Selasa, 30 September 2008
Mrs.Dash Baked Chicken Siciliano
Hello Neighbors!I am a big fan of Mrs. Dash seasoning blends because they are no-salt, no-MSG and they are tasty! The Mrs.Dash website has some terrific recipes and ideas for using the seasoning blends to punch-up ordinary meals. This recipe for Baked Chicken Siciliano comes from there and it is quick and delicious. Give it a try! For you 5 Day Pouch Testers this week save it for Day 5 or Day 6
Losing Weight After Age 45
Pamela has lost 13 inches from her waist. She's down to 118 pounds, from a high of 215 in July of 2007. She lost the weight by changing her diet and doing pool exercises. See her inspiring story and two other midlife weight loss stories at the Palm Beach Post.
Senin, 29 September 2008
Acne: Disease of Civilization
I often focus on the bigger facets of the disease of civilization. Things like cardiovascular disease and cancer, which are major killers and the subject of intensive research. But the disease of civilization is a spectrum of disorders that affects the body in countless ways, large and small.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
Acne: Disease of Civilization
I often focus on the bigger facets of the disease of civilization. Things like cardiovascular disease and cancer, which are major killers and the subject of intensive research. But the disease of civilization is a spectrum of disorders that affects the body in countless ways, large and small.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
Not bad
Ok, so I didnt wake up with £millions in the bank or a fine physique... yet anyway.
However, I am feeling * Not Bad *
This morning I went and got DS from Lotse and Csilla's where he had stayed for the weekend so we could do the hospital runs. Being Hungarian they are not too up to speed with the whole English education system of GCSE's, A Levels and NVQ's etc... so I spent an hour or so going over Their daughter Lili's possible education routes, had a coffee and come back home.
When I got home and it was about 12, and took a call from Mum saying that Dad was being moved to a 'normal' ward. I am in two minds about this. Its obviously good news because he is getting much better, but there again, the nurses swan around in their outdoor clothes and the cleanliness leaves a lot to be desired and its where he has picked up the previous 2 infections right? So its a bit of a catch 22.
Anyway, enough about all that rubbish, I am fed up with talking about it.
For lunch today I had home made carrot soup. In it was just carrot and onions and a bit of coriander, salt and pepper. I had 3lbs of carrots to use up, so made a whole cauldron of it last week. I also had a boiled egg with it too.
For a snack this afternoon I had an egg.
This evenings dinner is roast chicken (not for me!) and Broccoli, Romanesco, and cauliflower and potato and gravy. That's it. So I am being good.
I have also booked a fill for Sunday. Go me!
However, I am feeling * Not Bad *
This morning I went and got DS from Lotse and Csilla's where he had stayed for the weekend so we could do the hospital runs. Being Hungarian they are not too up to speed with the whole English education system of GCSE's, A Levels and NVQ's etc... so I spent an hour or so going over Their daughter Lili's possible education routes, had a coffee and come back home.
When I got home and it was about 12, and took a call from Mum saying that Dad was being moved to a 'normal' ward. I am in two minds about this. Its obviously good news because he is getting much better, but there again, the nurses swan around in their outdoor clothes and the cleanliness leaves a lot to be desired and its where he has picked up the previous 2 infections right? So its a bit of a catch 22.
Anyway, enough about all that rubbish, I am fed up with talking about it.
For lunch today I had home made carrot soup. In it was just carrot and onions and a bit of coriander, salt and pepper. I had 3lbs of carrots to use up, so made a whole cauldron of it last week. I also had a boiled egg with it too.
For a snack this afternoon I had an egg.
This evenings dinner is roast chicken (not for me!) and Broccoli, Romanesco, and cauliflower and potato and gravy. That's it. So I am being good.
I have also booked a fill for Sunday. Go me!
Hot Topics in The Neighborhood
Here are a few of our active conversations in the LivingAfterWLS Neighbor - your online safe haven circle of friends who are LIVING after Weight Loss Surgery:Autumn Awareness ChallengeJohnnyBGood Down 100 Pounds!5 Day Pouch Test Book: Coming November 5th!Tell Us Your Nickname at Fun FridayExercise and Accountability ChallengeOn-going Topic: Men and Weight Loss SurgeryTricks for eating out with
25-Years After WLS & the 5 Day Pouch Test
5 Day Pouch Test WebsiteOne of the questions I often receive in emails: "Is it too late for me to do the 5 Day Pouch Test?" and usually it is from someone who is three to five years post-op weight loss surgery. Last week Stardust53 joined the LivingAfterWLS Neighborhood to do the 5DPT and she is 25-years post-op. She successfully completed the five days and here is what she had to say:Last week
Minggu, 28 September 2008
Bonjour my fruities!
I am feeling particularly *random* this evening.
My adoring Daddy has been moved to the High Dependency Unit (HDU). This is in fact good news. Normal visiting hours have returned rather than the "Come any time, day or night, because we just don't know if they are gonna make it" visiting hours of the Intensive Care Unit.
So Mum has moved back home too, after being put up this week by a lovely friend who lived just across the road from the hospital. This means that she can get back to some kind of normality too and do her usual day to day things etc.
Dad is still wildly hallucinating, but apparently is easily pacified. He gets really upset mainly about being sued because Mum had a massive argument with all the nurses and doctors and my brother kicking all the doors in... I stress that this did NOT actually happen, but he thinks it did and is expecting court papers. Mum has to either go along with it or calm him down... whatever she feels best at the time. I guess its a kind of cold turkey. No wonder drug addicts are so messed up man - he's tripping his socks off!
Thanks to all my band buddies who have left messages and posts and stuff. I really cherished those little words of help, thanks so much. It means a lot to me that other people are there if need be.
Onto my weight. Oh man, I am thinking about self mutilation as a last ditch attempt. I have worked out that if I chop my legs off I will weigh about 12 stone. Hmmm might be worth it. This morning I weighed in at a WHOPPING 16 stone 11. That's just terrible. I was 15 stone 7 before I went on holiday in May. I have put on a lot of weight since I had that fill removed, so its obvious to me that I still am not at the right restriction. To be honest, I don't have a lot of restriction right now. I can eat toast, pitta, meat and all kinds of everything that I could not do when I had a bit more fluid in my band.
I am at the tragic point where all this stuff with my Dad happened right on the week where I could have gone back to Harley street and got a top up for free, so if I go at the weekend, I am going to have to pay which makes me feel really crap. I am of course worried that something has gone wrong again simply because of the weight gain, and I am getting to the point where I don't know whether I can carry on or not.
I don't know whether I can continue with this band journey or not, sometimes I genuinely wonder about the blissful life I could have by having all of the fluid removed and just getting on with my life, overweight or not, until I am in a better place. I know that I will return to my normal weight of around 18 stone or something, but right now I just cant handle NOT losing weight, so its like I don't even want to try. If I try to lose weight and fail, then I feel worse than if I didnt bother trying.
It seems like just when I get up that little bit of extra will power, something happens. 2 weeks ago I joined Weightwatchers, and I did it really well all day and then Tuesday rolled around and my Dad was taken into hospital, so for the last 2 weeks I have just wanted to eat . Full stop. Today I got my period too, and am feeling heavy, bloated and in pain. I have spent most of the day in bed with what feels like a cold, but kind of isn't anything productive...yet. Headache, hot and just tired out.
Today's food... 1ltr Orange Juice, 1 500g tub yogurt, bowl of rice pudding and jam, half bar of dairy milk chocolate and a glass of wine. Rubbish.
I want to wake up tomorrow, given that my Dad is on the road to recovery, with renewed energy, serious will power, and motivation to sort my fat out. I feel absolutely horrible. Eating high fat, sugary foods does not make me feel better at all. I don't know what I do it and I want to stop.
If I could wave a magic wand and have one wish granted right now it would be to make me satisfied eating less than 1000cals a day because it will make me a happier person, able to complete my daily duties rather than moping about depressed (apart from £several million in the bank, health and happiness for the universe and that kind of thing...)
With what has happened to my Dad and things that have happened to people I know, the awful things that go on in this world and even some serious other issues in my life that I don't write about here, you would think that I could get some darn perspective, but I can't!!! At the end of the day, this is my life and this is my problem and it doesnt matter what happens to anyone else in the world right now.
To be honest, that is why I havent written much on my blog. Every time I think I want to write in my blog, I end up feeling guilty for writing about such a petty problem (in the eyes of most other people I guess). Lets face it, being fat is seriously petty problem considered with cancer or warfare right? But, at the moment I really need to talk about it. I need to feel rubbish about my weight and mourn my weight gain. Gaining a stone since I had my fill removed has made me feel like someone in my family has died. I MOURN my weight loss. Litteraly. I just dont know how else to put it. I know that makes me look shallow and like I am totally unconsiderate of others, but I need to focus on me and how I feel right now. I am fed up with dealing with other problems or feeling bad about my own insignificant worries when actually to me they are the biggest problems in my life.
If my Mum wrote a blog, then she would have her problems laid out on view. Likewise others would do the same. I know that I should think "Wow, people are dying etc and this is all I have to worry about", but I can't seem to get that perspective. This being fat thing is a huge deal to me, and I feel guilty to some extent banging on about how awful I feel because I am fat. But I guess if I had a long nose, or club feet or a hump back or some other physical flaw, then that would pervade my life in the same way. I would wish to change that. I really can change the fact that I am fat - just by not eating. The equation is simple so why is putting pen to paper and writing the answer so DAMN difficult?
Why is it that when I feel upset about my weight, the one thing I want to do is eat?
Why is it that when I lose weight, the one thing I want to do is eat?
Why is it that when something happens that is terrible, I want to eat?
Why? What makes me this way?
I was trying to figure out why some people have the CAPACITY to eat, and do pig out, but don't get fat. It must be because they are not driven by emotional need. Others have the EMOTIONAL NEED to eat and don't get fat because they don't have the capacity to eat too much of the wrong thing at one time or over and over again. And why do some people have the CAPACITY & EMOTIONAL NEED?
It seems to me that anyone with both these PHYSICAL (capacity) and MENTAL (emotional need) states is Obese.
Lets fact it, we have all seen a scrawny bint completely pigging out at Pizza Hut or (like my brother) eating donuts for breakfast and lunch daily, but not putting on an ounce.
We have all seen a skinny mate crying about a lost boyfriend eating the contents of the fridge and wiping their chocolate covered mouth on the back of their hand.
But seemingly these people never do this ALL THE TIME. My brother, I have noticed will eat cakes for breakfast, have donuts for lunch and go home to a bacon sandwich, but when he gets full, he stops. Dead. He doesn't snack. When he is full he is full. That's it. So when you actually add up the cals he takes in in any one day, it only ever comes to about 2000. He eats NO vegetables, NO fruit, NO full meals. His eating is the most rubbish that I have ever come across, yet he is 6ft 4 and weighs in at 12 stone. Most likely Underweight!
What is this category? He doesn't have the capacity, nor does he have the Emotional Need. He is the category DEVOID, in that he eats to fuel his body only.
So there seems to be 4 categories.
DEVOID, CAPACITY, EMOTIONAL NEED, UNBALANCED
DEVOID - those who do not have the capacity to stuff themselves stupid. Those who do not/rarely have the emotional need to stuff themselves stupid.
CAPACITY - Those who have the capacity to stuff themselves, and do so on occasion. Those who do not have an emotional need to stuff themselves - the absence of which means these people are not heavily overweight.
EMOTIONAL NEED - Those who have an emotional need to overeat, and do so only occasions of that emotional need. Those who do not have the capacity to overeat to the extreme regularly.
UNBALANCED - Those who have both the capacity to overeat and the emotional need to overeat. One drives the other resulting in heavy overweight.
I have a friend who, when its her TOTM, or having a bad week at work, or an argument with her boyf, will go out for coffee and cakes and eat kids sweets and a bottle of wine, box of chocolates and really blow out and then doesn't gain weight because its not a lifestyle thing. Its a once in a blue moon. Normally she wont eat the next day because she is too stuffed from her overindulgence. There is nothing about guilt or anything like that.
Obviously there are fine differences between these groups but as a broad brush stroke, i think everyone could put themselves in one of them to a large degree.
I doubt anyone who has capacity and emotional need to overeat is thin. In fact I double dare them to tell me they are! I think as 'fatties' we are on a perpetual struggle. Its the mixture of physical and mental (dare I say problems) that give us our terrible situation. I thoroughly believe that it is NOT my fault that I am fat. I have a problem, or a syndrome or something. It makes me feel sick when some (usually very thin!!!!) people tell me that I can just sort myself by eating correct portions etc. I wish some serious scientists/doctors would actually try and work out what this is. I seriously think that they are onto something when they make a drug that curbs appetite (the Capacity problem) or a drug that makes us feel better like Prozac (the Emotional problem) but has anyone who has taken these drugs (I have) actually felt their appetite curbed, or better in mind frame enough to not want to eat their cadburys chocolate bar?
I don't think so.
There HAS to be a way to combat the deadly mixture of these two horrible things. For people with both Capacity and Emotional eating problems, its not going to be enough just to fix one or the other. There needs to be a wonder pill that makes us maybe radically NOT LIKE food, or for it to taste bad, whilst also curbing the appetite properly. Now, that is a drug that I would take any day.
Ask someone from the DEVOID category what they like about the dinner they are eating, and they will reply (more or less) "nothing". They don't get pleasure out of eating at all. The people of this category are always slim. Funny that.
Ask the UNBALANCED about what they like about their meal... you might want to get comfortable for some time!
Right now, I know that I am full, but I could SO eat a plate of singapore noodles and sweet and sour sauce! Wow, I need to go to bed before I do myself some more damage.
Being fat for me, truly is a form of self harm by proxy. I have to admit I often eat to punish myself. Oh my God I am a psycho.
My adoring Daddy has been moved to the High Dependency Unit (HDU). This is in fact good news. Normal visiting hours have returned rather than the "Come any time, day or night, because we just don't know if they are gonna make it" visiting hours of the Intensive Care Unit.
So Mum has moved back home too, after being put up this week by a lovely friend who lived just across the road from the hospital. This means that she can get back to some kind of normality too and do her usual day to day things etc.
Dad is still wildly hallucinating, but apparently is easily pacified. He gets really upset mainly about being sued because Mum had a massive argument with all the nurses and doctors and my brother kicking all the doors in... I stress that this did NOT actually happen, but he thinks it did and is expecting court papers. Mum has to either go along with it or calm him down... whatever she feels best at the time. I guess its a kind of cold turkey. No wonder drug addicts are so messed up man - he's tripping his socks off!
Thanks to all my band buddies who have left messages and posts and stuff. I really cherished those little words of help, thanks so much. It means a lot to me that other people are there if need be.
Onto my weight. Oh man, I am thinking about self mutilation as a last ditch attempt. I have worked out that if I chop my legs off I will weigh about 12 stone. Hmmm might be worth it. This morning I weighed in at a WHOPPING 16 stone 11. That's just terrible. I was 15 stone 7 before I went on holiday in May. I have put on a lot of weight since I had that fill removed, so its obvious to me that I still am not at the right restriction. To be honest, I don't have a lot of restriction right now. I can eat toast, pitta, meat and all kinds of everything that I could not do when I had a bit more fluid in my band.
I am at the tragic point where all this stuff with my Dad happened right on the week where I could have gone back to Harley street and got a top up for free, so if I go at the weekend, I am going to have to pay which makes me feel really crap. I am of course worried that something has gone wrong again simply because of the weight gain, and I am getting to the point where I don't know whether I can carry on or not.
I don't know whether I can continue with this band journey or not, sometimes I genuinely wonder about the blissful life I could have by having all of the fluid removed and just getting on with my life, overweight or not, until I am in a better place. I know that I will return to my normal weight of around 18 stone or something, but right now I just cant handle NOT losing weight, so its like I don't even want to try. If I try to lose weight and fail, then I feel worse than if I didnt bother trying.
It seems like just when I get up that little bit of extra will power, something happens. 2 weeks ago I joined Weightwatchers, and I did it really well all day and then Tuesday rolled around and my Dad was taken into hospital, so for the last 2 weeks I have just wanted to eat . Full stop. Today I got my period too, and am feeling heavy, bloated and in pain. I have spent most of the day in bed with what feels like a cold, but kind of isn't anything productive...yet. Headache, hot and just tired out.
Today's food... 1ltr Orange Juice, 1 500g tub yogurt, bowl of rice pudding and jam, half bar of dairy milk chocolate and a glass of wine. Rubbish.
I want to wake up tomorrow, given that my Dad is on the road to recovery, with renewed energy, serious will power, and motivation to sort my fat out. I feel absolutely horrible. Eating high fat, sugary foods does not make me feel better at all. I don't know what I do it and I want to stop.
If I could wave a magic wand and have one wish granted right now it would be to make me satisfied eating less than 1000cals a day because it will make me a happier person, able to complete my daily duties rather than moping about depressed (apart from £several million in the bank, health and happiness for the universe and that kind of thing...)
With what has happened to my Dad and things that have happened to people I know, the awful things that go on in this world and even some serious other issues in my life that I don't write about here, you would think that I could get some darn perspective, but I can't!!! At the end of the day, this is my life and this is my problem and it doesnt matter what happens to anyone else in the world right now.
To be honest, that is why I havent written much on my blog. Every time I think I want to write in my blog, I end up feeling guilty for writing about such a petty problem (in the eyes of most other people I guess). Lets face it, being fat is seriously petty problem considered with cancer or warfare right? But, at the moment I really need to talk about it. I need to feel rubbish about my weight and mourn my weight gain. Gaining a stone since I had my fill removed has made me feel like someone in my family has died. I MOURN my weight loss. Litteraly. I just dont know how else to put it. I know that makes me look shallow and like I am totally unconsiderate of others, but I need to focus on me and how I feel right now. I am fed up with dealing with other problems or feeling bad about my own insignificant worries when actually to me they are the biggest problems in my life.
If my Mum wrote a blog, then she would have her problems laid out on view. Likewise others would do the same. I know that I should think "Wow, people are dying etc and this is all I have to worry about", but I can't seem to get that perspective. This being fat thing is a huge deal to me, and I feel guilty to some extent banging on about how awful I feel because I am fat. But I guess if I had a long nose, or club feet or a hump back or some other physical flaw, then that would pervade my life in the same way. I would wish to change that. I really can change the fact that I am fat - just by not eating. The equation is simple so why is putting pen to paper and writing the answer so DAMN difficult?
Why is it that when I feel upset about my weight, the one thing I want to do is eat?
Why is it that when I lose weight, the one thing I want to do is eat?
Why is it that when something happens that is terrible, I want to eat?
Why? What makes me this way?
I was trying to figure out why some people have the CAPACITY to eat, and do pig out, but don't get fat. It must be because they are not driven by emotional need. Others have the EMOTIONAL NEED to eat and don't get fat because they don't have the capacity to eat too much of the wrong thing at one time or over and over again. And why do some people have the CAPACITY & EMOTIONAL NEED?
It seems to me that anyone with both these PHYSICAL (capacity) and MENTAL (emotional need) states is Obese.
Lets fact it, we have all seen a scrawny bint completely pigging out at Pizza Hut or (like my brother) eating donuts for breakfast and lunch daily, but not putting on an ounce.
We have all seen a skinny mate crying about a lost boyfriend eating the contents of the fridge and wiping their chocolate covered mouth on the back of their hand.
But seemingly these people never do this ALL THE TIME. My brother, I have noticed will eat cakes for breakfast, have donuts for lunch and go home to a bacon sandwich, but when he gets full, he stops. Dead. He doesn't snack. When he is full he is full. That's it. So when you actually add up the cals he takes in in any one day, it only ever comes to about 2000. He eats NO vegetables, NO fruit, NO full meals. His eating is the most rubbish that I have ever come across, yet he is 6ft 4 and weighs in at 12 stone. Most likely Underweight!
What is this category? He doesn't have the capacity, nor does he have the Emotional Need. He is the category DEVOID, in that he eats to fuel his body only.
So there seems to be 4 categories.
DEVOID, CAPACITY, EMOTIONAL NEED, UNBALANCED
DEVOID - those who do not have the capacity to stuff themselves stupid. Those who do not/rarely have the emotional need to stuff themselves stupid.
CAPACITY - Those who have the capacity to stuff themselves, and do so on occasion. Those who do not have an emotional need to stuff themselves - the absence of which means these people are not heavily overweight.
EMOTIONAL NEED - Those who have an emotional need to overeat, and do so only occasions of that emotional need. Those who do not have the capacity to overeat to the extreme regularly.
UNBALANCED - Those who have both the capacity to overeat and the emotional need to overeat. One drives the other resulting in heavy overweight.
I have a friend who, when its her TOTM, or having a bad week at work, or an argument with her boyf, will go out for coffee and cakes and eat kids sweets and a bottle of wine, box of chocolates and really blow out and then doesn't gain weight because its not a lifestyle thing. Its a once in a blue moon. Normally she wont eat the next day because she is too stuffed from her overindulgence. There is nothing about guilt or anything like that.
Obviously there are fine differences between these groups but as a broad brush stroke, i think everyone could put themselves in one of them to a large degree.
I doubt anyone who has capacity and emotional need to overeat is thin. In fact I double dare them to tell me they are! I think as 'fatties' we are on a perpetual struggle. Its the mixture of physical and mental (dare I say problems) that give us our terrible situation. I thoroughly believe that it is NOT my fault that I am fat. I have a problem, or a syndrome or something. It makes me feel sick when some (usually very thin!!!!) people tell me that I can just sort myself by eating correct portions etc. I wish some serious scientists/doctors would actually try and work out what this is. I seriously think that they are onto something when they make a drug that curbs appetite (the Capacity problem) or a drug that makes us feel better like Prozac (the Emotional problem) but has anyone who has taken these drugs (I have) actually felt their appetite curbed, or better in mind frame enough to not want to eat their cadburys chocolate bar?
I don't think so.
There HAS to be a way to combat the deadly mixture of these two horrible things. For people with both Capacity and Emotional eating problems, its not going to be enough just to fix one or the other. There needs to be a wonder pill that makes us maybe radically NOT LIKE food, or for it to taste bad, whilst also curbing the appetite properly. Now, that is a drug that I would take any day.
Ask someone from the DEVOID category what they like about the dinner they are eating, and they will reply (more or less) "nothing". They don't get pleasure out of eating at all. The people of this category are always slim. Funny that.
Ask the UNBALANCED about what they like about their meal... you might want to get comfortable for some time!
Right now, I know that I am full, but I could SO eat a plate of singapore noodles and sweet and sour sauce! Wow, I need to go to bed before I do myself some more damage.
Being fat for me, truly is a form of self harm by proxy. I have to admit I often eat to punish myself. Oh my God I am a psycho.
Kamis, 25 September 2008
Nonalcoholic Fatty Liver Disease
Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.
There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.
What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.
In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.
In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.
There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.
What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.
In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.
In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.
Nonalcoholic Fatty Liver Disease
Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.
There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.
What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.
In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.
In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.
There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.
What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.
In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.
In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.
Rabu, 24 September 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
Selasa, 23 September 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.
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!
Senin, 22 September 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!
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!
Jumat, 19 September 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
Kamis, 18 September 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.
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.
Clean Eating: It Works for Us
Every now and then a new product comes along and I think, "Wow! What a great idea." Well, just this week I held in hand my first copy of the Oxygen publication "Clean Eating" magazine. The subtitle: Improving your life one meal at a time.Finally! A mainstream magazine we can use to support, benefit and enhance our post surgical weight loss surgery way of life.Have you seen it yet?I have in hand
Rabu, 17 September 2008
Men and Weight Loss Surgery: Social Stigma?
We are having an interesting discussion on the Men & Weight Loss Surgery Message Board in the Neighborhood. Our new member ScottL, who is considering surgical weight loss. He presented statistics from the American Obesity Association that indicate men are not necessarily less obese than women, yet a significantly smaller population of men than women have obesity surgery. Scott asks the question
Senin, 15 September 2008
Evolution in Your Face
The debate between proponents of evolution and intelligent design (ID) rages on in certain parts of the US. It mostly centers around which one to emphasize, and whether to teach ID at all.
Here's how science is supposed to work: you get the best possible data, and then you create the most logical interpretation of it. I think all interpretations should be presented, including ID and antique scientific theories, but if we want to call it 'science class' then we shouldn't put on kid gloves for anything. The process of teaching science requires cultivating skepticism and independent thinking, and students should be allowed to come to their own conclusions with the facts in front of them.
What many people don't realize is that the facts point overwhelmingly toward evolution. Many American teachers have been tying their hands with the same wimpy anecdotes for decades. Evolution is not just about the fossil record and a few moths somewhere; it's a dynamic process that's happening around us at all times.
I'm constantly dealing with it in the lab. For example, sometimes by chance I'll create a mutant strain of yeast that grows slowly. I'll streak it out on a petri dish. Five days later, one out of twenty of the colonies growing on that plate will have mutated into faster-growing strains. These mutations are called 'suppressors' because they suppress slow growth. If I then take all the yeast on that plate and put them in liquid medium, by the next day, 99% of the cells will be of the faster-growing variety. The slow ones get left in the dust. That's natural selection.
Another example is antibiotic resistant bacteria. All you need is a selective pressure, in this case an antibiotic, and over time if an organism survives it will rise to the occasion. Bacteria are frighteningly rapid at adapting because there is a huge population of them and they have an extremely short generation time. But the same process applies to all organisms, usually on a longer timescale.
Science teachers should use the full repertoire of evidence supporting evolution, including allowing students to participate in natural selection experiments in yeast and bacteria. I think if students could see evolution, if it became tangible for them, they would realize the debate is a charade. Believe ID if you wish, but don't call it science.
Here's how science is supposed to work: you get the best possible data, and then you create the most logical interpretation of it. I think all interpretations should be presented, including ID and antique scientific theories, but if we want to call it 'science class' then we shouldn't put on kid gloves for anything. The process of teaching science requires cultivating skepticism and independent thinking, and students should be allowed to come to their own conclusions with the facts in front of them.
What many people don't realize is that the facts point overwhelmingly toward evolution. Many American teachers have been tying their hands with the same wimpy anecdotes for decades. Evolution is not just about the fossil record and a few moths somewhere; it's a dynamic process that's happening around us at all times.
I'm constantly dealing with it in the lab. For example, sometimes by chance I'll create a mutant strain of yeast that grows slowly. I'll streak it out on a petri dish. Five days later, one out of twenty of the colonies growing on that plate will have mutated into faster-growing strains. These mutations are called 'suppressors' because they suppress slow growth. If I then take all the yeast on that plate and put them in liquid medium, by the next day, 99% of the cells will be of the faster-growing variety. The slow ones get left in the dust. That's natural selection.
Another example is antibiotic resistant bacteria. All you need is a selective pressure, in this case an antibiotic, and over time if an organism survives it will rise to the occasion. Bacteria are frighteningly rapid at adapting because there is a huge population of them and they have an extremely short generation time. But the same process applies to all organisms, usually on a longer timescale.
Science teachers should use the full repertoire of evidence supporting evolution, including allowing students to participate in natural selection experiments in yeast and bacteria. I think if students could see evolution, if it became tangible for them, they would realize the debate is a charade. Believe ID if you wish, but don't call it science.
Evolution in Your Face
The debate between proponents of evolution and intelligent design (ID) rages on in certain parts of the US. It mostly centers around which one to emphasize, and whether to teach ID at all.
Here's how science is supposed to work: you get the best possible data, and then you create the most logical interpretation of it. I think all interpretations should be presented, including ID and antique scientific theories, but if we want to call it 'science class' then we shouldn't put on kid gloves for anything. The process of teaching science requires cultivating skepticism and independent thinking, and students should be allowed to come to their own conclusions with the facts in front of them.
What many people don't realize is that the facts point overwhelmingly toward evolution. Many American teachers have been tying their hands with the same wimpy anecdotes for decades. Evolution is not just about the fossil record and a few moths somewhere; it's a dynamic process that's happening around us at all times.
I'm constantly dealing with it in the lab. For example, sometimes by chance I'll create a mutant strain of yeast that grows slowly. I'll streak it out on a petri dish. Five days later, one out of twenty of the colonies growing on that plate will have mutated into faster-growing strains. These mutations are called 'suppressors' because they suppress slow growth. If I then take all the yeast on that plate and put them in liquid medium, by the next day, 99% of the cells will be of the faster-growing variety. The slow ones get left in the dust. That's natural selection.
Another example is antibiotic resistant bacteria. All you need is a selective pressure, in this case an antibiotic, and over time if an organism survives it will rise to the occasion. Bacteria are frighteningly rapid at adapting because there is a huge population of them and they have an extremely short generation time. But the same process applies to all organisms, usually on a longer timescale.
Science teachers should use the full repertoire of evidence supporting evolution, including allowing students to participate in natural selection experiments in yeast and bacteria. I think if students could see evolution, if it became tangible for them, they would realize the debate is a charade. Believe ID if you wish, but don't call it science.
Here's how science is supposed to work: you get the best possible data, and then you create the most logical interpretation of it. I think all interpretations should be presented, including ID and antique scientific theories, but if we want to call it 'science class' then we shouldn't put on kid gloves for anything. The process of teaching science requires cultivating skepticism and independent thinking, and students should be allowed to come to their own conclusions with the facts in front of them.
What many people don't realize is that the facts point overwhelmingly toward evolution. Many American teachers have been tying their hands with the same wimpy anecdotes for decades. Evolution is not just about the fossil record and a few moths somewhere; it's a dynamic process that's happening around us at all times.
I'm constantly dealing with it in the lab. For example, sometimes by chance I'll create a mutant strain of yeast that grows slowly. I'll streak it out on a petri dish. Five days later, one out of twenty of the colonies growing on that plate will have mutated into faster-growing strains. These mutations are called 'suppressors' because they suppress slow growth. If I then take all the yeast on that plate and put them in liquid medium, by the next day, 99% of the cells will be of the faster-growing variety. The slow ones get left in the dust. That's natural selection.
Another example is antibiotic resistant bacteria. All you need is a selective pressure, in this case an antibiotic, and over time if an organism survives it will rise to the occasion. Bacteria are frighteningly rapid at adapting because there is a huge population of them and they have an extremely short generation time. But the same process applies to all organisms, usually on a longer timescale.
Science teachers should use the full repertoire of evidence supporting evolution, including allowing students to participate in natural selection experiments in yeast and bacteria. I think if students could see evolution, if it became tangible for them, they would realize the debate is a charade. Believe ID if you wish, but don't call it science.
Minggu, 14 September 2008
After WLS: Not What I Was Expecting
I read and write a lot about weight loss surgery, and more importantly, LIVING after weight loss surgery. Recently I received an email from a disappointed post-surgical weight loss patient. This patient had only lost 10 (ten) pounds. She was discouraged and anxious. And she was 7 (seven) days post surgery ready to give the 5 Day Pouch Test a try since "the surgery did not work for her." How sad
Sabtu, 13 September 2008
9 Years Post Weight Loss Surgery
Hello Neighbors!Today marks nine years since I was gut-whacked; uh, I mean had laporoscopic gastric bypass surgery in San Diego, California. Nine years. You know, some times I do not remember what it was like to be morbidly obese. Then again, most of the time I never forget what being overweight was like.A couple of days ago I bought a new pair of denium jeans: size 8. I was pretty disgusted with
Jumat, 12 September 2008
Inactivity and Weight Gain
Every now and then I read a paper that restores a little bit of my faith in obesity research. Most of the papers I read in the field pay lip-service to the same tired old stories: thrifty genes; calories in, calories out; energy density; fat intake; gluttony and sloth. None of which make sense upon close examination. The "overweight is due to sloth" theory, in its many forms, is one of the most often repeated. The main evidence for it is that overweight people tend to move less than thin people, which seems to be true. Exercise also burns calories, which can come from fat.
It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around? Gary Taubes asked this question in Good Calories, Bad Calories. In other words, isn't it possible that metabolic deregulation could cause both overweight and a reduced activity level? The answer is clearly yes. There are a number of hormones and other factors that influence activity level in animals and humans. For example, the "Zucker fatty" rat, a genetic model of severe leptin resistance, is obese and hypoactive (I wrote about it here). It's actually a remarkable facsimile of the metabolic syndrome. Since leptin resistance typically comes before insulin resistance and predicts the metabolic syndrome, modern humans may be going through a process similar to the Zucker rat.
Back to the paper. Dr. Nicholas Wareham and his group followed 393 healthy white men for 5.6 years. They took baseline measurements of body composition (weight, BMI and waist circumference) and activity level, and then measured the same things after 5.6 years. In a nutshell, here's what they found:
I've pointed out before that the "we're fat because we exercise less" theory is probably incorrect. It's based on assumptions that fall apart on close examination. Exercise is healthy, but it's not the most effective way to achieve or maintain an optimal weight. The body compensates for the calories burned during exercise by a phenomenon known as "hunger". Certain obesity researchers have stubbornly tried to deny this, because it puts a kink in the "calories in, calories out" hypothesis, but anyone who has ever gotten out of their recliner knows it's true. I believe overweight is largely caused by diet composition. If that's the case, then changing diet composition is obviously going to be a more effective treatment than exercise, which doesn't address the root cause of the problem. This idea is supported by numerous diet intervention trials.
It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around? Gary Taubes asked this question in Good Calories, Bad Calories. In other words, isn't it possible that metabolic deregulation could cause both overweight and a reduced activity level? The answer is clearly yes. There are a number of hormones and other factors that influence activity level in animals and humans. For example, the "Zucker fatty" rat, a genetic model of severe leptin resistance, is obese and hypoactive (I wrote about it here). It's actually a remarkable facsimile of the metabolic syndrome. Since leptin resistance typically comes before insulin resistance and predicts the metabolic syndrome, modern humans may be going through a process similar to the Zucker rat.
Back to the paper. Dr. Nicholas Wareham and his group followed 393 healthy white men for 5.6 years. They took baseline measurements of body composition (weight, BMI and waist circumference) and activity level, and then measured the same things after 5.6 years. In a nutshell, here's what they found:
- Sedentary time associates with overweight at any given timepoint. This is consistent with other studies.
- Overweight at the beginning of the study predicted inactivity after 5.6 years.
- Inactivity at the beginning of the study was not associated with overweight at the end.
I've pointed out before that the "we're fat because we exercise less" theory is probably incorrect. It's based on assumptions that fall apart on close examination. Exercise is healthy, but it's not the most effective way to achieve or maintain an optimal weight. The body compensates for the calories burned during exercise by a phenomenon known as "hunger". Certain obesity researchers have stubbornly tried to deny this, because it puts a kink in the "calories in, calories out" hypothesis, but anyone who has ever gotten out of their recliner knows it's true. I believe overweight is largely caused by diet composition. If that's the case, then changing diet composition is obviously going to be a more effective treatment than exercise, which doesn't address the root cause of the problem. This idea is supported by numerous diet intervention trials.
Inactivity and Weight Gain
Every now and then I read a paper that restores a little bit of my faith in obesity research. Most of the papers I read in the field pay lip-service to the same tired old stories: thrifty genes; calories in, calories out; energy density; fat intake; gluttony and sloth. None of which make sense upon close examination. The "overweight is due to sloth" theory, in its many forms, is one of the most often repeated. The main evidence for it is that overweight people tend to move less than thin people, which seems to be true. Exercise also burns calories, which can come from fat.
It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around? Gary Taubes asked this question in Good Calories, Bad Calories. In other words, isn't it possible that metabolic deregulation could cause both overweight and a reduced activity level? The answer is clearly yes. There are a number of hormones and other factors that influence activity level in animals and humans. For example, the "Zucker fatty" rat, a genetic model of severe leptin resistance, is obese and hypoactive (I wrote about it here). It's actually a remarkable facsimile of the metabolic syndrome. Since leptin resistance typically comes before insulin resistance and predicts the metabolic syndrome, modern humans may be going through a process similar to the Zucker rat.
Back to the paper. Dr. Nicholas Wareham and his group followed 393 healthy white men for 5.6 years. They took baseline measurements of body composition (weight, BMI and waist circumference) and activity level, and then measured the same things after 5.6 years. In a nutshell, here's what they found:
I've pointed out before that the "we're fat because we exercise less" theory is probably incorrect. It's based on assumptions that fall apart on close examination. Exercise is healthy, but it's not the most effective way to achieve or maintain an optimal weight. The body compensates for the calories burned during exercise by a phenomenon known as "hunger". Certain obesity researchers have stubbornly tried to deny this, because it puts a kink in the "calories in, calories out" hypothesis, but anyone who has ever gotten out of their recliner knows it's true. I believe overweight is largely caused by diet composition. If that's the case, then changing diet composition is obviously going to be a more effective treatment than exercise, which doesn't address the root cause of the problem. This idea is supported by numerous diet intervention trials.
It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around? Gary Taubes asked this question in Good Calories, Bad Calories. In other words, isn't it possible that metabolic deregulation could cause both overweight and a reduced activity level? The answer is clearly yes. There are a number of hormones and other factors that influence activity level in animals and humans. For example, the "Zucker fatty" rat, a genetic model of severe leptin resistance, is obese and hypoactive (I wrote about it here). It's actually a remarkable facsimile of the metabolic syndrome. Since leptin resistance typically comes before insulin resistance and predicts the metabolic syndrome, modern humans may be going through a process similar to the Zucker rat.
Back to the paper. Dr. Nicholas Wareham and his group followed 393 healthy white men for 5.6 years. They took baseline measurements of body composition (weight, BMI and waist circumference) and activity level, and then measured the same things after 5.6 years. In a nutshell, here's what they found:
- Sedentary time associates with overweight at any given timepoint. This is consistent with other studies.
- Overweight at the beginning of the study predicted inactivity after 5.6 years.
- Inactivity at the beginning of the study was not associated with overweight at the end.
I've pointed out before that the "we're fat because we exercise less" theory is probably incorrect. It's based on assumptions that fall apart on close examination. Exercise is healthy, but it's not the most effective way to achieve or maintain an optimal weight. The body compensates for the calories burned during exercise by a phenomenon known as "hunger". Certain obesity researchers have stubbornly tried to deny this, because it puts a kink in the "calories in, calories out" hypothesis, but anyone who has ever gotten out of their recliner knows it's true. I believe overweight is largely caused by diet composition. If that's the case, then changing diet composition is obviously going to be a more effective treatment than exercise, which doesn't address the root cause of the problem. This idea is supported by numerous diet intervention trials.
Meet Charvie: My New Puppy
I try to focus this blog on weight loss surgery. But you know? I'm human and here is a really cool thing. We have brought home a new puppy and he is a sweetheart bundle of love. The following is from my personal journal September 3:The lights of our dog kennel building have been dark for two years, one month and two days. At twilight, on July 31, 2006 I shut the door to the building, not long
Delicious Wine Reductions for Cool Autumn Nights
So we've had weight loss surgery and are happily losing weight with a restricted diet and the improved ability to exercise. But you know, we didn't have taste bud surgery! We still have taste buds that crave delicious foods - we just want the foods we eat to be satiating and good for us.Let me tell you a culinary secret - it's in the wine! I'm not talking about wine in the glass, I'm talking
Kamis, 11 September 2008
A Few Numbers
I went to the doctor's office recently to get some tests done, so I could get a biochemical window into my health. Here's what came back:
I'll start from the top. The fasting insulin value is excellent; 2.3 is so low it's outside the "reference range" that's typically encountered. I don't have a trace of hyperinsulinemia, which implies a high degree of insulin sensitivity. I won't be developing metabolic syndrome anytime soon. My fasting blood glucose looks good, not much to say there.
The HbA1c reading is higher than I was hoping/expecting. It's "normal", but on the high end of normal. That could imply mild glucose intolerance. Perhaps a result of years of slamming myself with white flour and sugar. The other possibility is that my blood cells turn over more slowly than usual, which would artificially inflate the HbA1c number. I may buy a glucose meter so I can monitor my post-meal glucose. I wish I had HbA1c data from healthy non-industrial populations with which to compare. 5.8% does associate with a slightly higher risk of heart attack than 5% and below.
The lipid panel looks good. My total cholesterol is on the high side, mostly due to my extremely high HDL. My RN wrote "This is the highest HDL (high density lipoprotein, or 'good cholesterol') I've seen in 22 yrs of clinical practice!!" My triglycerides are very low, which also associates with low CVD risk. My LDL is on the high side, but it's probably the "non-atherogenic large, fluffy" LDL, judging by my HDL, triglyceride and insulin numbers. My triglyceride:HDL ratio and LDL:HDL ratio imply a low risk. Overall, the lipid panel looks very good to my eye.
However, I don't put a lot of faith in the predictive value of blood lipids. The studies that established links between blood lipids and CVD were typically performed in people eating the standard American diet. They don't necessarily imply the same risk in people eating an atypical diet like myself. Case in point, the Kitavans.
Here's a brief overview of my lifestyle:
- Fasting insulin: 2.3 uIU/mL
- Fasting glucose: 88 mg/dL
- HbA1c: 5.8%
- Total cholesterol: 252 mg/dL
- HDL: 111 mg/dL
- LDL (calculated): 131 mg/dL
- Triglycerides: 48 mg/dL
I'll start from the top. The fasting insulin value is excellent; 2.3 is so low it's outside the "reference range" that's typically encountered. I don't have a trace of hyperinsulinemia, which implies a high degree of insulin sensitivity. I won't be developing metabolic syndrome anytime soon. My fasting blood glucose looks good, not much to say there.
The HbA1c reading is higher than I was hoping/expecting. It's "normal", but on the high end of normal. That could imply mild glucose intolerance. Perhaps a result of years of slamming myself with white flour and sugar. The other possibility is that my blood cells turn over more slowly than usual, which would artificially inflate the HbA1c number. I may buy a glucose meter so I can monitor my post-meal glucose. I wish I had HbA1c data from healthy non-industrial populations with which to compare. 5.8% does associate with a slightly higher risk of heart attack than 5% and below.
The lipid panel looks good. My total cholesterol is on the high side, mostly due to my extremely high HDL. My RN wrote "This is the highest HDL (high density lipoprotein, or 'good cholesterol') I've seen in 22 yrs of clinical practice!!" My triglycerides are very low, which also associates with low CVD risk. My LDL is on the high side, but it's probably the "non-atherogenic large, fluffy" LDL, judging by my HDL, triglyceride and insulin numbers. My triglyceride:HDL ratio and LDL:HDL ratio imply a low risk. Overall, the lipid panel looks very good to my eye.
However, I don't put a lot of faith in the predictive value of blood lipids. The studies that established links between blood lipids and CVD were typically performed in people eating the standard American diet. They don't necessarily imply the same risk in people eating an atypical diet like myself. Case in point, the Kitavans.
Here's a brief overview of my lifestyle:
- Diet, in descending order of calories: added fats like butter, lard, coconut oil and olive oil. Starchy foods like root vegetables, winter squash, legumes and quinoa (latter two always soaked 12-24 hours). Meat, organs and fish, wild or pasture-raised. Pasture-raised eggs. Soaked raw almonds and toasted hazelnuts. Fresh and fermented vegetables. Cheese, yogurt and raw milk. Fruit. Unsweetened chocolate. I estimate my macronutrient intake to be roughly 50% fat, 37% carbohydrate and 13% protein.
- Exercise: I cycle commute 30 minutes a day, lift weights briefly 2-3 times a week, sprint once a week, and hike regularly.
- Meditation: several times a week.
- Sleep: 8.5 to 9 hours almost every night.
- Assorted hormesis: weekly 24-hour fast, exercise, cold water swims, sauna.
- Good friends, family, community, relaxation.
- I eat a LOT of saturated fat, yet my risk of heart attack is probably very low.
- A diet high in saturated fat that includes carbohydrate is compatible with excellent insulin sensitivity, at least in the context of an otherwise good lifestyle.
- I should look into my post-meal blood sugar.
A Few Numbers
I went to the doctor's office recently to get some tests done, so I could get a biochemical window into my health. Here's what came back:
I'll start from the top. The fasting insulin value is excellent; 2.3 is so low it's outside the "reference range" that's typically encountered. I don't have a trace of hyperinsulinemia, which implies a high degree of insulin sensitivity. I won't be developing metabolic syndrome anytime soon. My fasting blood glucose looks good, not much to say there.
The HbA1c reading is higher than I was hoping/expecting. It's "normal", but on the high end of normal. That could imply mild glucose intolerance. Perhaps a result of years of slamming myself with white flour and sugar. The other possibility is that my blood cells turn over more slowly than usual, which would artificially inflate the HbA1c number. I may buy a glucose meter so I can monitor my post-meal glucose. I wish I had HbA1c data from healthy non-industrial populations with which to compare. 5.8% does associate with a slightly higher risk of heart attack than 5% and below.
The lipid panel looks good. My total cholesterol is on the high side, mostly due to my extremely high HDL. My RN wrote "This is the highest HDL (high density lipoprotein, or 'good cholesterol') I've seen in 22 yrs of clinical practice!!" My triglycerides are very low, which also associates with low CVD risk. My LDL is on the high side, but it's probably the "non-atherogenic large, fluffy" LDL, judging by my HDL, triglyceride and insulin numbers. My triglyceride:HDL ratio and LDL:HDL ratio imply a low risk. Overall, the lipid panel looks very good to my eye.
However, I don't put a lot of faith in the predictive value of blood lipids. The studies that established links between blood lipids and CVD were typically performed in people eating the standard American diet. They don't necessarily imply the same risk in people eating an atypical diet like myself. Case in point, the Kitavans.
Here's a brief overview of my lifestyle:
- Fasting insulin: 2.3 uIU/mL
- Fasting glucose: 88 mg/dL
- HbA1c: 5.8%
- Total cholesterol: 252 mg/dL
- HDL: 111 mg/dL
- LDL (calculated): 131 mg/dL
- Triglycerides: 48 mg/dL
I'll start from the top. The fasting insulin value is excellent; 2.3 is so low it's outside the "reference range" that's typically encountered. I don't have a trace of hyperinsulinemia, which implies a high degree of insulin sensitivity. I won't be developing metabolic syndrome anytime soon. My fasting blood glucose looks good, not much to say there.
The HbA1c reading is higher than I was hoping/expecting. It's "normal", but on the high end of normal. That could imply mild glucose intolerance. Perhaps a result of years of slamming myself with white flour and sugar. The other possibility is that my blood cells turn over more slowly than usual, which would artificially inflate the HbA1c number. I may buy a glucose meter so I can monitor my post-meal glucose. I wish I had HbA1c data from healthy non-industrial populations with which to compare. 5.8% does associate with a slightly higher risk of heart attack than 5% and below.
The lipid panel looks good. My total cholesterol is on the high side, mostly due to my extremely high HDL. My RN wrote "This is the highest HDL (high density lipoprotein, or 'good cholesterol') I've seen in 22 yrs of clinical practice!!" My triglycerides are very low, which also associates with low CVD risk. My LDL is on the high side, but it's probably the "non-atherogenic large, fluffy" LDL, judging by my HDL, triglyceride and insulin numbers. My triglyceride:HDL ratio and LDL:HDL ratio imply a low risk. Overall, the lipid panel looks very good to my eye.
However, I don't put a lot of faith in the predictive value of blood lipids. The studies that established links between blood lipids and CVD were typically performed in people eating the standard American diet. They don't necessarily imply the same risk in people eating an atypical diet like myself. Case in point, the Kitavans.
Here's a brief overview of my lifestyle:
- Diet, in descending order of calories: added fats like butter, lard, coconut oil and olive oil. Starchy foods like root vegetables, winter squash, legumes and quinoa (latter two always soaked 12-24 hours). Meat, organs and fish, wild or pasture-raised. Pasture-raised eggs. Soaked raw almonds and toasted hazelnuts. Fresh and fermented vegetables. Cheese, yogurt and raw milk. Fruit. Unsweetened chocolate. I estimate my macronutrient intake to be roughly 50% fat, 37% carbohydrate and 13% protein.
- Exercise: I cycle commute 30 minutes a day, lift weights briefly 2-3 times a week, sprint once a week, and hike regularly.
- Meditation: several times a week.
- Sleep: 8.5 to 9 hours almost every night.
- Assorted hormesis: weekly 24-hour fast, exercise, cold water swims, sauna.
- Good friends, family, community, relaxation.
- I eat a LOT of saturated fat, yet my risk of heart attack is probably very low.
- A diet high in saturated fat that includes carbohydrate is compatible with excellent insulin sensitivity, at least in the context of an otherwise good lifestyle.
- I should look into my post-meal blood sugar.
Rabu, 10 September 2008
Hectic random musings
Lots have happened this week.
A round up...
We lost young Josh (I think I mentioned that before) and immediately advertised for a new housemate. We found one and Nicky has moved in. She is really nice. She is Korean and learning English at a school in the city. So every day is a delight for her as she tries something new - mainly in the food category, but everything English overwhelms her. She is so pleased to be able to stay in a 'typical English home'... Yeah! Laugh your heads off..that's right, typical. I think I would go for 'Crazy' or 'Bloody Mad' English family to be honest!
Anyhow, she is in, paid up and life is sweet on that score againthankfully as suddenly losing £320 a month overnight tends to put the willies up One!
Work - it's been fine, but I have noticed that I dread Wednesdays. This is because I have a family of acute nerds who in my opinion should:
a.) get personalities
b.) get social skills
c.) get some furniture (instead of having one small sofa and a massive Yamaha ONLY in a 25 x 14ft room!)
d.) get personalities
e.) and other stuff!
So, it was obviously with deep joy that yesterday rolled around after having a most beautiful 6 week rest from what must be the most inane geeky family in the world.
It had actually got mildly more bearable about a month before the holidays, when the mother of said geek family, actually stopped her lessons because she had too much work on. So, when I arrived at their empty chasm of an abode yesterday, I was thrilled when she told me she was starting again. Frankly, I would've liked to have known that I had to sqeeze an extra half hour into my schedule before hand, but there we go. So I smiled sweetly and thought of the fat cheque.
To be honest, the lesson actually went well, because I was dreading it. Yesterday morning, I sat down with DH and we had a massive chat about it. I was all for slinging in the towel (as I did not know that Mother wanted to kick start again!), but he said that maybe I should just regain control by putting them a little bit out of their comfort zones. Hmmm thinks I. This could work. I actually felt really good when I told each one, turn after happy turn, that we would be doing something different and not just sticking to the stuff they liked/was easy for them. It went surprisingly well.
When I feel in control, I feel ok about my job, but some of the upstarts I teach like to tell ME how it is. Obviously I have only been doing this for 13 Years... what do I know right? Anyway, long story short, yesterday was full of little mini victories for me. So I will endeavour to focus on the whole pay cheque thing, and just teach them, and not try not to groan outwardly when I sit for 2 hours on a hard stool and teach 4 people who have no opinion, or spark, or conversation, or passion for what they are learning and indeed paying for.
Also, yesterday my Dad had his reversal operation. He was diagnosed with bowel cancer back in the spring, remember? Well yesterday he had his colostomy bag reversed, and yesterday evening was sitting up in bed eating tomato and cheese sandwiches and ice cream with a big white bandage over the bit where the stoma has been these last 6 months. He is delighted. I have no idea when he gets out of hospital, but its not the big operation like it was last time thank goodness.
So, foodwise and bandwise...
Dunno. I have been sick a couple of times this week. I have been pretty good with my eating, no crap like crisps or biscuits or wine...
trying to remember my food for the week is hard. Yesterday I made ratatouille and rice for lunch, and in then evening we had fish and chips. I had 1/4 piece of cod, 6 chips, 1/2 sausage and 1/2 fish cake. I was actually full about 10 mins into the meal, but it was so yummy I cheated a little and followed every mouthful with a little sip of orange juice so that it made it wetter and would slip down. I know that's REALLY naughty, and I wont do it again, but it proves to me that I have restriction, and more than I did before Sunday's fill! I think I do have the restriction just about right now. I am gonna try and stop freaking that I haven't, because I honestly think I am about right. I am still 0.2ml below my highest fill level, so I think this could be about it, as I don't want to go back to where I was before!
After yesterdays dinner I felt horrid. I felt really bloated and awful. I lay in bed and I actually had tummy pain like I needed an alka seltzer, so that kind of food is just not doing it for me. So its back to meat and 3 veg again. I am not even going shopping tomorrow because I physically cannot get anything more in my cupboards or freezer. Its got to the point where I am going to the supermarket out of habit rather than necessity, so I am going to make what I can out of what we have for a week or so.
Tuesday! I remember now, I made purple sprouting soup followed by roast duck and green vegetables. I was sick after this meal.
Today, I don't know. it will have to be an oven job because of the schedule for today, and everyone will eat much earlier than me. I think I will make a quiche and salad. Easy peasy, and they can serve themselves then.
So that's just about it. I am taking Steven to the vet in half an hour to get his mini pom poms removed as he has taken to peeing on beds and washing and starting all that territorial 'Man Cat' rubbish. Hes a little young, but I just cant have cat pee on beds. NO NO NO.
My scales have run out of battery so I have no idea how I am doing since Sunday, and I am not going to worry until Sunday to get a good reading, so there we go. Over and out.
Post Script
After reading through this to check for errors, it has flagged up to me that I keep trying to PROVE the band. This has lead to my dawning realisation that if I keep trying to prove the band, I am over eating and therefore not going to lose weight. I can PROVE the band is ok by just eating normally and seeing the weight drop off. I have no idea why this hasn't dawned on me before, but now it has.
Resolution: I am gonna eat normally and prove my restriction is right by my weight loss, rather than keep eating until I feel I need to be sick. That's just plain madness!
A round up...
We lost young Josh (I think I mentioned that before) and immediately advertised for a new housemate. We found one and Nicky has moved in. She is really nice. She is Korean and learning English at a school in the city. So every day is a delight for her as she tries something new - mainly in the food category, but everything English overwhelms her. She is so pleased to be able to stay in a 'typical English home'... Yeah! Laugh your heads off..that's right, typical. I think I would go for 'Crazy' or 'Bloody Mad' English family to be honest!
Anyhow, she is in, paid up and life is sweet on that score againthankfully as suddenly losing £320 a month overnight tends to put the willies up One!
Work - it's been fine, but I have noticed that I dread Wednesdays. This is because I have a family of acute nerds who in my opinion should:
a.) get personalities
b.) get social skills
c.) get some furniture (instead of having one small sofa and a massive Yamaha ONLY in a 25 x 14ft room!)
d.) get personalities
e.) and other stuff!
So, it was obviously with deep joy that yesterday rolled around after having a most beautiful 6 week rest from what must be the most inane geeky family in the world.
It had actually got mildly more bearable about a month before the holidays, when the mother of said geek family, actually stopped her lessons because she had too much work on. So, when I arrived at their empty chasm of an abode yesterday, I was thrilled when she told me she was starting again. Frankly, I would've liked to have known that I had to sqeeze an extra half hour into my schedule before hand, but there we go. So I smiled sweetly and thought of the fat cheque.
To be honest, the lesson actually went well, because I was dreading it. Yesterday morning, I sat down with DH and we had a massive chat about it. I was all for slinging in the towel (as I did not know that Mother wanted to kick start again!), but he said that maybe I should just regain control by putting them a little bit out of their comfort zones. Hmmm thinks I. This could work. I actually felt really good when I told each one, turn after happy turn, that we would be doing something different and not just sticking to the stuff they liked/was easy for them. It went surprisingly well.
When I feel in control, I feel ok about my job, but some of the upstarts I teach like to tell ME how it is. Obviously I have only been doing this for 13 Years... what do I know right? Anyway, long story short, yesterday was full of little mini victories for me. So I will endeavour to focus on the whole pay cheque thing, and just teach them, and not try not to groan outwardly when I sit for 2 hours on a hard stool and teach 4 people who have no opinion, or spark, or conversation, or passion for what they are learning and indeed paying for.
Also, yesterday my Dad had his reversal operation. He was diagnosed with bowel cancer back in the spring, remember? Well yesterday he had his colostomy bag reversed, and yesterday evening was sitting up in bed eating tomato and cheese sandwiches and ice cream with a big white bandage over the bit where the stoma has been these last 6 months. He is delighted. I have no idea when he gets out of hospital, but its not the big operation like it was last time thank goodness.
So, foodwise and bandwise...
Dunno. I have been sick a couple of times this week. I have been pretty good with my eating, no crap like crisps or biscuits or wine...
trying to remember my food for the week is hard. Yesterday I made ratatouille and rice for lunch, and in then evening we had fish and chips. I had 1/4 piece of cod, 6 chips, 1/2 sausage and 1/2 fish cake. I was actually full about 10 mins into the meal, but it was so yummy I cheated a little and followed every mouthful with a little sip of orange juice so that it made it wetter and would slip down. I know that's REALLY naughty, and I wont do it again, but it proves to me that I have restriction, and more than I did before Sunday's fill! I think I do have the restriction just about right now. I am gonna try and stop freaking that I haven't, because I honestly think I am about right. I am still 0.2ml below my highest fill level, so I think this could be about it, as I don't want to go back to where I was before!
After yesterdays dinner I felt horrid. I felt really bloated and awful. I lay in bed and I actually had tummy pain like I needed an alka seltzer, so that kind of food is just not doing it for me. So its back to meat and 3 veg again. I am not even going shopping tomorrow because I physically cannot get anything more in my cupboards or freezer. Its got to the point where I am going to the supermarket out of habit rather than necessity, so I am going to make what I can out of what we have for a week or so.
Tuesday! I remember now, I made purple sprouting soup followed by roast duck and green vegetables. I was sick after this meal.
Today, I don't know. it will have to be an oven job because of the schedule for today, and everyone will eat much earlier than me. I think I will make a quiche and salad. Easy peasy, and they can serve themselves then.
So that's just about it. I am taking Steven to the vet in half an hour to get his mini pom poms removed as he has taken to peeing on beds and washing and starting all that territorial 'Man Cat' rubbish. Hes a little young, but I just cant have cat pee on beds. NO NO NO.
My scales have run out of battery so I have no idea how I am doing since Sunday, and I am not going to worry until Sunday to get a good reading, so there we go. Over and out.
Post Script
After reading through this to check for errors, it has flagged up to me that I keep trying to PROVE the band. This has lead to my dawning realisation that if I keep trying to prove the band, I am over eating and therefore not going to lose weight. I can PROVE the band is ok by just eating normally and seeing the weight drop off. I have no idea why this hasn't dawned on me before, but now it has.
Resolution: I am gonna eat normally and prove my restriction is right by my weight loss, rather than keep eating until I feel I need to be sick. That's just plain madness!
Senin, 08 September 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. I don't trust flax because paleolithic humans wouldn't have eaten anything like it, and it's full of phytoestrogens. 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 mealns 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 excellent health overall, 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
- Pacific islanders getting most of their fat from coconut and fish: 1:2 or less
- Inuit and other Pacific coast Americans: 1:4 or less
- Dairy-based cultures: 1:1
- 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. I don't trust flax because paleolithic humans wouldn't have eaten anything like it, and it's full of phytoestrogens. 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 mealns 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 excellent health overall, 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.
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. I don't trust flax because paleolithic humans wouldn't have eaten anything like it, and it's full of phytoestrogens. 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:
Except salmon oil, these are traditional fats suitable for cooking. Except schmaltz (chicken fat), they are relatively low in n-6. Next, vegetable oils:
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 mealns it has been bred for a high monounsaturated fat content at the expense of n-6. Here are the meats and eggs:
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 excellent health overall, 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
- Pacific islanders getting most of their fat from coconut and fish: 1:2 or less
- Inuit and other Pacific coast Americans: 1:4 or less
- Dairy-based cultures: 1:1
- 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. I don't trust flax because paleolithic humans wouldn't have eaten anything like it, and it's full of phytoestrogens. 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:
Except salmon oil, these are traditional fats suitable for cooking. Except schmaltz (chicken fat), they are relatively low in n-6. Next, vegetable oils: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 mealns it has been bred for a high monounsaturated fat content at the expense of n-6. Here are the meats and eggs: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 excellent health overall, 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.
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