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              Advocacy & Research for Unlimited Lifespans


Zero Gravity Orbital Habitation Causes Changes that are at Least Superficially Similar to Accelerated Aging

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#1 reason

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Posted 05 December 2015 - 01:38 AM

That old people will go into orbit to escape the rigors of gravity and thus live longer in their declining years was a staple of golden age and later science fiction. These works were written at a time in which our knowledge of human biochemistry - and the application of that knowledge to medicine - was crude in comparison to today. It is fascinating that we can say that for such a short span of years, a mere short lifetime past, but the differences between the medicine of the 1950s and the medicine of today are profound indeed. The writers of that time largely envisaged a future incorporating great gains in energy generation, and a consequent diaspora from Earth, while computation, medicine and the human condition remained much unchanged; older spacemen in the outer reaches struggling with heart disease in their fifties. Instead we found that expanding the generation, storage, transmission, and application of energy is very hard, and the largely unanticipated information revolution occurred instead. We lost the near future of cheap heavy lift to orbit and the solar system at our beck and call, but gained Moore's Law, biotechnology, nanotechnology, a pervasive internet, and medical progress that is in the early stages of conquering heart disease and may yet save us from all of degenerative aging.

As it turns out, retreating from the rigors of gravity may well have the opposite effect to that imagined by the authors of the last century. Among the alterations produced by orbital habitation in zero gravity are those that appear, at least superficially, much like accelerated aging of the cardiovascular system. The root causes have yet to be pinned down, since very few people are actually researching this topic, but since the onset of these symptoms is fairly rapid, I'd guess at the cause being more a matter of regulatory dysfunction than increased tissue damage, such as the presence of cross-links related to arterial stiffening in aging. Here I'll point out a few links to the work of one research group on this topic in recent years:

Waterloo to lead new experiment aboard International Space Station

The experiment will link changes in astronauts' hearts and blood vessels with specific molecules in the blood to determine why astronauts experience conditions that mimic aging-related problems and chronic diseases on earth. The findings will help identify important indicators for chronic disease and assist with the development of early interventions for people on earth. "We know that astronauts return from space with stiffer arteries and resistance to insulin, conditions affecting many adults as they age. For the first time, we will be able to track exactly how - and why - the body's blood vessels change, and use these findings to potentially improve quality of life and the burden of chronic disease."

"In space, astronauts' bodies show aging-like changes much faster than on Earth. The International Space Station provides a unique platform to study aging-related conditions providing insights that can be used to help understand some of the biggest health issues affecting society. Our research to date suggests that even though astronauts exercise every day, the actual physical demands of tasks of daily living are greatly reduced due to the lack of gravity. This lifestyle seems to cause changes in the vascular system and in the body's ability to regulate blood glucose that would normally take years to develop on earth."

U.Waterloo - Vascular Aging and Space Research Program

We study factors related to cardiovascular health with aging. One focus is on blood pressure regulation and its impact on brain blood flow to help us understand some of the factors that could contribute to falls in the elderly, especially those that occur on rising from bed. Another focus is on aging blood vessels. We have reported a strong link between peripheral arterial stiffness and a reduction in brain blood flow. Our space research program is very active. We recently completed the study Cardiovascular and Cerebrovascular Control on Return from the International Space Station (CCISS). We are currently collecting data for the project Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular).

Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular)

Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular) investigates the impact of long-duration space flight on the blood vessels of astronauts. Space flight accelerates the aging process, and it is important to understand this process to develop specific countermeasures. Data is collected before, during, and after space flight to assess inflammation of the artery walls, changes in blood vessel properties, and cardiovascular fitness.

Spaceflight can cause stiffening of the arteries, affecting the body's ability to control blood pressure. This investigation assessed the blood vessels of astronauts and found decreased flexibility of the carotid artery during flight. Researchers found no relationship between the level of physical fitness and this decrease. The experiment also provided data on the mechanisms behind increased arterial stiffness from spaceflight. Further research is needed to establish effective ways to counter the cardiovascular consequences of spaceflight and ultimately help treat increased arterial stiffness from aging on Earth, which can cause high blood pressure and organ damage.

Impaired cerebrovascular autoregulation and reduced CO2 reactivity after long duration spaceflight

Long duration habitation on the International Space Station (ISS) is associated with chronic elevations in arterial blood pressure in the brain compared with normal upright posture on Earth and elevated inspired carbon dioxide. Although results from short-duration spaceflights suggested possibly improved cerebrovascular autoregulation, animal models provided evidence of structural and functional changes in cerebral vessels that might negatively impact autoregulation with longer periods in microgravity. Seven astronauts (1 woman) spent 147 ± 49 days on ISS. Preflight testing (30-60 days before launch) was compared with postflight testing on landing day or the morning 1 or 2 days after return to Earth. The results indicate that long duration missions on the ISS impaired dynamic cerebrovascular autoregulation and reduced cerebrovascular carbon dioxide reactivity.

Recent findings in cardiovascular physiology with space travel

The cardiovascular system undergoes major changes in stress with space flight primarily related to the elimination of the head-to-foot gravitational force. A major observation has been that the central venous pressure is not elevated early in space flight yet stroke volume is increased at least early in flight. Recent observations demonstrate that heart rate remains lower during the normal daily activities of space flight compared to Earth-based conditions. Structural and functional adaptations occur in the vascular system that could result in impaired response with demands of physical exertion and return to Earth. Cardiac muscle mass is reduced after flight and contractile function may be altered. Regular and specific countermeasures are essential to maintain cardiovascular health during long-duration space flight.

View the full article at FightAging

#2 HighDesertWizard

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Posted 05 December 2015 - 07:15 PM

reason... As always, a great and informative article...


But I believe a statement you make doesn't fit the evidence... You write that "the root causes have yet to be pinned down, since very few people are actually researching this topic..." In fact, a good amount of science has been done about accelerated aging in space and the conclusions of that science fit with facts we already know about accelerated aging on earth. About what we already know and as just one example, I suggest a look at the graphic figure in this thread's opening post.


The bottom line... NF-kB Translocation and Cytokine Transcription is implicated in micro-gravity accelerated aging... A few studies highlighting the details of this emerging truth follow below...



Capacity of omega-3 fatty acids or eicosapentaenoic acid to counteract weightlessness-induced bone loss by inhibiting NF-kappaB activation: from cells to bed rest to astronauts, 2010


... We report here cellular, ground analogue, and spaceflight findings. We investigated the effects of EPA on differentiation of RAW264.7 monocyte/macrophage cells induced by receptor activator of NF-kappaB ligand (RANKL) and on activation of NF-kappaB by tumor necrosis factor alpha (TNF-alpha) or exposure to modeled weightlessness... In human studies, we evaluated whether NF-kappaB activation was altered after short-duration spaceflight and determined the relationship between intake of omega-3 fatty acids and markers of bone resorption during bed rest and the relationship between fish intake and bone mineral density after long-duration spaceflight. NF-kappaB was elevated in crew members after short-duration spaceflight, and higher consumption of fish (a rich source of omega-3 fatty acids) was associated with reduced loss of bone mineral density after flight (p < .05)...



Spaceflight alters expression of microRNA during T cell activation, 2011


Returning astronauts have experienced altered immune function and increased vulnerability to infection during spaceflights dating back to Apollo and Skylab suggesting that immune-suppression is a major barrier to safe, long-term human space habitation and travel. We present definitive evidence that early signal transduction events are inhibited by the microgravity (ug) environment of spaceflight. Human leukocytes were stimulated with T cell mitogens onboard the International Space Station using a 1g centrifuge as the Earth’s 1g control. Microarray analysis demonstrated significant (p< .05) differential expression of 54 genes in ug vs 1g conditions. Fifty percent of the genes most significantly inhibited in ug as compared to 1g showed marked over-representation of NFKB binding sites in their promoter regions. Qrtpcr confirmed that upregulation of key genes in the NFKB pathway were inhibited in ug. Inhibition of the NFKB pathway leads to activation dysfunction during spaceflight. Lack of immune response in microgravity occurs at the cellular level. In our recent spaceflight studies of early T cell activation, we have discovered that the expression of miRNAs in both man and mouse require gravity for appropriate regulation. MiRNAs expressed during activation in normal gravity (g), were down regulated in spaceflight. These data suggest that gravity may regulate T-cell activation by two separate mechanisms; promoter regions and microRNA.



The Rel/NF-κB pathway and transcription of immediate early genes in T cell activation are inhibited by microgravity, 2012


This study tested the hypothesis that transcription of immediate early genes is inhibited in T cells activated in μg. Immunosuppression during spaceflight is a major barrier to safe, long-term human space habitation and travel. The goals of these experiments were to prove that μg was the cause of impaired T cell activation during spaceflight, as well as understand the mechanisms controlling early T cell activation. T cells from four human donors were stimulated with Con A and anti-CD28 on board the ISS. An on-board centrifuge was used to generate a 1g simultaneous control to isolate the effects of μg from other variables of spaceflight. Microarray expression analysis after 1.5 h of activation demonstrated that μg- and 1g-activated T cells had distinct patterns of global gene expression and identified 47 genes that were significantly, differentially down-regulated in μg. Importantly, several key immediate early genes were inhibited in μg. In particular, transactivation of Rel/NF-κB, CREB, and SRF gene targets were down-regulated. Expression of cREL gene targets were significantly inhibited, and transcription of cREL itself was reduced significantly in μg and upon anti-CD3/anti-CD28 stimulation in simulated μg. Analysis of gene connectivity indicated that the TNF pathway is a major early downstream effector pathway inhibited in μg and may lead to ineffective proinflammatory host defenses against infectious pathogens during spaceflight. Results from these experiments indicate that μg was the causative factor for impaired T cell activation during spaceflight by inhibiting transactivation of key immediate early genes.


About this study...


Radiation induced nuclear factor kappa-B signaling cascade study in mammalian cells by improved detection systems, 2014


To enable long-term human space flight cellular radiation response to densely ionizing radiation needs to be better understood for developing appropriate countermeasures to mitigate acute effects and late radiation risks for the astronaut. The biological effectiveness of accelerated heavy ions with high linear energy transfer (LET) for effecting DNA damage response pathways as a gateway to cell death or survival is of major concern, not only for tumor radiotherapy but also for new regimes of space missions. Ionizing radiation modulates several signaling pathways resulting in transcription factor activation. NF-kappaB is one of the important transcription factors that respond to changes in the environment of a mammalian cell and plays a key role in many biological processes relevant to radiation response, such as apoptosis, inflammation and carcinogenesis.

Edited by HighDesertWizard, 05 December 2015 - 07:34 PM.

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