cron-web.org

[MR]

re: Hey leptin-loving TWITS: Say hello to the grave!; de Grey may need those bacteria that clean you up!

CRON4healthyfuture wrote:

> Hey, leptin-junkies!, just make sure you tell de Grey which plot you got, he wants to bat clean-up on the bacs that turn you into Krebs Cycle intermediates!
>

Er ... huh? Wha?

I'm not sure what this even means, but it seems to involve the notion
that de Grey is doing work that somehow involves Krebs cycle enzymes or
intermediates, on leptin, or on modifying metabolism in some related
way. I'm not aware that he is doing any such work at all, at all.

You are thinking of AUBREY de Grey of Cambridge, right? The constant
misrepresentation of his views would be explained if there were some
OTHER "de Grey" with whom you were confusing him ... maybe gardening
consultant A. (*Anthony*) de Grey ...?

-MR
> =-=-=-=-=-=-=-=-
>
> http://tinyurl.com/mza4z
>
> =--=-=-=--=-==--=
>
> "The inability to decrease leptin to the basal levels because of high estrogen after spawning could be in part responsible for the short life span of ayu." - PMID: 16506227
>
> =--=-=-=-=-=--==-
>
> http://tinyurl.com/lrjqb
>
> =--=--=-=-==-=-=--=
>
> "RESULTS: The elderly subjects with HBP had significantly higher leptin levels than the healthy elderly subjects (P = .02). Furthermore, in female elderly subjects we observed a statistically significant correlation between systolic blood pressure and leptin (r = 0.37, P = .003), as well as systolic blood pressure and age (r = 0.29, P = .02), but not with diastolic blood pressure. In male elderly subjects, there was no correlation between leptin and systolic blood pressure or leptin and diastolic blood pressure. However, hyperleptinemia as risk factor for HBP was nearly 5 times higher in men than in women (men, odds ratio = 18.0, 95% confidence interval 3.2-100.9, P < .001 vs women, odds ratio = 3.33, 95% confidence interval 1.4-7.4, P = .003). CONCLUSIONS: Our data suggest that hyperleptinemia was a significant risk factor for HBP elderly individuals, mainly in men." - PMID: 16454556
>
> =-=--=-=-=-=-=-=-
>
> http://tinyurl.com/n2krw
>
> =--==--==-=-=-=-=-
>
> "Evidence suggests that a clustering of sources of oxidative stress exists in obesity: hyperglycemia, hyperleptinemia, increased tissue lipid levels, inadequate antioxidant defenses, increased rates of free radical formation, enzymatic sources within the endothelium, and chronic inflammation." - PMID: 16302012
>
> =--==-=-=-=--=-=
>
> http://tinyurl.com/o2f2t
>
> =--===--==--==-
>
> "CONCLUSIONS: Our findings indicate that normotensive individuals with high normal BP have statistically significantly higher plasma leptin levels and lower numbers of human soluble leptin receptors. This observation may play a important role in the pathogenesis of cardiovascular events in this special group of patients and needs further investigation." - PMID: 16053999
>
> =--==--==--==-=--=-=
>
> http://tinyurl.com/rxeuy
>
> =-=-=-=-=--==---=-=-=-=
>
> "SUMMARY: Excess energy-intake leads to an expansion of adipose tissue, a hallmark of obesity. But morphology of the expanded adipose tissue differs across individuals, including the size of adipocytes. The presence of 'large' rather than 'small' adipocytes is associated with functional and structural abnormalities of adipose tissue. These include increased production of bioactive molecules, such as leptin, angiotensinogen, pro-inflammatory cytokines, and reactive oxygen species; insufficient capacity to accommodate excess energy-intake leading to ectopic fat storage in tissues and in turn insulin resistance and hyperinsulinemia; and augmented macrophage infiltration enhancing the production of pro-inflammatory cytokines and reactive oxygen species. Such a 'dysfunctional' adipose tissue may, in turn, induce activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system and oxidative stress and, hence, promote the development of obesity-associate
d
> hypertension." - PMID: 16481885
>
> =-=-=-=-=-=--==--=-=-==-
>
> http://www.jci.org/cgi/content/full/115/12/3579
>
> =-=-=-=-=--=-=-==-=-=-=-
>
> "These "weight-reduced" phenotypes are similar to those of leptin-deficient humans and rodents. We examined metabolic, autonomic, and neuroendocrine phenotypes in 10 inpatient subjects (5 males, 5 females [3 never-obese, 7 obese]) under 3 sets of experimental conditions: (a) maintaining usual weight by ingesting a liquid formula diet; (b) maintaining a 10% reduced weight by ingesting a liquid formula diet; and (c) receiving twice-daily subcutaneous doses of leptin sufficient to restore 8 am circulating leptin concentrations to pre-weight-loss levels and remaining on the same liquid formula diet required to maintain a 10% reduced weight. During leptin administration, energy expenditure, skeletal muscle work efficiency, sympathetic nervous system tone, and circulating concentrations of thyroxine and triiodothyronine returned to pre-weight-loss levels. These responses suggest that the weight-reduced state may be regarded as a condition of relative leptin insufficiency. Preve
nt
> ion of
> weight regain might be achievable by strategies relevant to reversing this leptin-insufficient state." - PMID: 16322796
>

[A1CR]

Mr. MR said:
>You're not, surely, saying that this proves something about CR or aging in nonobese, >non-leptin-resistant, nonasthmatic folks, are you?

No, MR, I am not the one who is saying it..........

THE FREAKIN' MD'S THAT RAN THE STUDY ARE THE ONES THAT ARE SAYING IT. WAKE UP!

If you eat until obese, you are going to increase your risk of developing asthma.

If you decide to CALORICALLY RESTRICT, you DECREASE your risk of asthma.

As an experiment, I want to see if anyone BESIDES MR similiarly believes that leptin can be so summarily disregarded. Anyone?

=-=-=-==-=-=-=-=-

"A lot of people have been wondering for many, many years why asthma is rising across the world, particularly in the developed world, and the obesity epidemic has been a near parallel to the asthma epidemic," said study author Dr. Akshay Sood, an associate professor of medicine at the University of New Mexico School of Medicine in Albuquerque. "A lot of epidemiologists have been wondering whether there is really a connection or just a strange coincidence."

"You don't need any more science to say you need to lose weight," Sood said.

[A1CR]

Posted on behalf of CRON4healthyfuture 2006-03-16:

C'mon, I want to hear some more of your smug "You surely don't believe...." crap on this one. =-=-==--
http://tinyurl.com/kbdsg
=-=-=-=-=--=
Methods We sensitized and challenged BALB/cJ mice with ovalbumin. Alzet® micro-osmotic pumps were implanted in the mice to deliver a continuous infusion of either saline or leptin (1.75 ìg/g/d). Two days later, the mice were challenged with either aerosolized saline or ovalbumin once per day for 3 days. We measured airway responsiveness, performed bronchoalveolar lavage, and obtained blood to measure serum leptin and IgE 24 or 48 hours after the last challenge. Results Leptin infusion increased serum leptin concentrations, which were increased further after ovalbumin sensitization and challenge. Ovalbumin challenge increased bronchoalveolar lavage fluid cells and cytokines, serum IgE, lung cytokine mRNA expression, and responses to inhaled, aerosolized methacholine. It is important to note that the changes in methacholine responsiveness and IgE were augmented in leptin- versus saline-infused mice. Conclusions These results indicate that serum leptin is increased during
allergic reactions in the airways and may play a role in the relationship between obesity and asthma.

[MR]

CRON4healthyfuture wrote:

> C'mon, I want to hear some more of your smug "You surely don't believe...." crap on this one. =-=-==--
> http://tinyurl.com/kbdsg

Glad to oblige!

The authors find that raising leptin to supraphysiologic levels enhances
the allergic response over and above the contribution of the natural
increase in leptin in response to such a challenge. They conclude:
--------------

Conclusions These results indicate that serum leptin is increased
*during allergic reactions in the airways* and may play a role in the
relationship between *obesity* and asthma.

------------

So, as with hyperinsulinemia, having extremely high leptin levels
associated with obesity is bad for one -- in particular, it may
contribute to asthma.

You're not, surely, saying that this proves something about CR or aging
in nonobese, non-leptin-resistant, nonasthmatic folks, are you?


Last time I said something pretty darned similar, you replied:

> No, MR, I am not the one who is saying it..........
>
> THE FREAKIN' MD'S THAT RAN THE STUDY ARE THE ONES THAT
> ARE SAYING IT. WAKE UP!

But they WEREN'T saying it; they were saying that (as you NOW rightly
summarize):

> If you eat until obese, you are going to increase your risk of
> developing asthma.

Right. But: ou're not, surely, saying that this proves something about
*CR or aging* in *nonobese*, *non-leptin-resistant*, *nonasthmatic*
folks, are you?

[A1CR]

posted on behalf of CRON4healthyfuture:

MR said:
> >*CR or aging* in *nonobese*, *non-leptin-resistant*, *nonasthmatic* folks,
> >are you?

Nonobese people who coordinate a calorically-restricted diet will have a
reduced risk of asthma as compared to the alternative. Your smartass reply
avoids this obvious conclusion.