Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.
This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.
Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).
Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.
Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.
Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!
Monday, September 22, 2008
Thursday, September 18, 2008
A New Toy
I bought a new toy the other day: a blood glucose meter. I was curious about my post-meal blood glucose after my HbA1c reading came back higher than I was expecting. A blood glucose meter is the only way to know what your blood sugar is doing in your normal setting.
"Glucose intolerance" is the inability to effectively control blood glucose as it enters the bloodstream from the digestive system. It results in elevated blood sugar after eating carbohydrate, which is not a good thing. In someone with normal glucose tolerance, insulin is secreted in sufficient amounts, and the tissues are sufficiently sensitive to it, that blood glucose is kept within a fairly tight range of concentrations.
Glucose tolerance is typically the first thing to deteriorate in the process leading to type II diabetes. By the time fasting glucose is elevated, glucose intolerance is usually well established. Jenny Ruhl talks about this in her wonderful book Blood Sugar 101. Unfortunately, fasting glucose is the most commonly administered glucose test. That's because the more telling one, the oral glucose tolerance test (OGTT), is more involved and more expensive.
An OGTT involves drinking a concentrated solution of glucose and monitoring blood glucose at one and two hours. Values of >140 mg/dL at one hour and >120 mg/dL at two hours are considered "normal". If you have access to a blood glucose meter, you can give yourself a makeshift OGTT. You eat 60-70 grams of quickly-digesting carbohydrate with no fat to slow down absorption and monitor your glucose.
I gave myself an OGTT tonight. I ate a medium-sized boiled potato and a large slice of white bread, totaling about 60g of carbohydrate. Potatoes and bread digest very quickly, resulting in a blood glucose spike similar to drinking concentrated glucose! You can see that in the graph below. I ate at time zero. By 15 minutes, my blood glucose had reached its peak at 106 mg/dL.
My numbers were 97 mg/dL at one hour, and 80 mg/dL at two hours; far below the cutoff for impaired glucose tolerance. I completely cleared the glucose by an hour and 45 minutes. My maximum value was 106 mg/dL, also quite good. That's despite the fact that I used more carbohydrate for the OGTT than I would typically eat in a sitting. I hope you like the graph; I had to prick my fingers 10 times to make it! I thought it would look good with a lot of data points.
I'm going to have fun with this glucose meter. I've already gotten some valuable information. For example, just as I suspected, fast-digesting carbohydrate is not a problem for someone with a well-functioning pancreas and insulin-sensitive tissues. This is consistent with what we see in the Kitavans, who eat a high-carbohydrate, high glycemic load diet, yet are extremely healthy. Of course, for someone with impaired glucose tolerance (very common in industrial societies), fast-digesting carbohydrates could be the kiss of death. The big question is, what causes the pancreas to deteriorate and the tissues to become insulin resistant? Considering certain non-industrial societies were eating plenty of carbohydrate with no problems, it must be something about the modern lifestyle: industrially processed grains (particularly wheat), industrial vegetable oils, refined sugar, lack of fat-soluble vitamins, toxic pollutants and inactivity come to mind. One could make a case for any of those factors contributing to the problem.
"Glucose intolerance" is the inability to effectively control blood glucose as it enters the bloodstream from the digestive system. It results in elevated blood sugar after eating carbohydrate, which is not a good thing. In someone with normal glucose tolerance, insulin is secreted in sufficient amounts, and the tissues are sufficiently sensitive to it, that blood glucose is kept within a fairly tight range of concentrations.
Glucose tolerance is typically the first thing to deteriorate in the process leading to type II diabetes. By the time fasting glucose is elevated, glucose intolerance is usually well established. Jenny Ruhl talks about this in her wonderful book Blood Sugar 101. Unfortunately, fasting glucose is the most commonly administered glucose test. That's because the more telling one, the oral glucose tolerance test (OGTT), is more involved and more expensive.
An OGTT involves drinking a concentrated solution of glucose and monitoring blood glucose at one and two hours. Values of >140 mg/dL at one hour and >120 mg/dL at two hours are considered "normal". If you have access to a blood glucose meter, you can give yourself a makeshift OGTT. You eat 60-70 grams of quickly-digesting carbohydrate with no fat to slow down absorption and monitor your glucose.
I gave myself an OGTT tonight. I ate a medium-sized boiled potato and a large slice of white bread, totaling about 60g of carbohydrate. Potatoes and bread digest very quickly, resulting in a blood glucose spike similar to drinking concentrated glucose! You can see that in the graph below. I ate at time zero. By 15 minutes, my blood glucose had reached its peak at 106 mg/dL.
My numbers were 97 mg/dL at one hour, and 80 mg/dL at two hours; far below the cutoff for impaired glucose tolerance. I completely cleared the glucose by an hour and 45 minutes. My maximum value was 106 mg/dL, also quite good. That's despite the fact that I used more carbohydrate for the OGTT than I would typically eat in a sitting. I hope you like the graph; I had to prick my fingers 10 times to make it! I thought it would look good with a lot of data points.
I'm going to have fun with this glucose meter. I've already gotten some valuable information. For example, just as I suspected, fast-digesting carbohydrate is not a problem for someone with a well-functioning pancreas and insulin-sensitive tissues. This is consistent with what we see in the Kitavans, who eat a high-carbohydrate, high glycemic load diet, yet are extremely healthy. Of course, for someone with impaired glucose tolerance (very common in industrial societies), fast-digesting carbohydrates could be the kiss of death. The big question is, what causes the pancreas to deteriorate and the tissues to become insulin resistant? Considering certain non-industrial societies were eating plenty of carbohydrate with no problems, it must be something about the modern lifestyle: industrially processed grains (particularly wheat), industrial vegetable oils, refined sugar, lack of fat-soluble vitamins, toxic pollutants and inactivity come to mind. One could make a case for any of those factors contributing to the problem.
Monday, September 8, 2008
A Practical Approach to Omega Fats
Hunter-gatherers and healthy non-industrial cultures didn't know what omega-6 and omega-3 fats were. They didn't balance nutrients precisely; they stayed healthy by eating foods that they knew were available and nourishing. Therefore, I don't think it's necessary to bean count omega fats, and I don't think there's likely to be a single ideal ratio of n-6 to n-3. However, I do think there's evidence for an optimal range. To find out what it is, let's look at what's been done by healthy cultures in the past:
I think there's a simple way to interpret all this. Number one, don't eat vegetable oils high in n-6 fats. They are mostly industrial creations that have never supported human health. Number two, find a source of n-3 fats that can approximately balance your n-6 intake. In practical terms, this means minimizing sources of n-6 and eating modest amounts of n-3 to balance it. Some foods are naturally balanced, such as grass-fed dairy and pastured lamb. Others, like coconut oil, have so little n-6 it doesn't take much n-3 to create a proper balance.
Animal sources of n-3 are the best because they provide pre-formed long-chain fats like DHA, which some people have difficulty producing themselves. Flax oil may have some benefits as well. Fish oil and cod liver oil can be a convenient source of n-3; take them in doses of one teaspoon or less. As usual, whole foods are probably better than isolated oils. Weston Price noted that cultures throughout the world went to great lengths to obtain fresh and dried marine foods. Choose shellfish and wild fish that are low on the food chain so they aren't excessively polluted.
I don't think adding gobs of fish oil on top of the standard American diet to correct a poor n-6:n-3 ratio is optimal. It may be better than no fish oil, but it's probably not the best approach. I just read a study, hot off the presses, that examines this very issue in young pigs. Pigs are similar to humans in many ways, including aspects of their fat metabolism. They were fed three diets: a "deficient" diet containing some n-6 but very little n-3; a "contemporary" diet containing a lot of n-6 and some n-3; an "evolutionary" diet containing a modest, balanced amount of n-6 and n-3; and a "supplemented" diet, which is the contemporary diet plus DHA and arachidonic acid (AA).
Using the evolutionary diet as a benchmark, none of the other diets were able to achieve the same fatty acid profile in the young pigs' brains, blood, liver or heart. They also showed that neurons in culture require DHA for proper development, and excess n-6 interferes with the process.
With that said, here are a few graphs of the proportion of n-6 in common foods. These numbers all come from nutrition data. They reflect the percentage n-6 out of the total fat content. First, animal fats:
.png)
Except salmon oil, these are traditional fats suitable for cooking. Except schmaltz (chicken fat), they are relatively low in n-6. Next, vegetable oils:
.png)
These range from very low in n-6 to very high. Most of the modern, industrially processed oils are on the right, while most traditional oils are on the left. I don't recommend using anything to the right of olive oil on a regular basis. "HO" sunflower oil is high-oleic, which means it has been bred for a high monounsaturated fat content at the expense of n-6. Here are the meats and eggs:
.png)
n-3 eggs are from hens fed flax or seaweed, while the other bar refers to conventional eggs.
A few of these foods are good sources of n-3. At the top of the list is fish oil, followed by n-3 eggs, grass-fed butter, and the fat of grass-fed ruminants. It is possible to keep a good balance without seafood, it just requires keeping n-6 fats to an absolute minimum. It's also possible to overdo n-3 fats. The traditional Inuit, despite their good overall health, did not clot well. They commonly developed nosebleeds that would last for three days, for example. This is thought to be due to the effect of n-3 on blood clotting. But keep in mind that their n-3 intake was so high it would be difficult to achieve today without drinking wine glasses full of fish oil.
- Hunter-gatherers living mostly on land animals: 2:1 to 4:1
- Pacific islanders getting most of their fat from coconut and fish: 1:2
- Inuit and other Pacific coast Americans: 1:4 or less
- Dairy-based cultures: 1:1 to 2:1
- Cultures eating fish and grains: 1:2 or less
I think there's a simple way to interpret all this. Number one, don't eat vegetable oils high in n-6 fats. They are mostly industrial creations that have never supported human health. Number two, find a source of n-3 fats that can approximately balance your n-6 intake. In practical terms, this means minimizing sources of n-6 and eating modest amounts of n-3 to balance it. Some foods are naturally balanced, such as grass-fed dairy and pastured lamb. Others, like coconut oil, have so little n-6 it doesn't take much n-3 to create a proper balance.
Animal sources of n-3 are the best because they provide pre-formed long-chain fats like DHA, which some people have difficulty producing themselves. Flax oil may have some benefits as well. Fish oil and cod liver oil can be a convenient source of n-3; take them in doses of one teaspoon or less. As usual, whole foods are probably better than isolated oils. Weston Price noted that cultures throughout the world went to great lengths to obtain fresh and dried marine foods. Choose shellfish and wild fish that are low on the food chain so they aren't excessively polluted.
I don't think adding gobs of fish oil on top of the standard American diet to correct a poor n-6:n-3 ratio is optimal. It may be better than no fish oil, but it's probably not the best approach. I just read a study, hot off the presses, that examines this very issue in young pigs. Pigs are similar to humans in many ways, including aspects of their fat metabolism. They were fed three diets: a "deficient" diet containing some n-6 but very little n-3; a "contemporary" diet containing a lot of n-6 and some n-3; an "evolutionary" diet containing a modest, balanced amount of n-6 and n-3; and a "supplemented" diet, which is the contemporary diet plus DHA and arachidonic acid (AA).
Using the evolutionary diet as a benchmark, none of the other diets were able to achieve the same fatty acid profile in the young pigs' brains, blood, liver or heart. They also showed that neurons in culture require DHA for proper development, and excess n-6 interferes with the process.
With that said, here are a few graphs of the proportion of n-6 in common foods. These numbers all come from nutrition data. They reflect the percentage n-6 out of the total fat content. First, animal fats:
.png)
Except salmon oil, these are traditional fats suitable for cooking. Except schmaltz (chicken fat), they are relatively low in n-6. Next, vegetable oils:.png)
These range from very low in n-6 to very high. Most of the modern, industrially processed oils are on the right, while most traditional oils are on the left. I don't recommend using anything to the right of olive oil on a regular basis. "HO" sunflower oil is high-oleic, which means it has been bred for a high monounsaturated fat content at the expense of n-6. Here are the meats and eggs:.png)
n-3 eggs are from hens fed flax or seaweed, while the other bar refers to conventional eggs. A few of these foods are good sources of n-3. At the top of the list is fish oil, followed by n-3 eggs, grass-fed butter, and the fat of grass-fed ruminants. It is possible to keep a good balance without seafood, it just requires keeping n-6 fats to an absolute minimum. It's also possible to overdo n-3 fats. The traditional Inuit, despite their good overall health, did not clot well. They commonly developed nosebleeds that would last for three days, for example. This is thought to be due to the effect of n-3 on blood clotting. But keep in mind that their n-3 intake was so high it would be difficult to achieve today without drinking wine glasses full of fish oil.
President’s Blog: My Personal Business Commitments
By Rik Ganderton - President & CEO
My Personal Business Commitments (PBCs) are available here.
I am sharing my PBCs as part of my accountability to the organization. These are the major things that we as an organization have set for ourselves to do this year. They have been developed directly from the Strategic Plan on-a-Page, which set our strategic direction and is posted on our public website and internal Intranet.
As a reminder, you'll recall we've said we intend "to be the best at what we do" and that:
- We will work as a team;
- Live our values every day;
- Relentlessly focus on quality in a health workplace;
- Maintain and strengthen core services and enhance centres of excellence;
- Deliver services within the context of the Central East Local Health Integration Network, Integrated Health Service Plan and Clinical Services Plan; and
- Live within our resources.
My Personal Business Commitments have been approved by our Board of Directors. By sharing these PBCs, we at Rouge Valley are cutting a new path that you are all a big part of.
Open communications has been a key of that path since I had the pleasure of joining the Rouge team in 2007.
I’m publishing my PBCs to help provide greater clarity for us all and to help each of us understand how our varied roles contribute to achieving our strategy at Rouge Valley. By focusing on achievement of these goals we will ensure that the day to day "noise," that we all face, will not distract us from our major objectives.
I want our vice-presidents, chiefs and all physicians, directors, managers and all staff and volunteers to see the very tangible targets the Board and I have set for me and for Rouge Valley itself.
PBCs have also been set by our senior team and are being cascaded throughout the leadership organization so that we are all aligned on our goals. The management team will be sharing their PBCs with their teams. The senior team has shared their individual goals with each other so that there is clarity and understanding between us.
By publishing my PBCs, and later those of our entire management team, all staff and physicians with be better able to work toward our common vision to be the best acute care community hospital.
We will continue to work as a team, at every level of Rouge Valley, to provide the best health care experience for our patients and their families.
PBCs are the tool we will use to provide clarity to the direction we have set our selves and how we will achieve and measure our success on that journey. They also make the links across management and staff, physicians, departments, campuses and disciplines.
The development of PBC's will become and annual exercise for the whole management team so that we have clear alignment of our actions to achieve our strategic intent of being "the best at what we do."
Please feel free to email me (rganderton@rougevalley.ca) any questions or thoughts you have about my PBCs.
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