Re: Re: Hypoadiponectinemia and obesity - keeping it straight

[Guest guest]

This discussion is circling on itself so perhaps there is another

viewpoint to consider.

Losing weight is difficult. You we control what we eat 24x7. This leaves

a lot of time we must distract ourselves from our hunger and what better

way than to search for " answers " . Sure finding an easier way could be

better than winning the lottery. We know the drug companies have been

pursuing this for a long time.

I don't think there is any dispute about the first order basic

mechanism. Eat too much food, gain weight. Eat less food than you need

and lose weight. It is only human nature to look for explanations other

than " I am somehow at fault for my present situation " (been there, done

that). The bottom line is it really doesn't matter and I have no desire

to impose my opinion on others or even consider blame.

Let's not get so invested in different causal scenarios that we lose

sight of the immediate issue of managing what we are eating today, and

tomorrow, and so on... That is what is really important.

Understanding the " why " is of academic interest but so far hasn't led to

any magic bullet short cuts (Hoodia anyone?).

Be well

JR

Rodney wrote:

>

>

> Hi Kayce:

>

> As you say, and as I had already noted in my earlier post:

>

> " hypoadiponetinemia is caused by the interaction of

> 1) genetic factors, and

> 2) environmental factors which also cause obesity "

>

> You added a third point of your own that I have not seen in the study.

>

> Of course the " environmental factors " referred to in that list is

> excessive food consumption resulting from an inexpensive, attractive

> and readily available food supply. Which causes obesity. Of course

> I certainly agree with that point in the study. As do a very large

> majority of the rest of the world's population.

>

> There is nothing we can do about our genetic inheritance. But even

> with poor genes, without the obesity adiponectin (ADPN) is not a

> problem. So in order to solve the ADPN problem people must solve the

> obesity problem which means restricting caloric intake. Which, of

> course, is what this entire site, , is all about!

>

> We know also that in obese people ADPN is low and in slim people it

> is high. And that it appears that ADPN is a key factor, perhaps THE

> key factor, that causes all the problems associated with insulin

> resistance, metabolic syndrome, CVD risk, inflammation/cancer and so

> on.

>

> We also know from several studies (15946462; 15917853;

> 15229336 ......... and there are plenty of others) that when weight

> is lost because of reduced caloric intake, ADPN levels rise, thereby

> solving the problem if the weight loss is pursued to levels

> associated with good health. So it cannot logically be argued that

> ADPN causes obesity, it is obesity (excessive caloric intake) that

> causes the problem of low ADPN .......... change the degree of

> obesity and a change in ADPN follows.

>

> Further, while you have previously acknowledged that the Laws of

> Thermodynamics must apply, it is unclear to me how you can reconcile

> that with your comment that : " but some people will retain fat more

> easily and more often then others eating similarly. " Certainly, poor

> intentinal absorption and much higher activity levels can make a

> difference in some cases. But given people at equal activity levels

> (obese people are not renowned for their athletic exploits, beyond

> carrying a huge amout of extra weight around with them) you can only

> blame obesity on intestinal absorption problems if you assume that

> everyone who is at a healthy weight excretes large amounts of what

> they eat, unabsorbed, and everyone who is obese absorbs just about

> every calorie they consume. Do you have any evidence to support this?

>

> And even if you did, it does not change the fact that in order for

> obese people to lower their weights to levels associated with good

> health and a lengthened life span, they have to consume fewer

> calories. And you can get a pretty good idea how many calories need

> to be cut by checking the data provided by -Benedict and

> Mifflin-St. Jeor. First, by running the numbers to determine the

> caloric intake that is associated with the present (obese) weight.

> Then running the numbers a few times to find what caloric intake is

> associated with an appropriate body weight.

>

> But you are waiting, I think, for someone to come along and invent a

> pill that will relieve you of having to make that effort. I hope it

> comes soon enough for you. I plan to eat an amount that maintains

> what my best guess is, is a healthy weight.

>

> Rodney.

>

>

> >

> > Hi Rodney,

> >

> > I am hurried today and hope I did not make any large errors or

> omissions

> > here.

> >

> > Before I contribute to this thread, I go on notice: I know that

> lowering

> > calories is required to reverse all types of obesity, presently.

> However,

> > there is increasing evidence that the seminar cause of all obesity

> is NOT

> > overeating, according to the standard recommendations for diet.

> Yes, if one

> > reduces calories low enough, weight reduction will occur, but some

> people

> > will retain fat more easily and more often then others eating

> similarly.

> > This paper sheds some light on one possible factor.

> >

> > 2nd sentence of abstract: " Hypoadiponectinemia, caused by

> interactions of

> > genetic factors such as SNPs in the Adiponectin gene and

> environmental

> > factors causing obesity, appears to play an important causal role

> in insulin

> > resistance, type 2 diabetes, and the metabolic syndrome, which are

> linked to

> > obesity. "

> >

> > From this (borne out in the rest of the paper) we know:

> >

> > hypoadiponetinemia is caused by the interaction of

> > 1) genetic factors

> > 2) environmental factors which also cause obesity

> > 3) but not necessarily the obesity itself - that may or may

> not be, but

> > is not stated

> > here

> >

> > and

> >

> > hypoadiponectinemia (not necessarily obesity) appears to be causal

> for

> > 1) insulin resistence

> > 2) type II diabetes

> > 3) metabolic syndrome

> >

> > and

> >

> > hypoadiponectinemia is associated with obesity (does not state

> whether or

> > not it is causative, and paper does not investigate that).

> >

> > and

> >

> > obesity may or may not be associated with type II diabetes, in a

> particular

> > person (e.g., not all obese people are diabetic)

> >

> > Nowhere in this paper did I see that obesity CAUSES

> hyadiponectinemia.

> >

> > Another paper,

> > http://care.diabetesjournals.org/cgi/content/abstract/26/6/1745?

> <http://care.diabetesjournals.org/cgi/content/abstract/26/6/1745?>

> ijkey=fe0d6d75be36b08d8449eee2c0ebb8b20c83db63 & keytype2=tf_ipsecsha

> >

> > states that adiponectin is a known predictor of type II diabetes in

> Pima

> > Indians. It does not say that obesity is.

> >

> > You gloss over the fact that the lowering of the Adiponectin is

> strongly

> > positively associated with various genes. It is in the presence

> of these

> > genes that the obesity, associated with diabetes type II, occurs -

> not

> > otherwise, despite food intake or obesity.

> >

> > I followed the citation given for the sentence you cite: " ....

> insulin

> > resistance caused by obesity, a state of increased adiposity " . You

> seem to

> > conclude from that sentence that the paper is stating that obesity

> causes

> > the insulin resistence, but the paper cited is not verifying that

> at all,

> > from the abstract. It is focused on the biochemical pathways under

> > discussion, not the cause of weight gain.

> >

> > We often assume that the sole cause of weight gain is calorie

> intake.

> > However, Ravussin's work shows (in a paper I cited yesterday) that

> in Pima

> > Indians, low resting metabolic rate PRECEDES obesity. So, you

> don't know

> > for sure, from the papers we have reviewed so far, whether low

> > adiponectinemia precedes obesity or not. We do know that it is

> inversely

> > related to weight gain, decreasing continuously as obesity

> increases. But,

> > nowhere in that paper was it verifed that weight gain PRECEDES

> > hypoadiponectinemia. If the root cause of the hypoadiponectinemia

> is

> > genetic, then of course, hypoadipondectinemia probably precedes

> weight gain,

> > and may be causitive of obesity in the presence of surplus food

> and/or other

> > environmental factors, regardless of whether obesity further lowers

> it,

> > which may also occur.

> >

> > And here is evidence that the fat is not the source of the problem,

> but

> > perhaps just another symptom of the problem:

> >

> http://mednewsarchive.wustl.edu/medadmin/PAnews.nsf/0/5CB0B012B243098F

> <http://mednewsarchive.wustl.edu/medadmin/PAnews.nsf/0/5CB0B012B243098F>

> 86256EAF007964F1

> >

> > I remain interested in what else we will discover here about the

> true and

> > complex nature of obesity.

> >

> > Best,

> > Kayce

> >

> >

[Guest guest]

Well said, ,

And we have examples of CRONies who use exercise at different levels, different supplements, different foods, low fat or low carbo diets, at least one claims a high protein diet. Their goals seem as diverse as there are people practicing CR.

In 20 years we'll know if there IS a best way to do CR.

Regards.

Re: [ ] Re: Hypoadiponectinemia and obesity - keeping it straight

This discussion is circling on itself so perhaps there is another viewpoint to consider.Losing weight is difficult. You we control what we eat 24x7. This leaves a lot of time we must distract ourselves from our hunger and what better way than to search for "answers". Sure finding an easier way could be better than winning the lottery. We know the drug companies have been pursuing this for a long time.I don't think there is any dispute about the first order basic mechanism. Eat too much food, gain weight. Eat less food than you need and lose weight. It is only human nature to look for explanations other than "I am somehow at fault for my present situation" (been there, done that). The bottom line is it really doesn't matter and I have no desire to impose my opinion on others or even consider blame.Let's not get so invested in different causal scenarios that we lose sight of the immediate issue of managing what we are eating today, and tomorrow, and so on... That is what is really important.Understanding the "why" is of academic interest but so far hasn't led to any magic bullet short cuts (Hoodia anyone?).Be wellJRRodney wrote:> > > Hi Kayce:> > As you say, and as I had already noted in my earlier post:> > " hypoadiponetinemia is caused by the interaction of> 1) genetic factors, and> 2) environmental factors which also cause obesity"> > You added a third point of your own that I have not seen in the study.> > Of course the "environmental factors" referred to in that list is> excessive food consumption resulting from an inexpensive, attractive> and readily available food supply. Which causes obesity. Of course> I certainly agree with that point in the study. As do a very large> majority of the rest of the world's population.> > There is nothing we can do about our genetic inheritance. But even> with poor genes, without the obesity adiponectin (ADPN) is not a> problem. So in order to solve the ADPN problem people must solve the> obesity problem which means restricting caloric intake. Which, of> course, is what this entire site, , is all about!> > We know also that in obese people ADPN is low and in slim people it> is high. And that it appears that ADPN is a key factor, perhaps THE> key factor, that causes all the problems associated with insulin> resistance, metabolic syndrome, CVD risk, inflammation/cancer and so> on.> > We also know from several studies (15946462; 15917853;> 15229336 ......... and there are plenty of others) that when weight> is lost because of reduced caloric intake, ADPN levels rise, thereby> solving the problem if the weight loss is pursued to levels> associated with good health. So it cannot logically be argued that> ADPN causes obesity, it is obesity (excessive caloric intake) that> causes the problem of low ADPN .......... change the degree of> obesity and a change in ADPN follows.> > Further, while you have previously acknowledged that the Laws of> Thermodynamics must apply, it is unclear to me how you can reconcile> that with your comment that : "but some people will retain fat more> easily and more often then others eating similarly." Certainly, poor> intentinal absorption and much higher activity levels can make a> difference in some cases. But given people at equal activity levels> (obese people are not renowned for their athletic exploits, beyond> carrying a huge amout of extra weight around with them) you can only> blame obesity on intestinal absorption problems if you assume that> everyone who is at a healthy weight excretes large amounts of what> they eat, unabsorbed, and everyone who is obese absorbs just about> every calorie they consume. Do you have any evidence to support this?> > And even if you did, it does not change the fact that in order for> obese people to lower their weights to levels associated with good> health and a lengthened life span, they have to consume fewer> calories. And you can get a pretty good idea how many calories need> to be cut by checking the data provided by -Benedict and> Mifflin-St. Jeor. First, by running the numbers to determine the> caloric intake that is associated with the present (obese) weight.> Then running the numbers a few times to find what caloric intake is> associated with an appropriate body weight.> > But you are waiting, I think, for someone to come along and invent a> pill that will relieve you of having to make that effort. I hope it> comes soon enough for you. I plan to eat an amount that maintains> what my best guess is, is a healthy weight.> > Rodney.> > > >> > Hi Rodney,> >> > I am hurried today and hope I did not make any large errors or> omissions> > here.> >> > Before I contribute to this thread, I go on notice: I know that> lowering> > calories is required to reverse all types of obesity, presently.> However,> > there is increasing evidence that the seminar cause of all obesity> is NOT> > overeating, according to the standard recommendations for diet.> Yes, if one> > reduces calories low enough, weight reduction will occur, but some> people> > will retain fat more easily and more often then others eating> similarly.> > This paper sheds some light on one possible factor.> >> > 2nd sentence of abstract: "Hypoadiponectinemia, caused by> interactions of> > genetic factors such as SNPs in the Adiponectin gene and> environmental> > factors causing obesity, appears to play an important causal role> in insulin> > resistance, type 2 diabetes, and the metabolic syndrome, which are> linked to> > obesity."> >> > From this (borne out in the rest of the paper) we know:> >> > hypoadiponetinemia is caused by the interaction of> > 1) genetic factors> > 2) environmental factors which also cause obesity> > 3) but not necessarily the obesity itself - that may or may> not be, but> > is not stated> > here> >> > and> >> > hypoadiponectinemia (not necessarily obesity) appears to be causal> for> > 1) insulin resistence> > 2) type II diabetes> > 3) metabolic syndrome> >> > and> >> > hypoadiponectinemia is associated with obesity (does not state> whether or> > not it is causative, and paper does not investigate that).> >> > and> >> > obesity may or may not be associated with type II diabetes, in a> particular> > person (e.g., not all obese people are diabetic)> >> > Nowhere in this paper did I see that obesity CAUSES> hyadiponectinemia.> >> > Another paper,> > http://care.diabetesjournals.org/cgi/content/abstract/26/6/1745? > <http://care.diabetesjournals.org/cgi/content/abstract/26/6/1745?>> ijkey=fe0d6d75be36b08d8449eee2c0ebb8b20c83db63 & keytype2=tf_ipsecsha> >> > states that adiponectin is a known predictor of type II diabetes in> Pima> > Indians. It does not say that obesity is.> >> > You gloss over the fact that the lowering of the Adiponectin is> strongly> > positively associated with various genes. It is in the presence> of these> > genes that the obesity, associated with diabetes type II, occurs -> not> > otherwise, despite food intake or obesity.> >> > I followed the citation given for the sentence you cite: "....> insulin> > resistance caused by obesity, a state of increased adiposity". You> seem to> > conclude from that sentence that the paper is stating that obesity> causes> > the insulin resistence, but the paper cited is not verifying that> at all,> > from the abstract. It is focused on the biochemical pathways under> > discussion, not the cause of weight gain.> >> > We often assume that the sole cause of weight gain is calorie> intake.> > However, Ravussin's work shows (in a paper I cited yesterday) that> in Pima> > Indians, low resting metabolic rate PRECEDES obesity. So, you> don't know> > for sure, from the papers we have reviewed so far, whether low> > adiponectinemia precedes obesity or not. We do know that it is> inversely> > related to weight gain, decreasing continuously as obesity> increases. But,> > nowhere in that paper was it verifed that weight gain PRECEDES> > hypoadiponectinemia. If the root cause of the hypoadiponectinemia> is> > genetic, then of course, hypoadipondectinemia probably precedes> weight gain,> > and may be causitive of obesity in the presence of surplus food> and/or other> > environmental factors, regardless of whether obesity further lowers> it,> > which may also occur.> >> > And here is evidence that the fat is not the source of the problem,> but> > perhaps just another symptom of the problem:> >> http://mednewsarchive.wustl.edu/medadmin/PAnews.nsf/0/5CB0B012B243098F > <http://mednewsarchive.wustl.edu/medadmin/PAnews.nsf/0/5CB0B012B243098F>> 86256EAF007964F1> >> > I remain interested in what else we will discover here about the> true and> > complex nature of obesity.> >> > Best,> > Kayce> >> >

[Guest guest]

At 11:39 AM 8/9/2006, you wrote:

Well said, ,

And we have examples of CRONies who use exercise at different levels,

different supplements, different foods, low fat or low carbo diets, at

least one claims a high protein diet. Their goals seem as diverse as

there are people practicing CR.

In 20 years we'll know if there IS a best way to do

CR.

The Best Way is always going to differ because even if, for example, it

were to be shown that EOD eating/fasting were somehow

" superior " to continual restriction (or the opposite), some

people will find one approch (or the other) untenable in terms of how

much they feel sorry for yourself.

If you feel sorry for yourself, you're not going to succeed at calorie

restriction long-term. Similarly, if you don't actually caloricly

restrict yourself, obviously you're not gaining anything. Whether 27%

restriction appears to be " perfect " 20 years from now or

the-more-the-merrier, as it appears now, with some kind of limit, the

final tolerance/success element is going to be one's level of

satisfaction with the restrictive regimen.

Happily, increases in restriction can be incremental as one's personal

" what makes me feel sorry for myself " changes, one hopes in the

direction of enabling greater restriction if so desired, so the crucial

element, at any point, is maintaining some modicum of restriction with at

least minimal enthusiasm; once that tipping point has been achieved, then

all things are eventually possible, potentially. Without it,

fuggedaboutit.

So probably the " best " way is always going to be an individual

work in progress regardless of what might seem to be the ideal to

eventually be shooting at.

Maco

[Guest guest]

> Well said, ,

Agreed

> And we have examples of CRONies who use exercise at

> different levels, different supplements, different

> foods, low fat or low carbo diets, at least one

> claims a high protein diet. Their goals seem as

> diverse as there are people practicing CR.

But, without speaking out of line, I think the one

thing we all do agree on, regardless of the above, is

that to practive CR-ON, especially the CR, and to lose

weight, you have to cut calories...

Regards

Jeff

[Guest guest]

I guess as long as that is not interpreted that we MUST lose weight or we must achieve a low BMI, we must get to x% body fat, we must run 5 miles, etc. I found a large leeway between the max I was eating and the min I could eat, without weight changes. And that's the message for me.

Those other things are health issues based on conventional medical criteria. However good, many are still argued in those circles and we know not how to apply them to CR.

I still firmly think that if there is a viable way to extend life, it is CR, and whether it works or not is not important. As long as I can do it and it doesn't threaten my life.

And many of the questions I had after reading the first LE book, are still not answered.

And to pick on your statement, I cut calories to find the lowest level where I DIDN'T lose weight.

Regards.

Re: [ ] Re: Hypoadiponectinemia and obesity - keeping it straight

> Well said, , Agreed > And we have examples of CRONies who use exercise at> different levels, different supplements, different> foods, low fat or low carbo diets, at least one> claims a high protein diet. Their goals seem as> diverse as there are people practicing CR. But, without speaking out of line, I think the onething we all do agree on, regardless of the above, isthat to practive CR-ON, especially the CR, and to loseweight, you have to cut calories...RegardsJeff

[Guest guest]

>>> And to pick on your statement, I cut calories to

> find the lowest level where I DIDN'T lose weight.

Thanks! but i agree. I dont want to lose

anymore weight either. And think sometimnes CR

should not be calorie " restriction " cause at some

point we stop restricting and maintain.. maybe Calorie

Reduction or Adequate Calories.

I dont know

Thanks again

Jeff

[Guest guest]

I mentioned in an earlier post that I too was angered, the first few

years after I lost weight, by obese individuals claiming that it was

different/harder/impossible for them to lose weight.

Upon reflection this may anger those of us who were formerly obese

because if true it would diminish our accomplishments that we are so

proud of. Perhaps if our body didn't remodel we could carry around folds

of extra skin as a badge of honor, but as it is people generally don't

even believe us when we tell them our former weight.

For the individuals who think they are different, this may be a little

like learning to ride a bike. If you are convinced you can't you won't,

but if you can balance well enough to stand, you can ride a bike.

Eating less is incredibly difficult. It's not like we can just stop

eating entirely " cold turkey " (interesting turn of phrase). Imagine

trying to break a heroin addiction by only shooting up half as much! The

good news is many here have managed to succeed (in at least the eating

less food one).

I have several theories why I was finally able to succeed but why

speculate. The important data point is that exposure to and learning

more about CRON/CRAN appears to be one very important factor. To all

that are still struggling with learning to ride their bike, keep trying,

it does get easier, while never effortless.

One hint/observation, it's impossible to eat food that isn't in your

house so your discipline needs to be marshaled for shopping. The only

way this wouldn't work is if you take ambien and go food shopping in

your sleep. There is surely a special place in heaven for mothers who

must feed rapacious teens while trying to manage their eating.

JR

Maco wrote:

>

>

> At 11:39 AM 8/9/2006, you wrote:

>

> The Best Way is always going to differ because even if, for example, it

> were to be shown that EOD eating/fasting were somehow " superior " to

> continual restriction (or the opposite), some people will find one

> approch (or the other) untenable in terms of how much they feel sorry

> for yourself.

>

> If you feel sorry for yourself, you're not going to succeed at calorie

> restriction long-term. Similarly, if you don't actually caloricly

> restrict yourself, obviously you're not gaining anything. Whether 27%

> restriction appears to be " perfect " 20 years from now or

> the-more-the-merrier, as it appears now, with some kind of limit, the

> final tolerance/success element is going to be one's level of

> satisfaction with the restrictive regimen.

>

> Happily, increases in restriction can be incremental as one's personal

> " what makes me feel sorry for myself " changes, one hopes in the

> direction of enabling greater restriction if so desired, so the crucial

> element, at any point, is maintaining some modicum of restriction with

> at least minimal enthusiasm; once that tipping point has been achieved,

> then all things are eventually possible, potentially. Without it,

> fuggedaboutit.

>

> So probably the " best " way is always going to be an individual work in

> progress regardless of what might seem to be the ideal to eventually be

> shooting at.

>

> Maco

>

>