Chiropractic + Naturopathic Doctor • December 2017 • Take 5

Health spending in Canada is expected to reach $6,604 per capita this year – or about $200 more per person compared to last year – according to a report released in November by the Canadian Institute for Health Information.

The report forecasts total health spending for the year to increase almost four per cent to $242 billion and equal 11.5 per cent of Canada’s gross domestic product, similar to last year.

The Institute said the growth rate is slightly higher than the annual average of 3.2 per cent that has been recorded since 2010.

The report said total health spending per person is expected to vary across the country, from $7,378 in Newfoundland and Labrador and $7,329 in Alberta to $6,367 in Ontario and $6,321 in British Columbia.

Hospitals, at 28.3 per cent, are expected to eat up the largest share of health dollars in 2017 – as they have since 1997 – followed by drugs at 16.4 per cent and physician services at 15.4 per cent.

Drug spending is expected to grow the fastest, reaching an estimated 5.2 per cent this year.

Physician spending growth is forecast to grow 4.4 per cent and spending on hospitals is estimated to grow by 2.9 per cent.

When compared to other countries, the Institute’s report said Canada’s health spending per person in 2015 was $5,681, similar to health spending in France Australia and the United Kingdom.

VICTORIA – British Columbia’s government has announced an expert task force to advise the province on how to eliminate medical premiums within four years.

The task force will be chaired by a University of Victoria professor who is an expert in applied economic research and policy analysis.

Paul Ramsey, a former NDP cabinet minister for health, environment and education, has also been appointed to the task force along with a law professor from the University of British Columbia.

The province’s Finance Minister Carole James said in a news release that Medical Services Plan premiums are unfair and place a significant burden on families.

The NDP already announced in its budget plans last fall that it aims to cut premiums by 50 per cent as of Jan. 1, 2018 which would annually save individuals up to $450 and families up to $900.

The task force is expected to deliver a final report to the government by March 31.

2018 is the year recreational marijuana will be legalized in Canada. Here are some interesting stats on pot.

BIRMINGHAM, Ala. – 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 it, 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.

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.

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 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, 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, 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 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 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 (CREB).

In turn, CREB activation increased autophagy – 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 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 systems supported the vital role for potassium to regulate vascular calcification through calcium signaling, CREB and autophagy.

A new Canadian study suggests teenage athletes who sustain concussions may still experience brain changes even after being cleared to return to play.

Researchers at Western University’s Schulich School of Medicine examined 17 bantam hockey players aged 11 to 14 who suffered concussions while playing. They studied MRIs the players received 24 to 72 hours after they were concussed, and then another set of MRIs three months later.

At the time of the second brain scans, the athletes showed no outward concussion symptoms and all had been cleared using the standardized return-to-play protocol. However, the researchers found the most-recent brain scans showed changes were still occurring in the athletes’ brains.

The changes related to damage to the brain’s white matter, the wiring that connects different parts of the brain.

“The minute you have that damage, that affects co-ordination between the different brain areas, it makes things like your balance or your vision or even some of your thought processes get disrupted,” said Dr. Ravi Menon, a biophysics professor who co-authored the study. That these changes continued to occur even after the young athletes were cleared to return to the game raises questions about the existing testing protocol, he said.

“We need more sensitive tests, because it’s unlikely that we’re going to give everyone an MRI on a routine basis.”

Dr. Lisa Fischer, who helped develop the post-concussive rehabilitation practice at Western’s Sports Medicine Clinic, said concussions are difficult to diagnose and treat because they are “truly a subjective injury.” Fischer hopes to participate in further research, with the eventual goal of developing an improved way to identify concussions.

The study also suggests that even months after suffering a concussion, young hockey players could be susceptible to second impact syndrome. Second impact syndrome is rare, but Fischer said it can cause permanent damage or even death.

There’s no conclusive proof identifying these brain abnormalities as a risk factor for second impact syndrome, and Fischer said she would urge parents not to panic and pull their kids out of sports.

“I don’t know that it’s worrying right now. I think it’s something that really needs more investigation,” she says.

Still, Menon says there’s no harm in being cautious and increasing recovery times for young athletes.