Brain repair diet

Do follow the anti-parasitic diet, eat whole foods rich in Vitamin C , A and E and get sufficient night time sleep. Avoid and run away from toxic people. Stay with nature and meet new friends. Make someone happy.  In nursing facilities, some seniors are suffering from sundowning syndrome, a state of acute mental confusion and behavioral change that takes place at the end of the day and into the night.  Since we synthesize cholesterol at night, eat a healthy fat food at night and use ways to calm the body for a good night sleep (dim the lights , except for a hallway night light) and stay with the seniors until he goes to sleep.


Omega-3 Fatty Acids, Vitamin E, Curcumin, and Caffeine

A number of studies point to the healthy effects of dietary factors on the brain. For example, fish-derived omega-3 fatty acids have been shown to improve cognition, plasticity, and recovery of neurons after traumatic brain injury. One of the most important forms of omega-3 fatty acids, docosahexaenoic acid (DHA), has been found to be a key component of neuronal membranes at sites of signal transduction at the synapse, suggesting that its action is vital to brain structure and function []. Evidence suggests that DHA serves to improve neuronal function by supporting synaptic membrane fluidity and function, and regulating gene expression and cell signaling []. Because the human body is not capable of producing its own DHA, supplementation of diet with foods rich in DHA is important in insuring proper function of neurons and in facilitating neuronal recovery after injury []. An additional benefit of omega-3 fatty acids which we observed in our studies is that they appear to reduce oxidative stress damage that results from trauma, indicating at the possibility of their application in assisting the recovery process [].

Another dietary supplement that has shown promise in protecting neurons is Vitamin E, found in certain oils, nuts, and spinach. Vitamin E functions as an antioxidant, reducing free radicals in the brain which would otherwise impede optimal function of neurons. Vitamin E has shown positive effects on memory performance in older people [], indicating its ability to maintain neuronal health. A different study similarly revealed the benefits of Vitamin E by showing a correlation between the amount of ingested Vitamin E and improved neurological performance, survival, and brain mitochondrial function in aging mice [].

Curcumin, a yellow curry spice, has also been suggested to enhance recovery events after brain trauma, displaying particular potency in preserving cognition. Curcumin was found to improve neuronal function in individuals afflicted with Alzheimer’s disease by reducing oxidative stress and amyloid pathology []. In addition, it was found to protect the brain from lipid peroxidation [] and nitric oxide-based radicals []. In accordance with these observations, our own studies have showed that the supplementation of curcumin into the diets of rats reduced the effects of experimental concussive injury on cognitive function tasks [].

Studies observing the effects of caffeine on neuronal regeneration and function are recently emerging. A new study shows that chronic, but not acute, treatment with caffeine protects the brain against injury in animal models of Parkinson’s disease and stroke by increasing glutamate release and inflammatory cytokine production [].

Caloric Intake

Cognition and plasticity of the brain have also been shown to be affected by caloric intake and the frequency of food consumption. Restriction of calories seems to increase levels of BDNF, resulting in improved neuronal function. Fasting every other day has been shown to protect neurons in the hippocampus against excitotoxicity-induced death []. In the study, rats put on an every-other-day-fasting diet for 2-4 months had hippocampus neurons that were much more resistant to degeneration induced by kainic acid, and greater preserved memory than rats fed ad lib.

Saturated-Fat Diet

While certain foods seem to contribute positively to neuronal health, diets that are rich in saturated fats appear to decrease levels of BDNF in the brain and lead in poorer neuronal performance. Molteni and colleagues have shown that rats fed a diet high in saturated fats and refined sugars (similar in content to the “junk food” that has become popular today) for a period of 1-2 months, performed significantly worse on the spatial learning mater maze test than rats fed a healthier diet that was low in fat and contained complex carbohydrates [].


Cancer cells prevent you from sleeping at night in order to survive

Cancer Overrides the Circadian Clock to Survive

Source: Medical University of South Carolina.

Tumor cells use the unfolded protein response to alter circadian rhythm, which contributes to more tumor growth, Hollings Cancer Center researchers at the Medical University of South Carolina (MUSC) find. A key part of the circadian clock opposes this process, according to a paper published online Dec. 11 in Nature Cell Biology.

For tumors to grow and spread, cancer cells must make larger than normal amounts of nucleic acids and protein, so they can replicate themselves. Yet in both normal and cancer cells that increase their synthesis of protein, a small percent of those proteins do not fold properly. When that happens, the cell activates its unfolded protein response (UPR), which slows down the making of new proteins while the misfolded proteins are refolded. Eventually, the buildup of misfolded proteins becomes toxic and leads to cell death. However, cancer cells have learned to use the UPR to slow protein synthesis when needed, in order to handle the backlog of misfolded proteins. This helps them survive in conditions that would kill normal cells.

This pattern of adaptation is often seen in tumor cells, according to J. Alan Diehl, Ph.D., the SmartState Endowed Chair in Lipidomics, Pathobiology and Therapy at the MUSC Hollings Cancer Center and senior researcher on the project. “What a tumor cell is doing is taking a pathway that’s already in the cell and using it to its advantage,” said Diehl.

Yet it was not clear exactly how cancer cells were able to use UPR activity to influence circadian rhythm. Diehl’s group found that the UPR and circadian rhythm are linked together to lead the clockwork of the cell and also that cancer cells use the UPR to manipulate the circadian clock in ways that allow them to survive conditions that are toxic to normal cells.

To start, Diehl and his fellow researchers formulated a new idea based on what was known about protein synthesis in the cell. First, as they knew, the UPR is altered in tumors, and second, cells establish a circadian rhythm to regulate metabolism by producing levels of certain proteins that rise and fall in coordination with natural cycles of light and dark. Third, other scientists had observed that circadian rhythm is altered in tumor cells. Since protein production is tied to circadian rhythm, Diehl’s group asked if misfolded proteins might change circadian rhythm in cancer cells.

In their first set of experiments, Diehl’s research team used chemicals to activate the UPR in osteosarcoma cells. They found that, when activated, the UPR changes levels of an important protein called Bmal1, which is a transcription factor that rises and falls with cycles of light and dark. As it does, it regulates the expression of major circadian rhythm genes. When cells were exposed to cycles of light and dark, Bmal1 levels peaked during dark hours. But when the UPR was chemically activated, Bmal1 stayed low during both light and dark phases, which caused a phase shift in the expression of circadian genes. When one of the main parts of the UPR machinery was absent in cells, the phase shift did not happen.

Next, the group found that the UPR functions much like a “middleman” between light-dark cycles and the ability of cells to establish a circadian rhythm from those cycles. Levels of the circadian protein Bmal1 continued to decrease, as the UPR was increasingly activated. In rodents that had their light-dark cycles suddenly reversed, Bmal1 stopped rising and falling – a clear sign that their circadian rhythms were disrupted. Shifts in light exposure activated the UPR in those rodents’ cells.

But what does that mean for the development of cancer? The team found that patients with breast, gastric or lung cancers survived longer when they had higher levels of Bmal1 protein. In myc-driven cancers, the UPR was causing the loss of Bmal1 protein, which caused the tumors to grow. Myc-driven tumors lost circadian rhythm, whereas normal cells maintained it. Conversely, high levels of Bmal1 overtook the UPR, thereby allowing protein synthesis to continue, which was toxic to tumor cells. In this way, Bmal1 directly encourages protein synthesis.

This is the first study showing that human cancer suppresses circadian rhythm by controlling protein synthesis through Bmal1. Cancer cells survived longer by using the UPR to suppress Bmal1 and short-circuit their circadian rhythms. These results are important for human biology, according to Yiwen Bu, Ph.D., a postdoctoral scholar in Diehl’s laboratory and first author on the paper. “Every single normal cell in our body has circadian oscillation,” said Bu. “We showed that resetting the circadian rhythms in cancer cells slows down their proliferation.”

Image shows a DNA strand.

Still, do changes in light-dark cycles contribute to the development of cancer in humans? It is not yet clear in patients if circadian shifts contribute to changes in the UPR and if that, in turn, contributes to the development of cancer. But these results could help clinicians boost the effectiveness of current cancer treatments, Diehl said.

“Physicians are beginning to think about timing delivery of therapies in such a way that, say, if we deliver a drug at a certain time of day, we’ll get better on-target effects on the cancer and less toxicity in the normal cells,” he said.


Source: Heather Woolwine – Medical University of South Carolina
Publisher: Organized by
Image Source: image is in the public domain.
Original Research: Abstract for “A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival” by Yiwen Bu, Akihiro Yoshida, Nilesh Chitnis, Brian J. Altman, Feven Tameire, Amanda Oran, Victoria Gennaro, Kent E. Armeson, Steven B. McMahon, Gerald B. Wertheim, Chi V. Dang, Davide Ruggero, Constantinos Koumenis, Serge Y. Fuchs & J. Alan Diehl in Nature Cell Biology. Published online December 11 2017 doi:10.1038/s41556-017-0006-y

Medical University of South Carolina “Cancer Overrides the Circadian Clock to Survive.” NeuroscienceNews. NeuroscienceNews, 28 December 2017.


A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival

The unfolded protein response (UPR) is a stress-activated signalling pathway that regulates cell proliferation, metabolism and survival. The circadian clock coordinates metabolism and signal transduction with light/dark cycles. We explore how UPR signalling interfaces with the circadian clock. UPR activation induces a 10 h phase shift in circadian oscillations through induction of miR-211, a PERK-inducible microRNA that transiently suppresses both Bmal1 and Clock, core circadian regulators. Molecular investigation reveals that miR-211 directly regulates Bmal1 and Clock via distinct mechanisms. Suppression of Bmal1 and Clock has the anticipated impact on expression of select circadian genes, but we also find that repression of Bmal1 is essential for UPR-dependent inhibition of protein synthesis and cell adaptation to stresses that disrupt endoplasmic reticulum homeostasis. Our data demonstrate that c-Myc-dependent activation of the UPR inhibits Bmal1 in Burkitt’s lymphoma, thereby suppressing both circadian oscillation and ongoing protein synthesis to facilitate tumour progression.

“A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival” by Yiwen Bu, Akihiro Yoshida, Nilesh Chitnis, Brian J. Altman, Feven Tameire, Amanda Oran, Victoria Gennaro, Kent E. Armeson, Steven B. McMahon, Gerald B. Wertheim, Chi V. Dang, Davide Ruggero, Constantinos Koumenis, Serge Y. Fuchs & J. Alan Diehl in Nature Cell Biology. Published online December 11 2017 doi:10.1038/s41556-017-0006-y

Sleep disorders and brain

Time of Day Influences Susceptibility to Infection

Time of Day Influences Susceptibility to Infection

Summary: A new study reveals we are more susceptible to infections at certain times of the day as our circadian rhythm affects the ability of the virus to spread and replicate.

Source: University of Cambridge.

We are more susceptible to infection at certain times of the day as our body clock affects the ability of viruses to replicate and spread between cells, suggests new research from the University of Cambridge. The findings, published today in the Proceedings of the National Academy of Sciences, may help explain why shift workers, whose body clocks are routinely disrupted, are more prone to health problems, including infections and chronic disease.

When a virus enters our body, it hijacks the machinery and resources in our cells to help it replicate and spread throughout the body. However, the resources on offer fluctuate throughout the day, partly in response to our circadian rhythms – in effect, our body clock. Circadian rhythms control many aspects of our physiology and bodily functions – from our sleep patterns to body temperature, and from our immune systems to the release of hormones. These cycles are controlled by a number of genes, including Bmal1 and Clock.

To test whether our circadian rhythms affect susceptibility to, or progression of, infection, researchers at the Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, compared normal ‘wild type’ mice infected with herpes virus at different times of the day, measuring levels of virus infection and spread. The mice lived in a controlled environment where 12 hours were in daylight and 12 hours were dark.

The researchers found that virus replication in those mice infected at the very start of the day – equivalent to sunrise, when these nocturnal animals start their resting phase – was ten times greater than in mice infected ten hours into the day, when they are transitioning to their active phase. When the researchers repeated the experiment in mice lacking Bmal1, they found high levels of virus replication regardless of the time of infection.

“The time of day of infection can have a major influence on how susceptible we are to the disease, or at least on the viral replication, meaning that infection at the wrong time of day could cause a much more severe acute infection,” explains Professor Akhilesh Reddy, the study’s senior author. “This is consistent with recent studies which have shown that the time of day that the influenza vaccine is administered can influence how effectively it works.”

In addition, the researchers found similar time-of-day variation in virus replication in individual cell cultures, without influence from our immune system. Abolishing cellular circadian rhythms increased both herpes and influenza A virus infection, a dissimilar type of virus – known as an RNA virus – that infects and replicates in a very different way to herpes.

Dr Rachel Edgar, the first author, adds: “Each cell in the body has a biological clock that allows them to keep track of time and anticipate daily changes in our environment. Our results suggest that the clock in every cell determines how successfully a virus replicates. When we disrupted the body clock in either cells or mice, we found that the timing of infection no longer mattered – viral replication was always high. This indicates that shift workers, who work some nights and rest some nights and so have a disrupted body clock, will be more susceptible to viral diseases. If so, then they could be prime candidates for receiving the annual flu vaccines.”

As well as its daily cycle of activity, Bmal1 also undergoes seasonal variation, being less active in the winter months and increasing in summer. The researchers speculate that this may help explain why diseases such as influenza are more likely to spread through populations during winter.

Diagram of the circadian clock.

Using cell cultures, the researchers also found that herpes viruses manipulate the molecular ‘clockwork’ that controls our circadian rhythms, helping the viruses to progress. This is not the first time that pathogens have been seen to ‘game’ our body clocks: the malaria parasite, for example, is known to synchronise its replication cycle with the host’s circadian rhythm, producing a more successful infection.

“Given that our body clocks appear to play a role in defending us from invading pathogens, their molecular machinery may offer a new, universal drug target to help fight infection,” adds Professor Reddy.


Funding: The research was mostly funded by the Wellcome Trust and the European Research Council.

Source: University of Cambridge
Image Source: This image is for illustrative purposes only and is licensed CC BY SA 3.0.
Original Research: Abstract for “Cell autonomous regulation of herpes and influenza virus infection by the circadian clock” by Rachel S. Edgar, Alessandra Stangherlin, Andras D. Nagy, Michael P. Nicoll, Stacey Efstathiou, John S. O’Neill, and Akhilesh B. Reddy in PNAS. Published online August 15 2016 doi:10.1073/pnas.1601895113

University of Cambridge. “Time of Day Influences Susceptibility to Infection .” NeuroscienceNews. NeuroscienceNews, 15 August 2016.


Cell autonomous regulation of herpes and influenza virus infection by the circadian clock

Viruses are intracellular pathogens that hijack host cell machinery and resources to replicate. Rather than being constant, host physiology is rhythmic, undergoing circadian (∼24 h) oscillations in many virus-relevant pathways, but whether daily rhythms impact on viral replication is unknown. We find that the time of day of host infection regulates virus progression in live mice and individual cells. Furthermore, we demonstrate that herpes and influenza A virus infections are enhanced when host circadian rhythms are abolished by disrupting the key clock gene transcription factor Bmal1. Intracellular trafficking, biosynthetic processes, protein synthesis, and chromatin assembly all contribute to circadian regulation of virus infection. Moreover, herpesviruses differentially target components of the molecular circadian clockwork. Our work demonstrates that viruses exploit the clockwork for their own gain and that the clock represents a novel target for modulating viral replication that extends beyond any single family of these ubiquitous pathogens.

“Cell autonomous regulation of herpes and influenza virus infection by the circadian clock” by Rachel S. Edgar, Alessandra Stangherlin, Andras D. Nagy, Michael P. Nicoll, Stacey Efstathiou, John S. O’Neill, and Akhilesh B. Reddy in PNAS. Published online August 15 2016 doi:10.1073/pnas.1601895113

Sleep , virus, cancer and parasites



Contrary to previous findings, new research finds no link between chronic fatigue syndrome and the viruses XMRV (xenotropic murine leukemia virus-related virus) and pMLV (polytropic murine leukemia virus). A study reveals that research that reported patients with chronic fatigue syndrome carried these two viruses was wrong and that there is still no evidence for an infectious cause behind chronic fatigue syndrome. READ MORE…