Thursday, September 25, 2014

                                               Zero-calorie sweeteners? Not so sweet....
                   Zero-calorie sweeteners may trigger blood sugar risk by screwing with gut bacteria

When artificial sweeteners are in the news, it’s rarely positive. In the last few years, sweeteners have been linked to everything from Type 2 diabetes to cardiovascular disease, high blood pressure, and stroke. Still, products like Splenda and Sweet‘N Low remain a cornerstone of many a weight-loss strategy, mostly because doctors don’t quite understand how sweeteners contribute to disease. That may soon change, however, as results from a study, published today in Nature, point to a possible mechanism behind these adverse health effects.

"Our results suggest that in a subset of individuals, artificial sweeteners may affect the composition and function of the gut microbiome" in a way that would lead to high blood-sugar levels, said Eran Elinav, an immunologist at the Weizmann Institute of Health in Israel and a co-author of the study, during a press conference yesterday. This, the researchers say, is bad for human health because when sugar levels are high in the blood, the body can’t break it down, so it ends up being stored as fat.

High blood sugar ends up being stored as fat.

To reach these conclusions, Elinav and his team first tested the effect of three common artificial sweeteners — aspartame, sucralose, saccharin — on rodents. They found that each of the sweeteners induced a change in blood sugar levels that surpassed that of the mice who consumed actual sugar. And later tests involving the main sweetening agent in Sweet‘N Low, saccharin, yielded similar results in both lean and obese mice.

But mammals don’t actually digest artificial sweeteners — that’s why they’re "calorie-free" — so the reasons why these mice were experiencing blood-glucose alterations was still mysterious, Elinav said. Still, the researchers had an idea: maybe the bacteria that lived in the guts of the mice were interacting with the sweeteners.

So the researchers performed several experiments to test their idea. In one, they gave antibiotics to mice who had been fed sweeteners regularly. Antibiotics kill gut bacteria, and when these mice had their microbial guests cleaned out, their blood sugar levels went back to normal. In another experiment, the scientists transplanted feces — a rich source of gut microbes — from sweetener-fed mice into rodents that had never consumed artificial sweeteners. The procedure caused the recipient mice to experience oddly high blood glucose, like the mice in the sweetener group. Finally, Elinav and his colleagues used genetic analysis to reveal that alterations in the composition of microbial colonies were also accompanied by changes in bacterial function — changes that could very well explain why the mice were experiencing such high blood sugar.

Findings in mice aren't nearly as convincing as findings in people

But findings in mice aren’t nearly as convincing as findings in people, so the researchers set out to investigate human sweetener consumption. In the first experiment, the researchers analyzed the blood-sugar levels and gut bacteria colonies of 381 participants. And, as expected, Elinav and his colleagues found that people who consumed sweeteners in large quantities also showed disturbances in several metabolic parameters — including increased weight — as well as distinct microbial changes in their guts.

The results from the second, much smaller human experiment might actually be the most illuminating.

"We followed for a single week a group of seven human volunteers who do not consume sweeteners as part of their normal diet," Elinav said. During that period, the researchers gave them a single dose of saccharin, and monitored their vitals. After just four days, half the participants showed microbial alterations and increases in blood sugar levels, he explained, "while the other subset had no meaningful effect immediately following the consumption of sweeteners."

In other words: some people are more susceptible to the effects of artificial sweetener than others.

A causal link

The handful of studies suggest that consuming non-caloric artificial sweeteners boosts the risk glucose intolerance in both humans and mice, as a result of changes in gut microbe function, the researchers wrote in their report. Yet, because of the preliminary nature of their results and the small number of human participants involved, they stopped short of suggesting that people change their eating habits. "By no means are we prepared to make recommendations as to the use and dosage of artificial sweeteners based on the results of this study," said Eran Segal, a study co-author also at the Weizmann Institute of Health.

Other researchers, however, were more forthcoming.

"People need to be much more mindful of what they are eating and drinking and make efforts to avoid products that have added sweeteners in any form" said Susan Swithers, a behavioral neuroscientist at Purdue University who wasn’t part of the Nature study, in an email to The Verge. The studies showed not only a causal link between the changes in the gut and artificial sweeteners, but that the observed changes happen quickly, she wrote.

"People need to be much more mindful of what they are eating and drinking."

Not everyone agrees with the design the researchers used to address the question about artificial sweeteners and weight gain. Christopher Gardner, a food scientist at Stanford University who didn’t participate in the study, says that the fact that the researchers gave the FDA's maximal acceptable daily intake of saccharin to the human participants — about 5 mg / kg body weight per day — isn’t ideal. In a real-life setting, that dose would be the equivalent to a 150-pound person consuming 42 12-ounce sodas per day, or 8.5 packets of pink Sweet 'n Low per day. "That may be ‘acceptable’ according to some set of guidelines," Gardner wrote in an email, "but it should be noted that realistically this is a very high dose they are using and one that wouldn't be consumed by a typical consumer."

Still, the idea that we might finally have an explanation for the adverse health effects seen in certain sweetener studies is worth paying attention to. Should the findings prove reproducible, doctors will be tasked with understanding why some people are susceptible to microbiome alterations, while others aren’t. And sweetener companies will have to address the criticism — in addition to rethinking their marketing strategies. "The work is important," Swithers said, "because it underscores the role that artificial sweeteners may play in contributing to the very problems they were designed to help."

By Arielle Duhaime-Ross

Tuesday, September 23, 2014

Sit Less, Live Longer? 
That's what the research shows.... Our front desk staff now uses adjustable desks from www.geekdesk.com that allow standing or sitting at work. Improves overall health and reduces back/neck pain. We walk our talk!! #geekdesk

If people need motivation to get up from their office chairs or couches and become less sedentary, two useful new studies could provide the impetus. One found that sitting less can slow the aging process within cells, and the other helpfully underscores that standing up — even if you are standing still — can be good for you as well. 

For most of us nowadays, sitting is our most common waking activity, with many of us sitting for eight hours or more every day. Even people who exercise for an hour or so tend to spend most of the remaining hours of the day in a chair.

The health consequences of this sedentariness are well-documented. Past studies have found that the more hours that people spend sitting, the more likely they are to develop diabetes, heart disease and other conditions, and potentially to die prematurely — even if they exercise regularly.
But most of these studies were associational, meaning that they found a link between sitting and illness, but could not prove whether or how sitting actually causes ill health. 

So for the most groundbreaking of the new studies, which was published this month in the British Journal of Sports Medicine, scientists in Sweden decided to mount an actual experiment, in which they would alter the amount of time that people spent exercising and sitting, and track certain physiological results. In particular, with this experiment, the scientists were interested in whether changes in sedentary time would affect people’s telomeres.

If you are unfamiliar with the componentry of your genes, telomeres are the tiny caps on the ends of DNA strands. They shorten and fray as a cell ages, although the process is not strictly chronological. Obesity, illness and other conditions can accelerate the shortening, causing cells to age prematurely, while some evidence suggests that healthy lifestyles may preserve telomere length, delaying cell aging. 

For the new experiment, the Swedish scientists recruited a group of sedentary, overweight men and women, all aged 68, and drew blood, in order to measure the length of telomeres in the volunteers’ white blood cells. Then half of the volunteers began an individualized, moderate exercise program, designed to improve their general health. They also were advised to sit less.

The other volunteers were told to continue with their normal lives, although the scientists urged them to try to lose weight and be healthy, without offering any specific methods. 

After six months, the volunteers all returned for a second blood draw and to complete questionnaires about their daily activities. These showed that those in the exercise group were, not surprisingly, exercising more than they had been previously. But they were also, for the most part, sitting substantially less than before. 

And when the scientists compared telomeres, they found that the telomeres in the volunteers who were sitting the least had lengthened. Their cells seemed to be growing physiologically younger.
Meanwhile, in the control group telomeres generally were shorter than they had been six months before. 

But perhaps most interesting, there was little correlation between exercise and telomere length. In fact, the volunteers in the exercise group who had worked out the most during the past six months tended now to have slightly less lengthening and even some shortening, compared to those who had exercised less but stood up more. 

Reducing sedentary time had lengthened telomeres, the scientists concluded, while exercising had played little role. 

Exactly what the volunteers did in lieu of sitting is impossible to say with precision, said Per Sjögren, a professor of public health at Uppsala University in Sweden, who led the study, because the researchers did not track their volunteers’ movement patterns with monitors. But “it’s most likely,” he said, that “sitting time was predominantly replaced with low-intensity activities,” and in particular with time spent standing up. 

Which makes the second new study of sedentary behavior particularly relevant. Standing is not, after all, physically demanding for most people, and some scientists have questioned whether merely standing up — without also moving about and walking — is sufficiently healthy or if standing merely replaces one type of sedentariness with another.

If so, standing could be expected to increase health problems and premature death, as sitting has been shown to do. 

To find out whether that situation held true, Peter Katzmarzyk, a professor of public health at the Pennington Biomedical Research Center in Baton Rouge, La., and an expert on sedentary behavior, turned to a large database of self-reported information about physical activity among Canadian adults. He noted the amount of time that the men and women had reported standing on most days over the course of a decade or more and crosschecked that data with death records, to see whether people who stood more died younger. 

The results, published in May in Medicine & Science in Sports & Exercise, are soothing if predictable. Dr. Katzmarzyk found no link between standing and premature death. Rather, as he writes in the study, “mortality rates declined at higher levels of standing,” suggesting that standing is not sedentary or hazardous, a conclusion with which our telomeres would likely concur. 

 Phys Ed Gretchen Reynolds on the science of fitness.

For more information on how to keep moving visit spechtpt.com
 
 

Thursday, September 18, 2014

To ease severe back pain, quit smoking

Posted by Leslie Orr-Rochester on December 7, 2012

U. ROCHESTER (US) — Quitting smoking offers significant relief to people suffering from severe back pain, new research suggests.

Published in the Journal of Bone and Joint Surgery, the study analyzed more than 5,300 patients followed for eight months during treatment of spinal disorders and showed that cigarette smokers reported far more pain than never-smokers or those who had quit.

Smoking cessation either prior to treatment or during the course of care was related to significant improvements in pain—a result that underlines the need for structured stop-smoking programs among the legions of patients who experience back pain due to degenerative disease, deformity, or musculoskeletal problems.

“We found that people who stopped smoking had meaningful benefit by reduction of their pain,” says Caleb Behrend, chief resident in the Department of Orthopaedics and Rehabilitation at the University of Rochester Medical Center. “The pain improvement is in addition to all the other benefits you gain from quitting.”

The relationship between pain and smoking is complex and full of contradictions. Nicotine has analgesic properties, for example, and yet clinical evidence shows that smokers are at higher risk for developing back pain and other chronic pain disorders, according to the American Society of Anesthesiologists.

Scientists already know that nicotine interacts with a family of proteins (nAChR), which have a key role in the central, and peripheral nervous system, and control anxiety and pain. Prolonged exposure to cigarettes upsets the function of these cells and eventually changes the way pain is processed, as well as impairing oxygen delivery to tissues, predisposing a person to bone and joint disorders such as osteoporosis, and inducing inflammation and depression. Smokers with spinal conditions also tend to have persistently more intense pain and more long-term disability.

he new study notes a daunting fact: Nearly all people will experience back pain at some point in their lives and many will seek medical care. Because the socioeconomic impact of spinal disorders (cost of care and lost productivity for patients) is so great, researchers want to find out if improvements in pain could be achieved with a cost-effective intervention such as smoking cessation.Researchers reviewed a prospectively maintained database of 5,333 patients, who completed questionnaires about pain at the initial doctors’ visit and at the time of discharge from care. Patients were treated with surgery, or with physical therapy, injections, over-the-counter medications, and home exercise programs. Physicians counseled all smokers to quit, and patients were referred to a smoking cessation hotline.

Of the 5,333 people, those who had never smoked or had quit some time ago reported less pain than smokers or those who had just quit. By the end of the follow-up period, the people who had recently quit or who quit during treatment showed significant improvements in pain. People who continued to smoke during treatment had no improvement in pain on all scales.

Younger people tended to comprise the group of current smokers and those who only decided to quit during treatment; this is consistent with other studies showing that smoking is associated with degenerative spine disease at a younger age.

Older patients tended to comprise the group who had never smoked or quit long ago.

The rate of smoking cessation was 22 percent, and research shows that up to 36 percent of patients with painful spinal disorders are able to quit with help from a structured program. A grant from the Southwestern Medical Foundation was used to create and maintain the patient database.

Source: University of Rochester

For more information on back pain, please visit spechtpt.com

Thursday, September 11, 2014

Zach Pereira earns Orthopaedic Specialist Certification!

Swansea, MA – Specht Physical Therapy Physical Therapist Zachary Pereira was certified as a Clinical Specialist in Orthopedic Physical Therapy (OCS) by the American Board of Physical Therapy Specialties (ABPTS). Roughly 6.5% of the physical therapists in the United States are Board Certified in a specialty and only 3.9% of therapists in the United States are Orthopedic Certified Specialists.

Board certification is granted by the American Board of Physical Therapy Specialists (ABPTS) and involves a rigorous examination process and provides assurance to patients and the medical community of a therapist’s skills and abilities.

Pereira is recognized for advanced knowledge, experience, and skills in the practice of orthopedic physical therapy and the conditions affecting bones, joints, ligaments, tendons, muscles and nerves. Similar to physician specialization, there are eight specialty areas in which physical therapists can be board certified. Those with this advanced certification are considered to have great depth of knowledge and skills in their specialty area of physical therapy.

“The certification process reaffirms my enthusiasm and dedication to continue pursuing the highest level of skill with which to best serve patients in Swansea and the surrounding area” Pereira said.  Mr. Pereira obtained his Masters in Physical Therapy from Springfield College in 2007 and joined the Specht Physical Therapy staff in 2009.


 Specht Physical Therapy is a privately owned physical therapy clinic in Swansea, Massachusetts dedicated to helping people of all ages get back to what they enjoy. For more information please contact Greg Specht, Clinical Director at Specht Physical Therapy at 508-675-3200 or visit our website at www.spechtpt.com.