As I said in my last post, let's see the full paper here and take a look at the raw data. Though LC/MS is a more accurate method, antibody purity is still an issue when you have GDF11 and myostatin 90% homologous.
BTW, my empirical data with my cohort shows that young people are very sensitive to GDF11 - a dose of only 4 ng can cause GERD and other inflammation issues. Older people can tolerate much higher doses. What does this suggest to you?
Look in your inbox for details on the latest Mayo research "Quantification of GDF11 and Myostatin in Human Aging and Cardiovascular Disease".
Some key parts of that study:
"Previous studies exploring the relationship of GDF11 to aging
have been contradictory. Thus, we utilized our quantitative LCMS/
MS assay to measure serum protein levels in 70 women
and 70 men, age 21–93. GDF11 levels did not statistically differ
as a function of age or sex (Figure 1B). MSTN levels were highest
in men in their 20s and statistically declined throughout subsequent
decades (p < 0.05) (Figure 1C). Female MSTN levels did
not change as a function of age (Figure 1C). Consistent with
our previous study (Bergen et al., 2015), young women had lower
circulating MSTN levels than young men (Figure 1C). As methods
used in several previous studies were unable to distinguish
GDF11 from MSTN, we also report combined GDF11 and
MSTN levels. GDF11 + MSTN levels declined in men (p <
0.05), but not women, throughout aging, in register with MSTN
levels (Figure 1D). When data from both sexes were combined,
we did not observe statistically significant differences in circulating
GDF11 + MSTN levels throughout aging (Figure 1E).
Notably, GDF11 represented, on average, 15.5% and 11.2% of
composite GDF11 + MSTN values for women and men, respectively.
Thus, GDF11 levels are not altered in women or men as a
function of age, and previous observations of age-dependent
decreases in GDF11 levels likely reflect changes in MSTN levels."
And regarding pathologies associated with high GDF11:
"We next interrogated potential associations between GDF11 and
MSTN levels and baseline comorbid conditions. Increased circulatingGDF11was
identified in a greater proportion of study participants
with diabetes (p = 0.019). 46% of individuals with high
GDF11 had diabetes, in contrast to only 14% with low levels.
Elevated GDF11 was also associated with a history of previous
cardiac conditions (p = 0.021),with a significant relationship drawn
with previous coronary artery bypass (p = 0.041). Participants with
the highest GDF11 levels at surgery had significantly higher New
YorkHeart Association (NYHA) class ranking than thosewith lower
GDF11 levels (p = 0.042) and were uniquely categorized as high
risk based on a mean Society of Thoracic Surgeons (STS) predicted
risk of mortality score greater than 8% (Thourani et al.,
2015) (p = 0.044) (Table 1). Critically,we did not identify differences
in aortic stenosis severity or related cardiac dysfunction, as
measuredbyejectionfraction,meangradient, aortic valve velocity,
valve area, valve area index, or left ventricular mass index, as a
function of circulatingGDF11 concentration (Table S5). In contrast
to GDF11, we were unable to draw any statistically significant
associations between MSTN and comorbid conditions, NYHA
classification, or mortality risk (Table 2)."
GDF11 is associated with frailty while aging:
"Frailty is a strong predictor of poor post-operative outcomes, yet
biomarkers of frailty have not been forthcoming. Accordingly,
we tested whether circulating GDF11 and MSTN protein levels
areassociatedwithfrailty statususingCardiovascularHealthStudy
(CHS) criteria, specified by unintentional weight loss, grip strength,
endurance,gait speed,andphysical activity (Friedetal., 2001).Participantswho
reported lowenergy and endurance had significantly
higher levels of circulating GDF11 than thosewho reported normal
energy (p < 0.001). A trend toward increased plasma GDF11 concentrations
was observed in individuals demonstrating unintentional
weight loss (p = 0.064) and low activity (p = 0.066), relative
to peers reporting no weight loss and normal activity (Figure 2B).
Similarly, individuals with slow gait (p = 0.150) and weak grip
strength (p = 0.163) appeared to possess higher GDF11 levels
than counterparts with normal gait and appropriate grip strength,
although these associations did not reach statistical significance.
Using the presence of three ormore CHS criteria as an operational
frailtydefinition,we comparedGDF11 concentrationsbetween frail
and non-frail study participants. Mean GDF11 levels increased by
21%as a function of frailty (p = 0.002) (Figure 2C). Unlike GDF11,
MSTN levels were not associated with frailty status (Table 2). To
evaluate whether the relationship between GDF11 and frailty remained
after adjusting for potential confounding demographic
and comorbidity characteristics, we applied a multivariable model
using a penalized stepwise logistic regression approach for variable
selection. After variable adjustment, GDF11 was still significantly
related to frailty (p = 0.003) (Table S6)."
This Mayo study uses the first really accurate technique for measuring GDF11 and GDF8 separately and precisely.
So, Steve, I totally get that you felt better on this hormone and also had increased cardiovascular exercise. But whatever it is that had this effect is something very hard to reverse engineer at this point. This Mayo study doesn't prove that if you inject GDF11 that you will get all of these disease conditions. This study doesn't even really prove that injecting GDF11 will increase your risk of these other conditions. But this Mayo study should really make you question that injecting GDF11 is a fountain of youth that will reverse any of your tissue aging. And who wants to be the guy on the block with the highest level of GDF11 circulating in your blood when this study is saying that those people all have terrible diseases and frailty as they age?
The basic science here just isn't finished.
Edited by pone11, 18 June 2016 - 01:49 AM.
Eish. I did not see that. Blond moment.
