Image credit: Women eating salad via Shutterstock

Scientists who study eating behavior have known for quite some time that the circumstances under which an individual eats affect how much is consumed. For instance, solitary diners tend to eat more than those who eat with companions [2]. How much one’s dinner companion eats, however, also influences eating behavior. Several studies have shown that humans are likely to eat more when dining companions consume more food, and that similarly, humans eat less when dining with companions who eat very little [3]. Several questions remain with regard to the influence of companions on eating behavior, including why the influence exists, and whether matching the intake of one’s companions is intentional or unconscious.

In the current study, researchers examined whether behavioral mimicry can account for these modeling effects of eating. They evaluated 70 young female pairs, coding for the total number of bites and the exact time at which each person took a bite. The scientists found that both women mimicked each other’s eating behavior; they were more likely to take a bite of their meal in within 5 seconds of their eating companion rather than eating at their own pace. This behavioral mimicry was found to be more prominent at the beginning (i.e. within the first ten minutes) rather than at the end of the meal (i.e. the last ten minutes).

According to the researchers, there are several possible explanations for these observations. Humans have a complex “mirroring network” that causes behavior-matching [4,5]. It’s possible that the pairs of women in the experiment were unconsciously matching one another bite-for-bite in order to create rapport. This possibility is supported somewhat by the observation that the mimicry was strongest in the first ten minutes of dining, a time during which the pairs would be developing a social rapport. The researchers also point out, however, that mimicking the eating behavior of a companion might be a mechanism by which the individual adjusts their caloric intake so as to avoid overeating; that is to say, the dining companion becomes a model for “appropriate eating.” While this is possible, it would require that the women consciously adjusted their eating patterns rather than responding unconsciously, which the researchers did not test. It’s highly unlikely that there would be an unconscious guard against overindulgence, given that until recently in human history, the challenge humans faced was in getting enough food (as opposed to controlling intake).

Regardless of the mechanism, however, the study suggests that eating with a companion who takes very few total bites of food may be a strategy for helping to control one’s own intake at a particular meal.

References

1. Hermans et al. Mimicry of Food Intake: The Dynamic Interplay between Eating Companions. PLoS One. 2012;7(2):e31027. Epub 2012 Feb 1.
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2. de Castro and Brewer. The amount eaten in meals by humans is a power function of the number of people present. Physiol Behav. 1992 Jan;51(1):121-5.
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3. Hermans et al. Modeling of palatable food intake. The influence of quality of social interaction. Appetite. 2009 Jun;52(3):801-4. Epub 2009 Mar 26.
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4. Chartrand et al. The chameleon effect: the perception-behavior link and social interaction. J Pers Soc Psychol. 1999 Jun;76(6):893-910.
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5. Lakin et al. Using nonconscious behavioral mimicry to create affiliation and rapport. Psychol Sci. 2003 Jul;14(4):334-9.
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February is American Heart Month. Sponsored by the American Heart Association, American Heart Month is a time to battle cardiovascular disease and educate people on what they can do to live heart-healthy lives. Heart disease, including stroke, is the leading cause of death for men and women in the United States.

How much do you know about the condition of your heart? Heart health awareness typically focuses on heart disease in older adults caused by an unhealthy diet and a lack of exercise. But what if you could be at risk for cardiac arrest and sudden death even though you are young and in shape?

Image credit: Heart arrhythmia via Shutterstock

Long QT syndrome (LQTS) is one of several sudden arrhythmia death syndromes, a class of conditions affecting the heart’s rhythm. People can be born with an inherited form of the syndrome or acquire it during their life. LQTS can cause sudden, uncontrollable, dangerous heartbeats in response to exercise or stress. LQTS can arise from mutation of one of several genes, including Potassium Channel, Voltage-gated, KQT-like Subfamily, Member 1 (KCNQ1); Potassium Channel, Voltage-gated, Subfamily H, Member 2 (KCNH2); and Sodium Channel, Voltage-gated, Type V, Alpha Subunit (SCN5A).

LQTS is common; approximately one in every 2,500 people has the disorder [1]. Some people don’t discover they have LQTS until the sudden unexplained death of a family member. However, if identified, LQTS can be treated with medications, limited physical activity, or, in some cases, medical devices or surgery [2].

Dr. Brian Delisle, a faculty member of the University of Kentucky’s College of Medicine, is studying the genetic form of LQTS in order to identify new treatments. According to Delisle, there are several types of the genetic form of LQTS, each caused by a different gene mutation. One form of LQTS syndrome, LQT2 (which involves mutations of the human ether-a-go-go related gene (hERG), also known as KCNH2), is caused by a mutation in a gene that codes for potassium channels in the heart’s cells. The mutation prevents the potassium channels from being transported to their proper place at the cell’s surface. As a result, the potassium channels cannot function properly.

In a recent study published in the American Journal of Physiology Cell Physiology, researchers from Delisle’s laboratory found that a distinct cellular compartment in cardiac myocytes (heart cells) negatively regulates the production and movement of LQT2 [3]. Delisle said:

We do have a series of drugs that can correct this … in cell systems. But the problem right now is that most of the drugs that do this actually cause the acquired form of Long QT.

Delisle hopes that by better understanding the mechanism preventing the proper transport of the potassium channels to the cell’s surface, other therapeutic approaches can be identified to correct this problem.

About the author: Julianne Wyrick is a senior biochemistry major at Asbury University. A 2011 Kentucky Academy of Sciences award winner for scientific research, following graduation Julianne plans to enter a health and medical journalism graduate program.

References

1. Long QT Syndrome. Sudden Arrhythmia Death Syndrome (SADS) Foundation. Accessed 2012 Jan 28.
2. Long QT Syndrome. Mayo Clinic. Accessed 2012 Jan 28.
3. Smith et al. Trafficking-deficient hERG K? channels linked to long QT syndrome are regulated by a microtubule-dependent quality control compartment in the ER. Am J Physiol Cell Physiol. 2011 Jul;301(1):C75-85. Epub 2011 Apr 13.
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Image credit: Skin care on the back via Shutterstock

Use of sunscreen is about more than just preventing painful burns. A single sunburn during childhood nearly doubles the risk of melanoma — a particularly aggressive and serious type of skin cancer — in adulthood [2], and reports indicate that at least half of all children experience at least one sunburn by age 11 [3].

Sunlight is crucial to life on Earth. Without the sun’s radiant energy, the planet would be an uninhabitable chunk of ice. Visible light from the sun fuels photosynthesis, the process by which plants make sugar from the molecules carbon dioxide and water. This provides food for herbivores and omnivores, which in turn provide food for higher consumers.

In essence, the sun is the ultimate source of food energy on the planet. Even the sun’s damaging rays — those in the ultraviolet region of the light spectrum — serve important purposes with regard to health and wellness. For instance, humans make vitamin D when ultraviolet light hits the skin.

Ultraviolet light, however, falls into the category of ionizing radiation, which means that it (like x-rays and like gamma radiation, which comes from nuclear reactions) is capable of breaking chemical bonds in molecules. When ultraviolet light hits the skin, it penetrates a short distance. The light can then break chemical bonds in biological molecules, including skin proteins and genetic material, or DNA. The former leads to the visible signs of aging associated with excess sun exposure, such as wrinkles and sagging skin. The latter ultimately leads to skin cancer.

One of the body’s natural protection mechanisms against overexposure to ultraviolet light is increased production of melanin, which is a chemical that makes the skin darker in color and helps protect the cell from further damage to DNA. For this reason, some people consider a tan protective against the sun, or even healthy. Darkening of the skin in response to sunlight, however, while protective to some extent, is also indicative of damage to the skin cells. It’s a bit like the body’s way of closing the barn door after (some of) the cows get out, since it takes cellular damage to stimulate the cell to produce more of the protective chemical melanin. Unfortunately, tans are seen as attractive. According to the Pediatrics study, the percent of children reporting liking to have a tan increased from 54 to 67% percent between 2004 and 2007, which could at least partially explain the decreased use of sunscreen during that same period of time.

As part of an effort to educate children and their parents about the damaging effects of the sun, the American Cancer Society promotes the slogan “Slip! Slop! Slap! And Wrap!” In longer form, the slogan reads: “Slip on a shirt, slop on sunscreen, slap on a hat, and wrap on sunglasses.” The Pediatrics findings, however, suggest that this message may not be reaching preadolescent children. The authors recommend finding new ways of encouraging sun-safe behavior in this demographic.

References

1. Dusza et al. Prospective Study of Sunburn and Sun Behavior Patterns During Adolescence. Pediatrics 2012;129:309–317.
2. Dennis et al. Sunburns and risk of cutaneous melanoma: does age matter? A comprehensive meta-analysis. Ann Epidemiol. 2008 Aug;18(8):614-27.
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3. Cokkinides et al. Trends in sunburns, sun protection practices, and attitudes toward sun exposure protection and tanning among US adolescents, 1998-2004. Pediatrics. 2006 Sep;118(3):853-64.
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Images in the mind image via Shutterstock

The media has widely reported recent research which shows that memory processes start to decline at 45 years of age [2]. With increasing attention paid to the impact of dementia on individuals, families, society and healthcare services, memory research is very much in the spotlight. Although it’s important to understand when memory starts to get worse, it’s also vital to come to grips with what happens to memory processes. This might give us clues to how to improve memory.

Memory is a complex set of processes, which may decrease at different rates or in different ways. Thus, Italian researchers at the University of Padua decided to focus on “working memory” — the part of memory that holds information at the ready so it can be processed (to go into “long-term memory”) or used to complete tasks. A now historical example would be looking up a number in a phone book before dialling it out — the numbers are held in working memory, like planes in a holding pattern, before coming in to land as we dialed the number. In real life, information often changes or gets supplemented. This means we have to update our working memory. This updating needs to remove no longer needed information and to retrieve the still needed information. The process then is rather complex and understanding how it works in people of different ages might provide clues as to what is happening as memory declines.

In the study, scientists aimed to examine any differences between younger and older participants in updating working memory. Data were collected from 26 “younger” adults (average age of 27.81 years) and 26 “older” adults (average age of 68.77 years). Because memory processes can work differently with different types of information, this experiment used verbal and visual tasks. In the verbal task, participants were asked to recall the last 4 letters in a string of letters read out to them. This sounds simple enough, so how does this test out the “updating” process? Participants did not know how long the string of letters would be, so every time another letter was given, they had to update their memory of the last 4 letters. The longer the list, the more updating required. Correct responses and incorrect recall of letters no-longer in the last 4 letters of the string were recorded. For the visual task, participants saw squares on a 5 by 5 table light up and had to recall the position of the last 4 lights in the sequence.

When only 4 items were given (so that no updating was required), older adults performed poorly on both the verbal and the visual task compared to younger adults. Older adults performed even worse on longer lists of items, where more updating was required. Older participants incorrectly updated their memory by stating that letters or light positions given earlier in the sequence were in the last 4 presented. Thus, it appears that older adults hold on to information that isn’t needed anymore.

This subtle finding is potentially very important — older participants aren’t forgetting things, rather they seem to be remembering too many things and therefore overloading the memory system. Additionally, it appears that in some cases, errors in memory did not reflect a failure of updating but sometimes simply that people waited until the end of the task before trying to recall. Older adults seemed to rely more often on the fact that recently provided information is held in the working memory quite well with the absence of great effort.

This research helps us to lift the lid on memory decline and to try to understand what is happening in more detail. Working memory performance is worse in older adults compared to younger adults. This itself is helpful, however the study also suggests that this is because memories are not being updated as efficiently and because older adults used less effort to keep items in the working memory.

Now, at this point, it’s always good to ask “so what?”. Well, first come the limitations of the study. From a single study we can’t infer too much. The study is an experiment and uses abstract tasks, which might not reflect real-life activities and therefore real-life cognitive processes. The researchers have inferred from the errors made to attempt to understand the processes, but that is the challenge of this type of research into processes that can’t be seen and people are not necessarily aware of these processes. Now, the so-what that is potentially very useful — a more in depth understanding of what is happening with older adults memory, we might be able to create training activities to enhance working memory based on updating and effort.

We accept that decline in body and mind is part of normal aging. However, there may be things we can do to slow or lessen these declines. Physical activity, healthy diets and staying active all seem to lessen the impact of aging. For psychological processes, research is required to understand how processes are declining. Although scientists are still exploring interventions to treat memory loss, the study reviewed here helps to understand what processes are active. Using working memory and engaging in updating of information and doing tasks that require effort to remember may be beneficial. So keep your working memory active and be wise by using effort to remember rather than tricks.

References

1. Fiore et al. Age differences in verbal and visuo-spatial working memory updating: Evidence from analysis of serial position curves. Memory. 2012 Jan;20(1):14-27. Epub 2011 Dec 2.
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2. Singh-Manoux et al. Timing of onset of cognitive decline: results from Whitehall II prospective cohort study. BMJ. 2011 Jan 5;344:d7622.
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Lose weight image via Shutterstock

Dr. Proietto runs a weight-loss clinic. In this most recent study, he recruited fifty obese individuals without diabetes or other serious illnesses into an intensive ten week weight loss program. After weight loss was achieved — study participants were required to lose ten percent of their body weight — they received dietary counseling to help them maintain their new weight. Dr. Proietto measured levels of a variety of hormones known to mediate appetite and got subjective ratings of appetite before the program began, immediately after it ended, and then again a year later.

Of the fifty people recruited, thirty-four were able to complete the study. Perhaps not surprisingly, Dr. Proietto found that the participants reported their “desire and urge to eat” as higher immediately after the weight loss regimen than it was before they had started. But distressingly, it was just as high a year later. What’s more, they reported being more preoccupied with thoughts of food, and less full, after a year than they had been just coming off of the diet.

The levels of nine different hormones were measured. Of these, leptin might be the best known. It is made by body fat, and thus functions as an indicator of energy stores. It acts in the brain to suppress hunger and increase metabolism. Leptin levels plummeted by 64% over the ten weeks that the study participants were dieting, and although they recovered somewhat over the course of the next year, they were still 35% lower than when the study began. The researchers noticed that as study participants put weight back on, their leptin levels rose. Ghrelin can be thought of as the opposite of leptin — whereas leptin suppresses feelings of hunger, ghrelin promotes them. And as such its levels were the opposite of leptin’s — for the ten weeks of the diet the participants’ ghrelin levels steadily rose, and although they fell over the course of the year, they ended up significantly higher than they were at the beginning of the study. The other hormones followed the same pattern established by these representatives; those that suppress appetite were reduced, while those that stimulate appetite were increased.

These hormonal changes indicate that a full year after these people lost weight, their bodies were trying to put it back on. Their bodies regarded this leaner state as akin to starvation, and treated their heavier body weights as normal. Their metabolism was not at all the same as that of someone who had always weighed this lower amount rather than achieving it by dieting.

A number of other studies have borne out this idea, that a weight-reduced body is quite different than one of the same size that had always been that way.

Last month, Tara Parker Pope expanded upon Dr. Proietto’s study in the in The New York Times Magazine. Ms. Parker Pope highlights some studies being done at Columbia University confirming that after people lose weight their muscles are more efficient — meaning that when doing the same activity as people who were always at that lower weight, they burn 20-25% fewer calories. And using brain scans, neuroscientists at Columbia have shown that images of food activate regions of the brain associated with reward more strongly in people after they have lost weight, while regions associated with control did not respond as strongly in these post dieters. Their brains are actively making food look more appealing, and undermining their will power, to get them to eat more — to get them back to their original weight.

The National Weight Control Registry tracks 10,000 people who have lost at least thirty pounds and kept it off for at least a year. Analysis of their habits reveals that to maintain their new lower weights, these individuals must in fact eat less, and exercise more, than those who naturally weigh the same amount. And that’s not really surprising: if you want to lose weight and keep it off, you have to permanently change your lifestyle. The lifestyle that you adopt to lose weight has to be one you’re prepared to maintain for the rest of your life. So as Ms. Parker-Pope notes in her article, it is not hopeless. It is not impossible to lose weight and then keep it off. It’s just really, really hard.

References

1. Sumithran P et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011 Oct 27; 365(17):1597-604.
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2. Rosenbaum M, Kissileff HR, Mayer LE, Hirsch J, Leibel RL. Energy intake in weight-reduced humans. Brain Res. 2010 Sep 2; 1350:95-102. Epub 2010 Jun 2.
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Osteoblasts, or bone cells, have been shown to grow into mature bone when subjected to mechanical stress. Scientists hypothesized that the same might hold true for other cell types. Adipocytes seemed the ideal test system for a number of reasons. Firstly, they are derived from the same embryonic progenitor cells as osteoblasts, so they might share similar properties. Moreover, adipocytes in the buttocks are known to be exposed to a large mechanical strain in a physiological setting — when we sit down. And lastly, obesity is such an immense health problem that any insight into its development could be clinically valuable.

To test their theory, researchers created a unique experimental apparatus in which two groups of cells could be cultured under identical conditions, but one group would be stretched and the other would not. The stretching of the cells mimicked the about half the degree of tissue compression that occurs in weight bearing postures. All of the cells were induced to differentiate by the addition of insulin, and cells were inspected almost daily. The researchers measured the numbers and sizes of lipid droplets in the two cell populations every two to three days over the course of three to four weeks. Within the first ten days of culture, the stretched cells differentiated about twice as fast as the non-stretched cells. Thereafter, the stretched cells contained lipid droplets that were about one and a half times as large — 50% more fat — as those in the non-stretched cells.

This is the first study to look at fat cells as they develop under sustained mechanical loading. The authors are quick to point out that cyclic or intermediate stretching — such as that attained during physical motion — has been shown to have the opposite effect; it actually inhibits the differentiation of preadipocytes and lipid production. They also note that future studies should try to determine if these results hold true in a more physiological setting, and if the cells might respond differently to different concentrations of insulin and glucose such as those that might be representative of a high calorie diet.

Nevertheless, the study is highly suggestive of yet another damaging effect of a modern, sedentary lifestyle. Dr. Gefen notes [2]:

Obesity is more than just an imbalance of calories. Cells themselves are also responsive to their mechanical environment. Fat cells produce more triglycerides, and at a faster rate, when exposed to static stretching.

Indeed, the findings indicate that we need to take our cells’ mechanical environment into account as well as pay attention to calories consumed and burned. Even people that eat a healthy diet and exercise will be negatively impacted by long periods of inactivity.

References

1. Shoham et al. Static Mechanical Stretching Accelerates Lipid Production in 3T3-L1 Adipocytes by Activating the MEK Signaling Pathway. Am J Physiol Cell Physiol. 2011 Oct 19.

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2. ‘Just chill?’ Relaxing can make you fatter. EurekAlert. 2011 Dec 1.

Two vitamins with which the article notes significant associated potential risk are vitamins E and A. Vitamin E is a fat-soluble antioxidant that exists in nature in several different forms.

The predominant form of vitamin E found in food sources, including leafy greens, nuts, and some oils, is called gamma-tocopherol. The predominant form in manufactured supplements, however, is alpha-tocopherol. Research suggests that alpha-tocopherol may actually block the activity of gamma-tocopherol, which at least partially explains some of the disturbing research findings associated with vitamin E supplementation. For instance, one study found vitamin E supplements increased the risk of prostate cancer in men by 17% [2], while another study found that vitamin E increased the risk of stroke by 22% and 10%, depending upon the type of stroke [3]. Yet a third study associated vitamin E supplementation with increased overall risk of mortality [4].

Vitamin A occurs in food in two major forms: preformed vitamin A and beta-carotene, which the human body uses to produce vitamin A. Like vitamin E, vitamin A is an antioxidant, though it also plays an important part in vision (particularly night vision) and in normal cell division and development. Food sources of beta-carotene include many fruits and vegetables (especially yellow-orange ones), while animal products such as milk and organ meat contain preformed vitamin A. Despite the importance of vitamin A in the diet, however, in supplement form, it is suspected to act as a pro-oxidant (the opposite of an antioxidant). Supplementation with beta-carotene and/or vitamin A has been found to be associated with or cause a number of negative outcomes. For instance, the study that associated vitamin E with increased overall risk of mortality found the same was true of vitamin A. Two studies found that vitamin A and beta-carotene supplements increased the incidence of lung cancer [5,6], while a third found an increased risk of prostate cancer associated with high blood levels of vitamin A [7].

The risks associated with vitamin E and A supplementation are somewhat disturbing. Without significant evidence to suggest that consuming these vitamins in supplement form confers any particular benefit to outweigh the risks, it’s difficult to rationalize recommending vitamin E and A supplements to the general population (those with absorption disorders and other disease processes that may require vitamin supplementation notwithstanding). In light of these findings, consumers using vitamin supplements that haven’t been prescribed or recommended by a healthcare practitioner may wish to discuss their choices with a doctor. Vitamins from food sources, of course, remain an important and healthy component of diet.

References

1. (No authors listed). Who should take vitamin supplements? Med Lett Drugs Ther. 2011 Dec 26;53(1380):101-3.
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2. Klein et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2011 Oct 12;306(14):1549-56.
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3. Schurks et al. Effects of vitamin E on stroke subtypes: meta-analysis of randomised controlled trials. BMJ. 2010 Nov 4;341:c5702. doi: 10.1136/bmj.c5702.
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4. Bjelakovic et al. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD007176.
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5. Omenn et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996 May 2;334(18):1150-5.
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6. Virtamo et al. Incidence of cancer and mortality following alpha-tocopherol and beta-carotene supplementation: a postintervention follow-up. JAMA. 2003 Jul 23;290(4):476-85.
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7. Mondul et al. Serum retinol and risk of prostate cancer. Am J Epidemiol. 2011 Apr 1;173(7):813-21. Epub 2011 Mar 9.
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Researchers at the University of Toronto recently performed a meta-analysis of three Finnish studies and found that children who chewed gum — or took other products laden with xylitol, including lozenges or syrup — had about a 25% lower risk of developing an ear infection compared to controls. The study is published in the Cochrane Database of Systematic Reviews [1].

Acute ear infections are the most common bacterial infections suffered by children in the United States and are the leading reason for antibiotic prescriptions. Such extensive use of antibiotics is extremely expensive, costing almost $3.8 million USD annually, and may contribute to the rise of antibiotic resistance among pathogenic strains of bacteria. Thus alternate treatments are desirable. A research group at the University of Toronto recently compiled a number of studies evaluating a daily dose of xylitol for the prevention of acute middle ear infections in children without acute upper respiratory infections attending day care centers.

Their literature search, which included randomized controlled trials, quasi-randomized controlled trials, unpublished studies, technical reports, dissertations, and abstracts from annual meetings, turned up eighty-four potential studies. Of these, only four met their eligibility criteria. All four were randomized controlled trials performed with 3,103 Finnish children in day care and published between 1998 and 2007.

They found that among healthy children, 8-10 g per day of xylitol in any form — gum, lozenges, or syrup — reduced the incidence of acute ear infections by 25% compared to children in the control group. Gum was notably the best (in the studies, children chewed two pieces of gum five times a day after meals for at least five minutes). However, since peak incidence of ear infection occurs when children are between six months and one year old, when they are too young to chew gum, the finding that other delivery methods can also work are valuable.

However, despite the significant preventative effect in healthy children, xylitol did not reduce the occurrence of acute ear infections in those children who already had acute upper respiratory tract infections. And although xylitol has been known to cause stomach distress, no adverse affects were reported by any children included in these studies.

The authors warn that since they only analyzed a few studies, and those were peformed by the same research group with a very homogenous group of children, they had insufficient data to generate any kind of treatment guidelines, such as how much xylitol is necessary or sufficient to prevent acute ear infections. But since chewing any kind of gum has also been found to boost mental performance and enhance alertness [2,3], perhaps teachers will be more tolerant of it in the classroom.

Ear infection risk factors

Ear infections are more likely to occur in the fall and winter when colds and flu are prevalent. Additional factors that put children at higher risk for ear infection include:

• Age (children between the ages of 6 months and 2 years are more susceptible to ear infections because of the size and shape of the eustachian tubes)
• Air quality (exposure to tobacco smoke or high levels of air pollution can increase the risk of ear infection)
• Allergies can cause inflammation in the airways and may contribute to ear infections
• Bottle-fed babies may have a higher risk for ear infections than breastfed babies
• Day care (close and frequent exposure of children to other children can pose a risk for ear infections)
• Ethnicity (American Indians and Inuits of Alaska and Canada have an increased risk of ear infections)
• Family history (the risk of ear infections increases if another member of the family has had ear infections)

References

1. Azarpazhooh et al. Xylitol for preventing acute otitis media in children up to 12 years of age. Cochrane Database Syst Rev. 2011 Nov 9;11:CD007095.
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2. Smith A. Effects of chewing gum on cognitive function, mood and physiology in stressed and non-stressed volunteers. Nutr Neurosci. 2010 Feb;13(1):7-16.
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3. Johnson et al. Chewing gum moderates multi-task induced shifts in stress, mood, and alertness. A re-examination. Appetite. 2011 Apr;56(2):408-11. Epub 2011 Jan 11.
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Elevated postprandial glucose (PPG) often precedes the development of type 2 diabetes, and is a risk factor for adverse cardiovascular events, independently of diabetes status. Thus, Dr. Catherine Mikus and her colleagues at the University of Missouri set out to precisely define the impact of reducing physical activity on PPG and glycemic variability in healthy, active volunteers as they went about their daily lives. The results of their study were recently published in the journal Medicine and Science in Sports and Exercise [1].

Twelve volunteers between the ages of twenty and thirty-five, eight men and four women, were recruited for participation. They were given pedometers to wear to count the number of steps they took each day, and glucose sensors were implanted under their skin and connected to continuous glucose monitors. They had to keep detailed diet and physical activity records for three days, and were instructed to maintain their regular physical activity patterns. Their glucose levels were taken 30 minutes and 60 minutes after meals. They then rested for a week, and then repeated the study protocol but this time they had to restrict their physical activity for three days. They significantly reduced the amount of time they spent walking, climbing stairs, and running — they pretty much just sat around. Four of the study participants did the protocols in reverse order — first the inactive period and then the active period — to reduce any effects of the sequence.

Only three days of reduced physical activity led to significant increases in postprandial glucose. The swings between the highest glucose levels and the lowest also increased, as did the length of time the postprandial blood glucose concentration stayed above target levels. Fasting plasma insulin was increased as well, and the researchers speculate that this may be because inactive people need more insulin to dispose of a given amount of glucose than an active person would require.

The scientists conclude that even short-term reductions in physical activity can result in robust changes in postprandial blood glucose concentrations and glycemic variability, and thus that regular physical activity plays an important role in the everyday maintenance of glycemic control. They note that although physical activity is generally assumed to improve health by promoting cardiorespiratory fitness and reducing fat, these factors are not impacted by a short-term change in physical activity. The role of physical activity in maintain glycemic control may thus be just as important as these other effects, as large fluctuations in blood glucose levels have been shown to have a number of deleterious effects that can help insulin resistance blossom into full blown type 2 diabetes. Interestingly, another study showed that reducing energy intake during reduced physical activity in order to maintain energy balance does not completely abrogate the effects of reduce physical activity on insulin sensitivity, so an energy imbalance cannot fully explain this phenomenon.

An obvious limitation of this study is its small sample size and the homogeneity of the participants. Further studies with larger cohorts are required to see if these findings hold up in a diverse population, and to see if factors like age, sex, body composition, ethnicity, type of physical activity, and glucose tolerance status impact the degree to which physical activity affects glycemic variability. But in this group, it is clear that physical activity is vital in maintaining stable glucose levels in the blood, and that reductions in physical activity can very quickly exert negative effects on glycemic control and insulin sensitivity.

References

1. Mikus et al. Lowering Physical Activity Impairs Glycemic Control in Healthy Volunteers. Med Sci Sports Exerc. 2011 Jun 28. [Epub ahead of print]
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A recent article published by Helen Tilbrook and colleagues in the Annals of Internal Medicine addresses the effectiveness of yoga — a combination of stretching, breathing, and exercise that falls into the CAM purview — in helping to relieve chronic low back pain [2]. The Tilbrook study is not the first of its kind; several studies have suggested that yoga may be effective for chronic back pain relief [see, for example, 3-5]. However, as Tilbrook and colleagues point out, the previous studies contained a variety of limiting factors that make it difficult to draw robust conclusions from their data.

The Tilbrook study was much larger than its predecessors, including a total of 313 participants. The participants were randomly assigned to either traditional back pain treatment or to attend a once-weekly yoga class each week for 3 months. During classes, the participants were taken through a series of poses appropriate to those with low back pain. They were also taught about relaxation and the philosophy of yoga, and were encouraged to practice yoga daily at home. To this end, participants were given a video yoga class to use in home practice.

One of the difficulties in addressing the efficacy of a pain relief technique is that pain can’t be objectively measured; patients must rank their own pain. However, a large back pain relief study previously demonstrated that a decrease in the Roland-Morris Disability Questionnaire (RMDQ, a questionnaire used to objectify the process of ranking pain and its effect on daily life) score of 1.57 points correlated to significantly improved quality of life [6]. The Tilbrook study found that the yoga group had significantly reduced back pain as compared to the group that received usual care. At three months (the end of the yoga program), the yoga group had an adjusted average RMDQ score that was 2.17 points lower than the average of the usual care group. At six and 12 months, the yoga group’s average adjusted RMDQ score was still lower than the average of the usual care group, by 1.48 and 1.57 points respectively.

While the results of the study are somewhat compelling in their support for yoga as a pain relief strategy, perhaps the most important finding of the study was that yoga appears to be quite safe for chronic sufferers of low back pain. Only 8 of the study participants reported adverse events that could potentially be attributed to yoga. As such, the risk-to-benefit analysis suggests that, given the possibility of pain relief and the minimal risk of injury, yoga is worth considering as an adjunct to other therapies in managing chronic low back pain.

References

1. Chronic Pain and CAM: At a Glance [NCCAM Research]. National Center for Complementary and Alternative Medicine. Accessed 2011 Dec 2.
2. Tilbrook et al. Yoga for chronic low back pain: a randomized trial. Ann Intern Med. 2011 Nov 1;155(9):569-78.
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3. Tekur et al. Effect of short-term intensive yoga program on pain, functional disability and spinal flexibility in chronic low back pain: a randomized control study. J Altern Complement Med. 2008 Jul;14(6):637-44.
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4. Sherman et al. Comparing yoga, exercise, and a self-care book for chronic low back pain: a randomized, controlled trial. Ann Intern Med. 2005 Dec 20;143(12):849-56.
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5. Galantio et al. The impact of modified Hatha yoga on chronic low back pain: a pilot study. Altern Ther Health Med. 2004 Mar-Apr;10(2):56-9.
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6. UK BEAM Trial Team. United Kingdom back pain exercise and manipulation (UK BEAM) randomised trial: effectiveness of physical treatments for back pain in primary care. BMJ. 2004 Dec 11;329(7479):1377. Epub 2004 Nov 19.
   View abstract