Nature Knows - Natural Nootropics

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CONTRIBUTED CONTENT — Antioxidants are a buzzword in health circles that sometimes deliver empty promises. But when it comes to autoimmune Hashimoto’s hypothyroidism, one antioxidant is a must-have in your protocol kit: Glutathione. Stock image | Photo by Inside Creative House/iStock/Getty Images Plus, St. George News Glutathione is considered the body’s master antioxidant, and at RedRiver Health and Wellness Center , it’s the supplement we tell our patients they need it to dampen autoimmune response and lower the risk of developing new autoimmune diseases.

Glutathione protects cells from damage, supports general detoxification, acts as a natural chelator for toxic heavy metals and environmental toxins and supports healthy immune system function. Glutathione works by protecting energy-producing factories inside cells called mitochondria.

Antioxidants are molecules that inhibit other molecules from going through oxidation, a chemical reaction that produces toxins called free radicals. Free radicals are unstable molecules that occur naturally but also enter our bodies through toxins in food, air, water and even medications. Left unchecked, free radicals damage cells, destabilize the immune system and contribute to the development of serious health problems.

Glutathione is a compound made by the body that protects cells and tissues from damage by free radicals. While the body makes glutathione, it can also be supplemented in absorbable forms or via nutrients that boost glutathione production.

Normally, our bodies should make enough glutathione to protect us. However, it’s common for glutathione to drop too low in our modern world. Even if we lead a very clean, nontoxic life, we cope with thousands of toxic chemicals in our daily environment, our food and our water. Sugary diets full of processed foods, food intolerances, leaky gut and undiagnosed infections are other examples of things that can deplete glutathione due to chronic inflammatory assaults on the cells.

Glutathione levels also decrease as we age, and our need for supplemental glutathione increases significantly. When glutathione production drops, you’re more vulnerable to developing autoimmune disease , chronic pain, chemical sensitivities, leaky gut and other immune-related disorders.

In fact, glutathione depletion is linked with a number of disease states and groups including the following: Aging.

Athletic overtraining.

Major injuries and trauma.

Patients with wasting diseases such as HIV /AIDS.

Lung cancer.

Gut-based diseases such as Crohn’s and ulcerative colitis.

Chronic fatigue syndrome.

Alcoholism and fatty liver disease.

Diabetes and low glucose tolerance.

Cancer.

One of the most important things you can do to improve glutathione status is to remove or mitigate stressors that deplete glutathione. These may include lack of sleep, smoking, food intolerances, diets high in sugars and processed foods, excess alcohol intake and hormone or immune imbalances.

If you have Hashimoto’s , this typically also means going on a gluten-free diet, as many studies show a connection between Hashimoto’s hypothyroidism and a gluten intolerance or celiac disease.

Additionally, research shows a link between poor glutathione status and autoimmune Hashimoto’s hypothyroidism .

Recycle glutathione to manage Hashimoto’s hypothyroidism

One of the most effective approaches to dampen autoimmune-related inflammation is to support your body’s ability to recycle glutathione. Recycling glutathione means your body takes existing glutathione that has already been used in self-defense and rebuilds it so it can work again to protect the body.

For glutathione to be recycled, it must be reduced. There are two main forms of glutathione in the body: reduced glutathione and oxidized glutathione.

When there is sufficient reduced glutathione in the cells, they sacrifice themselves to free radicals to protect cellular mitochondria. An enzyme called glutathione peroxidase then sparks the conversion of reduced glutathione to oxidized glutathione, a free radical itself.

If there is sufficient glutathione in the cell, the newly unstable oxidized glutathione pairs with available glutathione with the help of an enzyme called glutathione reductase. This sends it back to reduced glutathione status and gets it ready to return to service protecting cells.

Glutathione recycling helps balance immune function and shield thyroid tissue from inflammation and autoimmune attacks. Glutathione also helps repair damaged tissues, such as in the case of leaky gut. Supplementing to increase glutathione levels – the RedRiver clinical research observations Between all of our clinics, we see several hundred patients each day, which puts us at an unparalleled advantage when it comes to honing in on the best support for patients. Below is an overview of what’s available to boost glutathione levels and what we have seen work the best for our patients. Glutathione recycling Glutathione recycling is a good place to start to increase glutathione activity inside of cells. A variety of nutritional and botanical compounds have been shown to support glutathione recycling, such as the following: N-acetyl-cysteine, which quickly metabolizes into intracellular glutathione. L-glutamine, which helps generate glutathione. Alpha-lipoic acid, which recycles and extends the life span of vitamin C, glutathione and coenzyme Q10, all of which are needed for glutathione recycling. Selenium, which is a cofactor for the enzyme glutathione peroxidase that converts reduced glutathione to oxidized glutathione to protect cells. Milk thistle, which significantly increases glutathione and improves the ratios of reduced and oxidized glutathione. Gotu kola, which increases glutathione peroxidase and glutathione in general. Cordyceps, which supports glutathione synthesis and activates the glutathione enzyme cycle. Taken together, these botanicals and compounds activate the glutathione peroxidase and reductase enzymes to promote a healthy glutathione recycling system.I use a stand-alone product to support glutathione recycling containing all of these ingredients called Glutathione Recycler by Apex Energetics. This product was developed by Dr. Datis Kharrazian, who pioneered our modern understanding of Hashimoto’s and glutathione.We have found this product works best when used in conjunction with a liposomal glutathione blend, which I discuss below. Liposomal glutathione Stock image | Photo by Shidlovski/iStock/Getty Images Plus, St. George News We are very impressed with patients’ results from a liquid liposomal glutathione blend called Trizomal Glutathione by Apex Energetics, also formulated by Kharrazian. Trizomal Glutathione provides both bioactive glutathione and the glutathione precursor N-acetyl-cysteine, meaning it’s for comprehensive glutathione support.Although dosages vary depending on the degree of inflammation, we generally start people […]

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The urgency to remember a dangerous experience requires the brain to make a series of potentially dangerous moves: Neurons and other brain cells snap open their DNA in numerous locations — more than previously realized , according to a new study — to provide quick access to genetic instructions for the mechanisms of memory storage.

The extent of these DNA double-strand breaks (DSBs) in multiple key brain regions is surprising and concerning, says study senior author Li-Huei Tsai , Picower Professor of Neuroscience at MIT and director of The Picower Institute for Learning and Memory, because while the breaks are routinely repaired, that process may become more flawed and fragile with age. Tsai’s lab has shown that lingering DSBs are associated with neurodegeneration and cognitive decline and that repair mechanisms can falter .

“We wanted to understand exactly how widespread and extensive this natural activity is in the brain upon memory formation because that can give us insight into how genomic instability could undermine brain health down the road,” says Tsai, who is also a professor in the Department of Brain and Cognitive Sciences and a leader of MIT’s Aging Brain Initiative . “Clearly, memory formation is an urgent priority for healthy brain function, but these new results showing that several types of brain cells break their DNA in so many places to quickly express genes is still striking.”

Tracking breaks

In 2015, Tsai’s lab provided the first demonstration that neuronal activity caused DSBs and that they induced rapid gene expression. But those findings, mostly made in lab preparations of neurons, did not capture the full extent of the activity in the context of memory formation in a behaving animal, and did not investigate what happened in cells other than neurons.

In the new study published July 1 in PLOS ONE , lead author and former graduate student Ryan Stott and co-author and former research technician Oleg Kritsky sought to investigate the full landscape of DSB activity in learning and memory. To do so, they gave mice little electrical zaps to the feet when they entered a box, to condition a fear memory of that context. They then used several methods to assess DSBs and gene expression in the brains of the mice over the next half-hour, particularly among a variety of cell types in the prefrontal cortex and hippocampus, two regions essential for the formation and storage of conditioned fear memories. They also made measurements in the brains of mice that did not experience the foot shock to establish a baseline of activity for comparison.

The creation of a fear memory doubled the number of DSBs among neurons in the hippocampus and the prefrontal cortex, affecting more than 300 genes in each region. Among 206 affected genes common to both regions, the researchers then looked at what those genes do. Many were associated with the function of the connections neurons make with each other, called synapses. This makes sense because learning arises when neurons change their connections (a phenomenon called “synaptic plasticity”) and memories are formed when groups of neurons connect together into ensembles called engrams.

“Many genes essential for neuronal function and memory formation, and significantly more of them than expected based on previous observations in cultured neurons … are potentially hotspots of DSB formation,” the authors wrote in the study.

In another analysis, the researchers confirmed through measurements of RNA that the increase in DSBs indeed correlated closely with increased transcription and expression of affected genes, including ones affecting synapse function, as quickly as 10-30 minutes after the foot shock exposure.

“Overall, we find transcriptional changes are more strongly associated with [DSBs] in the brain than anticipated,” they wrote. “Previously we observed 20 gene-associated [DSB] loci following stimulation of cultured neurons, while in the hippocampus and prefrontal cortex we see more than 100-150 gene associated [DSB] loci that are transcriptionally induced.”

Snapping with stress

In the analysis of gene expression, the neuroscientists looked at not only neurons but also non-neuronal brain cells, or glia, and found that they also showed changes in expression of hundreds of genes after fear conditioning. Glia called astrocytes are known to be involved in fear learning, for instance, and they showed significant DSB and gene expression changes after fear conditioning.

Among the most important functions of genes associated with fear conditioning-related DSBs in glia was the response to hormones. The researchers therefore looked to see which hormones might be particularly involved and discovered that it was glutocortocoids, which are secreted in response to stress. Sure enough, the study data showed that in glia, many of the DSBs that occurred following fear conditioning occurred at genomic sites related to glutocortocoid receptors. Further tests revealed that directly stimulating those hormone receptors could trigger the same DSBs that fear conditioning did and that blocking the receptors could prevent transcription of key genes after fear conditioning.

Tsai says the finding that glia are so deeply involved in establishing memories from fear conditioning is an important surprise of the new study.

“The ability of glia to mount a robust transcriptional response to glutocorticoids suggest that glia may have a much larger role to play in the response to stress and its impact on the brain during learning than previously appreciated,” she and her co-authors wrote.

Damage and danger?

More research will have to be done to prove that the DSBs required for forming and storing fear memories are a threat to later brain health, but the new study only adds to evidence that it may be the case, the authors say.

“Overall we have identified sites of DSBs at genes important for neuronal and glial functions, suggesting that impaired DNA repair of these recurrent DNA breaks which are generated as part of brain activity could result in genomic instability that contribute to aging and disease in the brain,” they wrote.

The National Institutes of Health, The Glenn Foundation for Medical Research, and the JPB Foundation provided funding for the research.

Read more at news.mit.edu

Recall a phone number or directions just recited and your brain will be actively communicating across many regions. It is thought that working memory relies on interactions between these regions, but how these brain areas interact and properly represent memory has remained a mystery.

At Baylor College of Medicine, Dr. Nuo Li, assistant professor of neuroscience and a McNair Scholar, and his colleagues investigated the nature of the communication between brain regions involved in working memory and found evidence that a modular network organization is critical for persistent neural activity.

How brain regions communicate

Li and his colleagues were able to see that each hemisphere of the brain has a separate representation of a memory. However, the hemispheres are tightly coordinated on a moment-to-moment basis, resulting in highly coherent information across them during working memory.

In their study, the researchers engaged mice in a simple behavior that would require them to store specific information. They were trained to delay an instructed action for a few seconds. This time delay gave researchers the chance to look at brain activity during the memory process.

“We saw many neurons simultaneously firing from both hemispheres of the cortex in a coordinated fashion. If activity went up in one region, the other region followed closely. We hypothesized that the interactions between brain hemispheres is what was responsible for this memory,” Li said.

Li and his colleagues recorded activity in each hemisphere, showing that each one made its own copy of information during the memory process. So how are the two hemispheres communicating?

Li explained that through the use of optogenetics they were able to corrupt information in a single hemisphere, affecting thousands of neurons during the memory period. What they found was unexpected.

“When we disrupted one hemisphere, the other area turned off communication, basically preventing the corruption from spreading and affecting activity in other regions,” Li said. “This is similar to modern networks such as electricity grids. They are connected to allow for the flow of electricity but also monitor for faults, shutting down connections when necessary so the entire electrical grid doesn’t fail.”

In collaboration with Dr. Shaul Druckmann and Ph.D. student Byungwoo Kang at Stanford University, the researchers developed theoretical analyses and network simulations of this process, showing that this modular organization in the brain is critical for the robustness of persistent neural activity. This robustness could be responsible for the brain being able to withstand certain injuries, protecting cognitive function from distractions.

“Understanding redundant modular organization of the brain will be important for designing neural modulation and repair strategies that are compatible with the brain’s natural processing of information,” Li said.

Read the paper in the journal Cell.

/Public Release. This material comes from the originating organization and may be of a point-in-time nature, edited for clarity, style and length. View in full here .

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Wake up to this brain breakfast a few times a week and your noggin will thank you. If you want to start off the day benefiting your brain health, there’s one breakfast neurologists, neurosurgeons and other brain experts recommend overnight oats with walnuts and blueberries.

When making standard overnight oats , all you have to do is the following:

> Soak ½ cup rolled oats with 1 cup of almond milk.

Refrigerate overnight.

In the morning, top with fresh blueberries and walnuts.

You’re more likely to eat healthy when you have a nutritious breakfast waiting for you in the morning, and this easy one helps to boost your brain health from the get-go.

“The foods we eat directly relate to how our brain functions,” says Randall Wright, MD , a neurologist at Houston Methodist Hospital. “When it comes down to diet and eating, we are seeing now that it’s all about brain energy. The brain uses a large portion of energy compared to the rest of the body.”

That’s why it’s important to fuel your brain with foods that help it combat stress and damage, which is exactly what this powerhouse breakfast will help you do. Here are four benefits of an overnight oats breakfast with blueberries and walnuts.

The delicious blueberry can help guard your brain against damage and improve its long-term function. Brain experts tend to recommend three diets for a healthy brain — all of which recommend fruit, and one of which recommends blueberries specifically.

“Typically, when I speak to patients about diets they should focus on for brain health, there are three main diets I refer them to: the Mediterranean Diet, the MIND diet and the DASH diet,” says Philip Stieg, MD , a neurosurgeon and founder of the Weill Cornell Brain and Spine Center.

Here’s what you need to know about each of those diets: ​ The Mediterranean Diet ​: This diet is rich in fruits, vegetables, fish, high-fiber breads, whole grains and healthy fats, and is linked to lower rates of stroke, Alzheimer’s disease and other dementia, depression, stroke and Parkinson’s disease, per Michigan Medicine .

​ The DASH Diet ​: Also known as Dietary Approaches to Stop Hypertension, this diet focuses on foods that lower blood pressure and “bad” LDL cholesterol, and recommends vegetables, fruits, whole grains, fat-free or low-fat dairy products, poultry, beans, nuts and vegetable oils, per the National Heart, Lung, and Blood Institute . Dr. Stieg notes that diets that are healthy for the heart tend to be healthy for the brain, too.

​ The MIND Diet ​: The most famous diet for brain health, the MIND Diet (Mediterranean-DASH Intervention for Neurodegenerative Delay) is a hybrid of the DASH diet and Mediterranean diet and was formulated by researchers to emphasize foods that affect brain health. It includes plenty of vegetables, meat-free meals, nuts, occasional fish and olive oil, and specifically calls out blueberries, which have been linked to slower rates of cognitive decline, per the Mayo Clinic .

The MIND diet recommends two or more servings per week of any type of berry but calls out that blueberries may be potentially more beneficial. Older adults who ate the most blueberries and strawberries had the slowest rates of cognitive decline in a July 2012 study in the ​ Annals of Neurology ​ . The California Strawberry Commission partially funded the study, but it is worth noting because it reviewed data of over 16,000 participants from the Nurses’ Health Study over 20 years.

In the study, those who ate the most blueberries and strawberries delayed cognitive aging by up to 2.5 years. Anthocyanidins, which are a subclass of flavonoids, can cross the blood-brain barrier to accumulate in areas of the brain responsible for learning and memory, like the hippocampus.

“It’s clear that berries, and particularly blueberries, have direct benefits,” says Marwan Sabbagh, MD , an Alzheimer’s expert at the Cleveland Clinic. “Flavonoids are very potent free radical scavengers and antioxidants.”

In other words, flavonoids can help protect against the effects of oxidative stress and inflammation that naturally occur in your body. Your body creates free radicals, unstable molecules that cause oxidative stress (which in turn can lead to cell damage), when you digest food, exercise, smoke or are exposed to environmental factors like sunlight or air pollution, per the National Institutes of Health (NIH). Oxidative stress is thought to play a role in a variety of diseases, including those that affect the brain such as Alzheimer’s disease and Parkinson’s disease.

“The chemicals in blueberries are what the brain needs to protect itself,” Dr. Wright says. “When our diets don’t reflect that, that’s when disease may start.”

Antioxidants in blueberries can help prevent or delay cell damage in your body, but it’s best to get them through food — while diets high in antioxidant-rich fruits and vegetables have been shown to be healthy, antioxidant supplements have not been shown to be helpful in preventing disease, per the NIH.

Nuts like walnuts are rich in vitamin E , which is known for its brain-protective qualities, per the Mayo Clinic. The MIND Diet recommends eating a handful of nuts at least five times per week in place of processed snacks like chips — just opt for the raw, unsalted kind without added sodium, sweeteners or oils.

Walnuts, in particular, pack the most alpha-linolenic acid (ALA), a type of omega-3 fatty acid, than any other nut. They also have higher levels of polyphenolic compounds (a type of antioxidant) than any other nut. Both ALA and polyphenolic compounds may help lower oxidative stress and inflammation — which are two causes of cognitive decline, according to the American Society for Nutrition .

“The cells in our body have cell walls constructed of lipids, or fats,” Dr. Stieg says. “Good fats help construct a normal, healthy cell wall, so you want to make sure you have the appropriate fats in your diet.”

Eating more walnuts increased adults’ performance on cognitive tests, regardless of how old they were, in a December 2014 study in ​ The Journal of Nutrition, Health & Aging ​ […]

Read more at www.livestrong.com

Double-strand DNA breaks, which occur when the phosphate backbones of both DNA strands are hydrolyzed, are considered the most significant DNA damage and have been shown to increase the risk of cancer and other deadly diseases.

So, it’s surprising enough that previous research has shown the brain actually causes double-strand breaks (DSBs) when it is trying to create a fear-based memory. What’s even more shocking—and concerning—is the extent of these DSBs in multiple key brain regions, according to a new study by Li-Huei Tsai, professor of neuroscience at MIT and director of The Picower Institute for Learning and Memory.

In a new paper published in PLOS One , Tsai and colleagues show that while the breaks are routinely repaired, the process may become more flawed and fragile with age.

“We wanted to understand exactly how widespread and extensive this natural activity is in the brain upon memory formation because that can give us insight into how genomic instability could undermine brain health down the road,” said Tsai. “Clearly memory formation is an urgent priority for healthy brain function but these new results showing that several types of brain cells break their DNA in so many places to quickly express genes is striking.”

In the most recent study, researchers in Tsai’s lab gave mice low-power electrical zaps to the feet when they entered a box to condition a fear memory. Then, the team used several methods to assess DSBs and gene expression in the brains of said mice.

Compared with control mice, the creation of a fear memory in those who were zapped doubled the number of DSBs among neurons in the hippocampus and the prefrontal cortex, affecting more than 300 genes in each region—two brain regions known to form and store fear memories. Among the 206 affected genes common to both regions, many of the genes were associated with synapses.

“Many genes essential for neuronal function and memory formation, and significantly more of them than expected based on previous observations in cultured neurons are potentially hotspots of DSB formation,” the authors explain in the study.

Through RNA measurements, the researchers also demonstrated that an increase in DSBs correlated with increased transcription and expression of affected genes—including ones affecting synapse function—as quickly as 10 to 30 minutes after the foot shock exposure.

Surprisingly, the researchers also recorded gene expression changes in glia, or non-neuronal brain cells in the central nervous system. In glia, many of the DSBs that occurred following fear conditioning occurred at genomic sites related to the specific stress hormone glutocortocoid. Further tests revealed that directly stimulating glutocortocoid receptors could trigger the same DSBs that fear conditioning did. Moreover, blocking the receptors could prevent transcription of key genes after fear conditioning.

“The ability of glia to mount a robust transcriptional response to glutocorticoids suggest that glia may have a much larger role to play in the response to stress and its impact on the brain during learning than previously appreciated,” writes Tsai and her co-authors.

The scientists say more research will have to be done to prove that the DSBs required for forming and storing fear memories are a threat to later brain health, but their new study certainly adds evidence linking lingering DSBs with neurodegeneration and cognitive decline.

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