Vitamin D – Stroke Link

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Low vitamin D levels may not only increase a person’s risk of stroke, but lower their health post-stroke.

Low vitamin D has been associated in past studies with neurovascular injury (damage to the major blood vessels supplying the brain, brainstem, and upper spinal cord). Nils Henninger, from University of Massachusetts Medical School (Massachusetts, USA), and colleagues studied 96 stroke patients, assessing their blood levels of 25-hydroxyvitamin D (a marker of vitamin D status).  Stroke patients who had low vitamin D levels less than 30 ng/mL) showed two-times larger areas of dead tissue resulting from obstruction of the blood supply compared to patients with normal vitamin D levels. Further, for each 10 ng/mL reduction in vitamin D level, the chance for healthy recovery in the three months following stroke decreased by almost half, regardless of the patient’s age or initial stroke severity.

Article Source: http://www.worldhealth.net/news/vitamin-d-stroke-link/

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Testosterone may help men with multiple sclerosis

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A small pilot study suggests that testosterone treatment is safe, well tolerated and may reduce symptoms, slow brain degeneration and increase muscle mass in men with relapsing-remitting multiple sclerosis, the most common form of the disease, according to a report in the May issue of Archives of Neurology, one of the JAMA/Archives journals.

Multiple sclerosis is a progressive disease involving the immune and central nervous systems. MS and many other autoimmune diseases (in which the body attacks its own systems or tissues) are less common in men than in women, according to background information in the article. This is especially true during reproductive years. Sex hormones, including testosterone and estrogen, may be responsible for the difference. Testosterone has been shown to protect against an MS-like condition and other autoimmune diseases in animals.

Nancy L. Sicotte, M.D., of the David Geffen School of Medicine at UCLA, Los Angeles, and colleagues conducted a study of testosterone treatment in 10 men with relapsing-remitting MS, characterized by periods of neurologic symptoms (such as numbness or difficulty walking) followed by periods of remission. The men, who had an average age of 46, were enrolled in the study and then entered a six-month pre-treatment phase, during which symptoms were monitored but no therapies were administered. Then, each man applied 10 grams of a gel containing 100 milligrams of testosterone to his upper arms once daily for 12 months.

“One year of treatment with testosterone gel was associated with improvement in cognitive performance and a slowing of brain atrophy [deterioration],” the authors write. During the first nine months of the study–the period of time before the men began taking testosterone, plus the first three months of treatment, before it had time to take effect–brain volume decreased an average of -0.81 percent per year. In the second nine months, this decline slowed by 67 percent to an annual rate of -0.25 percent. “Because the protective effect of testosterone treatment on brain atrophy was observed in the absence of an appreciable anti-inflammatory effect, this protection may not be limited to MS, but may be applicable to those with non-inflammatory neurodegenerative diseases,” including amyotrophic lateral sclerosis or Lou Gehrig’s disease, the authors write.

In addition, lean body mass (muscle mass) increased an average of 1.7 kilograms (about 3.74 pounds) during the treatment phase. Participants did not report any adverse effects, there were no abnormalities in blood tests taken during the trial and the men’s prostate examination results remained stable.

“Overall, in this first trial of testosterone treatment in men with relapsing-remitting MS, the treatment was shown to be safe and well tolerated,” the authors conclude. “In addition, exploratory findings reported herein suggest a possible neuroprotective effect of testosterone treatment in men, which warrants further investigation.”

###

(Arch Neurol. 2007;64:683-688. Available pre-embargo to the media at www.jamamedia.org.)

Editor’s Note: This study was supported by grants from the National Multiple Sclerosis Society, the General Clinical Research Centers at Harbor-UCLA Medical Center, the Sherak Family Foundation and the Skirball Foundation. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Article Source: https://www.eurekalert.org/pub_releases/2007-05/jaaj-tmh051007.php

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Testosterone Therapy in Patients with Treated and Untreated Prostate Cancer: Impact on Oncologic Outcomes

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Purpose

Testosterone deficiency and prostate cancer have an increasing prevalence with age. However, because of the relationship between prostate cancer and androgen receptor activation, testosterone therapy among patients with known prostate cancer has been approached with caution.

Materials and Methods

We identified a cohort of 82 hypogonadal men with prostate cancer who were treated with testosterone therapy. They included 50 men treated with radiation therapy, 22 treated with radical prostatectomy, 8 on active surveillance, 1 treated with cryotherapy and 1 who underwent high intensity focused ultrasound. We monitored prostate specific antigen, testosterone, hemoglobin, biochemical recurrence and prostate specific antigen velocity.

Results

Median patient age was 75.5 years and median followup was 41 months. We found an increase in testosterone (p <0.001) and prostate specific antigen (p = 0.001) in the entire cohort. Prostate specific antigen increased in patients on active surveillance. However, no patients were upgraded to higher Gleason score on subsequent biopsies and none have yet gone on to definitive treatment. We did not note any biochemical recurrence among patients treated with radical prostatectomy but 3 (6%) treated with radiation therapy experienced biochemical recurrence. It is unclear whether these cases were related to testosterone therapy or reflected the natural biology of the disease. We calculated mean prostate specific antigen velocity as 0.001, 0.12 and 1.1 μg/l per year in the radical prostatectomy, radiation therapy and active surveillance groups, respectively.

Conclusions

In the absence of randomized, placebo controlled trials our study supports the hypothesis that testosterone therapy may be oncologically safe in hypogonadal men after definitive treatment or in those on active surveillance for prostate cancer.

Article Source: http://www.jurology.com/article/S0022-5347(16)30307-X/abstract

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NFL Players Searching For Painkiller Choices Hope For Relaxed Marijuana Ban

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Voters in seven more states said “yes” to marijuana this month. Pot now is legal for recreational or medicinal use in more than half the country.

It’s still against federal law and classified as a Schedule 1 drug, meaning U.S. officials consider marijuana to have a high risk of abuse or harm, and no accepted medical use in treatment. Also, it’s still banned in professional sports.

Many athletes hope that will change as momentum grows nationwide for legalization. That’s especially true in the National Football League, where pain is a constant companion. Advocates say marijuana could offer a safer and better way to manage the pain.

Powerful Painkillers

Football hurts. As a fan watching from home, that’s not always obvious — players collide, fall down, pop back up. They rarely wince or show weakness. That’s just not how it’s done in football.

Kyle Turley hurt plenty during his eight NFL seasons in the 1990s and 2000s. As an offensive lineman, he was involved in jarring collisions nearly every play when his team had the ball. He hurt after his career -– Turley sometimes walks with a cane. And in a recent video, he displayed one by one the bottles of powerful painkillers he used.

“Vicodin, Flexeril, Percocets, Vioxx, morphine,” Turley recited as he plopped the bottles down on a kitchen counter.

Turley says be became addicted to the drugs and depressed to the point of contemplating suicide.

Then last year, he quit the prescription painkillers and started using marijuana to manage his pain.

“Just this right here,” he says in the video, holding up a small marijuana bud. “That’s all you need. That’s about two hits.”

Maybe Help From The Union

The video is from a website for the Gridiron Cannabis Coalition. Turley helped start the group as a way to promote marijuana as a legal option for pain management in football. The effort may be gaining traction as the country’s acceptance of marijuana grows.

In the next couple of weeks, the NFL Player’s Association will announce it has formed a new committee to examine pain issues for players.

“Certainly given some of the medical research that’s out there,” says union executive George Atallah, “marijuana is going to be one of the substances that we take a look at.”

Safer And Better?

As it should be, says pain specialist Dr. Daniel Clauw. He’s a University of Michigan professor of anesthesiology who has studied cannabis and pain management for the past five years.

He says comparing the safety of marijuana and opioid painkillers — the kind Turley and so many other NFL players and retirees use — is no contest.

According to the Centers for Disease Control and Prevention, in 2014 more than 14,000 people died from overdoses involving prescription opioids.

“You can’t directly die from taking a cannabinioid, the way tens of thousands of people are directly dying from opioids each year in the U.S.,” says Dr. Clauw.

Dr. Clauw published a study this year of about 250 people who said they’d used marijuana and opioids for chronic pain. The subjects said as marijuana use went up, opioid use went down. Significantly.

“They noted on average a two-thirds decrease in their opioid dose,” says Dr. Clauw, adding, “they also noted that they just felt a lot better overall with respect to side-effect profile when their pain was being controlled largely with cannabinoids.”

Dr. Clauw says marijuana isn’t the only option for pain relief, nor is it a perfect alternative to opioids. Cannibis can be addictive, although much less so than narcotic painkillers.

“I’m really not as pro-cannabinoids as I am anti-opioids,” he says.

Still, with more research, Dr. Clauw and others could become more bullish on cannabis as a pain reliever.

Hard To Study

The kind of research needed is a mechanistic study, “Where we might want to look into the human brain to see exactly how cannabinoid is working or look at the subset of people that is going to respond best to a cannabinoid,” Dr. Clauw says. “In order to do those studies, we have to be able to administer the cannabis [to humans] in a controlled setting. Know the dose of it, know the strength.”

But scientists are limited in what they can do because of marijuana’s continuing Schedule 1 classification. Researchers have to get approvals from multiple agencies, a time-consuming process.

“It really is incredibly onerous on the part of the investigators to get all approvals you need to do research with Schedule 1 drugs,” Dr. Clauw says. “It has inhibited many of us from doing science on cannabinoids because we simply don’t want the hassles.”

Experts Disagree

In the absence of more stringent science, and more knowledge that potentially could change minds about marijuana, the Federal Government holds firm and the NFL maintains its ban.

The league tests for marijuana and suspends a player after four violations. The NFL issued a written statement on the subject, saying in part that the league would be open to reconsidering its policy, which it collectively bargained with the player’s union. But for now, the league’s medical experts haven’t recommended any changes.

“I don’t know where they’re getting their medical experts,” Dr. Clauw says. “I don’t know hardly anyone in the pain field that would be able to support the position that the NFL is taking, based on just scientific data.”

When asked to provide one of its experts for an interview, an NFL spokesman told NPR, “they don’t speak to the media.”

Meanwhile the professional football season rolls on, and the hurting continues as well. For players, and now their union, the search continues for better and safer ways to ease the pain.

Article Source: http://www.npr.org/2016/11/21/502610853/nfl-players-searching-for-painkiller-choices-hope-for-relaxed-marijuana-ban

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How metformin prevents tumors: UCSD researchers

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Researchers at University of California San Diego School of Medicine have identified a previously unknown mechanism that helps fortify the structure and tight junctions between epithelial cells — a basic cell type that lines various body cavities and organs throughout the body, forming a protective barrier against toxins, pathogens and inflammatory triggers. Breaches of this barrier can provoke organ dysfunction and development of tumors.

The findings, published online in the current issue of eLife by senior author Pradipta Ghosh, MD, professor in the departments of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine, and colleagues, helps illuminate why the widely prescribed anti-diabetic drug Metformin has repeatedly been shown to not only protect epithelial integrity in the face of stressors like inflammation, sepsis, hypoxia and harmful microbes, but also appears to prevent cancer.

Virtually all cell types possess cell polarity — the asymmetrical organization of their components and structures that makes it possible for them to carry out specialized functions. In epithelial cells, polarity determines how they form barriers. Loss of epithelial polarity impacts organ development and function and can initiate cancers.

The stress-polarity pathway, discovered and described in 2006 and 2007, is a specialized pathway mobilized only during periods of stress. It is orchestrated by a protein-kinase called AMPK that protects cellular polarity when epithelial cells are under energetic stress and an activator of AMPK called LBK1.

“The latter is a bona fide tumor suppressor,” said Ghosh. Mutations in LBK1 have been linked to cancers and loss of cell polarity. While the question of exactly how the energy-sensing LKB1-AMPK pathway maintains cell polarity during stress remained unknown for more than a decade, evidence accumulated that Metformin, an activator of the LKB1-AMPK pathway and a frontline treatment for type 2 diabetes, has beneficial effects on the epithelial lining and can potentially prevent cancer.

The new research, said Ghosh, provides “mechanistic insights into the tumor suppressive action of Metformin and the LKB1-AMPK pathway at a higher resolution.” Specifically, she and colleagues discovered that the stress-polarity pathway requires a key effector of AMPK — a protein called GIV/Girdin.

In cultured polarized epithelial cells, the authors demonstrated that AMPK and its activator Metformin exerted much of their beneficial effects via phosphorylating GIV and directing GIV to the tight junctions of the epithelial layer. Without such phosphorylation and/or targeting, the beneficial effects of AMPK, and its activator Metformin, were virtually abolished and the epithelial barrier became “leaky” and eventually collapsed. Mutants of GIV found in colon cancer that specifically abolish AMPK’s ability to phosphorylate GIV could trigger tumor cell growth in 3D matrigel.

“In summary, by identifying GIV/Girdin as a key layer within the stress-polarity pathway we’ve peeled another layer of the proverbial onion,” Ghosh said. “In the process, we’ve provided new insights into the epithelium-protecting and tumor-suppressive actions of one of the most widely prescribed drugs, Metformin, which may inspire a fresh look and better designed studies to fully evaluate the benefits of this relatively cheap medication.”

###

Co-authors of the study are: Nicolas Aznar, Arjun Patel, Christina Rohena, Ying Dunkel, Vanessa Taupin, Irina Kufareva, and Marilyn Farquhar, all at UC San Diego.

 

Article Source: http://www.stonehearthnewsletters.com/how-metformin-prevents-tumors-ucsd-researchers/diabetes/

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Is DMAE Missing from Your Anti-Aging Regimen?

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Dimethylaminoethanol (DMAE or deanol), is a compound that occurs in anchovies, salmon and sardines, and is believed to increase brain levels of the neurohormone acetylcholine, which facilitates the transmission of impulses between neurons (brain cells).

DMAE has been investigated as a treatment for several conditions since the 1950s, including attention deficit-hyperactivity disorder (ADHD) and the movement disorder known as tardive dyskinesia.

DMAE May Benefit Hyperactivity and Movement Disorders

A double-blind study involving 74 children with learning and behavior disorders including hyperactivity found improvement with DMAE, although the researchers were uncertain with regard to its mechanism of action.1

Research in rat cerebral cortex neurons exposed to acetylcholine or DMAE revealed similar excitatory responses in association with either compound, adding evidence to a cholinergic property for DMAE.2 In another study, rats that received choline or DMAE showed an increase in brain choline and acetylcholine.3 “This finding suggests that the concentration of free choline in the brain is below that which is necessary for a maximal rate of synthesis of acetylcholine, and raises the possibility that the availability of choline in brain may regulate the rate of synthesis of acetylcholine,” authors Dean R. Haubrich and colleagues note.

Tardive dyskinesia is a disorder characterized by involuntary, repetitive movement that is often the result of long term or high dose usage of antipsychotic pharmaceutical therapy. Early research involving individuals affected by this condition found therapeutic benefit for DMAE in some, but not all subjects.4

Failure of some patients to achieve the dramatic response observed in other patients involved in studies that evaluated DMAE has been suggested to be due to dosage inadequacies or other factors.5 In a study that compared the effects of one gram deanol (DMAE), two grams deanol, or a placebo daily for thirty days; only patients in the group that received the higher dose of DMAE exhibited a significant reduction in movement.6

The Anti-Aging Effects of DMAE

DMAE has been suggested to have an anti-aging effect. In 1973, researcher Richard Hochschild reported the finding of an extension of average lifespan of 27.3% and maximum lifespan of 39.7% in mice given a compound that immediately breaks down into DMAE and p-chlorophenoxyacetic acid, leading him to conclude that the effects observed in the study may be attributable to these byproducts.7

Research published in Mechanisms of Ageing and Development in 1980 reported the ability of DMAE to diminish cross-linking of proteins, a process that causes damage to cellular membranes in tissues, thereby contributing to aging.8 Author I. Nagy later confirmed the ability of DMAE to scavenge hydroxyl radicals, supporting its anti-aging properties.9

In mice, DMAE alone or in combination with one or two cholinergic drugs improved retention test performance.10 Lifelong administration of DMAE to mice has resulted in a reduction in the aging-associated pigment lipofuscin in the liver in comparison with untreated animals.11

In dementia patients, DMAE given three times daily for four weeks lessened behavioral changes, including those attributed to depression, anxiety, irritability and lack of initiative, in 10 out of 14 subjects.12

DMAE and Aging Skin

Interestingly, DMAE has been shown to benefit the appearance of the skin when applied topically. The compound appears to increase skin firmness.13 Whether these effects are long-lasting remains to be seen, however, one study found that several benefits obtained during a 16-week course of daily topical DMAE did not regress during a subsequent two-week period in which DMAE was not applied.14

According to author R. Grossman, improvements were observed in coarse wrinkles, under-eye circles, nasolabial folds and sagging skin on the neck. These visually assessed improvements have been confirmed by quantitative measures of skin strength. In another experiment, which involved mice and human volunteers, DMAE increased dermal thickness and collagen fiber thickness.15

DMAE is less of a household word these days, but worth keeping in mind. Because of its stimulating potential, low doses are suggested for those who choose to use it.

References:

  1. Lewis JA et al. Clin Pharmacol Ther. 1975 May;17(5):534-40.
  2. Kostopoulos GK et al. Psychopharmacol Commun. 1975;1(3):339-47.
  3. Haubrich DR et al. Life Sci. 1975 Sep 15;17(6):975-80.
  4. Bockenheimer S et al. Arch Psychiatr Nervenkr (1970). 1976 Sep 17;222(1):69-75.
  5. Stafford JR et al. Dis Nerv Syst. 1977 Dec;38(12 Pt 2):3-6.
  6. George J et al. Aust N Z J Psychiatry. 1981 Mar;15(1):68-71.
  7. Hochschild R. Exp Gerontol. 1973 Aug;8(4):185-91.
  8. Nagy I et al. Mech Ageing Dev. 1980 Sep-Oct;14(1-2):245-51.
  9. Nagy I et al. Arch Gerontol Geriatr. 1984 Dec;3(4):297-310.
  10. Flood JF et al. Neurobiol Aging. 1983 Spring;4(1):37-43.
  11. Stenbäck F et al. Mech Ageing Dev. 1988 Feb;42(2):129-38.
  12. Ferris SH et al. J Am Geriatr Soc. 1977 Jun;25(6):241-4.
  13. Uhoda I et al. Skin Res Technol. 2002 Aug;8(3):164-7.
  14. Grossman R. Am J Clin Dermatol. 2005;6(1):39-47.
  15. Tadini KA et al. Pharmazie. 2009 Dec;64(12):818-22.

Article Source:http://blog.lifeextension.com/2016/11/is-dmae-missing-from-your-anti-aging.html

 

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Why the Blood-Brain Barrier Is So Critical (and How to Maintain It)

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You all know about intestinal permeability, or “leaky gut.” The job of the gut lining is to be selectively permeable, allowing helpful things passage into the body and preventing harmful things from getting in. Nutrients get through, toxins and pathogens do not. Leaky gut describes the failure of this vetting process. But what about “leaky brain”?

A similarly dynamic barrier lies between the brain and the rest of the body: the blood-brain barrier. Since the brain is the seat of all the conscious machinations and subconscious processes that comprise human existence, anything attempting entry receives severe scrutiny. We want to admit glucose, amino acids, fat-soluble nutrients, and ketones. We want to reject toxins, pathogens, and errant immune cells. Think of the blood-brain barrier like the cordon of guards keeping the drunken rabble from spilling over into the VIP room in a nightclub.

The blood-brain barrier (or BBB) can get leaky, just like the gut lining. This is bad.

A compromised BBB has been implicated in many neurodegenerative diseases, like Alzheimer’s, Parkinson’s, and vascular dementia.

More generally, the BBB regulates passage of inflammatory cytokines into the brain, prevents fluctuations in serum composition from affecting brain levels, and protects against environmental toxins and infectious pathogens from reaching the brain. A leaky BBB means the floodgates are open for all manner of unpleasantries to enter the brain.

Some pathogens even wield chemical weaponry that blasts open the blood-brain barrier, giving them—and anything else in the vicinity—access to the brain. To prepare for that, you must support the integrity of your blood-brain barrier.

How?

Optimize your B vitamin intake

In adults with normal B vitamin levels, mild cognitive impairment, high homocysteine levels, and a leaky BBB, taking vitamins B12, B6, and B9 (folate) restored the integrity of the blood-brain barrier.

Review this post and make sure you’re getting the B vitamins you need. Primal folks tend to overlook them.

Nourish your gut

A leaky gut accompanies, and maybe causes, a leaky brain. Funny how that works, eh?

It’s a rodent study, but it’s quite illustrative: a fecal transplant from healthy mice with pristine BBB integrity to unhealthy mice with leaky BBB and pathogen-filled guts restored the integrity of the blood-brain barrier.

DIY fecal transplants are an extreme intervention. Until that becomes more feasible, simply eating more prebiotic fiber, experimenting with resistant starch, taking a quality probiotic, and eating fermented foods on a regular basis will get you most of the way there.

Eat plenty of magnesium

Okay, Sisson. Enough already with the magnesium. We get it! But magnesium can attenuate BBB permeability, even if you inject an agent explicitly designed to induce leaky blood-brain barriers.

This is yet another reason to eat enough magnesium-rich foods (like spinach, almonds, blackstrap molasses, winter squash), drink magnesium-rich mineral water (I love Gerolsteiner, but you can also just go down to the local Euro food market and check the labels for high-Mg waters), or take a good magnesium supplement (anything ending in “-ate” like magnesium glycinate or citrate).

Don’t eat a 40% cocoa butter diet

Rodents given a 40% saturated fat (from cocoa butter) diet experienced elevated BBB permeability.

Except wait: The remaining 60% of calories was split up between white sugar, wheat starch, casein, and dextrin (PDF). So this isn’t the type of 40% SFA diet you folks are eating.

Except wait again: Adding in either aged garlic extract, alpha lipoic acid (ALA), niacin, or nicotinamide completely abolished the increase in permeability.

It looks like a refined diet high in saturated fat and sugar/starch and absent any phytonutrient-rich plant foods like garlic or antioxidant supplements like ALA will cause elevated BBB permeability (in rodents). I’m not sure I’d recommend a 40% SFA diet either way, however. Balance is probably better.

Use phytonutrient-rich plants and spices

Recall the study from the last section where some garlic extract was enough to eliminate the bad BBB effects of a refined lab diet. That’s because aged garlic extract is particularly rich in phytonutrients with strong antioxidant effects. What about other fruits, vegetables, and spices with different phytonutrients—do those also help BBB function?

Curcumin (from turmeric) certainly helps. Astragalus root, used in many ancient medical traditions, can help. Sulforaphane, from cruciferous veggies like broccoli, Brussels sprouts, and cabbage, shows promise.

Drink coffee and/or tea

As phytonutrient-rich plants, they technically belong in the previous section, but coffee and tea are so special that they deserve their own space. Both are sources of caffeine, a noted protector of BBB integrity.

Supplements can help

Supplement forms of the aforementioned nutrients are worth a look. Also:

Alpha-GPC (a type of choline that readily crosses the blood-brain barrier) has been shown to reduce BBB permeability in hypertensive rats.

Inositol (which you can get from foods like egg yolks but not in very large amounts) improves BBB integrity. Another option is to consume phytate-containing foods; if you’ve got the right gut bacteria, you can convert phytate into inositol.

Berberine, noted anti-diabetic compound, reduces BBB permeability and increases resistance to brain damage following head trauma.

Control your blood pressure

Both acute and chronic hypertension increase BBB permeability. This means you’ll have to control your sleep and stress. You’ll need to reduce insulin resistance. Eat dark chocolate (the horror). Figure out if you’re salt-sensitive (you may even have to increase salt intake if it’s too low). Get enough magnesium (yes, again) and potassium.

Sleep

Sleep really is everything. You can’t avoid it, and if you skimp on it, things fall apart. The blood-brain barrier is no exception: sleep restriction impairs BBB function and increases permeability.

If you can’t stick to the bedtime you know is ideal, a little (0.25-0.5mg) melatonin can help set your circadian rhythm. Plus, supplementary melatonin may also preserve BBB integrity.

Don’t drink too much alcohol

Alcohol is a tough one. While I just wrote a big post explaining the merits of wine consumption, ethanol is undoubtedly a poison in high doses, and I derived real benefits when I gave it up for a few months. One way alcohol exerts its negative effects is by inducing BBB dysfunction. This allows both the pleasant effects of alcohol (low-dose ethanol migrating across the BBB and directly interacting with neurons, triggering endorphins and interacting with GABA receptors) and the negative effects (high-dose ethanol migrating across the BBB to damage the neurons, leaving the door open long enough for immune cells to sneak in and cause all sorts of trouble).

Stimulate your vagal nerve

After a traumatic brain injury or stroke, the resultant increase in BBB permeability floods the brain with inflammatory cytokines, causes swelling and neuronal death, and worsens the prognosis. Stimulating the vagal nerve after such an injury decreases the BBB permeabilityand improves the prognosis.

One treatment for epilepsy is to wear vagal nerve stimulators which send light electronic pulses to the nerve, akin to a pacemaker for the brain. Easier options include humming, cold water exposure (even just splashing the face can help), singing, chanting, meditating, deep breathing, coughing, moving your bowels (or summoning the same abdominal pressure required for said movement; girding your core for a heavy squat or deadlift should also work along the same lines), and many more.

Perhaps an entire post on the vagal nerve is in order. It’s an interesting area that impacts more than just the BBB.

Stop eating so often

Ghrelin is the hunger hormone. When you haven’t eaten in a while, ghrelin tells you that it’s time to eat. It also increases blood-brain barrier stability after (again) a traumatic brain injury.

So, never eat? No. But make sure to feel actual hunger. It’s the best spice, and it confers a whole host of other benefits, including better blood-brain barrier function. Heck, try intermittent fasting for the ultimate boost to ghrelin.

You might notice that a lot of the studies I cite involve traumatic brain injuries to rodents. Dropping a weight on a rat’s head or triggering a stroke in a mouse are two of the most reliable ways to induce BBB permeability. Brain injuries are also quite common in humans, and the BBB permeability that results is a major therapeutic target, but we can’t study it so easily in people. While acute and chronic BBB permeability are different beasts, and mice are not men, they operate along the same rough pathway.

That’s about it for today, folks. I hope you feel encouraged and able to fortify your blood-brain barrier. Don’t wait for cognitive decline to set in. Get started now.

How do you improve the integrity of your blood-brain barrier? Have you even considered it prior to today?

Thanks for reading!

Written By: By Mark Sisson  Article Source: http://www.marksdailyapple.com/why-the-blood-brain-barrier-is-so-critical-and-how-to-maintain-it/

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