On a good day, my shoulders, knees, and hips will dislocate two to five times apiece. The slightest bump into a table or door will bloom new bruises on my arms and legs or tear a gash in the thin skin on my hands. My blood pressure will plummet each time I stand, making me feel woozy, nauseated, and weak. I’ll have trouble focusing and remembering words. I’ll run my errands from underneath an umbrella to prevent an allergic reaction to the Sun.
I have Ehlers-Danlos Syndrome (EDS), Postural Orthostatic Tachycardia Syndrome (POTS), and Mast Cell Activation Syndrome (MCAS)—a trifecta of weird diseases. POTS, EDS, and MCAS are so obscure that many doctors have never even heard of them. But a 2016 study published in Nature Genetics might help change that: Researchers have found a genetic mutation that links all three conditions.
As concerns about health epidemics plague the nation, demand and sales of diet soda have plunged as consumers try to make better choices. As we reported, aspartame (the main sweetener for diet soda) is one of the most dangerous ingredients used in our food supply, causing seizures and a host of other health issues.
In a new study done over ten years and sampling 60,000 women, it was shown that women who drink two or more diet drinks a day have much higher cardiovascular disease rates and are more likely to die from the disease.
Many things cause oxidative stress. The body responds to things that endanger the body by oxidizing it. It secrete something called Reactive Oxygen Species. The end products are things like hydroxy radicals, peroxynitrites, and many other forms of oxidated products. They are designed to destroy things like pathogens or toxins that enter the body. Some toxins like mercury, aluminum,fluoride and the toxins in vaccine adjuvants are very difficult to remove from the body so they set off an endless cycle of oxidative stress. This can result in severe damage to the body. It can cause erosion of our gut, it can cause our blood brain barrier to become porous which leave things that could not normally access the brain to have dramatic effects. The blood brain barrier is difficult to cross, most chemicals and pathogens cannot cross it unless it has been compromised.
Evidence of how negatively fluoride can impact our health has been increasing in rapid pace throughout the past few years. People are hoping that by bringing awareness to this that somehow we can get sodium fluoride removed from the world’s water supply.
How host and microbial factors combine to structure gut microbial communities remains incompletely understood. Redox potential is an important environmental feature affected by both host and microbial actions. We assessed how antibiotics, which can impact host and microbial function, change redox state and how this contributes to post-antibiotic succession. We showed gut redox potential increased within hours of an antibiotic dose in mice. Host and microbial functioning changed under treatment, but shifts in redox potentials could be attributed specifically to bacterial suppression in a host-free ex vivo human gut microbiota model. Redox dynamics were linked to blooms of the bacterial family Enterobacteriaceae. Ecological succession to pre-treatment composition was associated with recovery of gut redox, but also required dispersal from unaffected gut communities. As bacterial competition for electron acceptors can be a key ecological factor structuring gut communities, these results support the potential for manipulating gut microbiota through managing bacterial respiration.
We read with great interest the article by Mathieu et al.1 entitled “Evidence for Cerebrospinal Fluid Entry Into the Optic Nerve via a Glymphatic Pathway,” recently published in Investigative Ophthalmology & Visual Science. The authors provided the first evidence of cerebrospinal fluid (CSF) entry via paravascular spaces into the orbital optic nerve in mice and concluded that this pathway may be highly relevant to optic nerve diseases, including glaucoma.1 We fully agree with this notion, and we believe that the “ocular glymphatic system” may also play a key role in the development of optic disc edema in astronauts.
Ophthalmic abnormalities including optic disc edema, globe flattening, choroidal and retinal folds, hyperopic refractive error shifts, and nerve fiber layer infarcts have been reported in astronauts returning from long-duration space flight on the International Space Station.2 Understanding factors contributing to this space flight-associated neuro-ocular syndrome (SANS) is one of the top priorities for the National Aeronautics and Space Administration (NASA), especially in view of future long-duration interplanetary space flight missions, including trips to Mars. Currently, the exact mechanisms causing SANS are unknown. These ophthalmic findings after long-duration space flight were initially referred to as the visual impairment and intracranial pressure (VIIP) syndrome,2 and a leading hypothesis is that VIIP is caused by elevated intracranial pressure (ICP) resulting from microgravity-induced cephalad fluid shifts leading to venous stasis in the head and neck.3,4 This stasis could cause impairment of CSF drainage into the venous system and cerebral venous congestion, both of which could lead to a rise in ICP.4 The resulting elevated ICP could lead to optic nerve sheath distention, globe flattening, and stasis of axoplasmic flow with optic disc swelling.4 We believe that the existence of an ocular glymphatic system offers an attractive additional explanation for how microgravity may cause optic disc edema in astronauts.
Decline of cognition and increasing risk of neurodegenerative diseases are major problems associated with aging in humans. Of particular importance is how the brain removes potentially toxic biomolecules that accumulate with normal neuronal function. Recently, a biomolecule clearance system using convective flow between the cerebrospinal fluid (CSF) and interstitial fluid (ISF) to remove toxic metabolites in the brain was described. Xie and colleagues now report that in mice the clearance activity of this so-called "glymphatic system" is strongly stimulated by sleep and is associated with an increase in interstitial volume, possibly by shrinkage of astroglial cells. Moreover, anesthesia and attenuation of adrenergic signaling can activate the glymphatic system to clear potentially toxic proteins known to contribute to the pathology of Alzheimer disease (AD) such as beta-amyloid (Abeta). Clearance during sleep is as much as two-fold faster than during waking hours. These results support a new hypothesis to answer the age-old question of why sleep is necessary. Glymphatic dysfunction may pay a hitherto unsuspected role in the pathogenesis of neurodegenerative diseases as well as maintenance of cognition. Furthermore, clinical studies suggest that quality and duration of sleep may be predictive of the onset of AD, and that quality sleep may significantly reduce the risk of AD for apolipoprotein E (ApoE) ɛ4 carriers, who have significantly greater chances of developing AD. Further characterization of the glymphatic system in humans may lead to new therapies and methods of prevention of neurodegenerative diseases. A public health initiative to ensure adequate sleep among middle-aged and older people may prove useful in preventing AD, especially in apolipoprotein E (ApoE) ɛ4 carriers.
The paravascular pathway, also known as the “glymphatic” pathway, is a recently described system for waste clearance in the brain. According to this model, cerebrospinal fluid (CSF) enters the paravascular spaces surrounding penetrating arteries of the brain, mixes with interstitial fluid (ISF) and solutes in the parenchyma, and exits along paravascular spaces of draining veins. Studies have shown that metabolic waste products and solutes, including proteins involved in the pathogenesis of neurodegenerative diseases such as amyloid-beta, may be cleared by this pathway. Consequently, a growing body of research has begun to explore the association between glymphatic dysfunction and various disease states. However, significant controversy exists in the literature regarding both the direction of waste clearance as well as the anatomical space in which the waste-fluid mixture is contained. Some studies have found no evidence of interstitial solute clearance along the paravascular space of veins. Rather, they demonstrate a perivascular pathway in which waste is cleared from the brain along an anatomically distinct perivascular space in a direction opposite to that of paravascular flow. Although possible explanations have been offered, none have been able to fully reconcile the discrepancies in the literature, and many questions remain. Given the therapeutic potential that a comprehensive understanding of brain waste clearance pathways might offer, further research and clarification is highly warranted.
The recent discovery of meningeal lymphatic vessels (LVs) has raised interest in their possible involvement in neuropathological processes, yet little is known about their development or maintenance. We show here that meningeal LVs develop postnatally, appearing first around the foramina in the basal parts of the skull and spinal canal, sprouting along the blood vessels and cranial and spinal nerves to various parts of the meninges surrounding the central nervous system (CNS). VEGF-C, expressed mainly in vascular smooth muscle cells, and VEGFR3 in lymphatic endothelial cells were essential for their development, whereas VEGF-D deletion had no effect. Surprisingly, in adult mice, the LVs showed regression after VEGF-C or VEGFR3 deletion, administration of the tyrosine kinase inhibitor sunitinib, or expression of VEGF-C/D trap, which also compromised the lymphatic drainage function. Conversely, an excess of VEGF-C induced meningeal lymphangiogenesis. The plasticity and regenerative potential of meningeal LVs should allow manipulation of cerebrospinal fluid drainage and neuropathological processes in the CNS.