Three 2023 studies to follow up mention of GDF11 in the Brain endothelial cells post. Two are selected for non-pharmaceutical interventions people can do on their own. Let’s start with a human exercise study:
“We explored the exercise-related regulation of Growth Differentiation Factor 11 (GDF11) in cerebrospinal fluid (CSF) and blood. Samples of serum, plasma, and CSF were obtained before and 60 min after acute exercise (90 min run) from twenty healthy young individuals. Additional serum and plasma samples were collected immediately after run. GDF11 protein content, body composition, physical fitness, and cognitive functions were evaluated.
Controversies regarding the role of GDF11 in aging originate mainly from the absence of a reliable, validated and widely accepted method of GDF11 detection. To support the reliability of our findings as well as to distinguish GDF11 from its close homologue GDF8, we determined GDF11 in CSF, serum, and plasma, by immunoblotting, using two different GDF11-specific antibodies, as well as GDF11/GDF8 non-specific antibody. These antibodies have been previously successfully used by others. Reliability of our findings is further supported by correlations between GDF11 in serum and plasma, as well as between GDF11 and serum GDF11/GDF8.
We report an association between levels of GDF11 and adiponectin in CSF as well as in serum after acute endurance exercise. These observations support potentially synergic effects of GDF11 and adiponectin on the brain. The experimental design we implement seems to represent a reliable model to study regulation of bioactive molecules, potential mediators of neuroprotective effects of exercise in the human brain.
We show for the first time a direct link between endurance exercise and GDF11 levels in human cerebrospinal fluid. This study provided the first albeit indirect (correlative) evidence on the putative role of GDF11 in promoting healthy aging in humans, by demonstrating a tight relationship between serum GDF11 and peak power output. We extend this observation by showing that the level of physical fitness is an important determinant of regulation of GDF11 by acute exercise.
In this work, we confirm in a bigger cohort our previous finding that blood-brain barrier permeability, as assessed by CSF/serum albumin ratio, is decreased after an acute bout of endurance exercise. We observed a modest positive correlation between CSF/serum albumin ratio and CSF/serum GDF11/GDF8 ratio, with a trend also for GDF11. However, exercise-induced changes of CSF/serum albumin ratio and that of GDF11 or GDF11/GDF8 did not correlate, indicating that there are other factors that could modulate levels of this growth factor rather than blood-brain barrier permeability.”
https://www.frontiersin.org/articles/10.3389/fendo.2023.1137048/full “Acute endurance exercise modulates growth differentiation factor 11 in cerebrospinal fluid of healthy young adults”
Next is a rodent study of intermittent fasting before and after cerebral ischemia:
“The present study focused on the cerebral angiogenesis effect of intermittent fasting (IF) on ischemic rats. Rats were fed within strict time periods for 8 h out of every 24 h, with free access to food between 0800 and 1600 h.
In the first step, we designed different time schedules (10 d, 1 month, and 3 months) of IF before middle cerebral artery occlusion (MCAO). We monitored whether IF accelerated neurobehavioral recovery and induced expression of endothelial cells after MCAO. Then we explored whether GDF11 and downstream signals mediated angiogenesis in the peri-infarct area.
We found that 3 months (p < 0.01) and 1 month (p < 0.05) of IF conditioning, respectively, markedly increased GDF11-positive cells in the peri-infarct area 3 d after MCAO compared with ad libitum dietary regimen. There were no significant differences between the cerebral ischemia (CI) + ad libitum group and the CI + IF 10-day group.
We also assayed plasma expression pattern of GDF11 protein. Plasma level of GDF11 protein was significantly upregulated in the IF dietary groups compared with the ad libitum dietary group 3 d after MCAO, which was consistent with the brain level. However, short-term CI + IF 10-day group results were not statistically different from CI + ad libitum group.
Taken together, our results strongly indicated that pretreatment of long-term IF might promote circulation of GDF11 and cerebral GDF11 protein during the post-ischemic, recovery period. Preoperative long-term IF might be beneficial for inducing cerebral angiogenesis in acute cerebral infarction.
These findings suggested that the longer the period of IF before MCAO, the better the protective effects after surgery.”
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0282338 “Long-term intermittent fasting improves neurological function by promoting angiogenesis after cerebral ischemia via growth differentiation factor 11 signaling activation”
Per Week 28 of Changing to a youthful phenotype with broccoli sprouts, using species maximum lifespan to estimate a human-equivalent multiplication factor that can be applied to a rat post-development time period is 122.5 years / 3.8 years = 32.2. Applying it to this study’s findings:
- 10 rat days (322 human days) of intermittent fasting provided little protection from cerebral ischemia;
- 1 rat month (32.2 human months) of intermittent fasting had better protection; and
- 3 rat months (a little over 8 human years) of intermittent fasting had even stronger protection.
Is it worth the hassle of intermittently fasting every day for years to prevent a future stroke, or better recover from one, or keep other subclinical / clinical diseases from accelerating, or keep aging from accelerating? This study also cited more immediate benefits of intermittent fasting.
Might be too late for a gradual approach for people who are already diseased or close, though, like subjects in this human study:
“We aimed to explore the correlation among serum GDF11, the severity of coronary artery lesions, and the prognosis of patients with ST-segment elevation myocardial infarction (STEMI). A total of 367 patients were enrolled and divided into control (n = 172) and STEMI (n = 195) groups. Control group fulfilled the following criteria:
- Presented with typical chest tightness, chest pain, or other discomfort symptoms on admission;
- Electrocardiogram examination suggested ST-T changes;
- Levels of myocardial injury markers did not suggest abnormalities; and
- The diagnosis of unstable angina was considered clinically valid.
14 variables that were significant in univariate logistic regression analysis were included in the subsequent multivariate logistic regression analysis. Multivariate analysis indicated that smoking, diabetes, C-reactive protein, homocysteine, and lipoprotein (a) were positively correlated with STEMI occurrence, whereas serum GDF11 and the Apolipoprotein A1-to-Apolipoprotein B ratio were negatively correlated with STEMI occurrence.
Serum GDF11 was negatively correlated with severity of coronary lesions, and was also an independent prognostic indicator of major adverse cardiovascular events in patients with STEMI.”
https://link.springer.com/article/10.1007/s12265-023-10358-w “Correlation Between GDF11 Serum Levels, Severity of Coronary Artery Lesions, and the Prognosis of Patients with ST-segment Elevation Myocardial Infarction” (not freely available)
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