Functional dyspepsia refers to painful and nonpainful symptoms that are perceived to arise in the upper digestive tract but are not secondary to organic, systemic or metabolic diseases. The symptoms of this syndrome often overlap with those of GERD and IBS, making its management far from simple. If Helicobacter pylori infection is diagnosed in patients with functional dyspepsia, it should be treated. In patients with mild or intermittent symptoms, reassurance and lifestyle advice might be sufficient; in patients not responding to these measures, or in those with more severe symptoms, drug therapy should be considered. Both PPIs and prokinetics can be used in initial empirical pharmacotherapy based on symptom patterns—a PPI is more likely to be effective in the presence of retrosternal or epigastric burning or epigastric pain, whereas a prokinetic is more effective in dyspepsia with early satiation or postprandial fullness. Although combinations of PPIs and prokinetics might have additive symptomatic effects, single-drug therapy is initially preferable. Antidepressants or referral to a psychiatrist or psychotherapist can be considered in nonresponders and in those whose symptoms have a marked effect on daily functioning. Despite extensive research, functional dyspepsia treatment often remains unsatisfactory. Better characterization of dyspeptic subgroups and understanding of underlying mechanisms will enable treatment advances to be made in the future.
Functional dyspepsia encompasses a myriad of painful and nonpainful symptoms perceived to arise in the upper digestive tract that are not secondary to organic diseases; its management is not simple
If Helicobacter pylori infection is diagnosed, it should be treated; a test and treat strategy is recommended in populations with a high prevalence of H. pylori infection
Lifestyle modifications can provide relief from symptoms in patients with mild or intermittent symptoms; drug therapy is the preferred option to treat severe symptoms or nonresponders
PPIs or prokinetics can be initial empirical pharmacotherapy: PPIs in the presence of retrosternal or epigastric burning or epigastric pain; prokinetics in dyspepsia with early satiation or postprandial fullness
Treatment of functional dyspepsia remains unsatisfactory; advances in our understanding of the pathophysiology of this disorder could enable targeted therapy in the future
This is a preview of subscription content, access via your institution
Open Access articles citing this article.
Schweizer Gastroenterologie Open Access 29 November 2022
Acupuncture and related therapies used as add-on or alternative to prokinetics for functional dyspepsia: overview of systematic reviews and network meta-analysis
Scientific Reports Open Access 04 September 2017
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Rent or buy this article
Prices vary by article type
Prices may be subject to local taxes which are calculated during checkout
Drossman, D. A. et al. U. S. householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact. Dig. Dis. Sci. 38, 1569–1580 (1993).
Nyren, O. et al. Economic costs of functional dyspepsia. Pharmacoeconomics 1, 312–324 (1992).
El Serag, H. B. & Talley, N. J. Health-related quality of life in functional dyspepsia. Aliment. Pharmacol. Ther. 18, 387–393 (2003).
Aro, P. et al. Anxiety is associated with uninvestigated and functional dyspepsia (Rome III) criteria in a Swedish population-based survey. Gastroenterology 137, 94–100 (2009).
Tack, J. et al. Functional gastroduodenal disorders. Gastroenterology 130, 1466–1479 (2006).
Castillo, E. J. et al. A community based, controlled study of the epidemiology and pathophysiology of dyspepsia. Clin. Gastroenterol. Hepatol. 2, 985–996 (2004).
Choung, R. S. et al. Do distinct dyspepsia subgroups exist in the community? A population-based study. Am. J. Gastroenterol. 102, 1983–1989 (2007).
Bisschops, R. et al. Relationship between symptoms and ingestion of a meal in functional dyspepsia. Gut 57, 1495–1503 (2008).
Stanghellini, V. et al. Risk indicators of delayed gastric emptying of solids in patients with functional dyspepsia. Gastroenterology 110, 1036–1042 (1996).
Tack, J., Bisschops, R. & Sarnelli, G. Pathophysiology and treatment of functional dyspepsia. Gastroenterology 127, 1239–1255 (2004).
Bredenoord, A. J. et al. Gastric accommodation and emptying in evaluation of patients with upper gastrointestinal symptoms. Clin. Gastroenterol. Hepatol. 1, 264–272 (2003).
Van Oudenhove, L. et al. Determinants of symptoms in functional dyspepsia: gastric sensorimotor function, psychosocial factors or somatisation? Gut 57, 1666–1673 (2008).
Koloski, N. A. et al. The brain–gut pathway in functional gastrointestinal disorders is bidirectional: a 12-year prospective population-based study. Gut 61, 1284–1290 (2012).
Tack, J. & Talley, N. J. Functional dyspepsia—symptoms, defintions and validity of the Rome III criteria. Nat. Rev. Gastroenterol. Hepatol. (in press).
Tack, J. & Talley, N. J. Gastroduodenal disorders. Am. J. Gastroenterol. 105, 757–763 (2010).
Talley, N. J. & American Gastroenterological Association. American Gastroenterological Association Medical Position Statement: evaluation of dyspepsia. Gastroenterology 129, 1753–1755 (2005).
Talley, N. J., Vakil, N. & Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the management of dyspepsia. Am. J. Gastroenterol. 100, 2324–2337 (2005).
Veldhuyzen van Zanten, S. J. et al. Evidence-based recommendations for short- and long-term management of uninvestigated dyspepsia in primary care: an update of the Canadian Dyspepsia Working Group (CanDys) Clinical Management Tool. Can. J. Gastroenterol. 19, 285–303 (2005).
Khademi, H. et al. Diagnostic accuracy of age and alarm symptoms for upper GI malignancy in patients with dyspepsia in a GI clinic: a 7-year cross-sectional study. PLoS ONE 7, e39173 (2012).
Rolff, H. C., Simonsen, L. R. & Rosenberg, J. Clinical findings confirm national guidelines regarding primary gastroscopy for upper gastrointestinal symptoms. Dan. Med. Bull. 58, A4363 (2011).
Breslin, N. P. et al. Gastric cancer and other endoscopic diagnoses in patients with benign dyspepsia. Gut 46, 93–97 (2000).
Malfertheiner, P. et al. Management of Helicobacter pylori infection—the Maastricht IV/ Florence Consensus Report. Gut 61, 646–664 (2012).
Lassen, A., Pedersen, F. M., Bytzer, P. & Schaffalitzky de Muckadell, O. B. Helicobacter pylori test-and-eradicate versus prompt endoscopy for management of dyspeptic patients: a randomized trial. Lancet 356, 455–460 (2000).
Ford, A. C. et al. Helicobacter pylori “test and treat” or endoscopy for managing dyspepsia: an individual patient data meta-analysis. Gastroenterology 128, 1838–1844 (2005).
Delaney, B. et al. Initial management strategies for dyspepsia. Cochrane Database of Systematic Reviews, Issue 4. Art. No.: CD001961. doi:10.1002/14651858.CD001961.pub3 (2005).
Lassen, A. T., Hallas, J. & Schaffalitzky de Muckadell, O. B. Helicobacter pylori test and eradicate versus prompt endoscopy for management of dyspeptic patients: 6.7 year follow up of a randomised trial. Gut 53, 1758–1763 (2004).
National Institute for Clinical Excellence. Dyspepsia: Managing Dyspepsia in Adults in Primary Care [online], (2004).
Mahadeva, S., Chia, Y. C., Vinothini, A., Mohazmi, M. & Goh, K. L. Cost-effectiveness of and satisfaction with a Helicobacter pylori “test and treat” strategy compared with prompt endoscopy in young Asians with dyspepsia. Gut 57, 1214–1220 (2008).
Talley, N. J. et al. Efficacy of omeprazole in functional dyspepsia: double-blind, randomized, placebo-controlled trials (the Bond and Opera studies). Aliment. Pharmacol. Ther. 12, 1055–1065 (1998).
Futagami, S. et al. Nizatidine improves clinical symptoms and gastric emptying in patients with functional dyspepsia accompanied by impaired gastric emptying. Digestion 86, 114–121 (2012).
Jarbol, D. E., Bech, M., Kragstrup, J., Havelund, T. & Schaffalitzky de Muckadell, O. B. Economic evaluation of empirical antisecretory therapy versus Helicobacter pylori test for management of dyspepsia: a randomized trial in primary care. Int. J. Technol. Assess. Health Care 22, 362–371 (2006).
Hu, W. H. et al. Comparison between empirical prokinetics, Helicobacter test-and-treat and empirical endoscopy in primary-care patients presenting with dyspepsia: a one-year study. World J. Gastroenterol. 12, 5010–5016 (2006).
Ang, T. L. et al. Helicobacter pylori eradication versus prokinetics in the treatment of functional dyspepsia: a randomized, double-blind study. J. Gastroenterol. 41, 647–653 (2006).
Moayyedi, P. et al. Pharmacological interventions for non-ulcer dyspepsia. Cochrane Database of Systematic Reviews, Issue 4. Art. No.: CD001960. doi:10.1002/14651858.CD001960.pub5 (2006).
Xiao, Y. L. et al. Prevalence and symptom pattern of pathologic esophageal acid reflux in patients with functional dyspepsia based on the Rome III criteria. Am. J. Gastroenterol. 105, 2626–2631 (2010).
Ladabaum, U. et al. Reappraisal of non-invasive management strategies for uninvestigated dyspepsia: a cost-minimization analysis. Aliment. Pharmacol. Ther. 16, 1491–1501 (2002).
Spiegel, B., Vakil, N. & Ofman, J. Dyspepsia management in primary care: a decision analysis of competing strategies. Gastroenterology 122, 1270–1285 (2002).
Rabeneck, L. et al. A double-blind, randomized, placebo-controlled trial of proton pump inhibitor therapy in patients with uninvestigated dyspepsia. Am. J. Gastroenterol. 97, 3045–3051 (2002).
Moayyedi, P. et al. The efficacy of proton pump inhibitors in non-ulcer dyspepsia: a systematic review and economic analysis. Gastroenterology 127, 1329–1337 (2004).
Wang, W. H. et al. Effects of proton pump inhibitors on functional dyspepsia: a meta-analysis of randomized placebo-controlled trials. Clin. Gastroenterol. Hepatol. 5, 178–185 (2007).
Sakaguchi, M. et al. Comparison of PPIs and H2-receptor antagonists plus prokinetics for dysmotility-like dyspepsia. World J. Gastroenterol. 18, 1517–1524 (2012).
Stanghellini, V. & Frisoni, C. Editorial: Reflux, dyspepsia, and Rome III (or Rome IV?). Am. J. Gastroenterol. 105, 2632–2634 (2010).
Moayyedi, P. et al. Eradication of Helicobacter pylori for non-ulcer dyspepsia. Cochrane Database of Systematic Reviews, Issue 2. Art. No.: CD002096. doi:10.1002/14651858.CD002096.pub5 (2006).
Mearin, F. et al. Levosulpiride and cisapride in the treatment of dysmotility-like functional dyspepsia: a randomized, double-masked trial. Clin. Gastroenterol. Hepatol. 2, 301–308 (2004).
Hallerback, B. I. et al. Dose finding study of mosapride in functional dyspepsia: a placebo-controlled, randomized study. Aliment. Pharmacol. Ther. 16, 959–967 (2002).
Vakil, N. et al. Tegaserod treatment for dysmotility-like functional dyspepsia: results of two randomized, controlled trials. Am. J. Gastroenterol. 103, 1906–1919 (2008).
Holtmann, G. et al. A placebo-controlled trial of itopride in functional dyspepsia. N. Engl. J. Med. 354, 832–840 (2006).
Talley, N. J. et al. Itopride in functional dyspepsia: results of two phase III multicenter, randomized, double-blind, placebo-controlled trials. Gut 57, 740–746 (2008).
Arts, J., Caenepeel, P., Verbeke, K. & Tack, J. Influence of erythromycin on gastric emptying and meal related symptoms in functional dyspepsia with delayed gastric emptying. Gut 54, 455–460 (2005).
Talley, N. J. et al. Failure of a motilin receptor agonist (ABT-229) to relieve the symptoms of functional dyspepsia in patients with and without delayed gastric emptying: a randomized double-blind placebo-controlled trial. Aliment. Pharmacol. Ther. 14, 1653–1661 (2000).
Foxx-Orenstein, A., Camilleri, M., Stephens, D. & Burton, D. Effect of a somatostatin analogue on gastric motor and sensory functions in healthy humans. Gut 52, 1555–1561 (2003).
Arts, J. et al. Efficacy of the long-acting repeatable formulation of the somatostatin analogue octreotide in postoperative dumping. Clin. Gastroenterol. Hepatol. 7, 432–437 (2009).
Tack, J. et al. A dose-ranging, placebo-controlled pilot trial of acotiamide in patients with functional dyspepsia. Neurogastroenterol. Motil. 21, 272–280 (2009).
Matsueda, K. et al. Clinical trial: dose-dependent therapeutic efficacy of acotiamide hydrochloride (Z-338) in patients with functional dyspepsia—100 mg t.i.d. is an optimal dosage. Neurogastroenterol. Motil. 22, 618–e173 (2010).
Matsueda, K. et al. A placebo-controlled trial of acotiamide for meal-related symptoms of functional dyspepsia. Gut 61, 821–828 (2012).
Kusunoki, H. et al. Therapeutic efficacy of acotiamide in patients with functional dyspepsia based on enhanced postprandial gastric accommodation and emptying: randomized controlled study evaluation by real-time ultrasonography. Neurogastroenterol. Motil. 24, 540–545 (2012).
Tack, J. & Janssen, P. Acotiamide (Z-338, YM443), a new drug for the treatment of functional dyspepsia. Expert Opin. Investig. Drugs 20, 701–712 (2011).
Hojo, M. et al. Treatment of functional dyspepsia with antianxiety or antidepressive agents: systematic review. J. Gastroenterol. 40, 1036–1042 (2005).
Otaka, M. et al. New strategy of therapy for functional dyspepsia using famotidine, mosapride and amitriptyline. Aliment. Pharmacol. Ther. 21 (Suppl. 2), 42–46 (2005).
Mertz, H. et al. Effect of amitriptyline on symptoms, sleep, and visceral perception in patients with functional dyspepsia. Am. J. Gastroenterol. 93, 160–165 (1998).
Tack, J. et al. Influence of the selective serotonin re-uptake inhibitor, paroxetine, on gastric sensorimotor function in humans. Aliment. Pharmacol. Ther. 17, 603–608 (2003).
van Kerkhoven, L. A. et al. Effect of the antidepressant venlafaxine in functional dyspepsia: a randomized, double-blind, placebo-controlled trial. Clin. Gastroenterol. Hepatol. 6, 746–752 (2008).
Dinan, T. G. et al. A double-blind placebo-controlled study of buspirone-stimulated prolactin release in non-ulcer dyspepsia—are central serotoninergic responses enhanced? Aliment. Pharmacol. Ther. 15, 1613–1618 (2001).
Coulie, B. et al. Role of nitric oxide in fasting gastric fundus tone and in 5-HT1 receptor-mediated relaxation of gastric fundus. Am. J. Physiol. 276, G373–G377 (1999).
Van Oudenhove, L., Kindt, S., Vos, R., Coulie, B. & Tack, J. Influence of buspirone on gastric sensorimotor function in man. Aliment. Pharmacol. Ther. 28, 1326–1333 (2008).
Chial, H. J. et al. Selective effects of serotonergic psychoactive agents on gastrointestinal functions in health. Am. J. Physiol. 284, G130–G137 (2003).
Tack, J., Janssen, P., Masaoka, T., Farré, R. & Van Oudenhove, L. Efficacy of buspirone, a fundus-relaxing drug, in patients with functional dyspepsia. Clin. Gastroenterol. Hepatol. 10, 1239–1245 (2012).
Miwa, H. et al. Efficacy of the 5-HT1A agonist tandospirone citrate in improving symptoms of patients with functional dyspepsia: a randomized controlled trial. Am. J. Gastroenterol. 104, 2779–2787 (2009).
Read, N. W. et al. Efficacy and safety of the peripheral κ agonist fedotozine versus placebo in the treatment of functional dyspepsia. Gut 41, 664–668 (1997).
Talley, N. J. et al. Asimadoline, a κ-opioid agonist, and satiation in functional dyspepsia. Aliment. Pharmacol. Ther. 27, 1122–1131 (2008).
Soo, S. et al. Psychological interventions for non-ulcer dyspepsia. Cochrane Database of Systematic Reviews, Issue 2. Art. No.: CD002301. doi:10.1002/14651858.CD002301.pub5 (2005).
Haug, T. T., Wilhelmsen, I., Svebak, S., Berstad, A. & Ursin, H. Psychotherapy in functional dyspepsia. J. Psychosom. Res. 38, 735–744 (1994).
Hamilton, J. et al. A randomized controlled trial of psychotherapy in patients with chronic functional dyspepsia. Gastroenterology 119, 661–669 (2000).
Calvert, E. L., Houghton, L. A., Cooper, P., Morris, J. & Whorwell, P. J. Long-term improvement in functional dyspepsia using hypnotherapy. Gastroenterology 123, 1778–1785 (2002).
Camilleri, M. Functional dyspepsia: mechanisms of symptom generation and appropriate management of patients. Gastroenterol. Clin. North Am. 36, 649–664 (2007).
Lacy, B. E. et al. Review article: current treatment options and management of functional dyspepsia. Aliment. Pharmacol. Ther. 36, 3–15 (2012).
Chial, H. J. et al. A nutrient drink test to assess maximum tolerated volume and postprandial symptoms: effects of gender, body mass index and age in health. Neurogastroenterol. Motil. 14, 249–253 (2002).
Abell, T. L. et al. Consensus recommendations for gastric emptying scintigraphy: a joint report of the Society of Nuclear Medicine and the American Neurogastroenterology and Motility Society. Am. J. Gastroenterol. 103, 753–763 (2008).
Camilleri, M. et al. Performance characteristics of scintigraphic measurement of gastric emptying of solids in healthy participants. Neurogastroenterol. Motil. http://dx.doi.org/10.1111/j.1365-29822012.01972.x.
Szarka, L. A. et al. A stable isotope breath test with a standard meal for abnormal gastric emptying of solids in the clinic and in research. Clin. Gastroenterol. Hepatol. 6, 635–643 (2008).
Odunsi, S. T. et al. Optimizing analysis of stable isotope breath tests to estimate gastric emptying of solids. Neurogastroenterol. Motil. 21, 706–738 (2009).
Bouras, E. P. et al. SPECT imaging of the stomach: comparison with barostat and effects of sex, age, body mass index, and fundoplication. Gut 51, 781–786 (2002).
Kindt, S. et al. Relationship between symptom pattern, assessed by the PAGI-SYM© questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia. Neurogastroenterol. Motil. 21, 1183–e105 (2009).
Delgado-Aros, S. et al. Contributions of gastric volumes and gastric emptying to meal size and post-meal symptoms in functional dyspepsia. Gastroenterology 127, 1685–1694 (2004).
The authors wish to thank Cindy Stanislav for secretarial assistance.
M. Camilleri declares no competing interests. V. Stanghellini has acted as a speaker for Alfa Wassermann, Almirall, Angelini, Janssen, Shire, and Takeda. He has acted as a consultant for Alfa Wassermann, Almirall, Angelini, Aptalis, Ironwood Pharmaceuticals, Norgine, Shire and Takeda. He has received research support from Alfa Wassermann, Almirall, Aptalis, Italchimici, Norgine, Shire and Sofar.
About this article
Cite this article
Camilleri, M., Stanghellini, V. Current management strategies and emerging treatments for functional dyspepsia. Nat Rev Gastroenterol Hepatol 10, 187–194 (2013). https://doi.org/10.1038/nrgastro.2013.11
This article is cited by
Schweizer Gastroenterologie (2023)
Digestive Diseases and Sciences (2022)
Akupunktur & Aurikulomedizin (2018)
Acupuncture and related therapies used as add-on or alternative to prokinetics for functional dyspepsia: overview of systematic reviews and network meta-analysis
Scientific Reports (2017)
Pathophysiological Abnormalities in Functional Dyspepsia Subgroups According to the Rome III Criteria
American Journal of Gastroenterology (2017)


Although many people love chubby newborn babies, the rise in “supersized” babies has doctors concerned.
Recently, babies born weighing more than 13 pounds at birth have made headlines. Earlier this month, a British mom in Spain gave birth to a 13-pound, 11-ounce daughter. Baby Maria Lorena is the new record-holder for heaviest baby born naturally in Spain. In February, a British woman gave birth naturally to a 15-pound 7-ounce son named George, making him the second heaviest baby in U.K. history to be born naturally.
Although heavy babies may run in some families, Harvard researchers at Children’s Hospital Boston found excess maternal weight gain is a strong predictor of high birth weight. The study was published in the British medical journal The Lancet.
The rising rates of obesity and higher rates of gestational diabetes that come with delay in childbearing are causing newborns to be heavier. Children who are born heavier have an increased risk of health issues, including a risk of obesity later in life.
“Since high birth weight, in turn, increases risk for obesity and diseases such as cancer and asthma later in life, these findings have important implications to general public health,” co-author David Ludwig, a Harvard Medical School associate professor of pediatrics and director of the Optimal Weight for Life (OWL) program at Children’s Hospital Boston, told the Harvard Gazette. “It’s appropriate for a baby to be born with some fat, but a baby born too fat indicates that the fetus developed in an abnormal environment during the most critical nine months of life.”
Babies weighing more than 4,000 grams or 8 pounds, 13 ounces are considered oversized. According to another report in the medical journal The Lancet, there’s been a 15 percent to 25 percent increase in babies born oversized in the past two or three decades in developed countries.
The study found that nearly 15 percent of babies born in Algeria, where maternal obesity is almost 30 percent, were oversized. Nearly 7 percent of babies born in China are considered oversized due to rising obesity rates among the Chinese.
Although oversized babies are becoming a trend around the world, doctors have been addressing the issue in the United States for years. The efforts have led to the average weight of full-term newborns (not born in multiples) to drop to around 7 pounds.
Caesarian sections for single babies in the United States have increased nearly 20 percent from 1996 to 2009, but the percent has remained around 32 percent since 2009.
Oversized babies can pose a risk for both mother and child during birth. The most common risk is shoulder dystocia. Average babies are born with their heads as the largest part of their body. However, oversized babies can have their shoulders grow to be larger than their head, which can cause the child to become stuck during delivery.
According to Dr. Robert Barbieri, a professor of obstetrics and gynecology at the Harvard Medical School and chief of obstetrics and gynecology at Harvard’s Brigham and Women’s Hospital, when babies get stuck during delivery, they can end up with fractured bones and can cause trauma to the mother.
Overweight mothers are also at an increased risk to develop diabetes during pregnancy. High blood sugar can cause the fetus to be born with low blood sugar, which can delay growth in the fetus.
“In some ways very large babies look more mature because of their size,” Dr. Hyagriv Simhan, chief of maternal fetal medicine and vice chairman for obstetrics at McGee Women’s Hospital at the University of Pittsburgh Medical Center, told NBC News. “But in terms of their lungs, they may be immature.”
Pregnant patients who are obese are encouraged by doctors to gain very little weight during pregnancy. There currently are clinical trials researching the impact of a drug that could help keep blood sugar low in pregnant women who are obese.
The heaviest baby born naturally according to “Guinness Book of World Records” was 23 pounds 12 ounces. Born to Canadian Anna Bates who was 7 foot 5.5 inches, the baby boy was 30 inches long and was born in her home in Seville, Ohio, on Jan. 19, 1879. The baby died 11 hours after birth. The heaviest baby to survive after childbirth weighed 22 pounds 8 ounces. Carmelina Fedele gave birth to the boy at Aversa, Italy, in September 1955.
- The Pac-12 football season nears kickoff
- Tips to get ready for a pain-free golf season
- Protect your family with these 7 home security features
- How to train like an Olympic swimmer
- 2016 Olympics: A guide to must-see TV events
- The bride's guide to feeling your best on your wedding day
- Deciding when you need knee surgery
- Celebrating Fourth of July is much cooler in these AZ towns
- Top ten road trip bathrooms in America
- Six things causing a pain in your neck
- 5 things to make your summer move easier
- Three elements of a strong timeshare exit guarantee
- Stretches and exercises for carpal tunnel syndrome
- The best Major League ballparks have their own personality
- Comparing the best regular seasons: The '96 Bulls and '16 Warriors
- 3 Arizona road trips and the vehicles to get you there
- Colon cancer is preventable. Check these signs and symptoms to stay healthy.
- 6 of the biggest skin cancer myths
- Affordable small home makeover ideas
- Locals helping locals: 6 success stories you need to know about
- Sunscreen facts that could save your life
- 6 energy saving hacks for your home
- 5 tips for choosing a company to end your timeshare
- Overlooked water tips to save you money
- 5 of the most adored gentlemen in professional sports today
- The real danger of sitting at your desk
- Most surprising NBA playoff performances of the last 40 years
- 11 classic baseball movies you must see again
- Finally getting rid of fat: 3 methods that actually work
- 4 reasons cancer survivors should focus on food


The Allegany County Department of Health is asking county residents to consider changing their normal holiday plans this year.
ALLEGANY COUNTY, N.Y. — As the number of COVID-19 cases continue to rise in the Western New York region, the Allegany County Department of Health is asking Allegany County residents to help stop the spread of the virus during the holiday season.
The Allegany County Department of Health is asking county residents to consider changing their normal holiday plans this year. The department of health is asking residents to consider having a small dinner with only those who live in your household, rather than having a large gathering of family and friends.
To further prevent the spread of COVID-19, the Allegany County Department of Health is recommending that Allegany County residents should ask family, friends and neighbors not to travel this Thanksgiving. In addition, any college students who are returning home should get a COVID-19 test before returning.
The department of health is also recommending the following low risk activities:
- Prepare traditional recipes for family, friends and/or neighbors — especially those who are at high risk of severe illness from COVID-19 — and deliver the food in a way that doesn’t involve contact with others.
- The department of health suggests leaving the food on their porch or doorway and calling to let them know it’s there. You can wave and talk from a distance.
- Drop off a holiday food basket filled with family favorite recipes and the ingredients to make them.
- Have a virtual dinner. Share recipes with friends and family so everyone can enjoy their favorites.
- Send pictures of your holiday meal.
- Shopping online rather than in person on Thanksgiving day or the days following.
- Watch sports events, parades and movies from home.
- Have a family game day.
The Allegany County Department of Health is reminding residents that when shopping for food for your holiday meal, to remember to wear a mask or face covering that covers your nose and mouth. Also remember to keep a social distance of six feet, to use hand sanitizer, and to try to shop when the stores are not busy.
Any Allegany County residents who have general COVID-19 questions may contact the Allegany County Department of Health at (585)268-9250 for more information.


Some Minnesota clinics out of flu vaccine
ST. PAUL, Minn. (AP) — The Minnesota Health Departments says there is no shortage of flu vaccine in the state — although some people haven't been able to get flu vaccine from their primary care clinics.
Kris Ehresmann, the department's infectious disease director, says flu vaccine is still available. But she says you may have to work a little harder to find it, because your primary provider might not have any right away.
Are you a newspaper subscriber but you don't have a Digital Access account yet? https://secure.forumcomm.com/?publisher_ID=40&event=subscriber/lookup.
You will need your subscription account number and phone number. Not sure if you have an account? Email us at firstname.lastname@example.org and we can help you.


Milton Keynes Eye Clinic Patient Support
Milton Keynes Hospital
H8 Standing Way,
Our volunteers are present at the eye clinic on Thursday and Friday mornings.
There is also an ECLO service at MK Hospital which is delivered by the Sensory Advice Resource Centre. The ECLO is present on Wednesday and Friday mornings.
Open Monday to Friday, 8.30am to 5.00pm
The clinic is located at Outpatients Entrance 6
Telephone: 01908 660 033 and ask for the Eye Clinic, ext 2829


Multidrug-Resistant Acinetobacter baumannii: An Emerging Health Threat in Aseer Region, Kingdom of Saudi Arabia
Objective. The study aims to determine the prevalence of multidrug-resistant A. baumannii in Aseer Region, Kingdom of Saudi Arabia. Methods. This study evaluated the antibiotic susceptibility of ninety-four (n = 94) clinical isolates of A. baumannii. The isolates were collected from the south region of Saudi Arabia, and notably Aseer Region, during the period from 15 October 2014 to 15 January 2015. The isolates were tentatively identified as A. baumannii by routine bench tests and were confirmed by using VITEK® 2 Compact. The latest instrument was used to identify antibiotic susceptibility of these isolates. Results. Antibiotic susceptibility in this study showed that 69% of these isolates were multidrug-resistant strains. Moreover, they were highly resistant to carbapenem drugs. Several strains of these isolates were found to be extremely resistant to test antibiotics and were only sensitive to one or two of them. Conclusion. High rate of multidrug-resistant A. baumannii bacteraemia has emerged in the south region of Saudi Arabia as an important health problem. Therefore, it is considered as a new threat in hospitals, which requires a tremendous effort to stop its escalation and spread.
Acinetobacter baumannii is a strictly aerobic, nonmotile, Gram-negative, nonfermentative, oxidase-negative, and catalase-positive organism. Within the healthcare settings, Acinetobacter baumannii has become a common pathogen, which can infect the respiratory tract, blood, soft tissues, and urinary tract of an individual. It is the etiological agent of nosocomial infections resulting in septicemia, meningitis, endocarditis, pneumonia, wound, and urinary tract infections [1, 2]. There are 32 Acinetobacter named and unnamed species, which have been identified . The Acinetobacter species cause infections, which are associated with increased morbidity and mortality rates [4, 5].
A. baumannii is tolerant to wide ranges of temperature, pH, and humidity. Studies have shown that this bacterium can survive on dry surfaces for 5 months, posing a challenge to hospital infection control measures ; therefore, this pathogen is considered as progressively important nosocomial pathogen, which can cause outbreak of serious infections. Despite the fact that the organism is often nosocomial, initial infection can be transmitted by patients, admitted from other hospitals [6, 7].
Almost 25 years ago, A. baumannii was found to be resistant against antimicrobial drugs, such as aminopenicillins, cephalosporins, first- and second-generation cephalosporins, cephamycins, aminoglycosides, ureidopenicillins, chloramphenicol, and tetracyclines. Strains of A. baumannii have started to acquire resistance to newly developed antimicrobial drugs and become prevalent in many hospitals . More recently, the term “extensively drug-resistant” A. baumannii (XDRAB) has been used to characterize bacterial isolates resistant to all authorized antibiotics except two categories of antibiotic such as tigecycline and polymyxins .
The possibility of A. baumannii isolation from hospitalized patients is related to some important factors, such as bacterial colonization, medical staff-to-patient ratio, and other ward characteristics . The current study was designed to determine the prevalence of multidrug-resistant A. baumannii in Aseer Region. Bacterial strains were isolated from patients who attended Aseer Central Hospital, Aseer Region, Kingdom of Saudi Arabia.
2. Materials and Methods
2. 1. Ethical Approval
This research was approved by Research Ethics Committee, College of Medicine, King Khalid University, Abha, Saudi Arabia.
2.2. Bacterial Isolates
94 clinical isolates of A. baumannii were collected from the south region of Saudi Arabia and notably Aseer Region (Figure 1) during the period from 15 October 2014 to 15 January 2015. All these strains were initially isolated and identified in Aseer Central Hospital laboratory and were sent to Department of Microbiology, College of Medicine, King Khalid University, for further assessment.
2.3. Media and Reagents
Two culture media were used in this experiment: blood agar (Oxoid Ltd., Basingstoke, and Hampshire, United Kingdom) and MacConkey agar (Oxoid). MacConkey agar was used as a selective and differential medium; while, blood agar was used for other processes, such as the sensitivity test. Biochemical reagents, such as catalase, oxidase, and indole, were used as initial identification tests.
2.4. Bacterial Identification and Purification
All clinical isolates were cultured on blood and MacConkey agar and then tested for Gram staining to identify Gram reaction and bacterial morphology. In order to ensure that all isolates are pure, they were cultured several times. Several biochemical tests were undertaken to confirm that all these isolates were belonging to A. baumannii, such as catalase, oxidase, and indole tests. Identification of all strains was done, using the automated VITEK 2 system (bioMérieux) following manufacturer instructions as briefly described below.
2.5. Antibiotic Susceptibility of A. baumannii
All isolates were tested for antibiotic susceptibility, using the automated VITEK 2 Compact system. All samples were cultured on blood agar, and then, a suspension was made for every isolate. Liquid suspension of all isolates was loaded on the VITEK system and left overnight to get the results. The next day, the results have illustrated the identification and antibiotic susceptibility of loaded samples.
VITEK 2 system was used for authenticating names of Acinetobacter species as described by the manufacturer (bioMérieux Inc., Durham, NC 27712, USA). The VITEK card contains 64 wells, which hold different fluorescent biochemical assays. Out of the 64, 20 were carbohydrate assimilation; 4 were phosphatase, urea, nitrate, and actidione tests. The VITEK 2 machine controlled the card automatically including the filling, sealing, and then transferring the cards into the linked incubator (35°C). Each output report is decoded according to a particular algorithmic system. The acquired results were compared to the ID-GN (identification of Gram-negative bacteria) databank. In case of most known Acinetobacter species with a clear cut profile, the system led to a correct identification of the unknown organism.
3.1. Identification of Tested Isolates
Colony characteristics of isolated colonies were obtained using blood and MacConkey agar. On MacConkey agar, colonies of A. baumannii appeared as a nonlactose fermenter. On blood agar, colonies of all isolates were appeared as nonpigmented, domed, and mucoid, with smooth-to-pitted surfaces in a diameter of 1-2 mm colonies. All strains of A. baumannii were found to be catalase positive and oxidase/indole negative. The isolates were tentatively identified as A. baumannii by routine bench tests and have been confirmed by using VITEK 2 Compact.
3.2. Antibiotic Susceptibility of A. baumannii
Antibiotic susceptibility testing has shown that 69% of these isolates were multidrug-resistant strains (Figure 1). 34 isolates were resistant to all antibiotics of interest and were only sensitive to colistin. The results have also shown that 15 of these isolates were only sensitive to colistin and a combination of trimethoprim and sulfamethoxazole, whereas 21 of isolates were sensitive to the combination of trimethoprim and sulfamethoxazole. One isolate and other two of them were resistant to all tested antibiotics except piperacillin and amikacin and tobramycin, respectively. The correlation between the number of isolates and their sensitivity to all tested antibiotics is shown in Figure 2.
Multidrug-resistant A. baumannii is currently a major cause of respiratory infections in intensive care unit patients. However, Acinetobacter was identified as a low-virulent pathogen, which infects mostly immunocompromised hosts; however, the emergence of resistant strains to antibiotics over the past several years has increased. Therefore, the concern toward this phenomenon has increased as well. MDR A. baumannii is recognized as one of the most difficult nosocomial pathogens to be treated and controlled [11, 12].
In this study, multidrug-resistant and extensively resistant A. baumannii strains have been isolated and identified in the southern region of Saudi Arabia. The study has shown that 74% of these isolates are multidrug-resistant strains. Among these MDR strains, approximately 50% are extensively drug-resistant isolates, which are sensitive to colistin and resistant to all other drugs of choice. This should raise the concern toward this potentially dangerous pathogen. The most effective antibiotic with high spectrum to treat A. baumannii is colistin (60%) and then the combination of trimethoprim and sulfamethoxazole (46%); these rates of spectrums were approximately compatible with previous studies .
A. baumannii isolates were extremely resistant to two carbapenem drugs: imipenem and meropenem. Among tested strains, only 5 (0.05%) and 4 (0.04%) isolates were susceptible to imipenem and meropenem, respectively. This process indicated that these isolates were more dangerous than previously identified MDR strains, which showed more than 90% susceptibility to both drugs .
Susceptibility of A. baumannii to carbapenems showed a clear drop, and it denotes a main epidemiological worry. The resistance mechanism was found due to class D OXA-type enzymes (oxa-23 and oxa-24/40) with carbapenemase activity . This fact made the medical choices very limited mainly based on polymyxin combinations with other antibiotics. Carbapenem-resistant Acinetobacter spp. have been described from many parts of the world, and Saudi Arabia is not an exception . These authors examined 64 Acinetobacter baumannii isolates during 2013 and 2014 from four different medical centers in Saudi Arabia and Egypt. All the isolates were found to be resistant to ceftazidime and ciprofloxacin. They reported the emergence of ST236 in Saudi Arabia and Egypt and the spread of distinct carbapenem-resistant A. baumannii clones belonging to ST884, ST945, and ST1096 in Saudi Arabia . Another study revealed a detailed molecular analysis of many isolates from Saudi Arabia including the detection of OXA-58 gene in five isolates and other OXA genes . A number of studies must be undertaken to eliminate extra emergence and distribution of this potent pathogen across the country. Some molecular projects are being processed and designed to study the type of antibiotic-resistant genes in these strains.
Higher rate of multidrug-resistant A. baumannii bacteraemia has emerged in the southern region of Saudi Arabia as an important health issue. Such a higher prevalence has now been considered as a new threat in the clinical settings, which requires a tremendous effort to stop its escalation and spread. The occurrence of Acinetobacter strains and the antimicrobial resistance degree continue to rise. The results among the patients, exposed to infections from these organisms, were discovered to be strong enough. Acinetobacter strains also indicated vast challenges for the healthcare facilities, public health, and elderly population.
Informed consent has been obtained from the participants before starting the procedures.
Conflicts of Interest
The authors declare that they have no conflicts of interest.
The authors would like to acknowledge microbiology staff at the laboratory of Aseer Central Hospital for their cooperation in passing these isolates to the laboratory.
L. S. Young, A. L. Sabel, and C. S. Price, “Epidemiologic, clinical, and economic evaluation of an outbreak of clonal multidrug-resistant Acinetobacter baumannii infection in a surgical intensive care unit,” Infection Control & Hospital Epidemiology, vol. 28, no. 11, pp. 1247–1254, 2007.View at: Publisher Site | Google Scholar
K. Montefour, J. Frieden, S. Hurst et al., “Acinetobacter baumannii: an emerging multidrug-resistant pathogen in critical care,” Critical Care Nurse, vol. 28, no. 1, pp. 15–25, 2008.View at: Google Scholar
A. M. Al Jarousha, A. H. El Jadba, A. S. Al Afifi, and Iyad A. El Qouqa, “Nosocomial multidrug-resistant Acinetobacter baumannii in the neonatal intensive care unit in Gaza City, Palestine,” International Journal of Infectious Diseases, vol. 13, no. 5, pp. 623–628, 2009.View at: Publisher Site | Google Scholar
C. Çelik, M. Gözel, F. Dayı, and E. Gültürk, “Increasing antimicrobial resistance in nosocomial pathogens; multidrug-resistant extensively drug-resistant and pandrug-resistant Acinetobacter baumannii,” Journal of Microbiology and Infectious Diseases, vol. 4, no. 1, pp. 7–12, 2014.View at: Publisher Site | Google Scholar
C. C. Chang, C. H. Lu, C. R. Huang et al., “Culture-proven bacterial meningitis in elderly patients in southern Taiwan: clinical characteristics and prognostic factors,” Acta Neurologica Taiwanica, vol. 15, no. 2, pp. 84–91, 2006.View at: Google Scholar
S. Al-Obeid, L. Jabri, M. Al-Agamy, A. Al-Omari, and A. Shibl, “Epidemiology of extensive drug resistant Acinetobacter baumannii (XDRAB) at Security Forces Hospital (SFH) in Kingdom of Saudi Arabia (KSA),” Journal of Chemotherapy, vol. 27, no. 3, pp. 156–162, 2015.View at: Publisher Site | Google Scholar
M. Aly, H. T. Tayeb, S. M. Al Johani et al., “Genetic diversity of OXA-51-like genes among multidrug-resistant Acinetobacter baumannii in Riyadh, Saudi Arabia,” European Journal of Clinical Microbiology & Infectious Diseases, vol. 33, no. 7, pp. 1223–1228, 2014.View at: Publisher Site | Google Scholar


Neurology Medical Center, Physicians
Mike Kreidie, M.D., F.A.A.N.
Dr. Kreidie is a diplomate of the American Board of Psychiatry and
He holds a teaching position at the University of California, Irvine as
an Associate Clinical Professor of Neurology. In addition, he held the position
of President of the Orange County Neurological Society, and member of
the Scientific Advisory Panel in Neurology of the California Medical
Association. He served as editor to the Lebanese Medical Journal, and
Science and Technology Journal.
Dr. Kreidie is an author and publisher of medical and scientific
Dr. Kreidie graduated from college and medical school with honors and
Dr. Kreidie was instrumental in founding teaching training programs and
training medical students, interns, and resident, while presenting many
seminars on various medical subjects.
As a practicing neurologists, Dr. Kreidie was responsible for a wide
variety of cares, including traumatic injury cases to the brain and
spine, stroke related illness, degeneration disease (Alzheimer's,
Parkinson's Disease), headache and pain syndrome, epilepsy, tumor, and
infections of the Nervous System.
Special expertise and training were undertaken performing
Electrodiagnostic Studies such as EEG, EMG, NCV, and EP's, as well as
Neuro-Radiology and sleep related disorders.
Dr. Kreidie is well respected in his community, having served the
population in Orange County since 1988.
International College, American University of Beirut, with Honors.
University of Cairo, School of Medicine, with distinction, 1970
Internship: Brooklyn Hospital, Down State Medical Center
New York University, New York, 1972-1973
Residency: Martinez Veteran's Administration Hospital
University of California, Davis, 1973-1974- Surgery
University of Alabama, Burmingham, 1974-1977 Neurology
Certification: Diplomate American Board of Psychiatry and Neurology
Fellow of the American Academy of Neurolegy
Qualified Medical Examiner
Private Practice in Mission Viejo since 1989
Mission Hospital and Regional Medical Center, Mission Viejo, CA
UCI Medical Center, Orange, CA,
Mission Hospital, Laguna Beach, CA
PROFESSIONAL MEMBERSHIPS HELD:
Associate Clinical Professor of Neurology, University of California,
President, Orange County Neurological Society, 1993-1994, 2004-2005
Diplomate, American Academy of Pain Management
Diplomate, American Board of Psychiatry and Neurology
Member, California Medical Association, Scientific Advisory Board.
Member, American Medical Association
Fellow Member, American Academy of Neurology
Member, Administrative Committee, UCI Medical Staff Association
Member, San Diego Head Injury Foundation.
ACADEMIC AND TEACHING BACKGROUND:
Associate Clinical Professor at University of California, Irvine
Supervisor, Epilepsy Clinic at University of California, Irvine
Mini-Fellowship on Sleep Disorders at University of California, Irvine
Visiting Fellowship in Carotid Ultra Sound & Doppler at University
of California, San Diego
Publication, Article on localized Lipodystrophy (American Journal of
Medical Director, Neurology Medical Center, California, U.S.A
Qualified Medical Examiner for the Sate of California, U.S.A.
Medical Disability Evaluator for the Veterans Administration, Birmingham
Prestigious memberships in the Medical Association.
Pioneered multiple educational papers and publishings of medical
Founded and Directed Electrodiagnostic and Imaging Centers.
Seminar on Multiple Sclerosis
Seminar on Vertigo and Balance
Presented a paper on Head Injury
Presented a paper on Sleep Disorder
Seminar on Neuro-ophthalmology
LICENSE TO PRACTICE:
Tung Buu, D.C.
Doctor of Chiropractic
Doctor of Chiropractic, California State Board, 03/2000 Doctor of Chiropractic Degree, Los Angeles College of Chiropractic 1999 (LACC), Whittier, California Summa Cum Laude, 12/1999 Student at Frankfurt Volkshochschule in Computer Sciences and German Languages 1990-1994
Medical Education: University of Saigon, Vietnam, School of Medicine, 1973-1978 Internship:, Cho-Ray Hospital
Premed: The Faculty of Sciences, University of Saigon, Vietnam Major in Biology, 1972-1973
Licenses, Awards and Distinctions
X-Rays Supervision and Operation License, Department of Health, 2000
Doctor of Chiropractic Diploma, 1999
Deutsch Als Fremdsprache Zertifkikat, Goethe Institute, Frankfurt
Germany, 1994 Physics-Chemistry-Biology Certificate, Saigon University, 1973
Main Doctor, The Citi Health Group, Westminster, California 2002-present Instructor, South Baylo University Anaheim California: 2000-present Instructor, Department of Anatomy, LACC, 2000-present Tutor, Department of Physiology, LACC, 2000 present Main Doctor, The Family Health Group, Long Beach California 2000-2002 Associate Doctor, CK Chiropractic, San Diego, California 2000-2002 Internship at the Center of Rehabilitation, California State University at Northridge (CSUN): Exercise therapy on stroke and other brain injured patients.
Internship at Doctor of Chiropractic Office, Long Beach CA 1999 Internship at LACC Health Center, Whittier CA 1999 Tutor and Teaching Assistant, department of Anatomy, LACC 1997-1999
Worker Compensation & Personal Injury Cases. Chiropractic treatment, Physiotherapy and Rehabilitation. Very experienced in Writing Medical/Chiropractic Report (W/C and P/I Cases) Instructor for Basic Sciences and Clinical Sciences, particularly in Human Anatomy, Physiology, and Nutrition. Internship in General Surgery
Yashruti, M.D., F.A.C.S.
Diplomate, American Board of Orthopedic Surgery Fellow, American Academy of Orthopedic Surgeons Fellow, American College of Surgeons
Medical Degree, M.D. American University of Beirut, Lebanon, 1959
Intership, American University Hospital, Beirut, 1957-1958
Residency, Pathology & General Surgery Upstate Medical Center,
Syracuse, New York, 1958-1960
Residency, Orthopedic, Upstate Medical Center,
Syracuse, New York, 1960-1961.
Residency Orthopedic Surgery, Lexington, Kentucky, 1961-1963
California, New York and Pennsylvania
Academic & Teaching Background:
Assistant Clinical Professor, Orthopedic Surgery,
Upstate Medical Center, Syracuse, New York, 1970-1986
Chief of Orthopedic Surgery, V.A. Hospital Medical Center
Syracuse, New York, 1973-1978
Orthopedic Surgery Staff, Community General Hospital,
Syracuse, New York, 1970-1986
Orthopedic Surgery Staff, University Hospital and Grouse Irving
Memorial Syracuse, New York, 1970-1986.
Orthopedic Surgery Staff, Chino Community Hospital,
Chino, California, 1986-present.
Orthopedic Surgery Staff, Pomona Valley Hospital
Pomona, California, 1987-1989
Member, California Orthopedic Association
Member, Association of V.A. Surgeon Member, New York State Society of Orthopedic Surgeons Member, Easter Orthopedic Association
Orthopedic Surgery, Syracuse, New York, 1970-1986
Orthopedic Surgery, Chino, California, 1986-1988
Medicolegal Practice, California, 1986-present


If you’re one of thousands of people who suffer from EMF sensitivity, the ability to get rid of your wireless router is one of the best reasons to embrace Cat6a cables.
You don’t really need Wi-Fi; with the right equipment, you can setup an Ethernet cable in every room you’ll work from. In addition to discouraging you from working on the couch, you’ll probably experience better sleep without your wireless router. That’s because melatonin – the substance that contributes to a good night’s sleep – is inhibited by the presence of electrosmog.
According to Dr. Mercola, many people with high sensitivity have a high amount of heavy metals in their system. “If you have accumulated toxic metals in your brain, your brain becomes like an antenna, picking up more cell phone radiation, which in turn can cause the microbes in your system to overreact and create more potent mycotoxins,” Dr. Mercola states. “This can create a never-ending vicious cycle between the microbes and metals in your body and your exposure to electromagnetic fields, which can lead to hypersensitivity.”
Do heavy metals cause your brain to function like an antenna? Does electrosmog inhibit melatonin? Does melatonin help sleeping (or the lack thereof, inhibit sleeping?)


Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a virus closely related to the SARS virus from 2002-03. Those affected may develop a fever, dry cough, fatigue, and shortness of breath. While the majority of cases result in mild symptoms, some can progress to pneumonia and multi-organ failure. The infection spreads from one person to others via respiratory droplets produced during coughing or sneezing. The World Health Organisation (WHO) has declared the 2019–20 coronavirus outbreak a Public Health Emergency of International Concern (PHEIC).
The disease was named COVID-19 by WHO in mid-February. This nomenclature is important to distinguish it from other forms of coronaviruses. Coronaviruses are fairly common and cause a variety of diseases in humans ranging from common cough and cold to severe pneumonia. Therefore, COVID-19 is a more accurate name for the disease caused by a specific strain of the fairly common coronavirus. However, several media outlets still use the term coronavirus. This nomenclature is wrong technically as it is a specific strain which leads to such a severe condition in humans. As an example, if someone is allergic to grapes, we do not say that the person is allergic to fruits because it is only a specific fruit to which the person is allergic to.
Alessandro Vespignani, director at the Laboratory for the Modeling of Biological and Socio-technical systems at the Northeastern University, has been working with researchers from all over the world to try and predict the potential spread of the disease. There is widespread panic relating to the spread of the disease. To control the situation, several steps have been taken by governments worldwide. These measures include the screening of passengers at the airport, setting up special helplines and special quarantines. Medical researchers are also working hard to develop a cure as soon as possible.


MBBS, MS - General Surgery, MCh - Neurosurgery
Consultant - Neurosurgery
39 Years Of Experience Neurosurgeon, Spine Surgeon
A Consultant at the department of Neurosurgery, Dr. Harshad Parekh has over two decades of rich professional experience in his field. Dr. Harshad Parekh has treated several patients suffering from neurological diseases in India and gives every patient the best of medical care. He has published several papers in India and abroad and is a member of prestigious medical associations. He believes in promoting health awareness and following a healthy lifestyle.
Consult fees ₹ 3000


After years of trying different approaches to losing weight, we understand how frustrating it can be for you to go through the same old diet and exercise routines without seeing any significant difference. Sometimes losing excess body weight and keeping it off requires more than simply changing habits.
We understand bariatric surgery is a life-changing decision and our team at the Georgia Bariatric Center at Coliseum Northside Hospital will be with you every step of the way. We are committed to providing you with the personalized care and attention you deserve.
We want you to be as prepared and as comfortable as possible for your surgery and your new life. To help guide you through this process, we create a step-by-step plan to your surgery.
Call our local Macon office at (478) 746-4646 or fill out the contact form below:
Our weight loss surgery options
Georgia Bariatric Center at Coliseum Northside Hospital is excited to offer you the latest weight loss surgery options. We offer a comprehensive program featuring several safe and highly effective minimally invasive weight loss surgery options, including gastric balloon, gastric sleeve and lap-band surgery.
Bariatric surgery alters the digestive process or reduces the amount of food the stomach can hold. There are a variety of bariatric options available today for treatment:
- Gastric balloon is placed into the stomach endoscopically without surgery. The balloon takes up space in the stomach, thereby making the patient eat less.
- Lap-band surgery is an adjustable band that is surgically placed around the top of the stomach that essentially functions like an hour glass. The band can be adjusted in the office to control the rate that food empties, providing a feeling of satisfaction after a small meal and affect hormones that regulate hunger.
- Robotic gastric sleeve is a minimally invasive surgery in which the surgeon removes about 75 percent of the stomach though a minimally invasive, robotic procedure. What remains of the stomach is a narrow tube or sleeve, which connects to the intestines normally. The stomach becomes much smaller, therefore food intake is restricted. Gastric sleeve is a simpler operation than gastric bypass and provides the patient with a lower risk of complications. Because the intestines are not affected, gastric sleeve does not affect how your body absorbs food or vitamins and minerals, so you're not likely to fall short on nutrients. However, watching protein intake and taking vitamins is generally recommended to maintain good health.
- Gastric Bypass (Laparoscopic and Robotic) is a surgery in which the surgeon creates a smaller stomach pouch and reroutes part of the small intestine. As a result, food bypasses a large portion of the stomach and some of the small intestine. Patients feel full sooner and do not absorb as many calories.
Weight loss surgery education
The education and support does not end after surgery; support groups and clinic visits are also available. The Center focuses on providing you with all the tools necessary for success to have a new healthy life.
Weight loss can not only improve your quality of life, but also prevent or lower your risk of developing life-threatening diseases. If your BMI is 35+, the threshold for obesity, and you have one or more serious health conditions, you may want to consider this effective weight loss solution.
Best of all, losing weight can lower your risk of developing diabetes, high blood pressure, arthralgia, back and joint pain. If you have these or other health conditions, losing excess weight may improve or even resolve these conditions.
Attend an information session
Free information seminars are provided quarterly for patients interested in seeking bariatric surgery as a weight loss option. We will cover surgery options, risks and benefits of the procedure and what your next steps are to begin the process. It is an informal discussion with time made available for questions and answers.
Call (478) 746-4646 to register to attend a FREE seminar.


ATLANTA – The average time that hospital emergency rooms patients wait to see a doctor has grown from about 38 minutes to almost an hour over the past decade, according to new federal statistics released Wednesday.
The increase is due to supply and demand, said Dr. Stephen Pitts, the lead author of the report by the Centers for Disease Control and Prevention.
“There are more people arriving at the ERs. And there are fewer ERs,” said Pitts, an associate professor of emergency medicine at Atlanta’s Emory University.
Overall, about 119 million visits were made to U.S. emergency rooms in 2006, up from 90 million in 1996 – a 32 percent increase.
Meanwhile, the number of hospital emergency departments dropped to fewer than 4,600, from nearly 4,900, according to American Hospital Association statistics.
Another reason for crowding is patients who are admitted to the hospital end up waiting in the ER because of the limited number of hospital beds, Pitts added.
A shortage of surgical specialists also contributes. So, too, does the difficulty many patients have in getting appointment to doctor’s offices – which causes some to turn to emergency departments, experts said.
“It takes me a month to get an appointment for my own doctor, and I’m a physician, for God’s sake,” said Dr. Ricardo Martinez, an Atlanta trauma physician. He is executive vice president of Schumacher Group, an organization that manages about 140 hospital emergency departments.
The amount of time a patient waited before seeing a physician in an ER has been rising steadily, from 38 minutes in 1997, to 47 minutes in 2004, to 56 minutes in 2006.
Pitts added that 56 minutes may be the average, but it’s not typical: The average was skewed to nearly an hour because of some very long waits.
“Half of people had waiting times of 31 minutes or less,” Pitts noted.
Researchers also found that there has not been any recent increases in the number of patients arriving by ambulance, or in the number of cases considered to be true emergencies.
Black patients visited emergency departments at twice the rate as whites in 2006. Among age groups, the highest visitation rates were for infants and elderly people aged 75 and older.
About 40 percent of ER patients had private insurance, about 25 percent were covered by state programs for children and about 17 percent were covered by Medicare, the report found. About 17 percent were uninsured.
Some more findings: Summer and winter were the busiest season in ERs, and the early evening – around 7 p.m. – tended to be the busiest time of day. There were geographic differences as well, with hospitals in the South having the highest ER visitation rates.
Also, half of hospital admissions in 2006 came through emergency departments, up from 36 percent in 1996.
“The ER has become the front door to the hospital,” said Pitts, a fellow at the CDC’s National Center for Health Statistics.
Some doctors said the report supports a call for increased governmental funding for hospital emergency services.
“Millions more people each year are seeking emergency care, but emergency departments are continuing to close, often because so much care goes uncompensated,” Dr. Linda Lawrence, president of the American College of Emergency Physicians, said in a statement.
“This report is very troubling, because it shows that care is being delayed for everyone, including people in pain and with heart attacks,” her statement added.
The results are based on a national survey of 362 hospital emergency departments.
On the Net:
The CDC report: http://www.cdc.gov/nchs


I was just wondering, as a diabetic do we have a greater chance of basic problems with our feet.. Arthritis? I have recently injured my big toe (a bottle fell on it). The swelling is gone, the burse is gone and I am still having minimal pain, little tingle like nerve pain. I did not see a dr. but now I am wondering if I should have?
Next Discussion: Just saying hi »


Upgrade to remove ads
Endocrine System (lecture)
Terms in this set (10)
C. the thymus produces hormone (thymosin), but it belongs to the lymphatic system
Which of the following is not a "true" endocrine organ?
A. pineal body
B. pituitary gland
D. adrenal gland
E. parathyroid gland
D. the kidney produces an exocrine product (urine) and two hormones (renin and erythropoietin).
WHich one of the following is a mixed (endocrine/exocrine) organ?
Which organ is matched with a hormone that it manufacture ?
A. adrenal gland-ACTH (adreocorticotropic hormone)
B. thyroid gland-thyrotropin
C. posterior lobe of pituitary gland-oxytocin
D. small intestine-secretion
E. stomach-gastric inhibitory polypeptide
B. A. is wrong because the hypothalamus produce more hormone thatn the pituitary gland. The problem with D is that ADH and oxytocin (produced by the hypothalamus) do not target the anterior pituitary gland.
Which statement is true regarding the pituitary gland?
A. It produces more hormones than any other structure in the body .
B. It manufactures seven hormone and releases nine into the bloodstream
C. It is suspended from the mesecephalon by a stalk of tissue termed the infundibulum.
D. It serves as a target for all of the hormones produced by the hypothalamus
E. if more than one of the above are true choos this response.
E. The thyroid gland is just inferior to the larynx.
Which statement is false regarding the thyroid gland ?
A. Its enlargement is called a goiter
B. it consists of two lobes connected by an isthmus
C. It produces T3, thryoxine and calcitonin
D. The parathyroid glands are embedded in it
E. It is positioned just above the larynx on the anterior aspect of the of the neck
F. All of them are correct
Parathryroid hormone elevates blood calcium leels by decreasing calcium loss in the urine, increasing the absorption of calcium from the small intestine, and by incresing the reabsorption of bone tissue by osteoclasts. Which one of the following is not a logical sequel to chronic hyperparathyroidism ?
A. increased release of calcitonin ( a hormone that decreases blood calcium levels)
B. weakened bone
C. loose teeth
E. hyperphosphaturia ( increased phosphate loss in urine)
F. If all are good choose F.
D. Hypersecretion of adrenal cortex hormones can cause it.
Which statement regarding the adrenal gland is false?
A. its cortex is divided into three named layers
B. it produces atecholamines and steroid hormones
C. its medulla releases epinephrine and norepiephrine
D. hyposecretion of adrenal cortex hormones produces a condition called cushings syndrome
E. each adrenal gland is positioned on the superior end of a kidney adjacent to the muscles of the back
E. Autocrine and paracrine regulators are biochemicals that do not fit the definition of hormones because they act within the same organ that produced them
Which statement regarding hormones is false?
A. most hormones are proteins or polypeptides
B. All hormones are carried to their targets by the bloodstream
C. hormones are secreted in minute quantities and are rapidly inactivated by being converted to other compounds
D. only the testis ovary and adrenal gland produce steroid hormones
E. autocrine and paracrine regulators are hormones
C. A and B both refer to the hypothalamohypohysial tract and E. is wrong because the portal system ends in the anterior lobe of the hypophysis (pituitary gland)
The hypothalamohypophysial portal system....
A. terminates in the posterior lobe of the pituitary gland
B. consists of axons of neurosecretory cells
C. carries a number of hypothalamic hormones to their target
D. is also known as the hypothalamohypophyisial tract
E. begins in the hypophysis and consists of blood vessels
C. The kidney produces erythropoietin and renin.
Which structure produces more than one hormone?
A. parathyroid gland
B. pineal gland
THIS SET IS OFTEN IN FOLDERS WITH...
Cardiovascular System ( lecture)
Lymphatic System ( Lecture )
Lab 5 Human Anatomy UVU
YOU MIGHT ALSO LIKE...
med term endocrine organs set 4
Unit 13 Endocrine System - hormones only
Unit 13 Endocrine System
Chapter 16 Endocrine System Test
OTHER SETS BY THIS CREATOR
Series 7 Master Study Guide
Regulation Section 2: Securities Exchange Act of 1…


Negative news is sensationalized, tragic acts hyped and anything that seems to be scary, gloomy or contradictory becomes popular amongst all of us immediately. There is plenty of research and data available supporting the fact that hostility, anger, depression, anxiety and isolation elevate the risk of cardiovascular disease. But are you all aware that the reverse is also true? Laughing aloud, a sense of humor and happiness are great ways to decrease stress hormone, reduce artery inflammation and increase HDL levels. Alongside reducing stress and tension it is also recommended to increase your laughter and happiness levels. According to the American Heart Association (AHA), the positive effects of laughter last 24 hours and there are several ways in which laughter can pave way to a healthier heart.
Laughing out loudly increases blood flow
Laughter increases blood flow by dilating inner lining of blood vessels known as the endothelium. When a person laughs, the act induces the release of beta-endorphins in the hypothalamus which in turn leads to the release of nitric oxide. Nitric oxide befriends the heart by dilating blood vessels, reducing inflammation and preventing formation of cholesterol plaque. Researchers in fact compare the changes in the endothelium caused due to laughter to be similar to the benefits of aerobic exercise or the use of cholesterol-lowering drugs such as statins. The only difference is that laughter is a reflex action that has an immediate effect unlike exercise or drugs.
Your ‘HaHa’ & ‘HoHo’ Decrease Stress Hormones
Laughing out aloud can indeed decrease stress hormones such as cortisol and epinephrine which are explained clearly in the website www.firsteatright.com. This advantage remains as a great value addition as otherwise stress causes blood vessels to constrict.
Laughing Enhances Immune System Functioning
Our immune system plays a pivotal role in safeguarding our body against diseases and disorders. This puts us in a critical position of keeping our immune system in the right form for performing their function properly. Laughing out increases the number of antibody-producing cells which increases the strength of the immune system.
Besides these, laughter reduces the negative response to stress and causes blood vessels in the body (this includes the heart too) to increase blood flow. These are some of the many benefits of laughter explored by researchers. There is also certain study material available that point out the fact that laughing out aloud can reduce the risk of heart attack.
When such are the crucial benefit of laughter, it’s better that we take efforts to laugh. For instance, we can try to look at the lighter/brighter side of things, watch something comical on TV or go to a comedy movie or try spending more time with loved ones who can make you laugh and be happy. Ultimately, we need to increase the happy hormones in our body, decrease the stress hormones and achieve the right balance of antibodies to safeguard our immune system.
AVOID FRAUD. EAT SMART.
+91 7846 800 800
Dietitian & Nutritionist Dr. Nafeesa Imteyaz.
Dr. Nafeesa's Blog @blogspot
- Written Testimonials
Diet & Nutrition
- Diabetes Reversal
- IVF IUI not needed for PCOS PCOD Infertility
Disease & Conditions
- Infertility | PCOS
- Diabetes Mellitus
- Kidney Problems
- Cardiovascular Diseases
- Liver Diseases
- Gastro intestinal disorder
- Metabolic Disorders
- Orthopedic Disorders
- Eating Disorders
- Dietary Recall
- Weight Record Filled By Clients
- Online Payment Transaction Details
- Online Clients Weight Check Form
- Our Program Package Service Charges
- Weight Record 2017 Clients
- Measurements sent by Clients
- Terms & Conditions Of Payment
- Thanks. Your Form is Submitted
- Video Testimonials
- Lifestyle & Wellness
- Lifestyle & Wellness Blog
- Allergy & Intolerance
- Weight Loss / Gain
- Weight Loss / Slimming Blog
- Disease & Conditions >
- Life Cycle Nutrition >
- Sports Nutrition >
- Integrity in Nutrition
- Knowledge Centre
© COPYRIGHT 2022. ALL RIGHTS RESERVED. FRST HEALTHCARE PVT LTD.
Dr. Nafeesa Imteyaz of First Eat Right clinic, is the Best Dietitian Nutritionist in Bangalore. Best Dietitian Nutritionist in Pune. Best Dietitian Nutritionist in Hyderabad. Best Dietitian Nutritionist in Chennai. Best Dietitian Nutritionist in Mumbai. Best Dietitian Nutritionist in Delhi. Best Dietitian Nutritionist in Kolkata.


Herpes: what you need to know about this family of viruses
LAST UPDATED: Oct 22, 2019
6 MIN READ
HERE'S WHAT WE'LL COVER
You probably didn’t want to be searching about herpes today, did you? Before you wipe your browser history, let’s answer your burning, itching questions about herpes, its symptoms, and what to do if you think you have it.
What is herpes?
Most people, when they say “herpes,” are referring to genital herpes. (You can skip ahead to everything about genital herpes if you’re worried about that sexually transmitted infection.) Herpes is actually the name for a whole family of viruses that cause a wide range of diseases. Called herpesviridae, members of this virus family are responsible for causing chickenpox, shingles, genital herpes, oral herpes (cold sores), and mononucleosis (“mono”), among many other diseases.
The name herpes comes from the Greek word herpein, which means “creeping” or “to creep.” This is in reference to the blisters that spread across the skin in many of the diseases that herpesviruses cause. And before you think the Greeks were ancient, humans and the herpesviruses go way back, back to even before we were human. Researchers at UCSD discovered that HSV-1 and HSV-2, the viruses that cause cold sores and genital herpes, infected Homo erectus, a precursor to modern humans, over 1.6 million years ago (Smith, 2014).
How many different types of herpes affect humans? How common are they?
Nine members of the herpesviridae virus family are known to infect humans. Conveniently, eight of them have been given the name human herpesvirus (HHV) and are numbered one through eight. The ninth—Herpes B virus—is incredibly rare but technically does infect humans. Let’s go over this fact sheet of the different viruses in this family.
Also known as herpes simplex virus-1 or HSV-1, this virus causes oral herpes (cold sores). HSV-1 is commonly spread person to person through kissing, sharing utensils, glasses, cups, water bottles, towels, lip balm, or razors, or through oral sex. It also causes some cases of genital herpes. It’s estimated that 3.7 billion people worldwide are infected by HHV-1. Learn more about cold sores here (WHO, 2017).
Also known as herpes simplex virus-2 or HSV-2, this virus causes genital herpes. HSV-2 infections are commonly transmitted from person to person during oral sex, anal sex, or vaginal sex. Genital herpes is one of the most common sexually transmitted infections (STIs), affecting more than 500 million people worldwide. Learn more about genital herpes here.
Also known as varicella-zoster virus or VZV, this virus causes chickenpox and shingles. Chickenpox is the form of the disease during the initial infection, and shingles occurs when it reactivates. Most people in the United States have either been vaccinated or were infected with VZV as a child. It’s estimated that 1 in 3 people will have shingles over their lifetime. There are effective vaccines for both chickenpox and shingles. Learn more about chickenpox and shingles here.
Also known as the Epstein-Barr virus or EBV, this virus causes infectious mononucleosis (“mono” or IM) among other diseases. EBV is tremendously prevalent—approximately 90–95% of all adults have previously been infected with EBV (Dunmire, 2018). EBV has also been associated with the development of certain cancers, including B and T cell lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma.
Also known as cytomegalovirus or CMV, this virus can commonly cause a mononucleosis-like syndrome. In people with compromised immune systems and newborns, however, CMV can cause a whole host of serious problems. CMV infections in a fetus can cause hearing loss, cerebral palsy, intellectual disability, vision impairment, and seizures. In people with acquired immunodeficiency syndrome (AIDS), CMV can infect the retina and cause vision loss, in a disease called CMV retinitis (Goldberg, 2015). CMV is also very common—in the United States, around 6 in 10 people have been infected with CMV before (Staras, 2006).
A virus with two subtypes, HHV-6A and HHV-6B, HHV-6 infects most children before age 2. The classic manifestation of an HHV-6 infection is called roseola infantum and causes a high fever for three to five days and is followed by a rash. HHV-6 infections usually result in only a minor illness. In the United States, over 90% of children have been infected by age 2 (Zerr, 2005).
HHV-7 infections are generally asymptomatic, but in the rare cases it does cause symptoms, it behaves like HHV-6. Over 95% of adults have been infected with HHV-7 (Wyatt, 1991).
HHV-8 infections are also usually asymptomatic in healthy people. More significantly, HHV-8 is associated with Kaposi sarcoma, a type of cancer of the blood vessels. Kaposi sarcoma is rare but can be seen in people with HIV once they have progressed to AIDS, transplant recipients, and cancer patients on chemotherapy.
B virus is an extremely rare form of herpes that comes from macaque monkeys. Only 50 cases of B virus have ever been documented, and only one case occurred from human-to-human contact (Cohen, 2019; CDC, 2019). Symptoms include fever, chills, muscle aches, fatigue, and headache. When B virus progresses, it can lead to severe brain damage and death.
What is genital herpes?
Let’s dive deeper into genital herpes, one of the most common sexually transmitted diseases. Genital herpes is caused by a viral infection, primarily by herpes simplex virus 2 (HSV-2), but can also be caused by herpes simplex virus 1 (HSV-1), the virus that also causes cold sores (oral herpes). The symptoms of genital herpes can vary significantly from person to person. Some people infected with genital herpes can have mild symptoms or no symptoms at all. Others experience severe, painful ulcers on their genitals, itching or burning with urination, fever, headache, flu-like symptoms, and swollen, painful lymph nodes.
Here are the facts you need to know about genital herpes:
Genital herpes typically looks like small pimples or blisters that will turn into painful ulcers or open sores. Herpes sores are found on the genitals and throughout the groin area. Over time, they will crust over and then form a scab. This lasts about 2–3 weeks before going away. The first time you get symptoms is usually the worst.
You can get recurrences of genital herpes multiple times a year. Stress, other illnesses, decreased immunity, sunlight, and fatigue can trigger recurrent herpes outbreaks.
HSV-2 infections are commonly transmitted during oral sex, anal sex, or vaginal sex. The highest chance of transmitting an HSV-2 infection is during an outbreak, but even when there are no symptoms, there’s still a chance of spreading the virus to your sexual partner. You can’t get infected from a toilet seat.
Latex condoms can reduce the risk of transmitting HSV-2, but there’s no way of eliminating the risk completely except through complete abstinence from sexual contact.
There are a few tests available to test for genital herpes. A viral culture tries to grow the virus from a swab of a suspected blister. A polymerase chain reaction (PCR) test tries to amplify and isolate viral DNA from a sample. Serological tests use a blood test to see if your immune system has responded to the infection.
There are three antiviral medicines commonly used to treat genital herpes—acyclovir, famciclovir, and valacyclovir (brand name Valtrex; see Important Safety Information). These medications are taken by mouth and can be used on an ongoing basis to prevent outbreaks, or they can be used to shorten an episode when taken at the first sign or symptom of an outbreak of herpes.
What is oral herpes?
Oral herpes, also called herpes labialis, is caused by a viral infection that causes small, painful blisters around the mouth and on the lips during an outbreak. These blisters—commonly called cold sores or fever blisters—are primarily caused by herpes simplex virus type 1 (HSV-1). HSV-1 is extremely common—worldwide, it’s estimated that 3.7 billion people are infected with HSV-1 (Looker, 2015).
Here are the facts you need to know about oral herpes:
Symptoms of oral herpes include small, fluid-filled blisters in and around the mouth that last around 1–2 weeks before going away. The first outbreak you get is usually the worst.
20–40% of those infected with HSV-1 will have recurrent cold sores (Spruance, 1977).
HSV-1 is transmitted from person to person via contact with sores, skin-to-skin contact, oral contact, or infected saliva. It’s common to spread HSV-1 through kissing, sharing utensils, glasses, cups, water bottles, towels, lip balm, or razors, or through oral sex.
You’re most infectious during an outbreak. However, you can still infect others with HSV-1 even if you don’t have any symptoms of oral herpes.
Usually, healthcare providers diagnose cold sores just by their physical exam, no testing required
Treatment options include oral as well as topical antiviral medicines for episodic treatment of an oral herpes outbreak.
Why is there no cure for herpes?
Herpesviruses share a trait that makes them very difficult to deal with. They are very good at evading your immune system (Huang, 2015). First, they have the ability to go into a latent phase, during which they hide out without doing much replication or damage to your cells. Second, they affect the MHC system, which allows them to hide in plain sight and lie to your immune system, telling it that the cells they infected are completely normal cells. Finally, some herpesviruses can use your cellular machinery to create a protein called cmvIL-10, which suppresses your immune system (Spencer, 2002).
Because of their stealth abilities, herpesviruses are usually lifelong infections. Your immune system is usually able to keep them in check and prevent them from causing symptoms of herpes infections most of the time. But when your immune system is compromised, or when you’re dealing with another illness, the virus can come back and wreak havoc. However, there are antiviral medications that can effectively treat herpesvirus infections.
If you have any medical questions or concerns, please talk to your healthcare provider. The articles on Health Guide are underpinned by peer-reviewed research and information drawn from medical societies and governmental agencies. However, they are not a substitute for professional medical advice, diagnosis, or treatment.
Centers for Disease Control and Prevention (CDC). (January 31, 2019). B Virus (herpes B, monkey B virus, herpesvirus simiae, and herpesvirus B). Retrieved from https://www.cdc.gov/herpesbvirus/index.html
Cohen, J. I. (January 23, 2019). B virus infection: Pathogenesis and Epidemiology. Retrieved from https://www.uptodate.com/contents/b-virus-infection#H2
Dunmire, S. K., Verghese, P. S., & Balfour, H. H. (2018). Primary Epstein-Barr virus infection. Journal of Clinical Virology , 102 , 84–92. doi: 10.1016/j.jcv.2018.03.001. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/29525635
Goldberg, D. E., Smithen, L. M., Angelilli, A., & Freeman, W. R. (2005). HIV-Associated Retinopathy In The HAART Era. Retina , 25 (5), 633–649. doi: 10.1097/00006982-200507000-00015. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/16077362
Huang, T., & Osterrieder, N. (2015). The herpesvirus stealth program. Oncotarget , 6 (26), 21761–21762. doi: 10.18632/oncotarget.5261. Retrieved from https://www.oncotarget.com/article/5261/
Looker, K. J., Magaret, A. S., May, M. T., Turner, K. M. E., Vickerman, P., Gottlieb, S. L., et al. (2015). Global and Regional Estimates of Prevalent and Incident Herpes Simplex Virus Type 1 Infections in 2012. PLOS One , 10 (10). doi: 10.1371/journal.pone.0140765. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/26510007
Smith, M. D., Kosakovsky Pond, S. L., Smith, D. M., & Scheffler, k. (2014, June 10). Herpes Infected Humans Before They Were Human. UC San Diego Health . Retrieved from https://health.ucsd.edu/news/releases/Pages/2014-06-10-herpes-origins-in-chimpanzees.aspx
Spencer, J. V., Lockridge, K. M., Barry, P. A., Lin, G., Tsang, M., Penfold, M. E. T., et al. (2002). Potent Immunosuppressive Activities of Cytomegalovirus- Encoded Interleukin-10. Journal of Virology , 76 (3), 1285–1292. doi: 10.1128/jvi.76.3.1285-1292.2002. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/11773404
Spruance, S. L., Overall, J. C., Kern, E. R., Krueger, G. G., Pliam, V., & Miller, W. (1977). The Natural History of Recurrent Herpes Simplex Labialis. New England Journal of Medicine , 297 (2), 69–75. doi: 10.1056/nejm197707142970201. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/194157
Staras, S. A., Dollard, S. C., Radford, K. W., Flanders, W. D., Pass, R. F., & Cannon, M. J. (2006). Seroprevalence of Cytomegalovirus Infection in the United States, 1988-1994. Clinical Infectious Diseases , 43 (9), 1143–1151. doi: 10.1086/508173. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17029132
World Health Organization (WHO). (January 31, 2017). Herpes simplex virus. Retrieved from https://www.who.int/en/news-room/fact-sheets/detail/herpes-simplex-virus
Wyatt, L. S., Rodriguez, W. J., Balachandran, N., & Frenkel, N. (1991). Human herpesvirus 7: antigenic properties and prevalence in children and adults. Journal of Virology , 65 (11), 6260–6265. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed?term=1656093
Zerr, D. M., Meier, A. S., Selke, S. S., Frenkel, L. M., Huang, M.-L., Wald, A., et al. (2005). A Population-Based Study of Primary Human Herpesvirus 6 Infection. New England Journal of Medicine , 352 (8), 768–776. doi: 10.1056/nejmoa042207. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/15728809


What Is Leaky Gut? (and 10 natural ways to help fix it)
It’s unavoidable. The more invested you are in your health, the more consumed you will become in this critically important part of your body. I’m talking about your gut. Yep, there it is: as you’ve probably heard a thousand times… good health begins in the gut. And that also means preventing “leaky gut.”
This is because the gut is a hub for digestion, absorption, immune function, mood regulation, brain function, heart health, and so on. The gut has been linked to so many different functions of the body, it is often referred to by medical professionals as the “second brain.” So, it only makes sense to make sure it’s in tip-top shape.
What is Leaky Gut?
How can you ensure your gut is healthy? Unfortunately, the gut is not like our hair or skin where we can physically see if it is healthy or not. Regardless, there are many factors which, over time, can cause the structure of the gut to become compromised, specifically when it comes to the gut lining or epithelium.
The intestinal epithelium is composed of a single layer of cells which have “tight junctions.” These tight junctions are protein structures that regulate the permeability of the intestine and selectively allow water and nutrients to pass through to be used throughout the body. 1 However, over time, these junctions can become “loose,” causing increased intestinal permeability, otherwise known as “leaky gut.” This means our once strong barrier between the gut and the bloodstream becomes weakened and unrefined. Now bacteria and toxins can leak into the bloodstream.
Leaky gut can cause an array of issues, including inflammation, bloating, fatigue, digestive issues, skin problems, and even stimulate an immune reaction to fend off the unknown particles entering the bloodstream. 2 This is concerning for overall health as leaky gut often accompanies other chronic health conditions, such as autoimmune diseases, skin conditions, migraines, food sensitivities, brain fog, chronic fatigue, celiac disease, and type 1 diabetes. 3,4,5
7 Things That Can Cause Leaky Gut
Despite recent attention revolving around leaky gut, research still needs to be done to truly understand what causes leaky gut and how we can treat it. Until then, professionals have a few suspect sources that can contribute to developing a leaky gut:
Stress has long been known to wreak havoc on the body as it can disrupt almost every system. When you’re stressed out, so is your body. However, when your body is stressed, it amps up your immune system, creating inflammation. Inflammatory flares cause wear on your digestive system and intestinal epithelium. 6
Non-steroidal anti-inflammatory drugs such as aspirin and ibuprofen have been shown to increase intestinal permeability. This is because NSAIDs appear to be toxic to the intestinal epithelium, potentially causing erosion and ulcers. 7
3. Excessive Alcohol
Alcohol consumption is regularly associated with increased intestinal permeability. This is because ethanol metabolism results in the formation of acetaldehyde. Acetaldehyde then damages the epithelium, which can result in excessive endotoxin (i.e., a toxin in a bacterial cell that’s released as the cell disintegrates, which can then lead to disease) passage through the bloodstream. 8,9
4. Processed Foods & Excessive Sugar
Processed foods are typically high in pro-inflammatory ingredients such as refined vegetable oils and carbohydrates. These lead to the growth of unhealthy gut bacteria that are linked to many chronic issues, including leaky gut. Further, a diet high in sugar, particularly added sugar in the form of fructose, harms the barrier function of the intestinal wall, thus causing increased permeability. 10,11
5. Nutrient Deficiencies
When you aren’t regularly consuming a varied diet filled with colorful fruits and veggies, it’s easy to develop nutrient deficiencies. Not getting all your essential nutrients can then harm the gut. Research has found that being deficient in certain nutrients such as zinc, vitamin A, and vitamin D can undermine the proteins in the epithelial lining, resulting in leaky gut. 12,13
Gluten is composed of proteins found in certain grains, such as wheat, rye, and barley. When you eat gluten, your small intestine may trigger the release of zonulin. Zonulin is a protein that regulates the tight junctions of your intestinal wall. However, releasing too much zonulin can cause these junctions to loosen, especially in people who are more sensitive, potentially creating increased intestinal permeability and leaky gut. 14,15
7. Overall Poor Gut Health
Poor gut health and an unhealthy gut microbiome can lead to gut infections and leaky gut. Low levels of good gut bacteria such as Bifidobacterium and Lactobacillus have been associated with increased intestinal permeability. 16 Also, when you ignore your gut health, infections such as Candida overgrowth can develop. Candida is yeast that naturally lives in your body in small amounts. But it can get overproduced and cause the breakdown of the intestinal walls, allowing it to penetrate the bloodstream. 17
10 Ways to Help Fix Leaky Gut Naturally
If you suspect you could be suffering from increased intestinal permeability (i.e., leaky gut), then you may want to begin paying more attention to your gut. Afterall, this is all the focus in the health community and will be for a long time to come. So if you haven’t already, it’s time to jump on the good gut bandwagon.
Again, as previously mentioned, more research still needs to be done to fully understand leaky gut and what to do about it. Nevertheless, there are several steps you can take that may improve gut health. Even if you don’t think your gut’s leaky, everyone can benefit from strengthening the framework and diversity of the gut. Not only will you feel better, but you may also boost your health as a whole.
Consider the following your Good Gut Guide:
- Avoid or at least limit processed foods. As noted above, a diet high in processed foods can decrease the diversity of your gut microbiome and create gut dysbiosis (or a microbial imbalance within the gut). Steering toward more natural and fresh foods will keep your gut healthy and happy.
- Cut down the added sugar. Added sugar is a known dietary evil, causing issues such as accelerated aging, weight gain, and increased risk for heart disease. But sugar also has a negative effect on your gut. Eating too much sugar can result in decreased microbiota diversity and inflammation. (Please note, the sugar found naturally in foods such as fresh fruits and dairy isn’t the problem—it’s the addition of refined sugars found so abundantly in processed foods that you’ll want to limit or remove.)
- Eat Fermented Foods. Fermented foods aid in the growth of beneficial gut bacteria. Some good sources include:
- Supplement Your Gut. Supplements can be a great way to jumpstart your way to a healthier gut. Probiotics, for example, may provide the gut with beneficial bacteria. BioTRUST’s ProX10 has 10 billion CFU daily of SIX “super strains” of probiotics.
- Get Plenty of Sleep. Not getting enough sleep or having poor quality sleep can disrupt your gut, and those who typically don’t get a good night’s rest have lower microbiota diversity. It is recommended that adults get at least seven hours of sleep each night.
- Hydrate. Staying properly hydrated is critical for the body to function properly. Further, drinking enough water helps lubricate joints, deliver nutrients, and is beneficial to mucosal lining of the intestines. Staying hydrated is also important for the balance of good bacteria in the gut. As we get older, we are at a higher risk of dehydration because older adults do not sense thirst as readily. It is recommended that the average healthy adult drink at least eight 8-ounce glasses of water a day—and 9 to 12 cups per day is an even better goal.
- De-stress. It is so easy to become overwhelmed and stressed in day-to-day life. However, it is important to take the time to lower your stress levels by going for a walk, socializing with friends, practicing mindful breathing, or anything else that helps you manage your stress. This is because stress has been shown to contribute to dysbiosis and intestinal permeability.
- Eat Mindfully. Eating on the go has become a norm as our schedules continue to fill up. However, taking the time to sit down and enjoy your food has been shown to be beneficial to gut health. This is because eating slowly allows your body to properly digest your food and helps avoid gut discomfort.
- Eat Your Veggies. Many vegetables are high in fiber, which acts as food for your good gut bacteria. Plus, vegetables contain vitamins and minerals, which help maintain a strong framework for your gut.
- Exercise. Exercise has countless benefits, including increasing the diversity in the gut microbiota. Those who exercise have been found to have an increase in gut microbes that reduce the risk of inflammatory diseases as well as type 2 diabetes, obesity, and heart disease. 18
Another supplement which has been linked to improved gut health is collagen. Collagen protein is an essential component of the digestive tract and helps maintain the structure of the gut lining. BioTRUST’s Ageless Multi-Collagen has 5 key types of collagen to help you gain the maximum benefits.
What is Leaky Gut? A Recap
Maintaining good gut health is, in fact, the key to a healthier you. Everyone can benefit from taking steps in the direction of better gut health. Whether you experience the symptoms of a leaky gut or just want to be your best self, the gut is an influential part of the body which should be prioritized on your path to wellness.


Designing space and lighting solutions for memory care facilities
In creating a dementia-friendly environment, the right lighting and space design can have an incredibly positive effect on resident quality of life. In fact, both artificial and natural light, as well as space design, can have an impact on emotional and psychological well-being.
How we integrate lighting design into dementia care homes
At Community Living Solutions, we’re dedicated to designing and building senior living communities that get to the heart of what our clients and their residents need. And when it comes to designing dementia-friendly environments, lighting design plays an integral role in not only creating a peaceful, healing environment but also making life easier for those who care for the residents.
Dementia care is complex and can be challenging to manage. So how is it possible that lighting and space—construction aspects that seem deceptively simple—make a difference? The answers may surprise you.
Biodynamic lighting allows us to harness daylight’s biological effects even in an environment with artificial lighting, like senior living communities. These biological effects are profound. Reduced exposure to daylight can lead to sleep problems, mood disorders and chronic fatigue. Meanwhile, biodynamic lighting allows us to mimic the variations of natural daylight through intentional design and light management. From a design and construction perspective, opportunities abound.
First, it’s important to note how lighting is shown to make a significant difference in the lives of senior living residents, in particular residents with dementia.
Tailored lighting intervention is proven to help those living with dementia
According to a recent 12-week study of multiple dementia care communities, increasing indoor exposure to daylight was shown to reduce depression among residents. More, it’s been found that exposure to the right amount of daylight is an effective non-drug treatment for those with dementia. Designing a space that allows for increased daylight exposure for residents could then feasibly improve quality of life for the 20 to 30 percent of individuals living with Alzheimer’s disease and related dementias (ADRD).
In addition, appropriately tailored lighting has been shown to alleviate sleep disturbances. Among individuals with ADRD, nighttime wandering is a common concern. By reducing sleep disturbances through lighting design for dementia care homes, facilities can also reduce this phenomenon. Less wandering results in a reduced risk of dangerous falls. Also, a tailored lighting design or intervention that stimulates the resident’s natural sleep and wakefulness cycles are shown to decrease what’s known as “sundowning,” or late-day confusion among dementia patients, while improving behavioral problems and lessening agitation. One recent study on lighting and Alzheimer’s patients showed at the end of just four weeks of lighting intervention, sleep disturbance and depression dropped significantly, and by the end of six months, sleep disturbance and depression scores dropped by half. Other studies have mirrored these findings while also noting decreased agitation scores.
The power of human-centric lighting
We all know that feeling we get when we’re outdoors and the sun just begins to dip below the horizon, the drowsiness that accompanies a rainy day or the joy of seeing the sun spread its golden light across the horizon in the morning. The role light plays in our mood and wellbeing is proven to us time and again, almost without us noticing it. With human-centric lighting, we design lighting while keeping in mind how it affects the many aspects of our lives. That means human-centric lighting is designed to optimize:
- Circadian rhythms
- Visual acuity
How well we can see is central to a number of our needs, from our sense of safety and wellbeing to our health, mood, task performance, social communication and aesthetic judgment. As a result, how we see and perceive our environment impacts our emotions, motivations, behavior and even our long-term memory.
Through biodynamic lighting in design for dementia care homes, we are able to send the appropriate cues to our bodies by mimicking the appropriate outdoor lighting for everything from dawn to daylight to dusk, including the nuances of an overcast sky, mid-afternoon sun rays and even sunset. Lighting “dose” can be adjusted for intensity, duration, timing and more, and it can be customized for individual environments, including resident rooms, community rooms and general areas.
Recommendations for creating dementia-friendly environments with light
Now that we recognize the potential for lighting in senior living environments and how it factors in dementia care, here are some recommendations for designing and building a dementia-friendly environment.
- Maximize resident exposure to daylight during the day, but especially in the morning
- Evenly illuminate spaces, to minimize contrast and especially shadows
- Minimize exposure to blue-rich light sources after 8 p.m.
- Use amber, or warm light sources, after sunset
- Create dark environments for sleeping
- Avoid using artificial light sources during the night
- Be mindful of quality of life over quantity of light
Facility design for dementia care homes
In addition to lighting interventions, use of space and purposeful wandering capability for residents improves quality of life for individuals with dementia. From an architectural perspective, it’s important to design a home-like environment for residents, one which engages the senses, reduces confusion and feels familiar. Common areas that feel homey, including living room-like spaces and comfortable dining areas, go a long way in comparison to the hospital-like environments in the past.
Purposeful wandering has been shown to reduce agitation and confusion. Incorporating purposeful wandering into your design can be done in several ways:
- Minimize dead-end corridors
- Create activity areas to encourage movement
- Design nourishment areas where residents have easy access to snacks
- Develop sitting nodes, for a sense of place
- Build interior, secured courtyards as a special focus for community spaces, and a safe place for residents to connect with nature
- Organize life stations for residents to display familiar images and items
- Incorporate memory boxes into wall spaces
Lighting and space: new frontiers in building a dementia-friendly environment
At Community Living Solutions, we’re eager to help you design the future of your dementia care home. From lighting to space design and more, our experts are ready to help you create a senior living community that provides the highest possible quality of life for residents while achieving your business goals.