Thought I'd picked a healthy breakfast option ...
Replies
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I think this abstract sums up the sources of my frustrated confusion on the issue. Note how they know what happens in rats, but humans seem to have different reactions, and they don't know what long term lower sugar consumption is going to do to us even though short term higher consumption does increase intrahepatic fat concentration. But also note that they mention moderate amounts as %10 of energy intake in the US and Europe. In 2010, teens and children were getting %16 of calories from added sugar. (source: http://www.cdc.gov/nchs/data/databriefs/db122.htm). I'm fascinated with the subject, and I want my liver to last a very long time, but there is a lot of contradictory information out there.
Summary
Fructose is mainly consumed with added sugars (sucrose and high fructose corn syrup), and represents up to 10% of total energy intake in the US and in several European countries. This hexose is essentially metabolized in splanchnic tissues, where it is converted into glucose, glycogen, lactate, and, to a minor extent, fatty acids. In animal models, high fructose diets cause the development of obesity, insulin resistance, diabetes mellitus, and dyslipidemia. Ectopic lipid deposition in the liver is an early occurrence upon fructose exposure, and is tightly linked to hepatic insulin resistance. In humans, there is strong evidence, based on several intervention trials, that fructose overfeeding increases fasting and postprandial plasma triglyceride concentrations, which are related to stimulation of hepatic de novo lipogenesis and VLDL-TG secretion, together with decreased VLDL-TG clearance. However, in contrast to animal models, fructose intakes as high as 200 g/day in humans only modestly decreases hepatic insulin sensitivity, and has no effect on no whole body (muscle) insulin sensitivity. A possible explanation may be that insulin resistance and dysglycemia develop mostly in presence of sustained fructose exposures associated with changes in body composition. Such effects are observed with high daily fructose intakes, and there is no solid evidence that fructose, when consumed in moderate amounts, has deleterious effects. There is only limited information regarding the effects of fructose on intrahepatic lipid concentrations. In animal models, high fructose diets clearly stimulate hepatic de novo lipogenesis and cause hepatic steatosis. In addition, some observations suggest that fructose may trigger hepatic inflammation and stimulate the development of hepatic fibrosis. This raises the possibility that fructose may promote the progression of non-alcoholic fatty liver disease to its more severe forms, i.e. non-alcoholic steatohepatitis and cirrhosis. In humans, a short-term fructose overfeeding stimulates de novo lipogenesis and significantly increases intrahepatic fat concentration, without however reaching the proportion encountered in non-alcoholic fatty liver diseases. Whether consumption of lower amounts of fructose over prolonged periods may contribute to the pathogenesis of NAFLD has not been convincingly documented in epidemiological studies and remains to be further assessed.
http://www.sciencedirect.com/science/article/pii/S2210740112001866
LOL "Data source and methods
Data from the National Health and Nutrition Examination Survey (NHANES) were used for these analyses. NHANES is a cross-sectional survey designed to monitor the health and nutritional status of the civilian noninstitutionalized U.S. population (9). The survey consists of interviews conducted in participants' homes, standardized physical examinations in mobile examination centers (MECs), and laboratory tests utilizing blood and urine specimens provided by participants during the physical examination. Dietary information for this analysis was obtained via an in-person 24-hour dietary recall interview in the MEC."
and lol at your abstract, how many people are consuming over 200g of fructose a day? And animal models? I wonder if DNL occurs at similar rates as humans or it's much much different?
There are other studies, including small scale human ones. I deliberately picked one that is difficult to read (as far as the abstract goes) and contradictory.
But since you don't like that one, let's have a human one:
http://www.mdpi.com/2072-6643/6/8/3187/htm
Dietary Fructose Reduction Improves Markers of Cardiovascular Disease Risk in Hispanic-American Adolescents with NAFLD
Abstract: Nonalcoholic fatty liver disease (NAFLD) is now thought to be the most common liver disease worldwide. Cardiovascular complications are a leading cause of mortality in NAFLD. Fructose, a common nutrient in the westernized diet, has been reported to be associated with increased cardiovascular risk, but its impact on adolescents with NAFLD is not well understood. We designed a 4-week randomized, controlled, double-blinded beverage intervention study. Twenty-four overweight Hispanic-American adolescents who had hepatic fat >8% on imaging and who were regular consumers of sweet beverages were enrolled and randomized to calorie-matched study-provided fructose only or glucose only beverages. After 4 weeks, there was no significant change in hepatic fat or body weight in either group. In the glucose beverage group there was significantly improved adipose insulin sensitivity, high sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) oxidation. These findings demonstrate that reduction of fructose improves several important factors related to cardiovascular disease despite a lack of measurable improvement in hepatic steatosis. Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials.
This one, too:
http://onlinelibrary.wiley.com/doi/10.1002/hep.26299/full
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in adults and children. A number of genetic and environmental factors are known to predispose individuals to NAFLD. Certain dietary sugars, particularly fructose, are suspected to contribute to the development of NAFLD and its progression. The increasing quantity of fructose in the diet comes from sugar additives (most commonly sucrose and high fructose corn syrup) in beverages and processed foods. Substantial links have been demonstrated between increased fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing evidence suggests that fructose contributes to the development and severity of NAFLD. In human studies, fructose is associated with increasing hepatic fat, inflammation, and possibly fibrosis. Whether fructose alone can cause NAFLD or if it serves only as a contributor when consumed excessively in the setting of insulin resistance, positive energy balance, and sedentary lifestyle is unknown. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added (fructose-containing) sugars. (Hepatology 2013;57:2525–2531)
How many do you want?
First study doesn't support your claim, 2nd one doesn't either unless correlations now = causation, although even the 2nd study's authors don't think that
Do you even science?
Like I said, how many do you want? A drop certainly doesn't fill a bucket, but increasingly the studies, however small and not always completely on point, are adding up. And I also said much is unknown and some contradictory (within the same studies, no less!).
By the way, you said earlier no one eats 200g of fructose a day, but I used to down a 2 liter of soda, then go on to have cake, ice cream, and cookies pretty much daily, so if I didn't quite get there, I was damn close. Who knows, I might already have liver damage, meaning the first study could be relevant to me. Quote: "Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials."
Furthermore:
Quote: However, some people develop NAFLD even if they do not have any risk factors. NAFLD affects up to 25% of people in the United States.
Source of second quote: http://www.liverfoundation.org/abouttheliver/info/nafld/
Who said no one eats 200g of fructose again, strawman much?
Oh love the references in that link you provided for that quote, oh wait there are none
You're right, you said 'how many' not no one. Well, I was one. And yes, I'm concerned about the possibility that my liver is fat because of that, or genetic factors, or both, based on what I've been reading and doing my best to learn.
So now you are someone that consumed 200g of fructose a day but before you said you're not sure. At least you're being consistent
I looked up grams of sugar in a 2 liter of soda this morning. But it's not all fructose, correct? It's a mix. %55 percent is fructose. So halve that, meaning over 100 grams of it was fructose. Then add in the cake, ice cream, and cookies, and I was almost certainly over 200 every day for the two years I was eating like an idiot. Yeah, I have reason to think I could have done some damage.
You'd need to have had roughly 166g of "sugar" in addition to the 2 liter to hit approx 200g of fructose a day. Perhaps you were consuming that much and certainly others do too, but what % do you think consumes that amount? If it's a small % then how realistic was the researcher for using that amount?
I'm not worried about everyone else, I'm worried about myself, at least in regard to that study. I know what I was eating. It was horrible. I'm pretty sure I did meet or exceed the 200g most days, not for sugar, but just fructose. So double it for how much sugar I was eating. It was ridiculous, I owe it to myself to take proper care of my liver now just in case I did damage. Plus I already know I picked the wrong parents. My family is rife with diabetes and many of the sufferers are not obese or even noticeably overweight.0 -
reachingforarainbow wrote: »So while its not always best to eat packaged sweetened yogurt (better to add it yourself, probably have less sugar), its not really that big of a deal. That sugar is looking at natural and added sugar. This is why it should be separated out (into natural and added sugar). It is accounting for lactose, which is a sugar. In regular nonfat, unsweetened milk, in a cup there is 12 grams of sugar... It's really only bad if its added sugar
ahhh yes the evil added sugars....your body does not distinguish between added sugar and natural sugar it is all the same at the molecular level....
Really? My body has no clue when I eat fructose with or without fiber? And it has no clue about the differences between fructose, glucose, and lactose?
If you're right, I'm wasting my time. If you're incorrect, then I should know any differences, too, and food labels should differentiate for us.
are sugar molecules different?
Does the liver treat different sugars differently or not? Does the digestive system act different in any way when we eat high fiber with fructose than when we don't?
so by that logic if I add table sugar to Metamucil it is then bad because added sugar, or is it good because fiber???
Do you actually know the answer? I'd like to hear you actually answer the question without more questions.
the answer to what..?
The part I quoted. Nevermind, you don't, I can see that. That's okay.
so you want me to answer a question that I posed to another poster?
my answer is that one form of sugar is not better than another...
sugar = sugar
so the answer to my question is that it does not matter0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party0
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I think this abstract sums up the sources of my frustrated confusion on the issue. Note how they know what happens in rats, but humans seem to have different reactions, and they don't know what long term lower sugar consumption is going to do to us even though short term higher consumption does increase intrahepatic fat concentration. But also note that they mention moderate amounts as %10 of energy intake in the US and Europe. In 2010, teens and children were getting %16 of calories from added sugar. (source: http://www.cdc.gov/nchs/data/databriefs/db122.htm). I'm fascinated with the subject, and I want my liver to last a very long time, but there is a lot of contradictory information out there.
Summary
Fructose is mainly consumed with added sugars (sucrose and high fructose corn syrup), and represents up to 10% of total energy intake in the US and in several European countries. This hexose is essentially metabolized in splanchnic tissues, where it is converted into glucose, glycogen, lactate, and, to a minor extent, fatty acids. In animal models, high fructose diets cause the development of obesity, insulin resistance, diabetes mellitus, and dyslipidemia. Ectopic lipid deposition in the liver is an early occurrence upon fructose exposure, and is tightly linked to hepatic insulin resistance. In humans, there is strong evidence, based on several intervention trials, that fructose overfeeding increases fasting and postprandial plasma triglyceride concentrations, which are related to stimulation of hepatic de novo lipogenesis and VLDL-TG secretion, together with decreased VLDL-TG clearance. However, in contrast to animal models, fructose intakes as high as 200 g/day in humans only modestly decreases hepatic insulin sensitivity, and has no effect on no whole body (muscle) insulin sensitivity. A possible explanation may be that insulin resistance and dysglycemia develop mostly in presence of sustained fructose exposures associated with changes in body composition. Such effects are observed with high daily fructose intakes, and there is no solid evidence that fructose, when consumed in moderate amounts, has deleterious effects. There is only limited information regarding the effects of fructose on intrahepatic lipid concentrations. In animal models, high fructose diets clearly stimulate hepatic de novo lipogenesis and cause hepatic steatosis. In addition, some observations suggest that fructose may trigger hepatic inflammation and stimulate the development of hepatic fibrosis. This raises the possibility that fructose may promote the progression of non-alcoholic fatty liver disease to its more severe forms, i.e. non-alcoholic steatohepatitis and cirrhosis. In humans, a short-term fructose overfeeding stimulates de novo lipogenesis and significantly increases intrahepatic fat concentration, without however reaching the proportion encountered in non-alcoholic fatty liver diseases. Whether consumption of lower amounts of fructose over prolonged periods may contribute to the pathogenesis of NAFLD has not been convincingly documented in epidemiological studies and remains to be further assessed.
http://www.sciencedirect.com/science/article/pii/S2210740112001866
LOL "Data source and methods
Data from the National Health and Nutrition Examination Survey (NHANES) were used for these analyses. NHANES is a cross-sectional survey designed to monitor the health and nutritional status of the civilian noninstitutionalized U.S. population (9). The survey consists of interviews conducted in participants' homes, standardized physical examinations in mobile examination centers (MECs), and laboratory tests utilizing blood and urine specimens provided by participants during the physical examination. Dietary information for this analysis was obtained via an in-person 24-hour dietary recall interview in the MEC."
and lol at your abstract, how many people are consuming over 200g of fructose a day? And animal models? I wonder if DNL occurs at similar rates as humans or it's much much different?
There are other studies, including small scale human ones. I deliberately picked one that is difficult to read (as far as the abstract goes) and contradictory.
But since you don't like that one, let's have a human one:
http://www.mdpi.com/2072-6643/6/8/3187/htm
Dietary Fructose Reduction Improves Markers of Cardiovascular Disease Risk in Hispanic-American Adolescents with NAFLD
Abstract: Nonalcoholic fatty liver disease (NAFLD) is now thought to be the most common liver disease worldwide. Cardiovascular complications are a leading cause of mortality in NAFLD. Fructose, a common nutrient in the westernized diet, has been reported to be associated with increased cardiovascular risk, but its impact on adolescents with NAFLD is not well understood. We designed a 4-week randomized, controlled, double-blinded beverage intervention study. Twenty-four overweight Hispanic-American adolescents who had hepatic fat >8% on imaging and who were regular consumers of sweet beverages were enrolled and randomized to calorie-matched study-provided fructose only or glucose only beverages. After 4 weeks, there was no significant change in hepatic fat or body weight in either group. In the glucose beverage group there was significantly improved adipose insulin sensitivity, high sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) oxidation. These findings demonstrate that reduction of fructose improves several important factors related to cardiovascular disease despite a lack of measurable improvement in hepatic steatosis. Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials.
This one, too:
http://onlinelibrary.wiley.com/doi/10.1002/hep.26299/full
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in adults and children. A number of genetic and environmental factors are known to predispose individuals to NAFLD. Certain dietary sugars, particularly fructose, are suspected to contribute to the development of NAFLD and its progression. The increasing quantity of fructose in the diet comes from sugar additives (most commonly sucrose and high fructose corn syrup) in beverages and processed foods. Substantial links have been demonstrated between increased fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing evidence suggests that fructose contributes to the development and severity of NAFLD. In human studies, fructose is associated with increasing hepatic fat, inflammation, and possibly fibrosis. Whether fructose alone can cause NAFLD or if it serves only as a contributor when consumed excessively in the setting of insulin resistance, positive energy balance, and sedentary lifestyle is unknown. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added (fructose-containing) sugars. (Hepatology 2013;57:2525–2531)
How many do you want?
First study doesn't support your claim, 2nd one doesn't either unless correlations now = causation, although even the 2nd study's authors don't think that
Do you even science?
Like I said, how many do you want? A drop certainly doesn't fill a bucket, but increasingly the studies, however small and not always completely on point, are adding up. And I also said much is unknown and some contradictory (within the same studies, no less!).
By the way, you said earlier no one eats 200g of fructose a day, but I used to down a 2 liter of soda, then go on to have cake, ice cream, and cookies pretty much daily, so if I didn't quite get there, I was damn close. Who knows, I might already have liver damage, meaning the first study could be relevant to me. Quote: "Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials."
Furthermore:
Quote: However, some people develop NAFLD even if they do not have any risk factors. NAFLD affects up to 25% of people in the United States.
Source of second quote: http://www.liverfoundation.org/abouttheliver/info/nafld/
Who said no one eats 200g of fructose again, strawman much?
Oh love the references in that link you provided for that quote, oh wait there are none
You're right, you said 'how many' not no one. Well, I was one. And yes, I'm concerned about the possibility that my liver is fat because of that, or genetic factors, or both, based on what I've been reading and doing my best to learn.
So now you are someone that consumed 200g of fructose a day but before you said you're not sure. At least you're being consistent
I looked up grams of sugar in a 2 liter of soda this morning. But it's not all fructose, correct? It's a mix. %55 percent is fructose. So halve that, meaning over 100 grams of it was fructose. Then add in the cake, ice cream, and cookies, and I was almost certainly over 200 every day for the two years I was eating like an idiot. Yeah, I have reason to think I could have done some damage.
You'd need to have had roughly 166g of "sugar" in addition to the 2 liter to hit approx 200g of fructose a day. Perhaps you were consuming that much and certainly others do too, but what % do you think consumes that amount? If it's a small % then how realistic was the researcher for using that amount?
I'm not worried about everyone else, I'm worried about myself, at least in regard to that study. I know what I was eating. It was horrible. I'm pretty sure I did meet or exceed the 200g most days, not for sugar, but just fructose. So double it for how much sugar I was eating. It was ridiculous, I owe it to myself to take proper care of my liver now just in case I did damage. Plus I already know I picked the wrong parents. My family is rife with diabetes and many of the sufferers are not obese or even noticeably overweight.
Except the study you referenced didn't show deleterious effects for 200g of fructose a day0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:
https://www.youtube.com/watch?v=UEA6ow1icDc
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Becky170467 wrote: »Fage - Total 0% Fat Greek Yogurt With Honey, 1 container (170g)
- Wrong
- 32g of SUGAR !!! 184 calories !!!
Had one of these for my afternoon snack today. Delicious.0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
LOLStig
http://community.myfitnesspal.com/en/discussion/988127/scientific-review-of-lolstigs-fat-chance
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According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
LOLStig
http://community.myfitnesspal.com/en/discussion/988127/scientific-review-of-lolstigs-fat-chance
If you don't like him, your CV in a relevant field better be equally as impressive as his, otherwise, who cares if you LOL?
Now if you want to post sources who do have equally impressive CVs and who don't work for the food industry, I'll be glad to have a new lecture to listen to. But otherwise, no.0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
LOLStig
http://community.myfitnesspal.com/en/discussion/988127/scientific-review-of-lolstigs-fat-chance
If you don't like him, your CV in a relevant field better be equally as impressive as his, otherwise, who cares if you LOL?
Now if you want to post sources who do have equally impressive CVs and who don't work for the food industry, I'll be glad to have a new lecture to listen to. But otherwise, no.
Except his BS has already been exposed by mult people with just as impressive CVs as his, only ignorant idiots use him to support their claims0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
LOLStig
http://community.myfitnesspal.com/en/discussion/988127/scientific-review-of-lolstigs-fat-chance
If you don't like him, your CV in a relevant field better be equally as impressive as his, otherwise, who cares if you LOL?
Now if you want to post sources who do have equally impressive CVs and who don't work for the food industry, I'll be glad to have a new lecture to listen to. But otherwise, no.
Except his BS has already been exposed by mult people with just as impressive CVs as his, only ignorant idiots use him to support their claims
Link to lecture to back your claim, please, with CV and disclosures of speaker. I will listen to it, and gladly, if you have it.0 -
alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/
Back to lurking in the thread.0 -
This thread needs to die. Or at least have some people take their discussion off-line.0
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mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?0 -
You do realize that the media hype about super foods and antioxidants is kind of just that- hype.According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
eat a balanced diet with variety- you'll be fine. Fruit doesn't win because it has more fiber or more "antioxidants".
Secondly... back on almost topic.
And someone PLEASE PLEASE PLEASE break down for me how low/no fat = no sugar??
why are we really shocked fat =/=sugar. I'm just really struggling to wrap my brain around all this.
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mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
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There are no "bad" foods at first, perhaps. But the longer you have diabetes the harder it can be to process certain things. At least that's what I'm currently finding out.
I hear you. For a beginning diabetic, I want a few rules ingrained (routine and balanced plate). If they start lopping off foods right at the beginning they've got the whole thing wrong. I overheard a nurse say that diabetics have to be their own lifetime coaches. Every meal and the timing of the meal is a choice. I became sensitized to my body's signals after a few months of diarizing and started associating things like sugary drinks and cakes to "feel like crap" later. I am sure you've discovered the stunning speed with which rice hits the system, for instance. BUT if I have my sugar punch in a shot glass chased with cheese and a cracker, chances are I'll be fine. Or if my rice is portioned to say, 1/4 cup with a mound of vegetables and a chicken breast, chances are it will metabolise decently.
I'm in remission now. A sweet here or there does not affect me. Even so, after years of tracking, I prefer my veggies over my fruit. Veggies are a lot less trouble.0 -
mamapeach910 wrote: »mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
If he doesn't have the education and experience in the area I'm interested in (liver health specifically in this case) why bother?0 -
mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
People who work in the fitness field also train hundreds of "regular" clients a year. Most people seek them out when their "named" diet fails miserably.0 -
mamapeach910 wrote: »mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
If he doesn't have the education and experience in the area I'm interested in (liver health specifically in this case) why bother?
Education? Did you look? He's got a Masters of Science in Nutrition. He's more than qualified. He's not just some random muscle-head.
0 -
mamapeach910 wrote: »mamapeach910 wrote: »mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
If he doesn't have the education and experience in the area I'm interested in (liver health specifically in this case) why bother?
Education? Did you look? He's got a Masters of Science in Nutrition. He's more than qualified. He's not just some random muscle-head.
That doesn't stack up against an MD and 20 some years medical experience with metabolic issues plus research. And Dr. Lustig isn't the only one lecturing on this issue, either. I'm finding more and more lectures from other professionals based on research findings in animals and humans.0 -
According to Lustig, fructose is as toxic to the liver as alcohol. But, fructose from fruit is fine because fiber............so does this mean I can add Metamucil to my whiskey and cheat the system. Let's party
Fruit also has antioxidants. Lustig states that the liver handles fructose better if the diet is high in antioxidants as well. Which it isn't going to be if someone is mostly living on cheese pizza and ice cream and soda.
Source:https://www.youtube.com/watch?v=UEA6ow1icDc
LOLStig
http://community.myfitnesspal.com/en/discussion/988127/scientific-review-of-lolstigs-fat-chance
If you don't like him, your CV in a relevant field better be equally as impressive as his, otherwise, who cares if you LOL?
Now if you want to post sources who do have equally impressive CVs and who don't work for the food industry, I'll be glad to have a new lecture to listen to. But otherwise, no.
Except his BS has already been exposed by mult people with just as impressive CVs as his, only ignorant idiots use him to support their claims
Link to lecture to back your claim, please, with CV and disclosures of speaker. I will listen to it, and gladly, if you have it.
Education
Ph.D., Purdue University, 1995, Foods and Nutrition
M.S., Indiana University, 1991, Nutrition Science
B.S., Indiana University, 1990, Nutrition Science
Research Areas
I have several areas of professional interest. I am particularly interested in the effects of diet and exercise on nutritional status (i.e., blood lipids, bone health and energy metabolism) as well as the effects of diet on exercise metabolism and performance. Lately, we have been working on several functional foods that may have influences on some of these issues. In particular, we have studied less refined sweeteners (e.g., honey, agave nectar, etc.) and oils (minimally refined soybean and corn oils) as well as foods such as dried plums, mushrooms, eggs, miracle fruit, pistachios, chocolate, pullulan and raisins and have dedicated much research to address the influences of L-alanine on exercise metabolism. Below are a few representative grants, publications, and presentations related to my research.
Selected Publications
Sheila Medina-Torne, Maria Rosario G. Araneta, Caroline A. Macera, Mark Kern, Ming Ji. Dietary factors associated with adiponectin in Filipino-American women. Ethnicity & Disease. In Press.
Tricia M. Nemoseck, Erin G. Carmody, Allison Furchner-Evanson, Marsa Gleason, Amy Li, Hayley Potter, Lauren M. Rezende, Kelly J. Lane, Mark Kern. Honey promotes lower weight gain, adiposity, and triglycerides than sucrose in rats. Nutrition Research. 2011. 31:55-60.
Janine M. Wong and Mark Kern. Miracle fruit improves sweetness of a low-calorie dessert without promoting subsequent energy compensation. Appetite. 2011. 56:163-166.
Leslie Howarth, Yumi Petrisko, Allison Furchner-Evanson, Tricia Nemoseck, Mark Kern. Snack selection influences nutrient intake, triglycerides and bowel habits of adult women. A pilot study. Journal of the American Dietetic Association. 2010. 110:1322-1327.
Allison Furchner-Evanson, Yumi Petrisko, Leslie Howarth, Tricia Nemoseck, Mark Kern. Type of snack influences satiety responses in adult women. Appetite. 2010. 54:564-569.
Nemoseck, T, Kern, M. Urinary calcium losses during high impact and resistance exercise training. Int J Sports Nutr Exerc Metab. 19(2):162-71, 2009.
Klein, J, Nyhan, WL, Kern, M. The effects of alanine ingestion on metabolic responses to exercise in cyclists. Amino Acids. 37(4):673-80, 2009.
Cheng, MH, Bushnell, D, Cannon, D, Kern, M. Regulation of appetite by exercise performed before or after meal consumption. Appetite. 52(1):193-8, 2009. Epub 2008 Sep 25.
Hill, KM, Braun, M, Kern, M, Martin, BR, Navalta, JW, Sedlock, DA, McCabe, L, McCabe, GP, Peacock, M, Weaver, CM. Predictors of calcium retention in adolescent boys. J Clin Endocrinol Metab. 93(12):4743-4748, 2008.
Kern, M, Heslin, CJ, Rezende, RS. Metabolic and performance effects of raisins versus sports gel as pre-exercise feedings in cyclists. J Strength Cond Res. 21(4):1204-7, 2007.
Kern, M., Broder, H.D., Edmondson, J.I., and Cannon, D.T. Diet composition does not alter energy expenditure, substrate metabolism or excess post-exercise oxygen consumption in healthy, non-exercise trained women. Nutr Res 27(11): 665-671, 2007.
Burger, K.S., Kern, M., Coleman, K.J. (2007) Characteristics of self-selected portion size in young adults. J Am Dietetic Assoc. 107:611-8.
Braun, M., B.R. Martin, B.R., Kern, M., McCabe, G.P., Peacock, M., Jiang, Z., Weaver, C.M. (2006) Calcium retention in adolescent boys on a range of controlled calcium intakes. Am. J. Clin. Nutr. 84:414-8.
Ischayek J.I. and Kern, M. (2006) US honeys varying in glucose and fructose content elicit similar glycemic indexes. J Am Dietetic Assoc. 106:1260-62.
Kern, M. Dietary intake of adolescent athletes and non-athletes. (2006) J Am Dietetic Assoc. 106:717-8.
Pernick, Y, Nichols, JF, Rauh, MJ, Kern, M, Ji, M, Lawson, MJ, Wilfley, D. (2006) Disordered eating among a multi-racial/ethnic sample of female high school athletes. J Adol Health. 38:689-95.
Kloss, R., Linscheid, J., Johnson, A., Lawson, B., Edwards, K., Linder, T., Stocker, K., Petitte, J., Kern, M. (2005) Effects of conjugated linoleic acid supplementation on blood lipids and adiposity of rats fed diets rich in saturated versus unsaturated fat. Pharmacological Research. 51:503-7.
Benado, M, Alcantara, C, de la Rosa, R, Ambrose, M, Mosier, K, Kern, M. Effects of various levels of dietary fructose on blood lipids of rats. In Review.
Kern, M., Ellison, D. Marroquin, Y., Ambrose, M., and Mosier, K. (2002) The effects of soy protein supplemented with methionine on blood lipids and adiposity of rats. Nutrition. 18:654-6.
Kern, M., Beuttenmuller, D., Diehl, S., McCormick, C, Ambrose, M. (2002) The effects of protein repletion at varied levels on the growth and nutritional status of protein restricted rats. Nutrition Research. 22;957-63.
Kern, M. (2001) An integrative research project for teaching research concepts and nutrition principles to college students. J Nutr Educ. 33:301-2.
Kern, M. Podewils, L.J., Vukovich, M., and Buono, M.J. (2001) Physiological response to exercise in the heat following creatine supplementation. J Exerc. Physiol. 4:18-27.
Weaver, C.M., Teegarden, D.T., Lyle, R.M., McCabe, G.P., McCabe, L.D., Proulx, W., Kern, M., Sedlock, D., Anderson, D.D., Hillberry, B.M., Peacock, M., and Johnston, C.C. (2001) Impact Of Exercise On Bone Health And Contraindication Of Oral Contraceptive Use In Young Women. Med. Sci. Sports Exerc. 33:873-880.
Misell, L.M, Lagomarcino, N.D., Schuster, V., and Kern, M. Chronic medium-chain triacylglycerol consumption and endurance performance in trained runners. (2001) J. Sports Med. Phys. Fitness. 41:210-215.
Kern, M., Harris, D.R., Broder, H., and Edmondson, J.I. (2000). Effects of an acute bout of exercise on high density lipoprotein cholesterol following consumption of a high or low fat diet. Sports Med. Training Rehab. 9:199-208.
Kern, M., Lagomarcino, N.D., Misell, L.M., Schuster, V. (2000). The effect of medium-chain triacylglycerols on the blood lipid profile of male endurance runners. J. Nutr. Biochem. 11:288-292.0 -
mamapeach910 wrote: »mamapeach910 wrote: »mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
If he doesn't have the education and experience in the area I'm interested in (liver health specifically in this case) why bother?
Education? Did you look? He's got a Masters of Science in Nutrition. He's more than qualified. He's not just some random muscle-head.
That doesn't stack up against an MD and 20 some years medical experience with metabolic issues plus research. And Dr. Lustig isn't the only one lecturing on this issue, either. I'm finding more and more lectures from other professionals based on research findings in animals and humans.
Except if he is a doctor and has 20 yrs experience, how does he get very basic things wrong?0 -
mamapeach910 wrote: »mamapeach910 wrote: »mamapeach910 wrote: »http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/"]http://alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/[/url]
Back to lurking in the thread.
Not even close to an equally impressive CV. And he works in the fitness field. How much of what he does is relevant to the average, non athlete American's health?
Forget the CV, please. Read his references, since he went to the trouble of making them.
If he doesn't have the education and experience in the area I'm interested in (liver health specifically in this case) why bother?
Education? Did you look? He's got a Masters of Science in Nutrition. He's more than qualified. He's not just some random muscle-head.
That doesn't stack up against an MD and 20 some years medical experience with metabolic issues plus research. And Dr. Lustig isn't the only one lecturing on this issue, either. I'm finding more and more lectures from other professionals based on research findings in animals and humans.
It is education enough to allow him to cull together research and form an argument on a subject regarding nutrition.
He cited PLENTY of other papers in the blog post I linked. You can read all of them for links to people with impressive enough medical credentials.
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So I've started reading this:
http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/
He has criticisms, but on some of the issues I'm most concerned with, he has agreements, too. For example:
"Another oversimplification Lustig makes is that fructose is “ethanol without the buzz,” and that fructose is toxic to the liver. This once again helps me illustrate my point that even in the case of alcoholic beverages, their risk or benefit to health is dose-dependent."
Okay, so this implies fructose is harmful to the liver at some dosage. He is criticizing in part because Lustig doesn't state the dosage. Well, no one knows exactly, but if there is a safe dosage, this implies there is such a thing as too much and that too much will harm the liver.
He complains: "I would add that fiber is only one of the numerous phytochemicals in fruit that impart health benefits. Thus, it’s not quite as simple as saying that fructose is evil, but once you take it with fiber, you’ve conquered the Dark Side."
But this means he acknowledges the benefits of fiber and other health benefits of fruit, too. He'd likely be scornful of posters here who try to equate a strawberry with ice cream to 'show' that all sugar from all sources is the same.
He says:
"I have a great deal of respect for Lustig’s professional accomplishments, and I share his concern for the nation’s penchant for sitting around and overconsuming food and beverages of all sorts. However, I disagree (as does the bulk of the research) with his myopic, militant focus on fructose avoidance. He’s missing the forest while barking up a single tree."
Well, in research and medicine, what is wrong with barking up a single tree, and then other researchers can broaden out. This is Lustig's career focus. Does that mean he's wrong, or just that others need to blaze other trails in nutrition to complete the picture? One person sure can't do it all.
He concludes by saying:
So, what’s the upper safe limit of fructose per day (all sources considered)? Again, this depends on a number of variables, not the least of which are an individual’s physical activity level and lean body mass. Currently in the literature is a liberal camp reporting that fructose intakes up to 90 grams per day have a beneficial effect on HbA(1c), and no significant effects are seen for fasting triacylglycerol or body weight with intakes up to 100 grams per day in adults [15]. The conservative camp suggests that the safe range is much less than this; roughly 25-40 grams per day [19]. Figuring that both sides are biased, the middle figure between the two camps is roughly 50 grams for adults (I’m talking about the general population, athletes with high energy demands can safely consume more).
Well I'd like to stack this up against the WHO recommendation and I'll have to go looking for more reasons on why they're going with the much lower %5. So I'm off to learn more!0 -
One more thing, I posted this before because Dr. Hu's assertion alarms me a helluva lot more than Dr. Lustig's:
http://www.npr.org/blogs/thesalt/2013/02/28/173170149/sugars-role-in-rise-of-diabetes-gets-clearer
"Hu notes that he was also surprised to see that other foods did not predict diabetes risk nearly as strongly as sugar in Lustig's study. "I don't know why this happened, because we know other foods are associated with diabetes risk – like highly refined grain products, white rice, bread, and other starchy foods. Those foods are not very different from sugar. But maybe sugar is a better indicator of certain dietary habits of a population."
Broadening out from just fructose as the problem only causes me more concern as far as diet since it just embraces even more foods.
Lustig also knows perfectly well that his research isn't the entire picture.
"Lustig himself is the first one to admit that proving that any one thing causes a disease, especially a chronic disease, is tricky business. And Lustig's co-author Sanjay Basu wrote on an epidemiology blog this week that "we can't 'prove causality' through any amount of statistics."0 -
Just interrupting this fascinating sugar battle to note that this thread forced me to go ALL THE WAY to my fridge to get a Fage 0% with honey for a bit of a lunch appetizer. I regret nothing. Mmmmmm. Delicious bee spit. Nom nom nom.0
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One more thing, I posted this before because Dr. Hu's assertion alarms me a helluva lot more than Dr. Lustig's:
http://www.npr.org/blogs/thesalt/2013/02/28/173170149/sugars-role-in-rise-of-diabetes-gets-clearer
"Hu notes that he was also surprised to see that other foods did not predict diabetes risk nearly as strongly as sugar in Lustig's study. "I don't know why this happened, because we know other foods are associated with diabetes risk – like highly refined grain products, white rice, bread, and other starchy foods. Those foods are not very different from sugar. But maybe sugar is a better indicator of certain dietary habits of a population."
Broadening out from just fructose as the problem only causes me more concern as far as diet since it just embraces even more foods.
Lustig also knows perfectly well that his research isn't the entire picture.
"Lustig himself is the first one to admit that proving that any one thing causes a disease, especially a chronic disease, is tricky business. And Lustig's co-author Sanjay Basu wrote on an epidemiology blog this week that "we can't 'prove causality' through any amount of statistics."
Thats funny alot of prominent low carb gurus are adding back "safe starches" to their diets and those include white rice and white potatoes...........hmmmm0 -
One more thing, I posted this before because Dr. Hu's assertion alarms me a helluva lot more than Dr. Lustig's:
http://www.npr.org/blogs/thesalt/2013/02/28/173170149/sugars-role-in-rise-of-diabetes-gets-clearer
"Hu notes that he was also surprised to see that other foods did not predict diabetes risk nearly as strongly as sugar in Lustig's study. "I don't know why this happened, because we know other foods are associated with diabetes risk – like highly refined grain products, white rice, bread, and other starchy foods. Those foods are not very different from sugar. But maybe sugar is a better indicator of certain dietary habits of a population."
Broadening out from just fructose as the problem only causes me more concern as far as diet since it just embraces even more foods.
Lustig also knows perfectly well that his research isn't the entire picture.
"Lustig himself is the first one to admit that proving that any one thing causes a disease, especially a chronic disease, is tricky business. And Lustig's co-author Sanjay Basu wrote on an epidemiology blog this week that "we can't 'prove causality' through any amount of statistics."
Thats funny alot of prominent low carb gurus are adding back "safe starches" to their diets and those include white rice and white potatoes...........hmmmm
Okay. But do you have any abstracts or lectures on why they're doing this?
Meanwhile, Dr. Lustig, at the end of the lecture I linked, does branch out from fructose and list a total of four concerns for liver health, one of which worries me since I'm on a low carb diet:
Transfats
Alcohol
Fructose
Branched-Chain Amino acids
I'd be less alarmed if he just stuck with sugar!
I'm eagerly looking forward to more information on branched-chain amino acids because I want to know how much is too much for my age, height, weight, gender, muscle mass, and activity level.
And if you have anything on potatoes of any variety helping my liver out, links, please.
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This discussion has been closed.
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