The Neuro-Protective Lifestyle

photo credit: Sadistos
Simple insomnia is one thing - but complex sleep-disorders like sleep-walking have kept people and scientists alike puzzled for decades…until now.

Finally, the Finnish Twin Cohort of some 11,220 subjects including some 3,000 twin pairs, is able to shed some scientific light on the genetic nature of sleep-walking.

But first–sleep-walking, (as you may already know), has nothing to do with walking.

Sleep-walking can consist of any number of seemingly purposeful behaviors such sitting up–eyes wide-open, going to the bathroom, dressing, undressing and occasionally even driving a car.

However “normal” the behavior appears, these people are still in deep, non-REM sleep and may stay that way for up to thirty minutes. Contrary to popular belief, waking a sleep-walker does not cause harm and in fact is highly recommended to remove them from a potentially dangerous situation (such as driving).

Here’s what “sleep-walking” looks like to a wide-awake observer (usually a family member)!

* Eyes open during “sleep”
* Blank look on face
* May sit up and appear “awake” during sleep
* Walking during sleep
* Detailed activity of any type during sleep i.e., arranging table items, using the phone
* No recall for the episode upon awakening
* Confused, disoriented upon awakening
* Sleep talking = nonsense

A normal sleep cycle has several distinct stages ranging from light drowsiness to a deep, deep sleep (if you’re lucky that is). Each night we normally go through several of these cycles.

Sleep walking (somnambulism) most often occurs during deep, non-REM sleep (stage 3 or stage 4) during the early part of the evening.

If “sleep-walking” behavior occurs during REM sleep (during the early morning hours), this is most likely a relatively new sleep disorder known as RBD (REM Behavior Disorder). With REM behavior disorder, people act out violent dreams and may injure their bed partner by punching, kicking or even jumping out of bed–all while still in REM sleep!

If that’s not weird enough, Bram Stoker’s Dracula may in fact have been inspired by his own observation of the automatic behaviors associated with sleep-walking and the works of several reknowned physiologists and physicians such as, David Ferrier, John Burdon-Sanderson, Thomas Huxley, and William Carpenter.

To these late-Victorian neurologists, these automatic behaviors suggested that humans were no more than “soulless machines” incapable of exercising free-will.

Thankfully, the truth lies somewhere between the two.

From a purely genetics standpoint, sleep-walking is 10 times more likely if a first-degree relative has a history of sleepwalking.

In fact, sleep-walking, from a sleep-disorders arousal standpoint, lies somewhere in between the sleep-state and the wake-state–not unlike Dracula’s trance-like vampiric behavior–a veritable mixed “state of being”.

As a final note, if you happen to be a sleep-walker without a family history of sleep-walking, consider cutting back on caffeine and alcohol. Try keeping a regular sleep schedule and if all else fails–keep a copy of Bram Stoker’s Dracula at your bedside. Pleasant dreams?

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photo credit: Digital Shotgun

Just in case you didn’t know, the blood-brain barrier (BBB), serves as a veritable “surge protector” guarding against certain drugs, chemicals and toxins that find their way into your blood stream.

Depending on the biochemical characteristics of specific molecules, they may never find their way into the brain. Good thing, since most drugs are medicines first and neurotoxins second.

But what exactly constitutes the blood-brain barrier?

Blood vessels in the brain (unlike the rest of the body) are lined with endothelial cells that form tight junctions where they meet.

In other words, the space between cells that line the blood vessels in the brain is so small as to only permit specific nutritional substances, and nothing else.

More specifically, size matters when it comes to the blood-brain barrier. Large proteins are excluded entirely and unless small molecules are lipophilic (soluble in fat), they too will be discriminated against. In short, the brain is very, very particular about what substances cross the blood-brain barrier and be thankful that’s the case.

All bets are off however when inflammation due to infection or any number of other diseases is present. Under these conditions, integrity of the blood-brain barrier is compromised and a neurotoxic “free-for-all” assault on the brain ensues.

Recent advances in nanomedicine seek to exploit this particular vulnerability of the blood-brain barrier by developing a drug delivery system utilizing nanoparticles. Unfortunately, nanoparticles themselves may ultimately be found to possess neurotoxic properties thus exemplifying the inherent truth the traditional French proverb:

“Plus ça change, plus c’est la même chose”, that is,

“the more things change, the more they stay the same”

So what’s an every-day-ordinary blood-brain barrier to do? Nano-neuro-nonsense on one hand or fledgling nutritional neuroscience on the other.

Well consider this for starters. Some of the most innocuous substances on planet earth serve as penultimate blood-brain barrier bolsterers. (I think bolsterers is a word).

Coffee, and the caffeine associated with it, has recently emerged as a neuroprotective agent. It’s clear now, the mechanism behind it’s neuroprotective properties includes caffeine’s ability to enhance the integrity of the BBB in addition to coffee’s inherent antioxidant properties.

Fortunately, flavonoids (a.k.a. phytochemicals, isoflavones, proanthocyanidines) can also traverse the BBB, bringing with them potent antioxidant and anti-inflammatory properties. The next time you enjoy fresh grapefruit juice, relish the bitterness. The citrus bioflavonoid naringenin accounts for both the bitterness and neuroprotective efficacy.

Not surprisingly, regular exercise improves BBB function even in the event of an ischemic stroke.

Ultimately, maintaining the integrity of the BBB may very well be the most effective way of ensuring life-long” cognitive reserve” and perhaps more importantly, establishing a neurobiological foundation for the “neuroprotective lifestyle”.

Coffee anyone?

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Depression can be difficult to treat.

Even with the most effective medications, a sixty percent response rate is considered exceptional. Worse yet for most people, continued treatment revolves around minimizing side-effects rather than aggressively addressing the circumstances that allowed the depression to develop in the first place.

To confound matters even more, recent studies suggest that for moderately depressed patients, new-generation anti-depressant medications function primarily as a placebo and clinically significant medication effects are reserved for only the most severely depressed.

Like most physicians, I have watched select patients benefit from SSRI and dopaminergic-type medications and marveled at their relatively rapid onset and ease of use. And, like most physicians, I’ve watched as patients gain weight, develop sexual side-effects and after prolonged drug therapy become less engaged and more dispassionate about life in general.

They are no longer sad — but they’re not happy either.

Now, recent studies in neuropsychopharmacology and nutritional neuroscience may help restore the chemical and informational imbalance that characterizes the current approach to anti-depressant therapy.

For example, from the Journal of Neuropsychopharmacology, scientists reveal how DHEA levels in the mesolimbic system of the brain up-regulate GABA receptors resulting in a pronounced anti-anxiety and anti-depressant effect.

In another study researchers at Boston University School of Medicine (BUSM) discovered that practicing yoga, in addition to it’s behavioral benefits is capable of elevating GABA (gamma aminobutyric acid) levels in the brain.

GABA is the brain’s primary inhibitory neurotransmitter and is thought to be the final common pathway for most anti-depressant, sedative and anesthetic-type medications. The GABA neurotransmitter system possesses the ability to counterbalance the action of excitatory neurotransmitters contributing to an overall calming effect. If yoga is just not your thing, GABA is available in capsule form without a prescription and the recommended dosage is 600-700 mg, 1-2 per day.

Nutritional neuroscience has also peered into the “mood-stabilizing” properties of omega-3 fatty acids. Epidemiological studies have confirmed that, the lower the intake of omega-3 fatty acids in a given population, the higher the incidence of major depressive disorders. The exact mechanism behind the mood stabilizing properties of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is unknown. Their effectiveness however, remains unquestioned. The recommended dosage is approximately 1.5 to 2 grams of EPA per day and less is more in this case since larger amounts have not been shown to be any more effective.

Not surprisingly, other nutritional deficiencies have been linked to depression, including folic acid and magnesium. Randomized, controlled trials have been conducted confirming the benefit of B12 and folic acid supplementation in the treatment of depression. While not as powerful, case studies in which patients received magnesium (glycinate or taurate) supplementation resulted in rapid resolution of major depression.

To sum it up - - if you “suddenly” find yourself on the Paxil, Prozac or Zoloft super-highway, remember you didn’t get there suddenly. This is the perfect time to introduce stress-management skills such as yoga to your daily routine. Ask your doctor about adding omega-3 fatty acid supplementation especially if you have a triglyceride disorder. DHEA is generally safe but may increase hormone levels if you are already taking estrogen or testosterone.

Finally, consider giving magnesium a try. Use it at bedtime for its sleep-inducing “side-effect” and wake up to a brighter day!

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