherlands). Doctors and nurses in those locations collected samples of DNA from each human subject and the DNA of their intestinal bacteria over about a two-year period. The researchers looked at thousands of microbial species and human genes.

The results showed that the human subjects’ DNA was linked to the bacteria in their intestines. Patients with IBD had lower biodiversity of bacteria and more opportunistic bacteria. In addition, this study confirmed the long time speculation that use of antibiotics is associated with a greater imbalance in the bacterial community in the intestines.

Thanks for reading!

Dr. Connie Wan

Journal Reference:  Dan Knights, Mark S Silverberg, Rinse K Weersma, Dirk Gevers, Gerard Dijkstra, Hailiang Huang, Andrea D Tyler, Suzanne van Sommeren, Floris Imhann, Joanne M Stempak, Hu Huang, Pajau Vangay, Gabriel A Al-Ghalith, Caitlin Russell, Jenny Sauk, Jo Knight, Mark J Daly, Curtis Huttenhower, Ramnik J Xavier. Complex host genetics influence the microbiome in inflammatory bowel disease. Genome Medicine, 2014; 6 (12): 107 DOI: 10.1186/s13073-014-0107-1

You must have noticed that your acne tends to flares up around stressful times—before a big test, a big meeting or during travel.  Often, the skin problems are accompanied with bowel movement problems.  I have experienced the phenomenon all my life and have heard many similar experiences from others.   For a longest time, I have been wondering if there is a connection between our skin, gut and stress.  Well, it turns out that the brain-gut-skin connection has been proposed by two brilliant scientists Stokes and Pillsbury over 70 years ago.

Drawing on the experimental evidence and clinical anecdotes similar to ones you and I have experienced, Stokes and Pillsbury hypothesized “a gastrointestinal mechanism’ in which the skin is influenced by emotional and nervous states. They proposed that emotional states such as depression, worry and anxiety could alter gastrointestinal tract function that leads to the alterations to the microbial flora, which in turn promotes local and systemic inflammation.  Citing research showing that as many as 40% of those with acne have hypochlorhydria, a condition that the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, Stokes and Pillsbury hypothesized that less than adequate stomach acid would set the stage for migration of bacteria from the colon towards the distal portions of the small intestine, as well as an alteration of normal intestinal microflora.  Further, Stokes and Pillsbury suggested that stress-induced alterations to microbial flora could increase the likelihood of intestinal permeability, which in turn sets the stage for systemic and local skin inflammation.

Based on the above hypothesis, Stokes and Pillsbury discussed the remedies for treating the skin conditions could include the “direct introduction of acidophil organisms in cultures such as those of Bacillus acidophilus”—basically taking pills of lactic acid bacilli tablets. They also proposed using “an acidophilus milk preparation” (basically yogurt) and “cod liver oil” (basically omega-3 supplements) to treat the skin conditions.

This is amazing considering that the gut microbiota was only recognized as a big part of human health in the past 10 years and only in the recent years that prebiotics (such as yogurt) and omega-3 supplements are recognized as healthy gut promoting means.  We will discuss more about evidences of brain-gut-skin connection in my next blog.

Thanks for reading.

Dr. Connie Wan

Our brain is well protected by a barrier termed the “blood-brain barrier (BBB).” The blood–brain barrier is a highly selective permeability barrier that separates the circulating blood from the brain extracellular fluid (BECF) in the central nervous system (CNS). The stuff that can pass through the blood-brain barrier are highly selective including water, some gases, lipid soluble molecules as well as glucose and amino acids that are crucial to neural function. The barrier exists to protect our brain from potential neurotoxins in the environment.

A recent study published in the journal Science Translational Medicine suggests that the gut microbes living in our guts can influence the integrity of the blood-brain barrier, meaning that the transport of molecules across the blood-brain barrier can be modulated by our gut microbes — which therefore play an important role in the protection of the brain.

In this study, the investigators compared the integrity and development of the blood-brain barrier between two groups of mice: the first group was raised in an environment where they were exposed to normal bacteria, and the second (called germ-free mice) was kept in a sterile environment without any bacteria. It was observed that the presence of the maternal gut microbiota blocked the passage of labeled antibodies from the circulation into the brain of the growing fetus; In contrast, in age-matched fetuses from germ-free mothers, these labeled antibodies easily crossed the blood-brain barrier and was detected within the brain.

The research also showed that the increased “leakiness” of the blood-brain barrier, observed in germ-free mice from early life, was maintained into adulthood. However, this “leakiness” was repaired when the mice received fecal transplantation from normal gut microbes. Understanding phenomena mechanistically, the researchers was able to show that the tight junction proteins, which are known to be important for the blood-brain barrier permeability, underwent structural changes and had altered levels of expression in the absence of gut bacteria.

The study concludes that gut microbiota can impact brain development and function and further underscore the importance of the maternal microbes during early life.  Since dietary structure impacts gut microbes, this means that what you eat does directly affect your brain health.

Thanks for reading.

Dr. Connie Wan

Journal Reference: V. Braniste, M. Al-Asmakh, C. Kowal, F. Anuar, A. Abbaspour, M. Toth, A. Korecka, N. Bakocevic, N. L. Guan, P. Kundu, B. Gulyas, C. Halldin, K. Hultenby, H. Nilsson, H. Hebert, B. T. Volpe, B. Diamond, S. Pettersson. The gut microbiota influences blood-brain barrier permeability in mice. Science Translational Medicine, 2014; 6 (263): 263ra158 DOI: 10.1126/scitranslmed.3009759

The relationship between gut microbes and human health is a hot research topic in the scientific community. Considering the number of gut microbes in one’s gut out numbers the total number of the human cells in one’s body by 10 to 1, it only makes sense that whatever the problems we might have, our gut microbes got to have something to do with it. A lot of the research seems to back this up.

Extensive research shows that bad gut microbes can cause obesity. In an article published in the journal Cell, a group of international researchers suggest that our genes influences whether we are fat or thin by shaping which types of microbes thrive in our gut.

In the study, funded by National Institutes of Health (NIH), the researchers sequenced the genes of microbes found in more than 1,000 fecal samples from 416 pairs of twins. The abundances of specific types of microbes were found to be more similar in identical twins, who share 100 per cent of their genes, than in non-identical twins, who share on average only half of the genes that vary between people. These findings demonstrate that genes influence the composition of gut microbes.

In addition, the researchers reported that host genetics have the most influence on a type of health-promoting bacterial family, which is more abundant in individuals with a low body weight than in obese individuals.  When the researchers treated mice with this microbe, the treated mice gained less weight than untreated mice, suggesting that increasing the amounts of this microbe may help to prevent or reduce obesity.

Up until now, variation in the abundances of gut microbes has been explained by diet such as the consumption of insoluble fibers versus highly processed food, the environment, lifestyle such as exercising, medical conditions such as antibiotics use and even health. This is the first study establishing that certain types of gut microbes are heritable — that their variation across a population is in part due to host gene variation, not just environmental influences.  Therefore, nature does work together with nurture to decide what and how we are.

Thanks for reading.

Dr. Connie Wan

Journal Reference: Julia K. Goodrich, Jillian L. Waters, Angela C. Poole, Jessica L. Sutter, Omry Koren, Ran Blekhman, Michelle Beaumont, William Van Treuren, Rob Knight, Jordana T. Bell, Timothy D. Spector, Andrew G. Clark, Ruth E. Ley. Human Genetics Shape the Gut Microbiome. Cell, 2014; 159 (4): 789 DOI:10.1016/j.cell.2014.09.053

Source: Informed Nutrition

Artificial sweeteners are a class of natural or synthetic compounds that are capable of interacting with sweet sensors on your tongue causing the sensing of sweet taste.  These compounds are used extensively as sugar substitutes in food and beverages to reduce the caloric content in these products and have long been promoted as aids to weight loss and diabetes prevention.  However, for years, data seems to suggest that non-caloric artificial sweeteners do not seem to assist in weight loss.  On the contrary, some studies actually suggest that artificial sweeteners may even have an opposite effect.

A study published on Nature magazine reported that artificial sweeteners, even though they do not contain sugar, nonetheless have a direct effect on the body’s ability to utilize glucose.   The researchers report that artificial sweeteners could actually hasten the development of glucose intolerance and metabolic disease, and they do so in a surprising way: by changing the composition and function of the gut microbiota — the substantial population of bacteria residing in our intestines.

In the study, the scientists gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the U.S. Food and Drug Administration (FDA). These mice developed glucose intolerance, as compared to mice that drank water, or even sugar water. Repeating the experiment with different types of mice and different doses of the artificial sweeteners produced the same results — these substances were somehow inducing glucose intolerance.

Knowing artificial sweeteners are not absorbed in the gastrointestinal tract but simply pass through while encountering trillions of the bacteria in the gut microbiota, the researchers wondered if the phenomenon is somehow caused by the artificial sweeteners’ effect on the gut microbiota.  To test the hyphothesis, the researchers treated mice with antibiotics to eradicate many of their gut bacteria; this resulted in a full reversal of the artificial sweeteners’ effects on glucose metabolism. Next, they transferred the microbiota from mice that consumed artificial sweeteners to germ-free mice — resulting in a complete transmission of the glucose intolerance into the recipient mice. This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host’s metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance in the germ-free mice. A detailed characterization of the microbiota in these mice revealed profound changes to their bacterial populations, including new microbial functions that are known to increase tendency of obesity, diabetes, and related metabolic syndrome in both mice and humans.

Does the human microbiome function in the same way?   The researchers looked at data collected from their Personalized Nutrition Project (www.personalnutrition.org), the largest human trial to date to look at the connection between nutrition and microbiota. Here, they uncovered a significant association between self-reported consumption of artificial sweeteners, personal configurations of gut bacteria, and the propensity for glucose intolerance. They next conducted a controlled experiment, asking a group of volunteers who did not generally eat or drink artificially sweetened foods to consume them for a week, and then undergo tests of their glucose levels and gut microbiota compositions.

The findings showed that many of the volunteers had begun to develop glucose intolerance after just one week of artificial sweetener consumption.  Similar to the mice study, the researchers discovered gut bacteria that induced glucose intolerance when exposed to the sweeteners from the composition of volunteers’ gut microbiota.

This study highlighted a fundamental irony on the diet coke consumption.  Consumers who drink diet coke are hoping for less calories and therefore less weight gain.  The observation that the artificial sweetener in the diet coke negatively impacts the gut microbiota population and in fact causes glucose intolerance and weight again might be a hard truth to swallow.

Thanks for reading.

Dr. Connie Wan

Journal Reference: Jotham Suez, Tal Korem, David Zeevi, Gili Zilberman-Schapira, Christoph A. Thaiss, Ori Maza, David Israeli, Niv Zmora, Shlomit Gilad, Adina Weinberger, Yael Kuperman, Alon Harmelin, Ilana Kolodkin-Gal, Hagit Shapiro, Zamir Halpern, Eran Segal, Eran Elinav. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 2014; DOI: 10.1038/nature13793
Source: Informed Nutrition

I admit that I have a “drinking” problem—I am addicted to green tea!  For me, it’s a taste that I’ve grown used to.  My dad was a big tea drinker.  As far as I could remember, the only “water” form I drank is tea, starting from daddy’s cup, of course.

Green tea is packed with antioxidants, to which most of the green tea health benefits have been attributed, including green tea’s anti-aging effect.  Recently, I had an honor of meeting a world leading gut microbiota expert.  Over the dinner, we chatted about carbohydrates (i.e., starch)’s effect on gut microbiota.  The professor told me that carbohydrates promote good gut microbiota population according to his research.  However, the problem is that carbohydrates in our food are highly processed and easily digested by starch hydrolyses (i.e., enzymes) in our mouth and stomach, very small amount of carbohydrates can survive the upper digestive track and reach our guts.  As a side effect, because the starch is so easily digested, the blood glucose tends to shoot up quickly during the meal, leading to glycemic shock for diabetics.

The discussion made me think that, if tea could inhibit the activity of starch hydrolyses, starch would be digested more slowly and more will reach gut promoting the healthy microbiota population.  With that, I started digging.  It turns out that green tea’s inhibition effect on starch digestion is a well-researched area.

As early as in 1998, Forsyth Dental Center researchers compared the inhibition effect of salivary amylase by black and green teas and their effects on the intraoral hydrolysis of starch.  It was found that both black and green teas inhibited amylase in human saliva.  Since salivary amylase hydrolyzes food starch to low molecular weight fermentable carbohydrates, experiments were carried out to determine whether tea decoctions would interfere with the release of maltose in food particles that became entrapped on the dentition. The results showed that tea consumption is effective in reducing the cariogenic potential of starch-containing foods such as crackers and cakes. Tea may reduce the tendency for these foods to serve as slow-release sources of fermentable carbohydrate.

In 2012, Penn State University researchers published a paper on “Molecular Nutrition & Food Research.” The paper examined the effect of co-administration of green tea polyphenol, (-)-epigallocatechin-3-gallate, on blood glucose levels following oral administration of common corn to fasted CF-1 mice.  It was found that green tea polyphenol significantly reduced postprandial blood glucose levels after administration of corn starch.   But the same effect was not observed on postprandial blood glucose following administration of maltose or glucose, suggesting that green tea polyphenol may modulate amylase-mediated starch digestion.

An article published in 2012 on J. Agric Food Chem by a group of researchers from Oregon State University evaluated the inhibitory effects of plant-based extracts including green tea, and white tea and their constituent flavan-3-ol monomers (catechins) on α-amylase and α-glucosidase activity, two key glucosidases required for starch digestion in humans. Results showed that tea extracts and catechin 3-gallates were potent inhibitors of α-glucosidase.

A group from Oxford Brookes University published a paper in 2013 on the International Journal of Food Science.  In the paper, the authors noted that green tea was the only tea shown to significantly reduce sugar release from white bread.

Therefore, green tea not only retards the wrinkle formation through its antioxidants’ radical scavenging effect but also reduces the starch digestion and prevents spiking of blood glucose level.  In addition, green tea allows more starch and carbohydrate nutrients to reach gut therefore promoting health gut microbiota population, which is known to have the effect of reducing systemic inflammation and stress.

If you are still not convinced of the benefits of drinking green tea, green tea is also shown to reduce risk of coronary heart disease,1 stroke incidence,2 chronic inflammation,3 and cancer incidence.4  So, before your next meal, order a green tea and start drinking your way to a perfect skin and a greater health.

Thanks for reading.

Dr. Connie Wan

Journal References:

1. K. J. Mukamal, K. MacDermott, J. A. Vinson, N. Oyama, W. J. Manning, and M. A. Mittleman, A 6-month randomized pilot study of black tea and cardiovascular risk factors, The American Heart Journal, 154(4), pp. 724.e1–726.e1, 2007.

2. S. O. Keli, M. G. L. Hertog, E. J. M. Feskens, and D. Kromhout, Flavonoids, antioxidant vitamins and risk of stroke: the Zutphen Study, Archives of Internal Medicine, 154, pp. 637–642, 1995.

3. V. Sharma and L. J. M. Rao, A thought on the biological activities of black tea, Critical Reviews in Food Science and Nutrition, 49( 5), pp. 379–404, 2009.

4. T. Kuzuhara, M. Suganuma, and H. Fujiki, Green tea catechin as a chemical chaperone in cancer prevention, Cancer Letters, 261 (1), pp. 12–20, 2008.

Source: Informed Nutrition