Get Moving to Keep Young

Sitting too long is no good. And exercise is good for us. We all know this and it’s something that Dr Shaun from Waverley Chiropractic Centre explains to every patient, old or young. New research from Brigham Young University is telling us exactly how much exercise impacts the aging process on a cellular level. Now that’s good to know!

It all comes down to tiny proteins called telomeres. Theses are the end bits of our chromosomes. “Each time a cell replicates, we lose a tiny bit of the endcaps. Therefore, the older we get, the shorter our telomeres [1].”

The study, lead by exercise science professor Larry Tucker, found that people who maintained consistently high levels of physical activity had significantly longer telomeres than those who were sedentary or even moderately active. At the extreme end of the comparison (i.e. Those with very high levels of physical activity vs. those who were sedentary) this amounted to 9 years difference in telomere length [2].  Between those who were highly active and those who were moderately so, the difference was a lesser but still hefty 7 years.

“Just because you’re 40, doesn’t mean you’re 40 years old biologically,” Tucker said. “We all know people that seem younger than their actual age. The more physically active we are, the less biological aging takes place in our bodies [1].”

What kind of activity? The study used benchmarks of 30 minutes jogging for women, and 40 minutes jogging for men, five days a week [1, 2].  Although the exact mechanism for the preservation of telomeres has not yet been pinpointed, Tucker speculated it could be tied to inflammation and oxidative stress.

“Previous studies have shown telomere length is closely related to those two factors and it is known that exercise can suppress inflammation and oxidative stress over time.

“We know that regular physical activity helps to reduce mortality and prolong life, and now we know part of that advantage may be due to the preservation of telomeres,” Tucker said. [1]”

The study is the second published this year that linked telomere length with physical activity levels. Researchers at the University of California (San Diego) School of Medicine looked at elderly women who sit for more than 10 hours a day [3]. They found these women to have cells that were “biologically older by eight years compared to women who are less sedentary [3].”

“Our study found cells age faster with a sedentary lifestyle. Chronological age doesn’t always match biological age,” said Aladdin Shadyab, PhD, lead author of the study with the Department of Family Medicine and Public Health at UC San Diego School of Medicine [3].”

Their benchmark for physical activity varied somewhat from that used by Tucker and his colleagues. Shadyab et al used 40 minutes of moderate to vigorous physical activity per day as their research parameter.

The study looked at nearly 1,500 women aged between 64 and 95, as part of a larger longitudinal study looking at determinants of chronic disease in postmenopausal women.

“We found that women who sat longer did not have shorter telomere length if they exercised for at least 30 minutes a day, the national recommended guideline,” said Shadyab. “Discussions about the benefits of exercise should start when we are young, and physical activity should continue to be part of our daily lives as we get older, even at 80 years old.”

So the answer for youth is very simple: get moving every day! It may keep you nearly a decade younger than your biological age, even on a cellular level.

References:

[1] “High level of exercise linked to nine years of less aging at the cellular level,” Medical Express, https://medicalxpress.com/news/2017-05-high-linked-years-aging-cellular.htmlretrieved May 15, 2017

[2] Tucker L (2017), “Physical activity and telomere length in U.S. men and women: An NHANES investigation,” Preventive Medicine (2017). DOI: 10.1016/j.ypmed.2017.04.027

[3] “Too much sitting, too little exercise may accelerate biological aging: study,” Medical Express, https://medicalxpress.com/news/2017-01-biological-aging.html retrieved May 15, 2017

Chronic pain and the brain

Chronic back problems are common place at Waverley Chiropractic Centre. Whether it’s due to unsuccessful previous treatment or it’s just been left too long, many patients present to Glen Waveley chiropractor, Dr Shaun Beovich with chronic back pain. Chronic back problems include pain which can be identified as a persistent ache anywhere on the back. Usually felt in the lower back area, chronic back pain can also cause stiffness, soreness and inflammation. The pain itself may range from mild to severe or from a dull ache to a sharp pain.

People with chronic back pain can often find it hard to undertake normal daily activities and this can affect general outlook on life. Chronic pain can create a perception of harmfulness, which may lead to reduced physical activity and a sense of disability or helplessness.

Chronic pain conditions are commonly associated with insomnia. Poor sleeping patterns and lack of sleep can exacerbate pain and impact quality of life.

What causes chronic back problems?
It is not always possible to identify the cause of back pain. Although pain from a direct injury (such as a sprain or strain) or a medical condition (like a slipped disc or sciatica) may be easier to identify, chronic back problems can also result from lifestyle choices.

People who lead inactive lives and have poor posture are more at risk of experiencing back pain due to prolonged strain on the back and spine.

Here is some interesting research on how the brain reacts to chronic pain. For more information contact Waverley Chirpractic Centre on 8839 5364 or book online at www.waverleychiro.com.au

Chronic pain amplifies the brain’s reaction to new injuries

 

Chronic pain in any one body part may distort the intensity with which a key brain region perceives pain everywhere else.

This is the finding of a study in rats, which was led by researchers at NYU Langone Medical Center, published in the journal eLife, and presented at the annual meeting of the American Pain Society.

Designed to help us avoid injury and be more likely to survive, our brains are wired to generate alarm when we are injured, and fear when we again encounter the same injury source.

The new study supports the theory that chronic pain rewires circuits in a brain region called the anterior cingulate cortex (ACC) to increase “aversion,” the amount of attention paid to, and alarm felt about, any given pain signal, say the study authors. Most previous studies have focused on nociception, the intensity of incoming sensory signals from say a burnt finger, instead of what the brain does with such signals once they arrive.

“We pursued this study because of what we saw in the clinic, where patients with chronic pain, say in the lower back, report much higher than normal pain after surgery in the knee or abdomen,” says Jing Wang, MD, PhD, vice chair for Clinical and Translational Research Department of Anesthesiology, Perioperative Care and Pain Medicine at NYU Langone. “Our study results argue that chronic pain causes distortion in how the ACC calculates pain intensity with system-wide consequences.”

As many as 1.5 billion people worldwide suffer from chronic pain, some from fibromyalgia and several other syndromes where patients are more sensitive to pain throughout the body for reasons unknown.

More Pain Everywhere

Past research had shown that a body part that is the source of chronic pain triggers greater than normal signaling activity in ACC nerve cells when that same area is injured again. The new study is the first to show that chronic pain in one locale causes a greater reaction to pain-causing stimuli throughout the body. Specifically, researchers found that chronic pain in one limb in rats increased the aversive response to acute pain stimuli in the opposite limb.

To understand these mechanisms behind this, Wang and colleagues stitched into a certain spot in the DNA of nerve cells in rats the code for a light-sensitive protein. At the same time, the team implanted electrodes in the AAC to measure nerve cell activity. With these elements in place, the team was able to shine light on the ACC, which reacted with the light-sensitive protein to adjust the activity of nerve cells there as rats encountered painful stimuli, judged their intensity, and learned to avoid them.

The researchers found that chronic pain dramatically increases ACC activity, and that artificially increasing AAC activity made the brain region’s response to low intensity pain stimuli larger than normal, such that it “bothered” the rat much more than it should. By the same token, turning down ACC nerve cell signaling returned the aversive behavioral response, which had been amplified by chronic pain, back to normal.

Beyond pain processing, the study results imply that chronic pain can magnify responses to stimuli that are aversive but not painful, like the responses to light that worsen migraines. Furthermore, the ACC is known to be involved in emotional processes and connected to many brain regions. That, combined with the current study results, suggests that chronic anxiety and depression may also amplify the attention and alarm attached to pain stimuli that would otherwise be too small to bother us, researchers say.

In zeroing in on the ACC, the research team has also provided a rational target for technologies like deep brain stimulation and transcranial magnetic stimulation, which deliver electric currents to reverse nerve cell signaling patterns that cause disease, says Wang. He and his colleagues are already working on related protocols designed to dial back the increased ACC activity linked to chronic pain, with clinical testing expected to begin in 2018.

Article: Chronic pain induces generalized enhancement of aversion, Qiaosheng Zhang, Toby Manders, Ai Phuong Tong, Runtao Yang, Arpan Garg, Erik Martinez, Haocheng Zhou, Jahrane Dale, Abhinav Goyal, Louise Urien, Guang Yang, Zhe Chen, Jing Wang, eLife, doi: 10.7554/eLife.25302, published 19 May 2017.