Re: Hypoadiponectinemia and obesity - keeping it straight

[Guest guest]

Wow. I think that may have important ramifications. Notice L. Fontana on the list of authors.

One is there must be a change in BMI. 20 liters is a lot of weight change. So does the BMI change not influence risk? That's like saying I get shorter due to aging, bone shortening, disk compaction, but it's assumed I can't use my original height in risk calc.

Secondly, it was always assumed that losing that ugly fat was responsible for the improvements and here we see that fat is only cosmetic. It has no health impact of itself, ergo, maybe there's a health benefit like storing stuff we don't really want in serum, (see Walford's toxin idea). Ergo, surgery is better than dieting to get it out, even though diet may be a benefit in other aspects, how do you diet when you just lost 44#?

Maybe the toxins are the main reason for the adipose growth.

Wonder how much to remove 10#? (ha)

regards.

[ ] Hypoadiponectinemia and obesity - keeping it straight

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/0/5CB0B012B243098F86256EAF007964F1I remain interested in what else we will discover here about the true and complex nature of obesity.Best,Kayce

..

[Guest guest]

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.

> >

> > Please read this again and try to understand the obese are

suffering

> a problem in hormone balance. They don't suffer from denial.

> > http://www.jci.org/cgi/content/full/116/7/1784?

>

maxtoshow= & HITS=10 & hits=10 & RESULTFORMAT= & fulltext=adiponectin & andorexa

c

>

tfulltext=and & searchid=1 & FIRSTINDEX=0 & sortspec=relevance & resourcetype=

H

> WCIT

> > Adiponectin and adiponectin receptors in insulin resistance,

> diabetes, and the metabolic syndrome

> >

> > Regards.

> >

>

>

>

>

>

>

>

>

[Guest guest]

Hi folks:

It would be nice if some time down the road we will be able to compare

the magnitude of the changes in our chemical test biomarkers (hsCRP,

fasting insulin, WBC, etc.) with those of the restricted rhesus

monkeys that are living 30% longer than their unrestricted pals.

Only then, I suspect, will we be able to get some kind of fix on what

our true degree of restriction really is, and then some idea of the

degree of lifespan extension we might possibly, on average, be able to

anticipate. (Making the assumption, of course, that the monkey data

are broadly transerable to humans.)

Rodney.