Category Archives: Government/Research

KO the KD? Results of Keto Diet for TBI Inconclusive

“Dinner today is going to be a big steak and, for dessert, a huge bowl of ice cream.”

The above meal may seem like a recipe for weight gain, but it is also a meal in tune with the ketogenic diet.  A diet trend for about a decade, the ketogenic diet (KD) seeks to, “mimic biochemical changes associated with starvation,” states the NIH. The basic idea of this diet is to limit the carbohydrates one consumes, and eat a diet of 80 – 90% fat, in order to put the body into a starvation state.  This extreme limitation of foods that are turned into glucose means that the metabolic source used for energy production must be changed by the body, so that it goes into a ketonic state.

People with chronic diseases/conditions have said that KD promotes their overall health, reduces their symptoms, slows their diseases progression and even may be a treatment for it.  In a 2008 study, titled Diet, Ketones and Neurotrauma, scientists noted, “This altered dietary approach may have tremendous therapeutic potential for both the pediatric and adult head injured populations.”  Since that time, over 20 studies have been done that show that KD both helps you lose weight and improves your health.  This year, in fact, the NIH reviewed past studies and performed new animal studies that showed, “The KD is an effective treatment for TBI recovery in rats and shows potential in humans… [however] the human trials did not establish much evidence with respect to the KD as a treatment for TBI.”  Again, the NIH concluded that further research is needed.

What has been determined is that the ketogenic diet is beneficial for some people who have particular neurological disorders – specifically children with epilepsy.  As far back as 1921, the KD diet was used as a treatment for epilepsy in children with positive results.  Since the diet is very strict it may be the last option, but it is still an option, especially for epilepsy – a disorder that can be caused or exasperated by traumatic brain injury.  Additionally, it seems that the ketogenic diet may be beneficial for treatment of diabetes, as it lowers blood sugar.  Diabetes has been shown both to be a possible consequence of brain injury or a possible cause of brain injury.  Even if a brain injury is not involved, the symptoms of hyperglycemia, the identifying mark of diabetes and other disorders, mimic those of TBI.  In fact, “Among the secondary complications, hyperglycemia (both peak glucose and persistent hyperglycemia) in TBI patients is one of the most common and correlates with the severity of the injury and clinical outcome.”  (However, the Cleveland Clinic notes that, “Eating a lot of sugar can lead to tooth decay, but it does not cause diabetes.”)

In reality, most people will embark on a diet at some point in their lives.  Even with all this inconsistent evidence, the ketogenic diet is still on trend, largely because of celebrity endorsements by such people as Kim and Kourtney Kardashian, Halle Berry, Gwyneth Paltrow and LeBron James.  Be aware though, that whenever you intake a greater amount of calories than your body needs, you will gain weight.  And even if you intake the correct number of calories, but not the right nutrients, your body will suffer.  This is even more true for those with severe and/or ongoing disorders/diseases, such as brain injury.

Investigating the Zombies in the Brain

This summer, a film, titled Tau, was released to movie theaters and explored the human trappings of implantation of artificial intelligence.  In August, UT Health San Antonio, formerly The University of Texas Health San Antonio, reported the human trappings of human intelligence, specifically in the brain: “Tau protein accumulation is the most common pathology among degenerative brain diseases, including… traumatic brain injury (TBI) and over twenty others.”

Simply explained, tau proteins are, “proteins that stabilize microtubules [and]… are abundant in neurons of the central nervous system.”  Related to brain injury, a high level of tau proteins results in poor recovery and, therefore, can possibly result in an ongoing cognitive decline.  The title of a 2012 NIH study further explains, Tau elevators in the brain extracellular space correlate with reduced amyloid-B levels and predict adverse clinical outcomes after severe traumatic brain injury.  This study notes that it was only the second study that was done on the subject, at the time.  However, since then, tau protein studies have become much more common, as can be seen by the above-mentioned quote.

Scientists now refer to tau proteins as zombie cells, as they, “can’t die but are equally unable to perform the functions of a normal cell.”  Unfortunately, they live as stressed, toxic senescent cells in the extracellular space of the brain, which means that while they are interesting to investigate, they are difficult to access.  However, just as scientists have discovered that eating protein-filled food like sushi is beneficial to the brain, scientists have developed a new means of brain study, referred to as SUSHI (super-resolution shadow imaging) that can access the extracellular space.  With the use of SUSHI, UT Health is currently attempting to develop a drug that clears tau tangles and zombie cells to improve brain function and structure following a traumatic brain injury and other brain diseases.  To this point, “The scientists at UT Health used senolytic drugs… to clear the senescent cells and tau tangles in [neurologically damaged] mice.”

* Also, this summer, across the ocean, Mario Negri Institute for Pharmacological Research of Milan and the University of Glasgow published the results of a study in which they determined a single brain trauma could result in widespread tau deposition.  According to the study, this is, “the first evidence for how a mechanical brain injury might evolve into chronic degenerative brain disease, including CTE.”  CTE is, of course, associated with American football, though this conclusion seems to indicate that the concern may be even greater.

New Study Walks Fast to Prove Benefit of Exercise after TBI

Rebecca M.

The National Institute of Health recently completed a study on the role of exercise in memory and cognitive skills for those with a traumatic brain injury.  Specifically, the goal of this study was to look at the benefits of exercise in 18-45 year old individuals with a TBI, at least 2 months after their injury and otherwise healthy.  Completed this summer at the main NIH Clinical Research site, this study was an exploration of previous findings that exercise after exposure to images enhances the participant’s subsequent recall and extended the study to include recall of words and logical cognition.  Notably, this study also looked at new ways to measure progress after a brain injury by examining the mechanism of the effect of using exercise biomarkers and the relatively new technology of fMRI.  In a parallel fMRI experiment, intended to explore the brain basis of the effect of exercise on memory, healthy volunteers viewed pictures, exercised at a high or low intensity, and then performed a recall task while in the scanner.

As of yet, the NIH has not published the study’s results.  However, this new study may well have similar findings to past ones.  Additionally, the use of newer biological tools will make an even stronger case that exercise, even walking fast, is well worth the time for adults living with a TBI to enhance their cognitive skills.

Preventing Pesticides from Killing Bugs and Brain Cells

A pesticide is “any substance used to kill, repel, or control certain forms of plant or animal life that are considered to be pests.”  No one denies the harm in ingestion of a pesticide.  However, the legality of using certain chemicals in pesticides has been long debated – at present, the chemical chlorpyrifos is of particular concern.

An active ingredient in some pesticides since 1965, chlorpyrifos is “used primarily to control foliage and soil-borne insect pests on a variety of food and feed crops.”  A Google search shows that it is sold under a variety of brand names.  In the past few years, chlorpyrifos has been a focus of concern because of a government-supported study conducted by the Columbia Center for Children’s Environmental Health at Columbia University.  One of the findings of this study confirms, “Children with high pesticide exposure cluster together to form a distinct behavioral phenotype… Cognitive and behavioral deficits associated with this phenotype may be mapped to alterations in brain regions and function.”

Legislation related to pesticide control was first introduced in Congress over a century ago in the Federal Insecticide, Fungicide, and Rodenticide Act.  Since its enactment in 1910, this legislation has been amended and new legislation regulating pesticide use has passed, such as the Food Quality Protection Act in 1996.  In November 2015, the EPA, with former head Gina McCarthy, proposed a ban on the use of neurotoxic chemical chlorpyifos on all food crops.  What then happened to this proposal is unclear.

During the tumultuous tenure of former EPA head Scott Pruitt, in 2017 and 2018, chlorpyrifos came to the pesticide forefront.  In 2017, Pruitt refused to sign off on a ban of the use of chlorpyrifos as a pesticide on food crops.  This decision, many say, is a sign of Pruitt siding with the “Pesticide Lobby”.  Groups such as the Environmental Working Group (EWG) have denounced and fought against Pruitt’s action, noting that, “The evidence is overwhelming that even small doses of chlorpyrifos can damage parts of the brain that control language, memory, behavior and emotion.”  Finally, last month, Pruitt’s decision was reversed by the United States Court of Appeals for the Ninth Circuit – the EPA now bans the use of chlorpyrifos on food crops.

While the above decision is a victory for food safety, the results of this legislation are not immediate.  Additionally, fruits and vegetables must still be washed before eaten both to eliminate any residual pesticide and to better the taste.  On the positive note, though, the EWG notes that, “the agency [has] put children’s health, strong science and the letter of the law above corporate interests.”

McCain’s Posthumous Charitable Hopes

In 2002, Senator John McCain was instrumental in establishing the Arizona-based nonprofit Translational Genomics Research Institute (TGen),  “a one-of-a-kind genomics research institute.” Unfortunately, the research focus of this institute later became all too important for McCain, as his diagnosis of brain cancer was announced last year.  After losing this year-long battle with glioblastoma*, Senator McCain was laid to rest near the US Naval Academy in Annapolis, Maryland on Sunday, September 2, 2018.  However, his service to America has not ended.

A visit to the memorial webpage of the late Senator provides not only a history of the man and synopses of the moments of honor that have occurred since his death on August 25, 2018, but also gives the visitor an opportunity to donate to two nonprofits specifically selected by McCain: The McCain Institute Foundation and the Translational Genomics Research Institute (TGen).

*According to the NIH, glioblastoma is, “the most common and aggressive malignant brain tumor in adults.”  As previously reported on this site, symptoms of brain malignancy, a.k.a. brain cancer, include headaches, seizures, speech difficulty, weakness and double vision – symptoms that can also be found following a traumatic brain injury.  The question as to whether there is a link between brain injury and brain cancer has been “long-debated”, as was remarked on in a 1979 NIH report.  Today the NIH continues this investigation.  Two years ago, they reported, “Epidemiological studies are equivocal on the possible link between trauma and increased risk of malignant glioblastoma… We propose a putative pathogenesis model that connects post-traumatic inflammation, stem and progenitor cell transformation, and glioblastoma.”

Mitigation for Morality and Murder

In the modern world, our understanding of science changes rapidly.  Law, at large, does not change so rapidly.  What has changed, in the past 20 years, is that defense lawyers have begun, during the trial and/or sentencing phases of court, to use brain damage/injury as a mitigating factor for criminal acts.

Brain injury was first introduced as a defense in 1966 for Charles Whitman, the so-called Texas Tower Sniper.  (Whitman stabbed his mother and his wife, shot to death 16 people at the University of Texas at Austin and shot and injured 31 others.  An autopsy upon his death found a tumor in his brain.)  Since the start of this century, the exploration into the effects of brain injury on what some may see as moral quandaries for those with neurological deficits has broadened.  Generally, what has been found is that head injury, specifically a brain lesion, can hinder executive functioning, which governs the ability to plan ahead, think things through, manage impulse, etc.  However, this is basic knowledge that applies to all brain injury survivors; tests specifically related to the unique brains of those who commit criminal acts are inconsistent.

In 2015, the NIH published a report, Does TBI Lead to Criminality?.  Their conclusion states, “The results support a modest causal link between traumatic brain injury and criminality.”  Investigations have shown that while brain injury is not a sufficient defense for a criminal act, it may be a mitigating circumstance in the sentencing phase of a trial – treatment versus incarceration.

Since then, brain damage/injury has often been used as a defense, most recently earlier this month: a convicted murderer in Ohio said, during sentencing, “Not everyone is fortunate enough to have a caring family or outside guidance… I am proof [that] a young person – beaten and abused physically, emotionally, and mentally – becomes the abuser.”   Though the defendant now admits to the killing of five women, the testimony of one of two testifying doctors states that because Kirkland MAY have a brain injury, he should not receive the strictest punishment, the death penalty.

Perhaps, though, the “brain injury” defense will relatively soon become a thing of the past.  The above-mentioned NIH report further concludes, “Reducing the rate of TBI… might have benefits in terms of crime reduction.”  (Since this report was released, more defendants have used brain damage as a mitigating factor for criminal acts.)  According to a UK study, approximately 50 to 70% of the incarcerated population has a brain injury.  That percentage is thought to be in the same realm as those imprisoned in America.  Given these astonishing statistics and the continuing government-sponsored and private research on brain injury prevention and recovery, the NIH’s conclusion seems a definite possibility.

(See also Massachusetts General Hospital – Center for Law, Brain & Behavior, “an academic and professional resource for the education, research, and understanding of neuroscience and the law.”)

MS: Cause, Effect or Comorbidity

Multiple sclerosis (MS) is presumed to be an autoimmune disorder, but beyond that, is not fully understood.  What is understood is some of the terrible symptoms that can occur with MS, including: blurred or double vision, muscle weakness, lack of coordination, imbalance, impaired walking/standing, speech impediments, tremors, hearing loss, difficulties with concentration, attention, memory, and poor judgement.  To those who read this blog and/or have personal knowledge of brain injury, the symptoms should be apparent, but for the purpose of this article it is necessary to spell out some of the symptoms of moderate to severe brain injuries: dilations of the pupils, seizures, slurred speech, weakness, loss of coordination, restlessness or agitation, chronic headaches, increased confusion, lightheadedness, dizziness, blurred vision, ringing in the ears, fatigue, behavioral or mood changes and trouble with memory, concentration, attention, and thinking.  As can be seen, even in these abbreviated lists, MS and TBI exhibit many of the same symptoms.  For this reason, it is not a surprise to find that the two may have a connection – however, the results of multiple NIH-funded studies on the subject have not, as of yet, been able to determine what exactly is this connection.

In 2006, for example, in a study titled “Risk of multiple sclerosis after head injury: record linkage study,” the NIH concluded: “There was no significant increase in the risk of MS at either short or long time periods after head injury.”  However, six years later, in 2012, the NIH released a study with the title: “Increased risk of multiple sclerosis after traumatic brain injury: a nationwide population-based study.”  In 2016, a study essentially took the middle-ground, concluding that, “The presence of comorbidities in patients with MS is associated with brain injury.”  (Therefore, they concluded that if someone has another disorder, as well as MS, they may be more likely to have a brain injury.)

The “cause or effect” confusion is recognized by researchers, as in 2017 a scientist at Harvard University remarked, “Some studies suggest that head injuries might be a risk factor for MS… On the other hand, it’s not an easy thing to study because researchers would never intentionally cause head injuries to see if they cause MS.”  However, this Harvard study did find that having a single concussion during childhood gave a person a 22% higher rate of MS and the percent was doubled for those who had more than one concussion.

Whether MS and TBI have a cause-and-effect relationship or not, their similar symptoms may mean that exercise is of particular benefit to those with multiple sclerosis, just as it is to those with brain injury.  To test this hypothesis, the NIH has funded a study at the University of Alabama at Birmingham and at the New Jersey-based Kessler Foundation specifically to determine the benefit of exercise training for cognitive deficits in MS.  The study will see if 3-months of treadmill walking for the participants improves their cognitive processing speed, brain volume, and functional connectivity.  “The study may provide the first Class 1 evidence for the effects of treadmill walking exercise training as a rehabilitative approach to cognitive deficits in people with multiple sclerosis,” says Brain Sandroff, PhD of UAB and principal investigator of the study.

Potential Biomarker of “Bad” Brain Injuries

Rebecca M.

It is often quite hard to determine how bad a brain injury is soon after it has happens, yet speed is needed for the best treatment of the injury, in order to have the best chance of recovery.  No one brain injury it quite like another.  Earlier this year, the National Institutes of Health (NIH) funded an important study about advances in the treatment of brain injuries.  Briefly, the study group identified that the brain lipid molecule, a type of fatty acid in brains, known as lysophosphatidic acid (LPA), significantly increased after a TBI in a preclinical animal model.  In general, fatty acids in the brain are thought to be important in brain function, but in excess, they are not healthy.  Moreover, the researchers found that LPA was elevated in areas associated with cell death and axonal injury, both major hallmarks of moderate and severe TBI.  The study was carried out at the David Geffen School of Medicine at UCLA.

If the results of this study holds for humans, it will give doctors a tool to ID right away if they are dealing with a moderate to severe brain injury, and not a mild one.  Though it has only been studied in animals, LPA could possibly be used as a biomarker of TBI, which could be particularly useful in cases when it is not clear if a brain injury has occurred.  (In some cases, such as a very bad car accidents, it is pretty clear that there has been a moderate to severe injury and cell death.  But that is not always the case, as with ABIs and other TBIs, it might less clear how bad the injury is without using a biomarker tool.)

Monitoring the LPA levels of a brain injury patient may allow neurologists to make smart and fast decisions with as many tools as needed medically, rather than having to guess about the severity, based on one factor – the amount of swelling.

New Technology, Same Problems

Last year, I reported on the secondary danger that can arise from using the shoulder-launched heavy artillery Carl Gustaf.  Carl Gustaf has a twin though – heavy artillery known as SMAW…  and, just like with Carl Gustaf, SMAW is strong enough both to blow up a tank and to cause severe brain injury to the shooter in the process.

Late last month, NPR reported on the effects the use of SMAW had on two former soldiers.  After every shot, you felt a “concussive wave”, one soldier said, before continuing to say “it’s an awesome thing”.  Based on this description, as well as these soldiers’ ongoing support for the military, one can see that “blaming” an institution that they love so much for their current deficits is a difficult thing for these soldiers.  For the same reason, many other soldiers find themselves in a conundrum when it comes to their opinion of the military.  (Statistics show, for example, that though enrollment in the military is at a low, retention is up.)  However, it seems that the military recognizes that, in some way, they, specifically their weaponry, are at fault for some injuries, as they keep putting more money into research (e.g. with animal models).  They also have set up a TBI Recovery Support Program and, as a member of that Program states, “If you talk to us in a year… I think we’re going to have exponential growth in our knowledge.”

However, is some of this concern over brain injury just unnecessary worry?  The soldiers NPR quotes in their article ask that question.  (This is very similar to the responses of some players, coaches and parents regarding brain injury in football.)

(Another interesting subject in the above-linked NPR article is the difficulty soldiers, who acquire a brain injury while not in combat, have in getting healthcare coverage for their recovery.)

Virginia Battles BI with Targeted Funds

Being home to the Pentagon, headquarters of the Department of Defense, Virginia has been the center of much brain injury research and treatment.  Having a background in pediatric neurology and a past residency at the Brooke Army Medical Center, a military hospital located in Texas, Governor of Virginia Dr. Ralph Northam has seen the short-term and long-term effects of brain injury.  Given this, Gov. Northam authored a proclamation for Brain Injury Awareness Month in March, stating, “WHEREAS, early, equal, and adequate access to care greatly increases the overall quality of life of Virginians with TBI, enabling them to return to home, school, work, and community.”

From 2014 to the present, “Virginia has received $3,573,485 in Federal TBI Planning, Implementation, and Implementation Partnership Grants. The State has provided $1,785,260 in matching support.”  However, this federal grant is set to expire after 2018.  Last week, Northam awarded a three-year $900,000 grant to the Virginia Department for Aging and Rehabilitative Services (DARS), earmarked for Brain Injury Services Coordination (BISC) Unit.  (Notes DARS Commissioner Kathryn A. Hayfield, this new grant is just another example of Virginia’s support for brain injury services, which has been ongoing since the 1980s.)  As it is, the goal of BISCU is to, “enhance the quality of life and vocational goals of persons with… brain injury.”  The goal of this grant is to go further than this, as the agency continues to enhance the “health, wellness and independence of people with TBI,” by enhancing “access to supports and services,” states Dr. Daniel Carey, Secretary of Health and Human Resources.