Wednesday, September 24, 2008
Refresher Course: 5 Day Pouch Test Soups
We get a lot of questions about the soups for the 5 Day Pouch Test. Here is an explanation directly from our forthcoming book: The 5 Day Pouch Test Owner's Manual. Many who have done the 5DPT and used the soups swear by them. Another question that I get frequently is, "Can I have the soups when I'm not doing the 5DPT?" The answer is a big resounding YES!Link to the Soup RecipesSoup
Tuesday, September 23, 2008
It's all happening in the Neighborhood
Autumn has arrived in the Northern Hemi and for me that means cool morning walks, beautiful colors as the leaves change and late-night tea in front of the fireplace. How are things in your neck of the woods? Our little calico, KeepHerKitty, is quite interested in the big round pumpkins just waiting to be carved.In the LivingAfterWLS Neighborhood the weather is always just right for over-the-fence
Agave Syrup
Anna brought up agave syrup in a comment on the last post, so I thought I'd put up a little mini-post so everyone can benefit from what she pointed out.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
My Dad is really really really REALLY ill.
Dunno where to start, but I guess the beginning. Here goes.
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
- Evening - pain in side and shoulder
- Night - could not sleep, excruciating pain
- Evening - A&E dept. given morphine to help pain. temperature, low BP, high pulse/heart rate obvious signs of infection as his body was in shock. Wound opened and blood & puss pour out and even spray my mother in the face!
- Night - wound stitches removed and scar opened up. A large amount of puss, blood and faeces removed from abdominal cavity through site of old stoma
- Night - Brought back from surgery straight to Intensive Care Unit (ICU) at approx 7pm. Completely our for the count on Life Support machine with respirator and 14 automatic drug administrators and untold monitors.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Monday, September 22, 2008
How to Fatten Your Liver
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!
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!
Friday, September 19, 2008
20gram Protein Drink! Refreshing!
Hello Neighbors!Will we ever get tired of talking about protein drinks?I have a new cocktail that is really tasty! And it is non-dairy. One reason I don't care much for most protein drinks is the texture of dairy and the digestive upset I get from dairy based food. Yesterday I came across Kellogg's "SpecialK2O Protein Water" that promises to take the edge off hunger. I purchased a 4-pack of
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 pump glucose into the tissues 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.
The bottom line is that my glucose control seems good, so I don't know why my HbA1c is on the high side. Maybe I have a slow rate of erythrocyte turnover?
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 pump glucose into the tissues 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.
The bottom line is that my glucose control seems good, so I don't know why my HbA1c is on the high side. Maybe I have a slow rate of erythrocyte turnover?
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.
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