Ministry Funding

By Rik Ganderton
President and CEO
Rouge Valley Health System

On Sunday, the Ministry of Health and Long-Term Care announced a $667 million funding boost for Ontario hospitals to address new beds, more surgeries and shorter wait times.

While the actual amount for Rouge Valley Health System is still be to announced by the Central East Local Health Integration Network, we are pleased to receive any additional funding and thank the Ministry.

It is important to note that this additional funding does not change our financial challenge. We remain focused on implementing our Deficit Elimination Plan so that we can effectively reduce our $78 million long-term debt and working capital deficit. These additional funds will be a positive first step in getting our financial house in order so that we can better focus on the future healthcare needs of our communities in west Durham and east Toronto.

Our plan is about more than simply reducing our debts and deficit. Rouge Valley is now focusing on performing at higher standards of effectiveness, as other hospitals do. You’ve heard me say it many times in our Town Halls, but it’s worth repeating: we know we can bring ourselves to the benchmarks of the best hospitals in Ontario—a top quartile performer rather than average, or worse. Rather than aiming for the median, or average, Rouge Valley is now striving for top-quartile performance in quality and effectiveness.

Having met many of you during the last year, I know we have the dedicated, high quality staff, physicians and volunteers to achieve this.

Details of our Deficit Elimination Plan are available on the Intranet.

Leptin

I've been puzzled by an interesting question lately. Why is it that certain cultures are able to eat large amounts of carbohydrate and remain healthy, while others suffer from overweight and disease? How do the pre-industrial Kuna and Kitavans maintain their insulin sensitivity while their bodies are being bombarded by an amount of carbohydrate that makes the average American look like a bowling ball?

I read a very interesting post on the Modern Forager yesterday that sent me on a nerd safari through the scientific literature. The paper that inspired the Modern Forager post is a review by Dr. Staffan Lindeberg. In it, he attempts to draw a link between compounds called lectins, found in grains (among other things), and resistance to the hormone leptin. Let's take a step back and go over some background.

One of the most-studied animal models of obesity is called the "Zucker" rat. This rat has a missense mutation in its leptin receptor gene, causing it to be nonfunctional. Leptin is a hormone that signals satiety, or fullness. It's secreted by fat tissue. The more fat tissue an animal has, the more leptin it secretes. Normally, this creates negative feedback that causes it to eat less when fat begins to accumulate, keeping its weight within a narrow range.

Zucker rats secrete leptin just fine, but they lack leptin receptors in their brain. Their blood leptin is high but their brain isn't listening. Thus, the signal to stop eating never gets through and they eat themselves to morbid obesity. Cardiovascular disease and diabetes follow shortly thereafter, unless you remove their visceral fat surgically.

The reason Zucker rats are so interesting is they faithfully reproduce so many features of the disease of civilization in humans. They become obese, hypometabolic, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome. So here's a rat that shows that leptin resistance can cause something that looks a whole heck of a lot like the disease of civilization in humans.

For this model to be relevant to us, we'd expect that humans with metabolic syndrome should be leptin-resistant. Well what do you know, administering leptin to obese people doesn't cause satiety like it does in thin people. Furthermore, elevated leptin predicts the onset of obesity and metabolic syndrome. It also predicts insulin resistance. Yes, you read that right, leptin resistance may come before insulin resistance.

Interestingly enough, the carbohydrate-loving Kitavans don't get elevated leptin like europeans do, and they don't become overweight, develop insulin dysfunction or the metabolic syndrome either. This all suggests that leptin may be the keystone in the whole disease process, but what accounts for the differences in leptin levels between populations?

Hydration: Attempt Only Under Medical Supervision

I've noticed how the word "hydration" has crept into the popular lexicon in the last decade or so. Before that, we were so primitive, we just "drank water". Now you need a PhD just to put a glass to your lips. I'm not sure I'm qualified!

I've been hearing so many people, including health professionals, tell me to drink 8 glasses of water a day for my entire life. In my middle school health class, I was told by my hydrophilic teacher that I should be urinating every hour and my urine should always be clear. For my whole life, I've thought it was nonsense. Yet the message has reached people. Walk around any college campus and you'll see undergrads faithfully carrying around their endocrine-disrupting plastic-water everywhere they go.

You see, our bodies have this very sophisticated mechanism to ensure water homeostasis. It's called thirst. If we need so much water to be healthy, why aren't we thirsty more often?

I skimmed through a paper today in the Journal of the American Society of Nephrology that reviews the evidence for health benefits from drinking more water than your thirst demands. Their conclusion: there's no evidence to suggest it helps anything. Water is just a nice harmless placebo.

The term "hydration" has helped fuel a whole industry to satisfy our need for hydration technology. Gatorade claims it hydrates better than water. It must be the high-fructose corn syrup and yellow #5... And make sure to bring your "hydration pack" when you go on your 20 minute jog; you might get lost and end up in the Kalahari desert!

I actually think the water craze isn't totally harmless. Drinking large amounts of water with a meal interferes with digestion by diluting digestive enzymes and stomach acid. Drinking a tall beer does the same. Wine is better because it tends to be a smaller volume.

As far as I'm concerned, with minor exceptions, the only thing to drink is water. I'll have an occasional glass of wine, beer or whole raw milk, but 99% of what I drink is good old-fashioned dihydrogen oxide.

The only time I drink a large amount of water without being thirsty is if I'm about to do vigorous exercise or spend time outside in hot weather.

Thanks to Snap for the CC photo.

Low-carb Review Article

The other day, I came across this nice review article from the American Journal of Clinical Nutrition. It gives a thorough but accessible overview of the current state of research into carbohydrate-restricted diets, without all the fatophobic mumbo-jumbo. It points out a few "elephants in the room" that the mainstream likes to ignore. First of all, the current approach isn't working:

The persistence of an epidemic of obesity and type 2 diabetes suggests that new nutritional strategies are needed if the epidemic is to be overcome.

They claim that preagricultural diets were low in carbohydrate:

In contrast to current Western diets, the traditional diets of many preagricultural peoples were relatively low in carbohydrate (1, 2). In North America, for example, the traditional diet of many First Nations peoples of Canada before European migration comprised fish, meat, wild plants, and berries. The change in lifestyle of several North American aboriginal populations occurred as recently as the late 1800s, and the numerous ensuing health problems were extensively documented (3-5). Whereas many aspects of lifestyle were altered with modernization, these researchers suspected that the health problems came from the change in nutrition—specifically, the introduction of sugar and flour.

But of course, many of them were very high in carbohydrate, and these cultures seemed in fine health as well.

Carbohydrate reduction leads to a normalization of appetite:

It may also be that the mere lowering of serum insulin concentrations, as is seen with LCDs, may lead to a reduction in appetite. In support of this idea, several studies have found that insulin increases food intake, that foods with high insulin responses are less satiating, and that suppression of insulin with octreotide leads to weight loss (27-29).

I can't believe it; all that fat isn't going to clog my arteries??

Several outpatient diet studies have shown reductions in CVD risk factors after an 8–12-wk LCKD, during weight loss, and during weight maintenance (21, 60-62).

The last paragraph is a zinger:

We emphasize that strategies based on carbohydrate restriction have continued to fulfill their promise in relation to weight loss and that, contrary to early concerns, they have a generally beneficial effect on most markers of CVD, even in the absence of weight loss. In combination with the intuitive and established efficacy in relation to glycemic control in diabetics, some form of LCD may be the preferred choice for weight reduction as well as for general health.