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.
Sunday, September 28, 2008
Thursday, September 25, 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.
Wednesday, September 24, 2008
Refresher Course: 5 Day Pouch Test Soups
We get a lot of questions about the soups for the 5 Day Pouch Test. Here is an explanation directly from our forthcoming book: The 5 Day Pouch Test Owner's Manual. Many who have done the 5DPT and used the soups swear by them. Another question that I get frequently is, "Can I have the soups when I'm not doing the 5DPT?" The answer is a big resounding YES!Link to the Soup RecipesSoup
Tuesday, September 23, 2008
It's all happening in the Neighborhood
Autumn has arrived in the Northern Hemi and for me that means cool morning walks, beautiful colors as the leaves change and late-night tea in front of the fireplace. How are things in your neck of the woods? Our little calico, KeepHerKitty, is quite interested in the big round pumpkins just waiting to be carved.In the LivingAfterWLS Neighborhood the weather is always just right for over-the-fence
Agave Syrup
Anna brought up agave syrup in a comment on the last post, so I thought I'd put up a little mini-post so everyone can benefit from what she pointed out.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
My Dad is really really really REALLY ill.
Dunno where to start, but I guess the beginning. Here goes.
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
- Evening - pain in side and shoulder
- Night - could not sleep, excruciating pain
- Evening - A&E dept. given morphine to help pain. temperature, low BP, high pulse/heart rate obvious signs of infection as his body was in shock. Wound opened and blood & puss pour out and even spray my mother in the face!
- Night - wound stitches removed and scar opened up. A large amount of puss, blood and faeces removed from abdominal cavity through site of old stoma
- Night - Brought back from surgery straight to Intensive Care Unit (ICU) at approx 7pm. Completely our for the count on Life Support machine with respirator and 14 automatic drug administrators and untold monitors.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Monday, September 22, 2008
How to Fatten Your Liver
Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.
This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.
Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).
Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.
Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.
Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!
This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.
Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).
Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.
Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.
Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!
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