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Protein and Insulin Sensitivity
Replies
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stevencloser wrote: »Something interesting I found while looking for examples of large scale studies.
https://www.edge.org/response-detail/25497
And the thing with nutrition is that a "proper" nutritional intervention study is way harder to do, which the article sortof mentions too. With a new drug, easy you give one group the drug the other a placebo, done. You can scale that up as you wish. There's no way the control group would somehow get the drug or that the experimental group has a high amount of people who simply don't take it. For nutritional intervention you'd have to monitor every participant 24/7 for weeks to months. That's just not feasible.
Good point. Although it's not that simple; many drug interventions are treating conditions that can be affected by other factors (example a blood pressure tablet trial would need to factor variables like diet, cardiac function, exercise, concurrent medications etc so a large subject group can help in looking at overall response across a population, not just a handful of participants) ... but really diverging from the actual topic here.,
I guess I'm critiquing nutritional studies in the same way I would a medical intervention/drug trial. I'm not sure that's a bad thing but I do respect the points made about the difficulty in large studies.
But even a study of 100 people would be more convincing. Or 200 ... 36 is kinda just, meh.
With these small studies though, just because they may be the best model researchers can realistically produce doesn't automatically make them good evidence.
One way to increase the strength of the conclusions would be to replicate the experiment, several times and compare the data. But then wouldn't the cost of that be as prohibitive as a large no of participants?
I dunno. I just think a finding such as this (or anything really) should be viewed in the context of the study limitations.
That's all
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I thought this article may be of interest. It is mainly dealing with protein intake/sarcopenia but does talk about IR a little towards the end.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760315/
Cheers, h.
Sorry- not a scientific bone in my body.2 -
I dunno. I just think a finding such as this (or anything really) should be viewed in the context of the study limitations.
But as stevencloser said, you are applying standards that aren't used in nutrition studies normally (in part because the goal is different than for the large scale drug studies -- they aren't trying to get a drug approved). If you can show that other nutrition studies follow your model and this one departed from it, sure, but I don't think you can -- virtually every nutrition study that gets discussed is small like this one or one of the large correlation studies, which is why things like the Health Care Professional studies and the information from them are given such importance despite the problems with them.
Also NO ONE should claim that the result of one of these nutrition studies proves anything (and neither the people doing this study nor me, who linked it) said otherwise. They try out ideas and typically result in findings that look interesting to explore further, as well as more questions. That's actually one thing that sometimes drives me crazy on MFP, that people will toss up some study (mice lose more weight eating during the day and not at night, overweight women with an exercise intervention lose less weight than those without it) and insist it proves some point that it clearly does not. But to insist that it lacks value and isn't worth doing is not true either -- goes way too far in the other way. There are presumably enough people to demonstrate statistically significant differences, and then more work needs to be done.3 -
middlehaitch wrote: »I thought this article may be of interest. It is mainly dealing with protein intake/sarcopenia but does talk about IR a little towards the end.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760315/
Cheers, h.
Sorry- not a scientific bone in my body.
That was a good read. I'm bookmarking it.1 -
This topic is over my head but fascinating. Looking forward to more responses about why these results might have turned out the way they did. Obviously this one small study doesn't prove anything (no one study does) and OP didn't suggest it did. The affect of protein on insulin comes up here a lot, so I think this study is interesting to pick apart!0
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lemurcat12 wrote: »I dunno. I just think a finding such as this (or anything really) should be viewed in the context of the study limitations.
But as stevencloser said, you are applying standards that aren't used in nutrition studies normally (in part because the goal is different than for the large scale drug studies -- they aren't trying to get a drug approved). If you can show that other nutrition studies follow your model and this one departed from it, sure, but I don't think you can -- virtually every nutrition study that gets discussed is small like this one or one of the large correlation studies, which is why things like the Health Care Professional studies and the information from them are given such importance despite the problems with them.
Also NO ONE should claim that the result of one of these nutrition studies proves anything (and neither the people doing this study nor me, who linked it) said otherwise. They try out ideas and typically result in findings that look interesting to explore further, as well as more questions. That's actually one thing that sometimes drives me crazy on MFP, that people will toss up some study (mice lose more weight eating during the day and not at night, overweight women with an exercise intervention lose less weight than those without it) and insist it proves some point that it clearly does not. But to insist that it lacks value and isn't worth doing is not true either -- goes way too far in the other way. There are presumably enough people to demonstrate statistically significant differences, and then more work needs to be done.
If you read my replies, I have acknowledged my bias but furthermore also acknowledge that small studies may trigger further research ... replicates studies ... 'further work' as you say.
Sure, a human study is better than rats. Kinda. Rats are actually psysiologically similar to humans (and easier to control variables) and finding of animal trials are often then used to see if the same apples to people. I'm not saying animal trials are good evidence. They do have their place.
As do small scale human trials.
Are either 'good' evidence though? No.
I have never at any point said this trial lacks 'value'. I have said it is not broad enough to provide evidence or draw conclusions from.
I think you - like me - are essential expressing frustration about people (lay people, the media etc) drawing conclusions based on what is poor quality evidence or skewed interpretation of same.
With this article - great talking point, yes.
Clinical evidence? No.
Further research? Sure.
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One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.3
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lemurcat12 wrote: »I dunno. I just think a finding such as this (or anything really) should be viewed in the context of the study limitations.
But as stevencloser said, you are applying standards that aren't used in nutrition studies normally (in part because the goal is different than for the large scale drug studies -- they aren't trying to get a drug approved). If you can show that other nutrition studies follow your model and this one departed from it, sure, but I don't think you can -- virtually every nutrition study that gets discussed is small like this one or one of the large correlation studies, which is why things like the Health Care Professional studies and the information from them are given such importance despite the problems with them.
Also NO ONE should claim that the result of one of these nutrition studies proves anything (and neither the people doing this study nor me, who linked it) said otherwise. They try out ideas and typically result in findings that look interesting to explore further, as well as more questions. That's actually one thing that sometimes drives me crazy on MFP, that people will toss up some study (mice lose more weight eating during the day and not at night, overweight women with an exercise intervention lose less weight than those without it) and insist it proves some point that it clearly does not. But to insist that it lacks value and isn't worth doing is not true either -- goes way too far in the other way. There are presumably enough people to demonstrate statistically significant differences, and then more work needs to be done.
If you read my replies, I have acknowledged my bias but furthermore also acknowledge that small studies may trigger further research ... replicates studies ... 'further work' as you say.
Sure, a human study is better than rats. Kinda. Rats are actually psysiologically similar to humans (and easier to control variables) and finding of animal trials are often then used to see if the same apples to people. I'm not saying animal trials are good evidence. They do have their place.
As do small scale human trials.
Are either 'good' evidence though? No.
I have never at any point said this trial lacks 'value'. I have said it is not broad enough to provide evidence or draw conclusions from.
I think you - like me - are essential expressing frustration about people (lay people, the media etc) drawing conclusions based on what is poor quality evidence or skewed interpretation of same.
With this article - great talking point, yes.
Clinical evidence? No.
Further research? Sure.
As far as I can see, we are in agreement, I'm just summarizing what I think we both agree on for the more general audience to follow in case they are missing what we are discussing since it is rather important.
The gold standard for nutritional research is the metabolic ward study were you can pretty much get a single, independent variable manipulation. When these show up they are great but they are usually the same type of small batch, short-term studies due to cost and ability to find participants willing to be voluntarily incarcerated for a month or so.
I would say that the big difference I see here is that nutritional studies merely provide evidence to a small piece of the puzzle, which is rather large, while drug trials are trying to access as much of the big picture as possible and the scope is considerably smaller compared to human nutrition. Bringing a drug to market costs hundreds of millions of dollars and that's just not in the purview of nutritional research unfortunately.3 -
Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.0 -
middlehaitch wrote: »I thought this article may be of interest. It is mainly dealing with protein intake/sarcopenia but does talk about IR a little towards the end.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760315/
Cheers, h.
Sorry- not a scientific bone in my body.
I've seen one of the related studies to this (a mouse study) and isn't really what you might think. This is a rather controversial theory by a minority of researchers who believe that in order to trigger muscle synthesis that you require a minimum of around 20g of protein at one sitting (with maximum effect at 30g) with 5g of it being Leucien and that carbohydrates don't work to spur synthesis in adults as it does in children. However, this isn't what the balance of evidence shows, which is that timing is not very important but rather the total intake of protein per day and that carbohydrates do help to spur muscle synthesis in adults as would be expected when you look at the biochemistry of cell signaling.
I'm not convinced about the protein timing aspect but having a higher protein diet seems to be reasonable.1 -
Wheelhouse15 wrote: »middlehaitch wrote: »I thought this article may be of interest. It is mainly dealing with protein intake/sarcopenia but does talk about IR a little towards the end.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760315/
Cheers, h.
Sorry- not a scientific bone in my body.
I've seen one of the related studies to this (a mouse study) and isn't really what you might think. This is a rather controversial theory by a minority of researchers who believe that in order to trigger muscle synthesis that you require a minimum of around 20g of protein at one sitting (with maximum effect at 30g) with 5g of it being Leucien and that carbohydrates don't work to spur synthesis in adults as it does in children. However, this isn't what the balance of evidence shows, which is that timing is not very important but rather the total intake of protein per day and that carbohydrates do help to spur muscle synthesis in adults as would be expected when you look at the biochemistry of cell signaling.
I'm not convinced about the protein timing aspect but having a higher protein diet seems to be reasonable.
Well that's good, because I like carbs with my protein
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Wheelhouse15 wrote: »Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.
I guess IR may be seen that way, but as a "defense mechanism" is not that smart, since the final outcome is diabetes.0 -
@Wheelhouse15 thanks for your feedback. As I said I am not too well educated/read on the sience of nutrition. (Read not at all)
Interpretation from the good people on this forum is, at times, priceless, and always educational.
Thanks for the comments on the daily intake of protein being the important factor ( even for us older people) not the amount ingested at one time- I was curious about that.
@GottaBurnEmAll, what is steak without a baked potato!
Cheers, h.1 -
Gianfranco_R wrote: »Wheelhouse15 wrote: »Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.
I guess IR may be seen that way, but as a "defense mechanism" is not that smart, since the final outcome is diabetes.
That's because it's most likely meant to put a short term stop on storage, but people just keep overfeeding.3 -
Gianfranco_R wrote: »Wheelhouse15 wrote: »Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.
I guess IR may be seen that way, but as a "defense mechanism" is not that smart, since the final outcome is diabetes.
Not all adaptations we have are beneficial in the modern era. I suspect that this wasn't an issue among our ancestors who lived in a much less food rich environment and starvation was the real issue. Packing on a bit of extra fat was the exception during our evolution.
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Wheelhouse15 wrote: »Gianfranco_R wrote: »Wheelhouse15 wrote: »Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.
I guess IR may be seen that way, but as a "defense mechanism" is not that smart, since the final outcome is diabetes.
Not all adaptations we have are beneficial in the modern era. I suspect that this wasn't an issue among our ancestors who lived in a much less food rich environment and starvation was the real issue. Packing on a bit of extra fat was the exception during our evolution.
Exactly. So far as your endocrine system and brain are concerned, your name is Ugg, and you live in a cave, and might have to wrestle a bear for the next salmon you eat. The "land of plenty" isn't part of our biological programming just yet.1 -
Gallowmere1984 wrote: »Wheelhouse15 wrote: »Gianfranco_R wrote: »Wheelhouse15 wrote: »Gallowmere1984 wrote: »One other really odd thing that is suggested here that's kind of annoying me: insulin is a storage hormone. Having a temporary resistance to it helps (not hinders) weight loss, assuming calories are kept constant. This is part of the reason that clenbuterol and the ephedrine/caffeine stacks work as well as they do. They temporarily reduce insulin sensitivity, making storage more difficult. Insulin resistance in the obese is a symptom, not a cause.
It is an interesting point that most people miss: when you have increased insulin sensitivity it's systemic meaning that both muscle and fat cells are more sensitive so adipose cells becomes more efficient at storing fat. This reduce ability to store fat might be one of the few mechanisms to fight excessive weight gain that we actually have developed. Of course, it never defeats CICO but it might change the energy balance slightly.
I guess IR may be seen that way, but as a "defense mechanism" is not that smart, since the final outcome is diabetes.
Not all adaptations we have are beneficial in the modern era. I suspect that this wasn't an issue among our ancestors who lived in a much less food rich environment and starvation was the real issue. Packing on a bit of extra fat was the exception during our evolution.
Exactly. So far as your endocrine system and brain are concerned, your name is Ugg, and you live in a cave, and might have to wrestle a bear for the next salmon you eat. The "land of plenty" isn't part of our biological programming just yet.
Good thing we live in modern times because the bear wrestling part sounds ok but I hate salmon.
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I read through the actual study, and found this:Therefore, we conducted an RCT to evaluate the effect of dietary protein intake on body composition and insulin sensitivity by providing a protein supplement to subjects during weight loss to minimize the potential confounding influences of differences in overall diet composition on our outcome measures.
I'm not finding details on what type of protein supplement was given, but the results make me think it was whey. If it was, then I just have to say, "No kitten!" If it wasn't whey, then perhaps some of the interest in the results can be explained... but it is really hyped even in the original authors' own words. It almost makes me think that the authors realized there was nothing new but really wanted to publish something, so they just made it sound like there is some wild new correlation. At best, this shows there is value in additional research. It proves nothing at this point.0
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