Bananas and avocados — foods that are rich in potassium — may help protect against pathogenic vascular calcification, also known as hardening of the arteries.
University of Alabama at Birmingham (UAB) researchers have shown, for the first time, that reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice. Such arterial stiffness in humans is predictive of heart disease and death from heart disease, and it represents an important health problem for the nation as a whole.
The UAB researchers also found that increased dietary potassium levels lessened vascular calcification and aortic stiffness. Furthermore, they unraveled the molecular mechanism underlying the effects of low or high dietary potassium.
Such knowledge of how vascular smooth muscle cells in the arteries regulate vascular calcification emphasizes the need to consider dietary intake of potassium in the prevention of vascular complications of atherosclerosis. It also provides new targets for potential therapies to prevent or treat atherosclerotic vascular calcification and arterial stiffness.
A UAB team led by Yabing Chen, professor of pathology and a research career scientist at the Birmingham VA Medical Center, explored this mechanism of vascular disease three ways: living mice fed diets that varied in potassium, mouse artery cross-sections studied in culture medium with varying concentrations of potassium, and mouse vascular smooth muscle cells grown in culture medium.
Working from living mice down to molecular events in cells in culture, the UAB researchers determined a causative link between reduced dietary potassium and vascular calcification in atherosclerosis, as well as uncovered the underlying pathogenic mechanisms.
The animal work was carried out in the atherosclerosis-prone mouse model, the apoliprotein E-deficient mice, a standard model that is prone to cardiovascular disease when fed a high-fat diet. Using low, normal or high levels of dietary potassium – 0.3 per cent, 0.7 per cent and 2.1 per cent weight/weight, respectively –the UAB team found that the mice fed a low-potassium diet had a significant increase in vascular calcification. In contrast, the mice fed a high-potassium diet had markedly inhibited vascular calcification. Also, the low-potassium mice had increased stiffness of their aortas, and high-potassium mice had decreased stiffness, as indicated by the arterial stiffness indicator called pulse wave velocity, which is measured by echocardiography in live animals.
The different levels of dietary potassium were mirrored by different blood levels of potassium in the three groups of mice.
When researchers looked at arterial cross-sections in cultures that were exposed to three different concentrations of potassium, based on normal physiological levels of potassium in the blood, they found a direct effect for the potassium on arterial calcification within arterial rings. Arterial rings in low-potassium had markedly enhanced calcification, while high-potassium inhibited aortic calcification.
“The findings have important translational potential,” said Dr. Paul Sanders, professor of nephrology in the UAB Department of Medicine and a co-author, “since they demonstrate the benefit of adequate potassium supplementation on prevention of vascular calcification in atherosclerosis-prone mice, and the adverse effect of low potassium intake.”
In cell culture, low potassium levels in the culture media markedly enhanced calcification of vascular smooth muscle cells. Previous research by several labs including Chen’s group has shown that calcification of vascular smooth muscle cells resembles the differentiation of bone cells, which leads to the transformation of smooth muscle cells into bone-like cells.
So the UAB researchers tested the effect of growing vascular smooth muscle cells in low-potassium cell culture. They found that the low-potassium conditions promoted the expression of several gene markers that are hallmarks of bone cells, but decreased the expression of vascular smooth muscle cell markers, suggesting the transformation of the vascular smooth muscle cells into bone-like cells under low-potassium conditions.
Mechanistically, they found that low-potassium elevated intracellular calcium in the vascular smooth muscle cells, via a potassium transport channel called the inward rectifier potassium channel. This was accompanied by activation of several known downstream mediators, including protein kinase C and the calcium-activated cAMP response element-binding protein, or CREB.
In turn, CREB activation increased autophagy – the intracellular degradation system – in the low-potassium cells. Using autophagy inhibitors, the researchers showed that blocking autophagy blocked calcification. Thus, autophagy plays an important role in mediating calcification of vascular smooth muscle cells induced by the low-potassium condition.
The roles of the CREB activation and autophagy signals were then tested in the mouse artery cross-section and living-mouse models, with low, normal or high levels of potassium in the media or diet. Results in both of those systems supported the vital role for potassium to regulate vascular calcification through calcium signaling, CREB and autophagy.
Besides Chen and Sanders, co-authors of the paper, “Dietary potassium regulates vascular calcification and arterial stiffness,” published in JCI Insight, are Yong Sun, Chang Hyun Byon and Youfeng Yang, UAB Department of Pathology; Wayne E. Bradley, Louis J. Dell’Italia and Anupam Agarwal, UAB Department of Medicine; and Hui Wu, UAB Department of Pediatric Dentistry. Sanders, Agarwal and Chen are also members of the Research Department, Veterans Affairs Birmingham Medical Center.
Motorcyclists in Ontario are three times more likely to be injured in a collision than people in automobiles, 10 times more likely to suffer serious injuries and those injuries will cost more to treat, a new study suggests.
The study from researchers at the University of Toronto, Sunnybrook Health Sciences Centre and the Institute for Clinical Evaluative Science was published in the Canadian Medical Association Journal.
It tracked Ontario adults who went to hospital because of a motorcycle or automobile crash from 2007 through 2013 and calculated the costs of their treatment over a two-year period.
It found treatment of a motorcycle crash’s injuries will cost, on average, nearly twice as much – $5,825 – as those suffered by a person in a car, pegged at $2,995.
“We found that motorcyclists were much more likely to have severe extremity injuries – even mangled extremities or traumatic amputations,” said Dr. Daniel Pincus, an orthopedic resident physician at Sunnybrook who is one of the study’s authors.
The rate of injury was triple for motorcycle crashes compared with automobile crashes – 2,194 injuries a year per 100,000 registered motorcycles as opposed to 718 injuries annually per 100,000 registered automobiles.
“When a crash does happen the result seemed to be more devastating consistently for a motorcyclist,” Pincus said.
The study looked at 26,831 patients injured in motorcycle crashes and 281,826 injured in car crashes, and excluded patients from outside the province.
It found 81 per cent of patients who were in motorcycle crashes were men compared with car crash patients, who were 57 per cent female.
The study’s authors said they hope the higher medical costs associated with motorcycle crash injuries provide incentive to improve motorcycle safety.
“Despite publicly available data indicating that the risk associated with driving a motorcycle is much greater than that associated with driving an automobile, this knowledge has not translated to improvements in motorcycle safety,” the authors said.
The study also pointed to statistics indicating that motorcycles, on average, are driven only a fifth the distance of a car in Ontario and, Pincus said, are much more dangerous than cars on a per-kilometre basis.
Research quoted in the study found that between 2000 and 2010, automobile crash deaths decreased by 55.1 per cent in 19 developed countries, while deaths and injuries in motorcycle crashes remained stable during the same time period.
But Pincus said the motorcycle crash statistics in Ontario “have gotten worse.”
“The number of people dying related to motorcycle crashes in Ontario is worse today than it was in 1997,” he said. “Some of it will never be preventable as motorcycle trauma’s always going to be worse.”
As the holiday season is fast approaching we would like to take this opportunity to thank you for your faith in our commitment to your health and well being.
This year we are again sponsoring a family in our community to help give them a very Merry Christmas. We have put together items needed for each family member on the gift tags on our Christmas tree. Please help us by choosing a tag when you are in the clinic next and dropping off the item to our office by December 15th. Please attach a gift tag to the unwrapped gift so we know who it should go to. You can also help us reach our goal by donating any appropriate non-perishable food items or grocery store gift certificates.
Thank you in advance and wishing you and your good health and happiness!
A large Canadian study has found that contrary to popular belief, a diet that contains a moderate amount of fat is linked to a reduced risk of premature death compared to the much-touted low-fat diet.
The study by researchers at McMaster University in Hamilton also found that eating a high-carbohydrate diet is associated with an increased risk of dying early.
Findings from the Prospective Urban Rural Epidemiology study of more than 135,000 people in 18 countries suggest that dietary guidelines should focus on reducing carbohydrate consumption, rather than fat intake.
Lead author Dr. Mahshid Dehghan says the healthiest diet would be made up of 50 to 55 per cent carbs and 35 per cent total fat, including both saturated and unsaturated fats.
A second McMaster study found that eating three to four servings of fruit, vegetables and legumes per day has a similar benefit in reducing the risk of premature death as eating the currently recommended five-plus servings.
Both studies were presented Tuesday at the European Society of Cardiology Congress in Barcelona and are published in The Lancet.
There is a host of scientific studies linking magnesium to many different health conditions, but reviewing these effects one by one is overwhelming and confusing. Instead, it’s more helpful to look at magnesium’s underlying physiological mechanisms. Understanding what magnesium does fundamentally will let us better understand how insufficient magnesium levels might affect our bodies and our daily lives. Magnesium’s hundreds of roles can be roughly categorized into four basic functions:
Magnesium activates enzymes
We are kept alive by trillions of chemical reactions that occur inside the body. Carbohydrates are broken up and harvested for energy. New tissue is created. Cellular waste products are removed. New strands of DNA are synthesized. This collection of chemical processes is called metabolism. The speed a reaction occurs will depend on factors like temperature, pressure, solubility and concentration of molecules. We use these factors every day. You might notice that sugar dissolves in hot water faster, or refrigerating food will slow the rate of decay. When you make a campfire, a hotter flame will burn wood faster.
Our metabolism needs to occur at a certain rate to keep us alive. but we don’t have the liberty of turning the body into a raging furnace to speed up these reactions, not without causing a lot of damage anyway. That’s where enzymes come in.
Enzymes are bits of protein that catalyze and regulate almost all metabolic reactions. As catalysts, they reduce the energy needed to spark a chemical reaction and speed up reactions. Without enzymes, reactions that would normally take milliseconds to occur might take hours or days. Some enzymes require additional ions or molecules called co factors to function. Without a co factor bound to its structure, an enzyme may float dormant and be unable to catalyze any reactions. Magnesium is a co factor for several important enzymes in the body, like DNA/RNA plymerases used to transcribe new DNA/RNA strands, and guanylate cyclase, used to regulate the movement of minerals across cell membranes.
A 1968 estimate suggested that magnesium was a required co factor for 300 enzymatic reactions. This figure is found in many medical texts and quoted in many scientific papers. Since then, many more enzymes that rely on magnesium have been identified. A search of today’s enzymatic databases reveals over 600 enzymes that magnesium is a co factor for and another 200 enzymes that need magnesium to be activated.
2. Magnesium creates cellular energy
Arguably the most important enzymes that magnesium is a co factor for are the ones that produce cellular energy. These enzymes form a series of pathways (glycolysis, Kreb’s cycle, phosphorylation) that convert organic compounds like glucose sugars into smaller molecules called adenosine triphosphate (ATP). ATP acts as our main unit of cellular energy.
Every one of our hundred trillion cells manufactures ATP to store and shuttle intracellular energy. ATP stores a tremendous amount of potential energy in the bonds of the second and third phosphate groups. When the cell wants to carry out a function like cellular division or transport molecules across the cell membrane, it breaks this bond and releases the energy.
We use a tremendous amount of ATP all the time. The typical adult only stores about 50g of ATP in the body so each ATP molecule is recycled over a thousand times a day. Since cellular pathways are magnesium dependent, we need quite a bit of magnesium on hand to fuel a continuous production of ATP.
3. Magnesium helps to create, repair and protect DNA and proteins
When a protein needs to be created, specific DNA nucleotide sequences are read and copied (transcribed) onto another molecule called RNA. The RNA strand is then moved out of the nucleus where enzyme-like organelles called ribosomes use it as a guide to synthesize chains of amino acids that form the desired protein.
This protein synthesis relies on all sorts of enzymes to work, from helicases that open up the DNA strand to be read, to RNA polymerases that create RNA based on the original DNA sequence, to protein kinases. Magnesium is a co factor for most of these critical enzymes. The ribosome, while not technically an enzyme, is the most important catalyst for stitching together amino acids into proteins. Lots of magnesium is needed to keep this complex riboprotein stable.
Without enough magnesium, protein is impaired. And since protein is used for most of the structural components and nearly all metabolic functions in the body, a lack of proteins can have widespread consequences.
4. Magnesium in the cell membrane regulates concentrations of other minerals
Some of those 3751 proteins dot the surface of our cell membranes and perform a variety of roles, like receiving signals from hormones (signal transduction), enzymatic activity and transporting things across the membrane. In particular, magnesium-dependent proteins are used to facilitate the transport of different minerals into and out of cells, acting as gates for sodium (Na+), potassium (K+), and calcium (Ca+).
Many of these are active transporters, for instance pumping sodium out of cells even though it’s against the concentration gradient.
Imagine a flooding basement. Water naturally flows downhill, so you’ll need a pump to move the water out of the basement, against the flow of gravity. Magnesium-powered ion pumps shunt sodium, against its concentration gradient out of the cell to maintain normal concentrations of sodium and potassium in and out of the cell. Just like the water pump in your basement, the ion pumps in your body are necessary to restore homeostasis and balance.
Source: Fall 2017: Vol 3. No. 2 Nd Notes – Magnesium & Me pgs. 3-5
Did you know that at least half of pregnant women experience back pain? And 10% of those report discomfort severe enough to disrupt their daily routines. The good news is that there are steps you can take to protect your back during pregnancy.
What causes pregnancy-related back pain in the first place?
When pregnant, it’s normal to gain more than 30 pounds. This extra weight places considerable stress on your back, feet, ankles and knees. As your baby grows, your core abdominal muscles become stretched and cannot stabilize your posture as well as they did before.
In the third trimester, levels of a hormone called “relaxin” increase by a factor of ten. Relaxin loosens your joints to allow the pelvis to accommodate the enlarging uterus. These loose joints force the muscles of the back and pelvis to work overtime to keep you upright and balanced, leading to back pain.
Try these tips to help minimize your risk of back pain:
1. Exercise
Exercise can go a long way to increase muscle support for an aching back. A health care practitioner should always be consulted before starting a new exercise regimen. Low impact cardiovascular activities, such as swimming, walking, or stationary cycling can help relieve pain and maintain fitness.
2. Sleep Position
Sleep on your left side to reduce the pressure of your uterus on the large blood vessels in your abdomen, optimizing blood flow to both you and the baby.
3. Pillow Position
Place a pillow between your knees to take pressure off your lower back when sleeping on your side.
4. Support Your Body
With the added weight, support has never been more important. Wear flat, supportive shoes and use a lumbar support pillow in your chair at home or work. If you sit at a computer or desk, walk around for a few minutes each hour.
5. Take Breaks
Take frequent, short breaks with your feet elevated. Adequate rest restores your energy and gives your back a chance to relax.
(Content provided by the Ontario Chiropractic Association)
How to spot – and treat – these troublesome conditions
If the human body were a marionette. the tendons would be its strings. These cord-like structures connect your muscles to your bones, letting you move your body when your muscles contract. In popular parlance, painful tendons are called tendinitis (which is defined as the inflammation of a tendon). However, the most common tendon problem isn’t just cause by inflammation. It’s an overuse injury that involves tissue degeneration and swelling related to water retention, so the preferred clinical term for it is “tendinopathy.”
Near the tendons are your bursae, cushiony, fluid-filled sacs that allow for smoother gliding in the spots where your tendons and other moving parts would otherwise rub against your bones. When a bursa gets inflamed, a condition known as “bursitis,” it can feel similar to tendinopathy, with localized pain and swelling. Tendon troubles usually cause pain only during movement, where bursitis might hurt even at rest.
Anyone can suffer from these conditions, but the risk increases with age. The main cause for both bursitis and tendinopathy is repetitive stress. They could be triggered by poor postural habits, shoveling for hours or clenching your hands around the steering wheel while driving. People who repeat the same movements constantly – musicians, gardeners, golfers – are more at risk. If a job or hobby is contributing to the problem, an occupational therapist could suggest adjustments to your tools, work space or body positioning.
Commonly affected areas include the shoulders, wrists, ankles and knees. Unlike arthritis, tendinopathy and bursitis can usually improve. To speed up the healing process, you should “reduce activity in the affected area to a level that does not overly irritate the tendon,’ says Dr. Seth O’Neill, a physiotherapist affiliated with the Chartered Society of Physiotherapy in the U.K. “However, total rest isn’t ideal because tendons, like muscles, waste when you rest them too much.”
A good rule of thumb: if a particular movement provokes prolonged pain and swelling, cut back on it until the flare-up is tolerable. You can also ice the area regularly for the first few days and take anti-inflammatories such as Aspirin or ibuprofen. If your pain doesn’t subside after a month or so, see a doctor. Longer-lasting tendinopathy or bursitis may call for physical therapy, physical supports (a can, brace or splint) or, in severe cases, surgery.
(Readers Digest: November 2017. Pg. 18 “Health – Tendinopathy or Bursitis?)
A motor vehicle accident can have devastating consequences. Recovering psychologically and physically from the trauma of a car crash can be a difficult process that may take a long time. But it’s not a journey that has to be taken alone, as chiropractors can help a patient as they free themselves from pain and get back to leading an active healthy life.
Dr. Barbara Rodwin is very familiar with the arduous rehab many patients have to go through. An Ottawa based chiropractor who has been practicing for over 20 years now, Dr. Rodwin’s clinic specializes in a biomechanical approach to therapy, looking at the movement and function of the whole body. Her staff includes a registered massage therapist, a naturopath and a kinesiologist in order to provide a variety of perspectives and skill sets in helping patients heal.
Matt Morling would unfortunately need to rely on all of their skills and more. Five years ago, Matt was involved in a severe accident when another driver hit his vehicle head on. This devastating crash took the life of his grandmother and left Matt with fractures to his neck, left femur, ribs and, according to Dr. Rodwin, “the most extensive fractures to both feet I have ever seen.”
Following the accident, Matt was wheelchair bound for over two months, much of it spent in a rigid neck brace. And this was only the beginning of his road to recovery. When Matt went to see Dr. Rodwin, he had limited mobility, at times being in a wheelchair or on crutches due to the pain and difficulty of walking. The specialists at the hospital initially told him he was in danger of permanent paralysis, or at the very least, never being able to properly walk, much less run or engage in athletic activities, for the rest of his life.
“Matt’s treatment involved a number of different therapies and practitioners working in tandem,” said Dr. Rodwin. “I provided active release and other manual therapies, our RMT provided massage therapy, while our kinesiologist helped get Matt back on his feet by analysing his balance and gait with force plate analysis and providing custom orthotics that had to account for a screw that was protruding from his heel.”
Dr. Rodwin also referred Matt to physiotherapists to help provide exercises and stretches to help with his rehabilitation. This inter-professional approach to rehabilitation proved its value when Matt was complaining of pain due to one of his screws. The hospital specialists determined the screws were properly placed but Dr. Rodwin’s assessment found some warning signs. She had Matt sent for further X-rays, which revealed that the screws were sticking into his adductor muscles.
The path to rehabilitation is the road to getting back to doing the things you love to do. “Mobility is so important,” says Dr. Rodwin. “Being able to move and get around pain free is such a psychological boost and can help motivate patients to succeed with the rehab process.”
Today Matt is fully mobile and only comes in to Dr. Rodwin’s clinic around once a month for maintenance purposes. He has hardly any scar tissue present in his joints, his mobility is solid and all of his fractures have healed nicely. An avid golfer, he is back on the golf course playing 18 holes whenever he wants. Best of all, Matt was recently married, and was able to celebrate this once in a lifetime occasion by dancing all night long in the company of his friends and loved ones. “When I heard Matt was able to dance his wedding night away, I got goose bumps,” says Dr. Rodwin. It’s hard to find a more powerful illustration of the impact a dedicated team of healthcare professionals can have on someone’s life.
An illness, an accident, or even just getting older can limit a person’s capacity for exercise. Rest is an essential component of healing, but it also atrophies muscles.
“People who are unable to exercise due to, for example, a recent surgery or illness, lose as much as three percent of their muscle mass per week,” said Dr. Esther Dupont-Versteegden of the University of Kentucky’s College of Health Sciences (CHS). “That doesn’t sound like much, but it can make recovery much more difficult, especially for the elderly.”Dupont-Versteegden and her UK CHS colleague Dr. Tim Butterfield have been testing an inexpensive, non-invasive treatment that appears, in preliminary studies, to aid in the recovery of muscle mass and reduce muscle atrophy: massage.
“Don’t run out and get a massage when you read this,” she laughed. “It might make you feel good, but it won’t turn you into a body builder.”
Proteins are the basic building blocks of all of the body’s tissues, especially muscle. The complicated metabolic process that turns protein into muscle, called protein synthesis, increases muscle cell size, which in turn strengthens muscle fibers. But one of the crucial ingredients for muscle growth is exercise.
“However, there are times and circumstances in which exercise is not possible, because of a severe illness or surgery, for example” Dupont-Versteegden said. “Our research proposes that massage may stave off atrophy, even if you aren’t able to get up and move around. ”
According to Butterfield, it appears that massage mimics the effect of exercise by sending signals to the muscle to begin protein synthesis. But perhaps even more tantalizing: massaging one limb seems to confer benefit to its corresponding muscle on the other side as well.
“We’re not sure why yet, but if we could understand the mechanisms for this crossover effect it could have real healing benefits for patients with wounds to one limb – for example, car accident victims or wounded soldiers,” Butterfield said.
Their initial work is promising enough to garner a five-year, $2.1 million grant from the National Center for Complementary & Integrative Health to further their study in conjunction with Drs. Benjamin Miller and Karyn Hamilton from Colorado State University.
The loss of skeletal muscle mass and the inability to recover from atrophy are major contributors to disability and a major factor in the elderly’s loss of independence, Dupont-Versteegden said.
“If we can identify new, cost-effective ways to reduce disability and improve overall health, that’s an all-around win.”
The Village Chiropractic Clinic consists of a group of knowledgeable, and friendly professionals that have worked as a team to help me obtain and maintain my optimal health goal through chiropractic and massage therapy.
