The facts on our improved Mental Health model

By Rik Ganderton
President and CEO

Our improved model for mental health care at Rouge Valley Health System has received much media coverage.
But lost or buried is the fact that the new model will improve mental health care by –
• Increasing expert mental health crisis intervention services from 12 hours (8 on weekends) to 16 hours a day, seven days a week at the Ajax and Pickering Campus.
• Maintaining our outpatient services at Ajax and Pickering Campus. Outpatient Mental Health Care serves the vast majority of mental health patients
• Continuing access to all mental health services, including emergencies, through our Ajax and Pickering Campus
• Consolidating specialized Mental Health Nursing expertise for inpatient care so that more hours of nursing care will be provided to those patients who require treatment on an in-patient basis.
• Adding a further eight beds to General Medicine at the Ajax and Pickering Campus to improve patient flow and reduce wait times in our Emergency Department.
We are also exploring alternate patient care uses for the space that will be vacated in the Ajax and Pickering Campus. Among the alternate uses is the possible addition of more medical beds at our Ajax and Pickering Campus to further reduce Emergency Department Wait Times. These would require additional funding which we are discussing with the LHIN.

THE NEXT THREE YEARS
Furthermore, there has also been a considerable amount of misrepresentation by some parties as to the number and nature of jobs we must eliminate over the next three years. The facts are –
• 220 positions will go over three years: 60 at the Ajax and Pickering Campus; and 160 at the Centenary Campus.
• Of the 60 jobs at Ajax and Pickering Campus, 36 are Mental Health staff who will be re-employed at Centenary Campus; in other words they are not losing their jobs.
• Of the total positions being eliminated over the next 3 years, 72 are nursing. However, the nurses currently filling those positions will have the opportunity to move into newly funded positions such as those required for the expansion of the specialized Neonatal Intensive Care Unit (14) and the Ajax and Pickering Campus (60) as well as the other options described below.
It is our strongly held belief that almost no person will have to leave RVHS involuntarily. Our normal staff turnover rate is about five per cent a year, which represents 150 positions a year. In addition we will –
• Fill vacancies in areas not being restructured.
• Provide early retirement and voluntary exit packages in accordance with our collective agreements, which cover more than 90% of our staff.
• Provide retraining to support redeployment.
• Fill new positions created by our expansion projects.
Our three-year plan represents changes for the better. Rouge Valley will be a top performer in the healthcare system. We will deploy staff at similar levels to our best performing peers. We will improve the quality of care we deliver and reduce wait times in our Emergency Departments. We will live within the money provided to us.
We know we can do this because we have compared ourselves against other Ontario hospitals. We have seen how they treat patients more quickly, with better service quality and lower resource use than Rouge Valley. As we do this we will continue to grow our services in conjunction with the directions of the Central East Local Health Integration Network.

More Liver

It's time to celebrate your liver. It's a hard-working organ and it deserves some credit.

One of the liver's most important overall functions is maintaining nutrient homeostasis. It controls the blood level of a number of macro- and micronutrients, and attempts to keep them all at optimal levels.

Here's a list of some of the liver's functions I'm aware of:

• Buffers blood glucose by taking it up or releasing it when needed
• A major storage site for glycogen (a glucose polymer)
  
• Clears insulin from the blood
• Synthesizes triglycerides
• Secretes and absorbs lipoprotein particles ("cholesterol")
• Stores important vitamins: B12, folate, A, D, E, K (that's why it's so nutritious to eat!)
• Stores minerals: copper and iron
  
• Detoxifies the blood
• Produces ketone bodies when glucose is running low
• Secretes blood proteins
• Secretes bile
• Converts thyroid hormones
• Converts vitamin D (D3 --> 25(OH)D3)
  

The liver is an all-purpose metabolic powerhouse and storage depot. In the next post, I'll give you a recipe for it...

The Liver: Your Metabolic Gatekeeper

As I've been learning more about the different blood markers of metabolic dysfunction, something suddenly occurred to me. Most of them reflect liver function! Elevated fasting glucose, low HDL cholesterol, high LDL cholesterol, high triglycerides and high fasting insulin all reflect (at least in part) liver function. The liver is the "Grand Central Station" of cholesterol and fatty acid metabolism, to quote Philip A. Wood from How Fat Works. It's also critical for insulin and glucose control, as I'll explain shortly. When we look at our blood lipid profile, fasting glucose, or insulin, what we're seeing is largely a snapshot of our liver function. Does no one talk about this or am I just late to the party here?!

I read a paper today from the lab of C. Ronald Kahn that really drove home the point. They created a liver-specific insulin receptor knockout (LIRKO) mouse, which is a model of severe insulin resistance in the liver. The mouse ends up developing severe whole-body insulin resistance, dramatically elevated post-meal insulin levels (20-fold!), impaired glucose tolerance, and elevated post-meal and fasting glucose. Keep in mind that this all resulted from nothing more than an insulin resistant liver.

LIRKO mice had elevated post-meal blood glucose due to the liver's unresponsiveness to insulin's command to take up sugar. Apparently the liver can dispose of one third of the glucose from a meal, turning it into glycogen and triglycerides. The elevated fasting glucose was caused by insulin not suppressing gluconeogenesis (glucose synthesis) by the liver. In other words, the liver has no way to know that there's already enough glucose in the blood so it keeps on pumping it out. This is highly relevant to diabetics because fasting hyperglycemia comes mostly from increased glucose output by the liver. This can be due to liver insulin resistance or insufficient insulin production by the pancreas.

One of the interesting things about LIRKO mice is their dramatically elevated insulin level. Their pancreases are enlarged and swollen with insulin. It's as if the pancreas is screaming at the body to pick up the slack and take up the post-meal glucose the liver isn't disposing of. The elevated insulin isn't just due to increased output by the pancreas, however. It's also due to decreased disposal by the liver. According to the paper, the liver is responsible for 75% of insulin clearance from the blood in mice. The hyperinsulinemia they observed was both due to increased secretion and decreased clearance. Interestingly, they noted no decline in beta cell (the cells that secrete insulin) function even under such a high load.

Something that's interesting to note about these mice is they have very low blood triglyceride. It makes sense since insulin is what tells the liver to produce it. Could this have something to do with their lack of beta cell dysfunction?

The really strange thing about LIRKO mice is that their blood glucose becomes more normal with age. Strange until you see the reason: their livers are degenerating so they can't keep up glucose production!

LIRKO mice reproduce many of the characteristics of type II diabetes, without degenerating completely into beta cell death. So insulin resistance in the liver appears to reproduce some elements of diabetes and the metabolic syndrome, but the full-blown disorders require other tissues as well. As a side note, this group also has a skeletal muscle-specific insulin receptor knockout which is basically normal. Interesting considering muscle tissue seems to be one of the first tissues to become insulin resistant during diabetes onset.

So if you want to end up like your good pal LIRKO, remember to drink high-fructose corn syrup with every meal! You'll have fatty liver and insulin resistance in no time!

I have a lot more to say about the liver, but I'll continue it in another post.

Book Review: Blood Sugar 101

I just finished reading "Blood Sugar 101" by Jenny Ruhl. It's a quick read, and very informative. Ruhl is a diabetic who has taken treatment into her own hands, using the scientific literature and her blood glucose monitor to understand blood sugar control and its relationship to health. The book challenges some commonly held ideas about diabetes, such as the notion that diabetics always deteriorate.

She begins by explaining in detail how blood glucose is controlled by the body. The pancreas releases basal amounts of insulin to make glucose available to tissues between meals. It also releases insulin in response to carbohydrate intake (primarily) in two bursts, phase I and phase II. Phase I is a rapid response that causes tissues to absorb most of the glucose from a meal, and is released in proportion to the amount of carbohydrate in preceding meals. Phase II cleans up what's left.

In a person with a healthy pancreas, insulin secretion will keep blood glucose under about 130 mg/dL even under a heavy carbohydrate load. The implications of this are really interesting. Namely, that blood glucose levels will not be very different between a person who eats little carbohydrate, and one who eats a lot, as long as the latter has a burly pancreas and insulin-sensitive tissues.

Most Americans don't have such good control however, hence the usefulness of low-carbohydrate diets. This begs the question of why we lose blood sugar control. Insulin resistance seems like a good candidate, maybe preceded by leptin resistance. As you may have noticed, I'm starting to think the carbohydrate per se is not the primary insult. It's probably something else about the diet or lifestyle that causes carbohydrate insensitivity. Grain lectins are a good candidate in my opinion, as well as inactivity.

Diabetics can have blood glucose up to 500 mg/dL, that remains elevated long after it would have returned to baseline in a healthy person. Ruhl asserts that elevated blood sugar is toxic, and causes not only diabetic complications but perhaps also cancer and heart disease.

Heart attack incidence is strongly associated with A1C level, which is a rough measure of average blood sugar over the past couple of months. It makes sense, although most of the data she cites is correlative. They might have seen the same relationship if they had compared heart attack risk to fasting insulin level or insulin resistance. It's difficult to nail down blood sugar as the causative agent. More information from animal studies would have been helpful.

Probably the most important thing I took from the book is that the first thing to deteriorate is glucose tolerance, or the ability to pack post-meal glucose into the tissues. It's often a result of insulin resistance, although autoimmune processes seem to be a factor for some people. Doctors often use fasting glucose to diagnose diabetes and pre-diabetes, but typically you are far gone by the time your fasting glucose is elevated!

I like that she advocates a low-carbohydrate diet for diabetics, and lambasts the ADA for its continued support of high-carbohydrate diets.

Overall, a good book. I recommend it!

Scientist Discovers that Only Pills can Control Hypertension

I went to a presentation today by a prominent hypertension researcher. His talk began with a slide that had two pictures side-by-side: one of the late fitness advocate Jim Fixx, and the other of Winston Churchill. Fixx was a marathon runner, while Churchill was inactive, overweight and had a famous appetite. Fixx died of a sudden heart attack at 52, while Churchill lived to 90. The presenter went on to state that this is an example of how genes control CVD risk, implying that despite Fixx's exercise, his genes had condemned him to an early death.

I wanted to jump up and yell "I think you're leaving out the alternate hypothesis: running marathons and eating junk food isn't healthy!" But instead I suffered quietly through what ended up being an inane yet informative presentation.

His lab looks for gene variations that affect blood pressure (BP). There's a huge amount of money and research going into this. His lab and others have come up with two classes of mutations:

• Common allele variants that have an insignificant but measurable effect on blood pressure.
• Rare genetic mutations that have a significant effect on BP. The most common affects 1 in 2,000 people in the US.

Despite truckloads of funding and research, they have yet to uncover any gene or combination of genes that accounts for even a fraction of hypertension in Americans. So what's the next step? Keep looking for genes.

There is certainly a genetic component to hypertension, but it is only expressed in an unhealthy environment.  Hypertension is tightly linked to lifestyle. It's a quintessential aspect of the "disease of civilization". It's highly responsive to carbohydrate restriction, as a number of clinical trials have shown. Remember the Kuna? They don't get hypertension when they live a non-industrial lifestyle (despite eating more salt than the average American), but as soon as they move to the city their hearts explode. It's been demonstrated in a number of other similar cases as well. Genetics are clearly not responsible.

Don't get me wrong, I do think genetics can modify a person's response to a poor lifestyle. But when the lifestyle is healthy, the vast majority of these differences fade away. I have a more thorough discussion of this point here.

If you give just the right dose of poison to a group of animals, 50% will die and 50% will survive (called the EC50 dose). You might then conclude that genetics had determined who lived and died. You wouldn't be wrong, but you'd be missing the point that what killed them was the poison.

The thing that really bothers me about this thinking is it's disempowering. The presenter suggested that the reason for the difference between Fixx and Churchill was their genes. If genes have us in such a tight grip, why bother trying to live well? The only logical solution is to pop hypertension pills and eat cake all day.

My guess is that if they had lived a more natural lifestyle, Fixx would have made it to 90 and Churchill would have been fit and lean.

By Rik Ganderton
President and CEO

So much to say. Firstly, my thanks and thanks from our executive team and the Board of Directors to our nurses, security, physicians and all staff involved in handling a significant incident in our Emergency Department at the Centenary campus on April 16.

We placed the Centenary Emergency Department on redirect status following the incident in which a patient seriously injured himself late that morning. Staff and physicians responded immediately to the situation and in handling the redirection of ambulances and emergency patients like the professionals they are.

OUR RECOVERY CONTINUES
We have been busy in healthcare partner and public consultations concerning our improved new model of mental health care delivery.

Much has been reported in the media. For clarity, please reference the information posted on our web site since March 25.
From the consultations, we have been able to better define issues, such as transportation of patients and families, which we will address during the next five months before our improved model of mental health care is put into place.

It’s important that our patients, families and communities—in addition to all of you—know that this model represents better access to our services by:

• Increasing crisis services from 12 to 16 hours a day, seven days a week at both campuses;
• Maintaining our outpatient services, which serves the majority of mental health patients at both campuses;
• Ensuring access to all mental health services, including emergencies, continues at each campus;
• Pooling expertise for inpatient care.
Our Rouge Valley Ajax and Pickering mental health information page has much more detail on this.

More information is available online at www.rougevalley.ca and at www.centraleastlhin.on.ca.

FUNDING
We have received funding from the provincial government as announced on April 13. That funding is not new and will not change our need to become more effective as we move up to the standards of the best community hospitals in Ontario.
We also remain focused on implementing our Deficit Elimination Plan so that we can effectively reduce our $78 million long-term debt and working capital deficit.

You’ve heard me say it many times in our Town Halls, but it’s worth repeating: we know we can perform with the best hospitals in Ontario—a top quartile performer rather than average, or worse. Rouge Valley is striving to be among the best of Ontario community acute care hospitals in both 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.”

Real Food V: Sauerkraut

Sauerkraut is part of a tradition of fermented foods that reaches far into human prehistory. Fermentation is a means of preserving food while also increasing its nutritional value. It increases digestibility and provides us with beneficial bacteria, especially those that produce lactic acid. Raw sauerkraut is a potent digestive aid, probably the reason it's traditionally eaten with heavy food.

Sauerkraut is produced by a process called ‘anaerobic’ fermentation, meaning ‘without oxygen’. It’s very simple to achieve in practice. You simply submerge the cabbage in a brine of its own juices and allow the naturally present bacteria to break down the sugars it contains. The process of ‘lacto-fermentation’ converts the sugars to lactic acid, making it tart. The combination of salt, anaerobic conditions, and acidity makes it very difficult for anything to survive besides the beneficial bacteria, so contamination is rare. If it does become contaminated, your nose will tell you as soon as you taste it.

Store-bought sauerkraut is far inferior to homemade. It's soggy and sterile. Ask a German: unpasteurized kraut is light, crunchy and tart!

My method is inexpensive and requires no special equipment. I've tested it many times and have never been disappointed.

Materials

• Wide-mouth quart canning jars (cheap at your local grocery store)
• Beer bottles with the labels removed, or small jars that fit inside the canning jars
• Three tablespoons of sea salt (NOT iodized table salt-- it's fatal to our bacteria)
• Five pounds of green cabbage

Recipe

1. Chop cabbage thinly. Ideally the slices should be 2 mm or so wide, but it doesn’t matter very much. You can use a food processor, mandolin or knife.
2. Put all the cabbage together in a large bowl and add the salt. If the salt is not very dense (sometimes finely ground sea salt can be fluffy), you can add up to 5 tablespoons total. Mix it around with your hands. Taste some. It should be good and salty.
3. Let the salted cabbage sit in the bowl for 30 minutes or so. It should be starting to get juicy.
4. Pack the cabbage tightly into the canning jars. Leave 2-3 inches at the top of the jar. When you push on the cabbage in the jar, you should be able to get the brine to rise above the cabbage. Try to get rid of air bubbles.
5. Put water into the beer bottles and place them into the canning jars. The weight of the bottles will keep the cabbage under the brine. It’s okay that some of the brine is exposed to the air; the cabbage itself is protected.
6. Let it sit for 2 weeks at room temperature! As the fermentation proceeds, bubbles will form and this will raise the level of the brine. This is normal. You might get some scum on top of the liquid; just check for this and scrape it off every few days. It won’t affect the final product. If the brine drops to the level of the cabbage, add salt water (1 tsp/cup, non-chlorinated water) to bring it back up.
7. Taste it! It should be tart and slightly crunchy, with a fresh lactic acid flavor. If fully fermented, it will keep in the fridge for a long time.

Here are some photos from making sauerruben, which is like sauerkraut but made with turnips:

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.