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Edited by Russell L. Blaylock, M.D. Blaylock Wellness Report Living a Long, Healthy Life November 2016 Vol. 13, No. 11 Key Points • Glutamate regulates brain, but is harmful in excess • Bacopa increases number of connections between brain cells • Damage from Parkinson’s reduced with bacopa • Study: Alzheimer’s symptoms improve when treated with bacopa • Alzheimer’s patients oſten suffer from ‘silent seizures’ • Bacopa lowers stress hormones that cause depression PLUS • New, superpowered vitamin B ASK DR. BLAYLOCK • How do you cure cluster headaches? • What treats tinnitus? In the last three decades, scientists have learned a great deal about the molecular mechanisms of disease. What we have found is that many seemingly unrelated disorders have several common mechanisms, including inflammation and excitotoxicity. This means that altering just a few factors could improve or even reverse a number of terrible diseases. A growing number of natural compounds have shown varying degrees of protection against brain-damaging conditions such as strokes, multiple sclerosis, brain trauma, brain inflammation, and neurodegenerative disorders like Alzheimer’s dementia, Parkinson’s disease, ALS, and even aging. Yet for many who already have brain disorders, the question is: Are there ways to promote brain healing and repair damage already done? Increasingly, the answer is yes. In this month’s issue of The Blaylock Wellness Report, I will focus mainly on one such compound, bacopa monnieri (also called Brahmi, Indian pennywort, and water hyssop), but will also touch on others that show tremendous potential for brain repair and healing. Restoring Memory Bacopa has been used for centuries, primarily as a memory aid. Most studies of the compound have been conducted on animal models of dementia. There have also been some human studies, using either healthy individuals or those with varying degrees of memory impairment. In one animal model, researchers used the amnesia drug scopolamine to induce memory loss. Scopolamine was used in the 1960s to bring on what they called a “twilight sleep” in women during labor, so they would not remember their pain. The drug causes both retrograde and anterograde amnesia in animals — that is, the loss of memories that formed just before being given the drug and the inability to form new memories aſter the drug is given. The researchers found that bacopa restored memory by altering several Bacopa: Natural Compound Stimulates and Repairs the Brain The

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Edited by Russell L. Blaylock, M.D.

Blaylock Wellness ReportLiving a Long, Healthy Life

November 2016 Vol. 13, No. 11

Key Points• Glutamate regulates brain,

but is harmful in excess

• Bacopa increases number of connections between brain cells

• Damage from Parkinson’s reduced with bacopa

• Study: Alzheimer’s symptoms improve when treated with bacopa

• Alzheimer’s patients often suffer from ‘silent seizures’

• Bacopa lowers stress hormones that cause depression

PLUS

• New, superpowered vitamin B

ASK DR. BLAYLOCK

• How do you cure cluster headaches?

• What treats tinnitus?

In the last three decades, scientists have learned a great deal about the molecular mechanisms of disease. What we have found is that many seemingly unrelated disorders have several common mechanisms, including inflammation and excitotoxicity. This means that altering just a few factors could improve or even reverse a number of terrible diseases.

A growing number of natural compounds have shown varying degrees of protection against brain-damaging conditions such as strokes, multiple sclerosis, brain trauma, brain inflammation, and neurodegenerative disorders like Alzheimer’s dementia, Parkinson’s disease, ALS, and even aging.

Yet for many who already have brain disorders, the question is: Are there ways to promote brain healing and repair damage already done? Increasingly, the answer is yes.

In this month’s issue of The Blaylock Wellness Report, I will focus mainly on one such compound, bacopa monnieri (also called Brahmi, Indian pennywort, and water hyssop), but will also touch on others that show tremendous potential for brain repair and healing.

Restoring MemoryBacopa has been used for centuries, primarily as a memory aid. Most

studies of the compound have been conducted on animal models of dementia.

There have also been some human studies, using either healthy individuals or those with varying degrees of memory impairment.

In one animal model, researchers used the amnesia drug scopolamine to induce memory loss. Scopolamine was used in the 1960s to bring on what they called a “twilight sleep” in women during labor, so they would not remember their pain. The drug causes both retrograde and anterograde amnesia in animals — that is, the loss of memories that formed just before being given the drug and the inability to form new memories after the drug is given.

The researchers found that bacopa restored memory by altering several

Bacopa: Natural Compound Stimulates and Repairs the Brain

The

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brain mechanisms involved in memory formation.1-3

Other successful animal models used different methods to interfere with memory, which demonstrates that the memory-enhancing effect of bacopa was not limited to a single type of model.4-8

If only one type of animal model had been used, we might be able to conclude that bacopa had limited effectiveness. But the fact that it works with many types of models shows that bacopa is affecting basic mechanisms in the brain that control memory.

A number of other studies have explored these mechanisms. For example, it has been shown that bacopa dramatically increases the brain’s production of a major brain repair compound called brain-derived neurotrophic factor (BDNF).9, 10

Another way that bacopa preserves and protects memory mechanisms is to restore neurotransmitters that are essential for memory formation. These include serotonin, acetylcholine, and glutamate, as well as their receptors.11-13

The Brain’s Double-Edged SwordGlutamate is the most abundant neurotransmitter

in the brain, regulating the receptors of other neurotransmitters such as dopamine, serotonin, norepinephrine, and acetylcholine.

This complex interaction is what gives the brain its incredible ability to respond in myriad ways and do all the wondrous things we often take for granted

— thinking, remembering, walking, making music, composing poetry, appreciating art, being creative, and experiencing love, compassion, fear, grief, and many other emotions.

Glutamate receptors also play a major role in memory, especially the development of memories from experience (called long-term potentiation, or LTP).

The glutamate receptor system in the brain is composed of a very complex mixture of receptor types, each in turn made up of a number of subcomponents. Not only are there many types of glutamate receptors, but they are also constantly changing.

And yet, glutamate is also one of the most destructive compounds in the brain — but only when it is found in excess outside of brain cells. That’s why it’s so important to avoid the monosodium glutamate (MSG) found in so many processed foods.

The destruction of brain cells by glutamate is called excitotoxicity because it causes the cells to become extremely excited, ultimately leading to their death.

The brain has elaborate systems that help maintain glutamate levels outside of brain cells at very low concentrations. Unfortunately, many things — such as toxic metals (lead, mercury, aluminum, and tin), strokes, brain trauma, autoimmune diseases, tumors, and brain inflammation — can interfere with these protective mechanisms, leading to varying degrees of brain injury by glutamate.

In fact, if we look at each of these conditions, the

Please note: All information presented in The Blaylock Wellness Report (including answers to reader questions) is for informational purposes only, and is not specifically applicable to any individual’s medical problem(s), concerns, and/or needs. No content is intended to be a substitute for professional medical advice, diagnosis, or treatment. All information presented in The Blaylock Wellness Report should not be construed as medical consultation or instruction. You should take no action solely on the basis of this publication’s contents. Readers are advised to consult a health professional about any issue regarding their health and well-being. Any action you take on the basis of the information provided is solely at your own risk and expense. The opinions expressed in The Blaylock Wellness Report do not necessarily reflect those of Newsmax Media, Inc.

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central event in all of them is inflammation. Brain inflammation is basically driven by special cells called microglia, which are scattered unevenly throughout.

Normally, microglia cells are in a semi-resting state. I say semi-resting, because we have now learned that they are always quite active, sending out probing extensions that sample the brain’s environment to make sure all is well — particularly making sure glutamate levels are not too high.

If the brain is damaged in some way or exposed to things like mercury, aluminum, or certain pesticides, these microglia cells can become fully activated. In such an activated state, they can become destructive to the brain’s cells and connections.

Interestingly, they can become activated in quite restricted parts of the brain or they can be diffusely activated throughout the brain. In Parkinson’s disease, — at least early on — microglial activation is restricted to just a few brain areas.

Being immune cells, microglia also contain all the mechanisms for inflammation. They can inflame and trigger excitotoxicity at the same time they are acting as immune cells — a condition called immunoexcitotoxicity.14

The microglia also contain anti-inflammatory compounds that reduce inflammation to prevent too much damage from occurring.

Or at least that’s how it’s supposed to work.But many medical conditions can cause microglia

cells to become stuck in a destructive mode, which leads to chronic neurodegeneration as we see in Alzheimer’s dementia, Parkinson’s disease, and many other neurological disorders.

Because microglia cells play such an important role in neurodegenerative diseases, strokes, brain trauma, inflammatory brain diseases, and toxic metal-related brain injury, a great deal of research is being directed at ways to calm microglia or convert them to a reparative mode in which they fix damage to the brain.

A number of natural compounds do just that, including bacopa.

Another dementia-causing medical condition, diabetes, is also greatly improved by bacopa. Using special animal models of diabetes, researchers found that bacopa could significantly improve the memory and stop learning deterioration seen in diabetic animals.15

Bacopa has the potential of improving many neurological problems associated with diabetes. By significantly improving the antioxidant network within the hippocampus of the brain and reducing the process of lipid peroxidation, bacopa adds a great deal of protection against neurodegeneration of critical areas of the brain.

It also stimulates the growth of brain cell communication pathways, lowers damaging excess nitric oxide, and improves blood flow to the brain — all major problems associated with diabetes.

Fighting DementiaTwo processes play the greatest role in dementia-

causing diseases such as Alzheimer’s and Lewy body dementia — inflammation and excitotoxicity. These two processes are linked.

What Is Bacopa and What Can It Do?

Bacopa monnieri is a creeping herb native to wetlands (ponds, bogs, and marshes) of eastern and southern India, Australia, Europe, Africa, Asia, and North and South America. Analysis of the plant’s leaves demonstrates a number of compounds of the triterpenoid saponin type. The most studied and beneficial compounds are called bacoside A and bacoside B.

Bacopa has been used for thousands of years for a number of ailments, but mainly to improve memory.

It has been found to have a number of useful properties, such as reducing inflammation, as an antioxidant, improving blood flow, protecting against neurodegeneration, and stimulating healing of damaged neurons and nerve cell connections (synapses). It is also an antidepressant, and reduces pain and anxiety.

Extensive testing using very high doses in both animals and humans demonstrated a very high margin of safety and no serious side effects — even when used in children. It has not been tested for safety in pregnant women.

The most beneficial supplements are those extracted using water or methanol. Most studies were conducted using a form called CDRI-08, which is available without a prescription — at least for now.

Other high quality forms are also available.

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In most cases, inflammation occurs first (or at the same time), and then triggers excitotoxicity.16, 17 This interaction of inflammation and excitotoxicity (immunoexcitotoxicity) drives the destruction of the neuron connections and the eventual destruction of the neurons themselves.

This chronic process can last for decades and accelerates as the dementia progresses.

In one study, bacopa was found to increase the connections between neurons (dendritic arborizations) in the hippocampus, the site of memory formation in the brain.18

One of the earliest events in all neurodegenerative diseases is a loss of brain cell connections, which can occur years or even decades before the neurons themselves are lost.

This long delay, before the actual destruction of the brain cells, means that if immunoexcitotoxicity is halted soon enough, the connections can be repaired — mainly by compounds such as BDNF, which is produced by special brain cells. Bacopa stimulates these cells to release greater quantities of BDNF.

Bacopa has also been tested in animal models of human Alzheimer’s disease. Beta-amyloid, a toxic compound that accumulates in the brains of people with Alzheimer’s, has been shown to stimulate inflammation within the brain. Bacopa reduces the toxicity of beta-amyloid, thus protecting brain cells.19-21

Bacopa protects the brain in a number of other ways, such as:

• Improving mitochondrial energy production• Reducing brain oxidative damage• Reducing inflammation• Reducing lipid peroxidation• Improving blood flow in the brain• Reducing excessive nitric oxide levels• Reducing enzymatic destruction of acetylcholine

(which is essential for memory)• Reducing excitotoxicityIt also stimulates the brain’s ability to change

throughout life — called brain plasticity — and increases the level of protective antioxidant enzymes.22-26

In one study using an animal model of Alzheimer’s disease, bacopa not only reduced the amount of amyloid accumulating in the brain, it also reduced learning deficits and improved long-term spatial

memory, which is used to remember where you have been and how to get places.27

Reducing Parkinson’s Disease DamageOne of the recently discovered links to Parkinson’s

disease is exposure to pesticides. Of these, the best researched is the pesticide rotenone, which destroys the areas of the brain involved in Parkinson’s disease — called the striatum and substantia nigra.

The destruction of these brain areas happens mainly by the activation of microglia and a subsequent development of high levels of inflammatory cytokines, free radicals, lipid peroxidation, and excitotoxicity.

In one study using mice, researchers found that brain damage by rotenone could be significantly reduced by feeding the animals bacopa,28 which raised the level of a powerful brain-protecting molecule called glutathione in the critical areas of the brain.

Loss of glutathione is an early indicator in the brains of Parkinson’s patients.

Bacopa also protected dopamine levels, which are low in Parkinson’s disease brains.

Another pesticide, called paraquat, also is linked to Parkinson’s disease risk. Bacopa also reduced damage by paraquat on the type of cell damaged in Parkinson’s — called dopaminergic neurons.29, 30

In one animal model of Parkinson’s disease, bacopa reduced damage in these same cells by limiting alpha-synuclein accumulation (a marker for Parkinson’s disease) and preventing degeneration of dopamine-releasing cells.31

In another type of Parkinson’s animal model, researchers found that bacopa prevented loss of glutathione and lowered elevated levels of lipid peroxidation in the substantia nigra of animals exposed to the toxic agent.32

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It also restored other important antioxidant enzymes in the substantia nigra.

Ginkgo biloba has also been shown to protect against the brain damage in Parkinson’s animal models.

In combination with bacopa, ginkgo could be expected to add considerable protection.33

Bacopa has also been shown to protect dopamine receptors in the brain, which are severely depleted by Parkinson’s disease.34

One of the chemicals that produce a Parkinson’s-like disease in both animals and humans is called MPTP. This compound damages mitochondria within the substantia nigra and activates microglia — a combination that greatly magnifies the destructive effects of excess glutamate.

Bacopa has been shown to block the damage to mitochondria, raise glutathione levels, increase dopamine levels, and increase the levels of other antioxidant enzymes — all things that can greatly benefit a Parkinson’s patient.35

A number of other natural compounds also offer protection to the parts of the brain associated with Parkinson’s disease. These include curcumin, quercetin, naringenin, hesperidin, baicalein, and silymarin.

Used in combination, they could provide even better protection.

Improving Alzheimer’s SymptomsOne of the few studies on patients with Alzheimer’s

disease used bacopa in a randomized, double-blind, placebo-controlled trial of 104 people. They were given a combination of bacopa, sea buckthorn, and a special yam species (air potato) — or a placebo.36 The study also included 97 healthy subjects.

The researchers used a number of intelligence and cognitive tests to evaluate the participants.

They also tracked a number of inflammatory markers, such as homocysteine levels, C-reactive protein, TNF-alpha levels, and measures of lipid peroxidation; measures of the antioxidant network, such as glutathione, glutathione peroxidase, and superoxide dismutase.

The study lasted 12 months.They found that the Alzheimer’s patients given

bacopa showed significant improvement in cognitive function, including immediate word recall, attention span, and activity function.

Delayed word recall was not improved, but depression — which can be a major problem in Alzheimer’s patients — was remarkably improved.

Most impressive was the dramatic fall in measures of inflammation.

This is critical because inflammation is a major driving force for progression of Alzheimer’s, and is

Human Studies Using BacopaSeveral trials have been conducted

to see if human beings’ memory could be improved by supplementing with bacopa.

The trials used two types of subjects: one group used normal, healthy people, and other trials were conducted on those with impaired memory secondary to either aging or neurodegeneration.

Studies of short-term bacopa use generally did not result in significant improvement in memory. However, a 90-day double-blind placebo-controlled trial of 62 people found significantly improved spatial working memory and better rapid visual memory processing.

Working memory is what allows people to hold onto new information so that it can be processed, analyzed, and used to understand what that information means.

Another impressive study subjected 24 healthy volunteers to a six cognitively demanding tests in a double-blind, placebo-controlled environment.

The dose of bacopa used was either 320 or 640 mg (versus a placebo).

Even at the lower dose, the researchers saw significant improvement in the cognitive function of the participants. What makes this study especially

important is that by using a series of demanding tests, the researchers not only measured the subjects’ cognitive brain function, but also the ability to maintain concentration and mental function under demanding conditions.

Yet another study measured if bacopa could improve a person’s memory function during a period of life when memory problems frequently arise.

Researchers gave 465 elderly people between ages 60 to 75 years 300 mg a day of bacopa or placebo for 12 months. The study found a significant improvement in their memory.

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directly linked to excitotoxicity, which does most of the damage.

The earlier the treatment is started, the more dramatic the results would be.

In fact, if bacopa were taken before any Alzheimer’s symptoms appeared, you could expect significant prevention of cognitive impairment in a patient.

Interestingly, the researchers saw significant improvement in cognitive function in the healthy elderly as well — especially in delayed word recall, attention span, and functional activity.

Inflammation markers in the healthy elderly also fell dramatically.

As we age, our bodies become progressively more inflamed. This is suspected to be the reason for the high incidence of neurodegenerative diseases with aging.

Bacopa has also been tested among children suffering from mental retardation. It had impressive results in terms of improving behavior and memory.37

Some clinical studies of patients with a number of types of neurological disorders have shown significant and sometimes dramatic improvement when the inflammatory brain cytokine TNF-alpha levels are lowered by bacopa.38-40

Treating and Preventing StrokesBrain damage caused by ischemic strokes

(due to a blocked artery) has many of the same destructive processes as neurodegenerative diseases. Like neurodegenerative diseases, we see immunoexcitotoxicity and microglial activation at center stage.

In the past, we thought that stroke damage in the brain was mainly caused by a lack of blood supply to that part of the brain affected by the blocked blood vessel.

But we now know that a great deal of the damage

comes from activated microglia causing intense inflammation and excitotoxicity around the area of the blocked vessel.

Activation of microglia occurs very rapidly after a stroke and can persist for a long period. As long as the microglia are activated, they will continue to release powerful pro-inflammatory compounds (cytokines, chemokines, and interferon) as well as glutamate. This combination first destroys the connections between brain cells and then the brain cells themselves.

Knowing that most of the damage is delayed, researchers have been searching for ways to turn off the activated microglia and lower levels of inflammatory cytokines and excitotoxins in the brain immediately after a stroke.

Among several other naturally occurring compounds, bacopa is quite effective for accomplishing this task.

One study using rats found that bacopa significantly reduced the neurological impairment, reduced the amount of brain damage (infarct volume), and reduced swelling of the brain.41

Bacopa has also been shown to increase blood flow to the brain without raising blood pressure.42

Because bacopa raises the antioxidant network enzymes in the brain and has powerful anti-inflammatory effects, it should be useful not only for treating strokes, but for preventing them.

Inhibiting SeizuresBacopa has been studied in a number of

animal models of human-type seizures. Most have demonstrated significant benefits in reducing or even completely blocking seizures.

What is most impressive in these studies is that they used a wide variety of seizure models, indicating that bacopa inhibits the basic mechanisms that drive all seizures.

A note from Dr. Blaylock: Advertisements for various supplements may appear in the newsletter or attached to the newsletter. I have nothing to do with these advertisements and do not endorse them. The only

supplements I endorse are those that I list in the newsletter. This is not to say that I object to the supplements; it’s just that I am not familiar with the supplements being advertised.

Please note that this advice is generic and not specific to any individual. You should consult with your doctor before undertaking any medical or nutritional course of action.

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Exactly how bacopa inhibits seizures is still under much study. But many mechanisms have been discovered. It is understood that suppressing overactivation of glutamate receptors in the area of the brain involved in the seizures is critical.

In some studies, bacopa altered the sensitivity and expression of a class of glutamate receptors, thereby inhibiting seizures.43, 44

Other studies have shown that bacopa alters other neurotransmitter receptors, such as serotonin receptors, that are also associated with seizures.45

Another receptor that is important for understanding epilepsy is the GABA receptor, which calms the brain circuits, thus preventing seizures.

In both animals and humans, GABA receptors are deficient in the parts of the brain affected by the seizure.

One study found that bacopa restored the normal balance of GABA receptors in animals that had experienced seizures, preventing further seizures from occurring.46

You also have to appreciate that not all seizures are recognizable. People don’t always fall to the floor and jerk or writhe.

In a number of cases, a person may not even be aware of a seizure (called silent seizures). Or the person may experience nothing more than momentary lapses of attention that quickly pass and are attributed to a “wandering mind.”

In addition, a seizure may result in a strange behavioral outburst such as anger, crying, or inappropriate laughter, or a person may simply become withdrawn and contentious.

Studies have shown that Alzheimer’s dementia patients experience silent seizures quite frequently. That may explain many of their behavioral quirks, as well as contributing to their deterioration.

In such cases, bacopa would not only reduce brain inflammation, excitotoxicity, free radical damage, lipid peroxidation, and beta-amyloid accumulation, it would also quiet their silent seizures.

Reversing DepressionIt is suspected that brain inflammation and

excitotoxicity are playing significant roles in depression — especially major depression.

Studies have shown that most antidepressant

medications reduce brain inflammation. In fact, that might be how they work.

Many antidepressants also partially block excitotoxicity, which is associated with depression.

This explains the memory loss often associated with major depression, suggesting atrophy of the hippocampus of the brain, which is the area most concerned with memory formation.

A number of studies have shown that bacopa acts as a significant antidepressant.

In most such studies, scientists used a mouse model of depression.

You may be wondering: How does one know when a mouse is depressed?

Mice show certain behaviors with depression, just like people — for instance, loss of interest in eating, no interest in social interaction, inactivity, and other signs.

In one mouse study, researchers found that bacopa could significantly reverse depression in the animals after two weeks.47

Stress — especially chronic, unrelieved stress — is also a major cause of depression. In today’s world, we are all under increased stress.

One study put rats under either acute or chronic stress, and researchers found that bacopa was able to significantly reverse depression by raising levels of the brain repair compound BDNF.48

People with depression have been shown to have low levels of BDNF.

People under stress also have much higher levels of corticosterone — a steroid hormone produced in the adrenal glands — that persist for prolonged periods. This can damage neurons in the hippocampus.

Several studies have shown that bacopa can lower corticosterone levels in stressed animals.49

Depression is frequently accompanied by anxiety. The brain structure centrally involved with anxiety is called the amygdala, an almond-shaped nucleus tucked within the temporal lobe of the brain.

This structure is also involved with memory — especially control of memories of terrifying or traumatic events, such as we see with post-traumatic stress disorder (PTSD).

Studies have shown that bacopa significantly improves and stimulates the growth of connections within amygdala brain circuits.50

Finally, bacopa has been found to be useful in cases

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of other psychiatric conditions, such as psychotic behavior and even ADHD.51, 52

It has also been shown to significantly reduce depression associated with withdrawal from morphine.53

Protecting the Brain from Toxic MetalsBacopa has been shown to significantly protect

the brain from three toxic metals, two of which — aluminum and mercury — are commonly found in vaccines.

The third, lead, is commonly found in household dust and many other sources.

All three are found in most peoples’ brains. In some cases, the levels are unquestionably toxic.

Because these toxic metals are ubiquitous in the environment, and because they accumulate in the brain, finding a way to reduce their toxicity is critical for everyone’s brain health.

Aluminum is found in many medicinal products that can be obtained both over the counter and by prescription. It is also found in many foods (especially as a food dye), vaccines, and teas.

Medications with aluminum that are inhaled, such as nasal sprays, are especially dangerous because the metal is transported via the nasal (olfactory) nerves directly into the three parts of the brain most damaged by Alzheimer’s disease:

• Entorhinal area• Hippocampus• Prefrontal cortexSeveral studies have shown that much of the

damage done to the brain by aluminum is secondary to aluminum-induced lipid peroxidation (oxidation of brain fats), microglial activation, and suppression of brain-protective antioxidant network compounds.

Researchers found that bacopa could dramatically reduce the damage caused by aluminum by preventing lipid peroxidation and significantly restoring antioxidant enzymes to normal levels.54, 55

Electron microscope studies have also shown dramatic protection of the brain from damage by aluminum.

Studies using animals also demonstrated significant restoration of memory in aluminum-exposed animals that received bacopa.56

Similar protection against brain damage caused by lead has also been demonstrated.

In one impressive study, rats were exposed to lead acetate for four weeks. They were then either given the chelator DMSA alone, bacopa alone, or a combination of DMSA and bacopa over a seven-day period.

The researchers examined four areas of the animals’ brains — cerebellum, frontal cortex, hippocampus, and brain stem.57

They found extensive protection against lead-

Good Diet Prevents Retina DiseaseSome glaucoma cases have

normal intraocular pressure, and are not improved by medications. In some cases, lowering the pressure will not stop the progressive destruction of the retina. These observations demonstrate that the problem is not pressure alone. It is important to maximize the antioxidant network of the eyes, reduce inflammation, block excitotoxicity, and increase energy production by the retina.

By doing these things, intraocular pressure is lowered and blood flow

can be improved within the retina. A good diet is a better method

for getting nutrients than taking supplements. The supplements are important if you already have a disorder or have a strong family history of eye problems. The principle goal for your diet is to reduce inflammatory foods, such as sugar and other high glycemic foods. Avoid omega-6 oils, pesticide/herbicide exposure, and red meats as much as possible. Drink only purified water and white or green tea, and avoid fluorinated

water and drinks. Increase your intake of kale, spinach, collard greens, and parsley.

These vegetables have very high levels of lutein and some zeaxanthin. They reduce macular degeneration and protect against retinal damage from glaucoma.

While vegetables have the highest levels of lutein, the best absorption of carotenoids comes from egg yolks. You should eat eggs at least two times a week. But do not scramble them, as this exposes the phospholipids to oxidation.

BLAYLOCK TIP

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induced brain damage with all three treatments. In fact, animals’ brains were close to normal.

Methylmercury is a highly absorbable form of mercury that does extensive damage to the brain, especially the cerebellum.

Similar damage is caused by ethylmercury, the form used in many vaccines.

Studies have shown that bacopa prevented the cerebellar damage caused by exposure to methylmercury in experimental animals. It also prevented loss of memory and reduced activity seen with mercury exposure.58

Great Promise of BacopaBecause bacopa powerfully inhibits the release of

inflammatory chemicals (cytokines) from activated microglia, it promises to become a major brain-protecting agent.

It offers great hope in treating a tremendous number of neurological conditions such as:

• Strokes• Alzheimer’s disease• Parkinson’s disease• ALS• Huntington’s disease• Lewy body dementia• Brain trauma• Multiple sclerosis Bacopa is also a promising treatment for

autoimmune diseases and toxic chemical exposures.59, 60

As I have written often, inflammation is a central process in a great many diseases and other types of ailments. In general, things that calm inflammation make people better.

Inflammation and excitotoxicity (immunoexcitotoxicity) play major roles in pain, especially chronic pain.

Bacopa has been shown to significantly reduce pain, even the pain of arthritis.61-63

Bacopa also dramatically improves wound healing, which would be very important for diabetics because they have great difficulty healing wounds.64

The reason this compound promotes healing is that it has antimicrobial properties, which help prevent wound infections.

In addition, bacopa has been shown to improve sperm quality and sperm cell number, lowers elevated

cholesterol, and improves stamina with intense exercise.65-68 Several studies have shown a significant anticancer effect of bacopa.69, 70

Studies in both animals and humans (including children) have shown bacopa to be very safe.71, 72

It is important to emphasize that when using bacopa, you should allow at least six weeks for the maximal effects to occur. In most cases, it does not work rapidly.

REFERENCES1. Rai R et al. Evid Based Complement Alternat Med 2015;2015:254303. 2. Pandareesh MD et al. Neurochem Res 2016;41(5):985-99. 3. Saraf MK et al. Evid Based Complement Alternt Med 2011;2011;236186.4. Rani A, Prasad S. Evid Based Complement Alternat Med 2015:2015: 347978.5. Wetchateng T, Piyabhan P. J Med Assoc Thai 2015;98:Suppl 2:S56-63. 6. Le XT et al. J Ethnopharmacol 2015;164:37-45. 7. Dwivedi S et al. Evid Based Complement Alternat Med 2013:2013: 294501.8. Le et al. Neurochem Res 2013;39(10):2201-15.9. Preethi J et al. Front Pharmacol 2016;7:doi: 10.3389/jphar.2016.00166.10. Kumar S, Mondal AC. Neurochem Res 2016; epub ahead of print.11. Charles PD et al. J Ethnopharmacol 2011;134(1):55-61. 12. Piyabhan P et al. ClinExpPharmacolPhysiol 2016;doi:111/1440/1681.12658. 13. Uabundit N et al. J Ethnopharmacol 2010;127(1):26-31.14. Blaylock RL. Surg Neurol Int 2013:4:118. 15. Khan MB et al. Metab Brain Dis 2015;30:115-127.16. Blaylock RL, Maroon J. Surg Neurol Int 2011;2:107. 17. Blaylock RL. Surg Neurol Int 2013;4:118.18. Vollala VR et al. Rom J MorpholEmbryol 2011;52(3):879-86.19. Limpeanchob N et al. J Ethnopharmacol 2008;120(1):112-7. 20. Mannangatti P, Naidu KN. AdvNeurobiol 2016;12:323-36. 21. Saini N et al. Neurochem Res 2012;37(9):1928-37.22. Pandareesh MD et al. Cytotech 2014;68:157-72. 23. Saraf M et al. Neuroscience 2008;155:476-84. 24. Pandareesh MD, Anand T. Neurochem Res 2014;39(5):800-14. 25. Shinomol GK et al. Phytomedicine 2011;18(4):317-26. 26. Kamkaew N et al. Phytother Res 2013;27(1):135-8.27. Li Y et al. Aging 2016;8(3):521-33. 28. Shinomol GK et al. Cell MolNeurobiol 2012;32(3):455-65.29. Singh M et al. ToxicolSci 2012;125(1):219-32. 30. Hosamani R et al. NutrNeurosci 2014; abstract.31. Jadiya P et al. BiochemBiophys Res Commun 2011;413(4):605-10. 32. Shobana C et al. Cell MolNeurobiol 2012;32(7):1099-112.33. Ahmad M et al. J Neurochem 2005;93(1):94-104.34. Thomas RB et al. Cell MolNeurobiol 2013;33(8):1065-74.35. Nellore J et al. J Neurodegener Dis 2013;2013:972391.36. Sadhu A et al. Clin Drug Investig 2014;34(12):857-69.37. Dave UP et al. Ind J Pediatr 1993;60:423-28.38. Tobinick E et al. CNS Drugs 2012;26(12):1051-70. 39. Tobinick E. CNS Drugs 2011;25(2):145-55. 40. Tobinick E. Curr Alzheimer Res 2007;4(5):550-2.41. Liu X et al. RestorNeurolNeurosci 2013;31(2):109-23.42. Kamkaew N et al. Phytother Res 2013;27(1):135-8.43. Paulose CS et al. Neurochem Res 2008;33(9):1663-71. 44. Khan R et al. Epilepsy Behav 2008;12(1):54-60.45. Krishnakumar A et al. Neurochem Res 2015;40(1):216-25.46. Mathew J et al. Neurochem Res 2011;36(1):7-16.47. Mannan A et al. BMC Complement Alternat Med 2015;15:337.48. Banerjee R et al. Psychiatry Investig 2014;11(3):297-306.49. Sheikh N et al. J Ethnopharmacol 2007;111(3):671-6.50. Vollala VR et al. Cinic 2011;66(4):663-71.51. Chatterjee M et al. PharmacolBiol 2015;53(12):1850-60. 52. Dave UP et al. Adv Mind Body Med 2014;28(2):10-5.53. Rauf K et al. Phytother Res 2014;26(6):937-9. 54. Nannepaga JS et al. Chin J Physiol 2014;57(5):279-85. 55. Jyoti A, Sharma D. Neurotoxicol 2006;27(4):451-7.56. Thippeswamy AH etv al. Acupunct Meridian Stud 2013;6(4):208-13.57. Velaga MK et al. Drug ChemToxicol 2014;37(3):357-64.58. Sumathi T et al. Cell MolNeurobiol 2012;32(6):979-87.59. Nemetchek MD et al. J Ethnopharmacol 2016;doi:10.1016/j.jep.2016.07.073.60. Williams R et al. Food Funct 2014;5(3):517-20.61. Bhaskar M, Jagtap AG. In J Ayurveda Res 2011;2(1):2-7. 62. Rauf K et al. Curr Med Chem 2013;20(8):1028-37. 63. Viji V et al. Phytother Res 2010;24(9):1377-83.64. Murthy S et al. Biomed Res Int 2013:2013:972028.65. Patel SK et al. J Ethnopharmacol 2016; doi:10.1016/j.jep/2016.07.26.66. Kamesh V, Sumthi T. Asian Pac J Trop Med 2012;5(12):949-55. 67. Anand T et al. Phytother Res 2012;26(4):587-93. 68. Kalyani M et al. J Nat Med 2013;67(1):123-36.69. Mallick MN et al. J Pharm BioalliedSci 2015;7(4):325-8. 70. Peng L et al. Phytothere Res 2010;24(6):864-8.71. Sireeratawong S et al. BMC Complement Altern Med 2016;16:249. 72. Sharma R et al. J Res EducInd Med 1987;1:12.

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Benfotiamine: Superpowered Vitamin B1It doesn’t happen often, but sometimes a synthetic

vitamin has properties that are superior in some ways to the natural vitamin.

A synthetic form of vitamin B1 (thiamine) called benfotiamine (S-benzoylthiamine-O-monophosphate) has some incredible properties that are especially beneficial for a number of neurological conditions.

Originally, this vitamin was designed by Japanese scientists to treat alcoholic neuropathy; a very painful and crippling nerve condition.

But now it is considered a superior treatment for diabetes-related polyneuropathy and other diabetic complications such as nephropathy (kidney damage), retinopathy (loss of vision) and cardiac angiopathy (heart failure).

Deficiencies of thiamine are associated with Alzheimer’s dementia, Parkinson’s disease, ALS, multiple sclerosis, and diabetes.

Benfotiamine is more fat-soluble than natural thiamine and therefore easily enters the brain and nerves. In animal models of Alzheimer’s disease, benfotiamine was able to significantly reduce amyloid deposits in the brain.

One of the central events in the vast majority of neurological conditions is prolonged microglial activation. Benfotiamine has been shown to inhibit microglial activation and prevent the release of damaging chemicals from microglia, such as nitric oxide, inflammatory prostaglandins, and inflammatory cytokines.

It also increases the release of a powerful anti-inflammatory cytokine called IL-10.

About ‘The Blaylock Wellness Report’In this age of deteriorated civility, lack of respect

for elders, and general obsession among far too many to insult those they do not know or agree with, I feel a need to clear up some rumors that are floating

around the Internet — mainly that I do not write this newsletter; that it is written by others and I merely edit each issue.

I do this for clarification, not that my enemies will in any way be convinced by my assurances. But that is the nature of modernity.

I choose all the subjects I write about, I do all the research myself, and I choose and read all the studies I quote as references. I write the entire newsletter and answer all the reader questions myself and then an editor at Newsmax arranges the newsletter as per its design. They do suggest a few changes in some sentences for clarity, but I make all final editorial changes.

I analyze the studies and also add my own experiences from the 30 years I have been in the medical field — which includes my internship,

neurosurgical residency, and 24 years of neurosurgical practice.

I did not practice natural medicine in addition to neurosurgery, as some have stated. I did utilize many natural treatments during my years of neurosurgical practice.

After I retired from practicing neurosurgery, I spent two years running a full-time natural medicine practice, and then fully retired from clinical practice.

I have written four books on natural health subjects (none were ghostwritten), several chapters in medical and surgical texts and continue to write articles for medical and scientific journals. I also review submitted articles for several medical journals.

In addition, I serve as an assistant-editor-in-chief for the journal “Surgical Neurology International” (SNI), and serve on the neuroscience editorial staff of SNI.

I also serve on the editorial staff of other medical journals.

I hope I have set the record straight for those who really care.

Health and Nutrition Updates

‘It doesn’t happen often, but sometimes a synthetic vitamin has properties that are superior in some ways to the natural vitamin. Benfotiamine has some incredible properties for neurological conditions.

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November 2016 The Blaylock Wellness Report Page 11

NewsmaxHealth.com

Can I Take Immune Supplements?Q: You wrote that immune stimulants shouldn’t be taken for chronic inflammatory demyelinating polyneuropathy (CIDP). I take a lot of supplements for my immune system against stage 3 colon cancer. Are they making the symptoms of CIDP worse?

— Lowell K., Guildford, United Kingdom

A: Chronic inflammatory demyelinating polyneuropathy is a neurological disorder that causes weakness and poor sensory function in the arms and legs. The greatest danger in CIDP, an autoimmune nerve disorder, is from humoral immune stimulation.

The most effective immune stimulant for cancer is beta-glucan, which is a cellular immune stimulant that does not worsen autoimmune disorders. Try the beta-glucan, and if the condition worsens, taking fish oil will reverse it and within a week the immune enhancement will subside.

In such cases, it may be more important to depend on cancer inhibitors, such as curcumin, quercetin, ellagic acid, baicalein, tocotrienols, and hesperidin in combination.

This constitutes a very powerful anticancer combination. The B vitamins, including benfotiamine, would be important.

Do I Have to Worry About Glutamate?Q: I’m thinking about taking sulbutiamine to prevent Alzheimer’s. But I’ve heard it increases glutamate activity. Do I have to worry about harmful effects from increased glutamate activity?

— Albert Y., Vancouver, B.C.

A: The one study that looked into the effects of

sulbutiamine (which is composed of two thiamine molecules linked by sulfur) found no increase in glutamate activity and an actual decrease in one form of glutamate receptor.

The compound is similar to benfotiamine (see “Benfotiamine: Superpowered Vitamin B1,” page 10) but a lot more expensive. I would use benfotiamine instead.

Should I Stop Taking Tocopherol?Q: I serve as a missionary in Indonesia and have Parkinson’s. I take a supplement that has alpha-tocopherols, but no tocotrienols. Should I stop taking it?

— Ruth M., Bandung, Indonesia

A: Bless you for your service to our Lord. It is not that alpha-tocopherol itself is harmful, it just is not as beneficial as the mixed tocopherols, the type God made. It is best to take the tocotrienols and tocopherols at different times of the day, because they can interfere with each other’s absorption.

How to Treat Cluster Headaches?Q: My 30-year-old son has been suffering from cluster headaches since he was 18. Is there something he can do to get relief? Can he change his diet or take certain supplements?

— Cathy B., Fort Smith, Ark.

A: These types of headaches appear to be related to migraine headaches, and therefore are linked to the immunoexcitotoxic process and microglial activation. Hypoglycemia is also linked to these headaches, and is a major trigger.

Avoid sugar and high-glycemic foods. Magnesium will reduce the incidence and severity of the

Ask Dr. BlaylockAttention Blaylock Readers:Dr. Blaylock welcomes any questions or comments you would like to share.Each month, he will select a few to be published and answered in the newsletter.Please remember that he cannot answer every question.When submitting a question or comment, please include full name, city, and state.Please e-mail the doctor at: [email protected].

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headaches. The slow-release magnesium malate — two tablets three times a day — is best.

For severe episodes, mix 250 mg magnesium citrate/malate in 6 ounces of water and drink twice a day as an additional protective boost.

It is also critical to avoid all sources of excitotoxin food additives and foods high in glutamate. High dose B vitamins, especially thiamine and riboflavin will reduce episodes.

Supplements for Cancer?Q: My husband, age 64, was diagnosed with multiple myeloma five years ago. He had a three-year remission, but recently relapsed. Can you recommend supplements for him?

— Camille A., Nampa, Idaho

A: Multiple myeloma responds well to a number of natural compounds. Curcumin, quercetin, baicalein, hesperidin, ellagic acid, and beta-glucan all inhibit this cancer — especially when used in combination.

Curcumin and quercetin should be added to

extra virgin olive oil to enhance absorption. Empty two capsules of 500 mg each into a tablespoon of oil and take four times a day. Avoid omega-6 oils, sugar, glutamine, and glutamate.

What Should I Do for Tinnitus?Q: I developed bilateral tinnitus two years ago. Do you know of any supplements or pharmaceuticals that could reduce the effects of this disorder?

— Robert M., Lufkin, Texas

A: There are several things that help tinnitus. Vinpocetine in a dose of 20 mg a day has had the most success. Ginkgo biloba has also had some success and can be added to vinpocetine. Both have mild anticoagulant effects and should not be added to other anticoagulants. DHA, 1,000 mg a day, can also help reduce inflammation and heal the nerve. The B vitamins can also repair the nerve.

A number of prescription medications and aspirin worsen the tinnitus. You should also avoid glutamate additives in foods and aspartame. Caffeine and other stimulants worsen the symptoms.

About Dr. BlaylockDr. Russell Blaylock is a nationally recognized, board-certified neurosurgeon, health practitioner, author, and

lecturer. He attended the Louisiana State University School of Medicine in New Orleans and completed his internship and neurosurgical residency at the Medical University of South Carolina in Charleston, S.C. For 25 years, he has practiced neurosurgery in addition to having a nutritional practice. He recently retired from his neurosurgical duties to devote his full attention to nutritional studies and research. Dr. Blaylock has authored four books on nutrition and wellness, including “Excitotoxins: The Taste That Kills,” “Health and Nutrition Secrets That Can Save Your Life,” “Natural Strategies for Cancer Patients,” and his most recent work, “Cellular and Molecular Biology of Autism Spectrum Disorders,” edited by Anna Strunecka. An in-demand guest for radio and television programs, he lectures extensively to both lay and professional medical audiences on a variety of nutrition related subjects.

He is the 2004 recipient of the Integrity in Science Award granted by the Weston A. Price Foundation. He serves on the editorial staffs of the Surgical Neurology International and the Journal of American Physicians and Surgeons, official publication of the Association of American Physicians and Surgeons. He also serves as an assistant editor-in-chief for the journal Surgical Neurology International. He was also a lecturer for the Foundation on Anti-Aging and Regenerative Medicine. At present, he is a reviewer for the journal Food & Chemical Toxicology and other journals.

Dr. Blaylock previously served as clinical assistant professor of neurosurgery at the University of Mississippi Medical Center in Jackson, Miss.

To renew or subscribe to The Blaylock Wellness Report go to: NewsmaxHealth.com/Newsletters or call 1-800-485-4350

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