Getting the COVID-19 vaccine and a new exercise bike to keep stable in the fight against Huntington’s disease

 

In my fight against Huntington’s disease, I have strived to delay the inevitable onset by working hard to keep my overall health stable. This strategy has included avoiding potential shocks to my system.

 

Now the leading cause of death in the United States, COVID-19 poses a threat to all of us. As a 61-year-old HD asymptomatic gene carrier, I have religiously followed recommendations on social distancing, mask use, and handwashing.

 

As a university professor, I have taught online since March 2020. The pandemic has rocked universities’ finances and employees’ benefits. Despite serious precautions by the schools, the coronavirus has surged among some students, including at my campus, the University of San Diego.

 

On February 6, I got a last-minute opportunity to get vaccinated with the Moderna COVID-19 vaccine. A San Diego nonprofit clinic that was following guidelines to first vaccinate individuals 65 and over announced around midday that not enough people from that group had responded, thus making available extra doses that needed to be injected that day. Educators and healthcare workers were invited to get that first of two doses.

 

My wife Regina, an instructional coordinator for the San Diego Unified School District, and I jumped at the chance. After a two-hour wait, including filling out forms and questionnaires, we received our shots! We were jubilant. Getting vaccinated also felt like an extra gift for Regina: February 6 was her birthday.

 

 

Gene Veritas, aka Kenneth P. Serbin, receiving an injection of the Moderna COVID-19 vaccine (selfie by Gene Veritas)

 

As one of the tens of millions of Americans now at least partially vaccinated, I am protecting not only my health, but also limiting the spread of the pandemic. (For an expert discussion of the ethics of COVID-19 vaccination, including the phenomenon of “vaccine guilt,” click here.)

 

I was also proud to get the Moderna vaccine because its RNA-based approach resembles some of the treatment strategies being tried in HD clinical trial programs. Furthermore, the scientist-written HDBuzz website has urged HD-affected individuals to get vaccinated for COVID-19.

 

Though I had a sore arm and felt a queasy for a couple of days, I have felt normal since. We are scheduled to get the required second shot on March 6. I also have participated voluntarily in the federal government’s V-safe After Vaccination Health Checker, a mobile phone app including questions about pain and other potential side effects.

 

An innovative, ‘neurobic’ spin bike

 

Four days after our COVID shots, technicians delivered and set up our long-awaited new exercise machine, the Peloton Bike+, which has a screen for watching online classes.

 

Regina and I have always prioritized exercise. This has become ever more important as we have aged. When we had a backyard pool built in 2009, I insisted on installing a Fastlane swim device so that I could exercise vigorously.

 

I have varied my exercise – swimming, walking, riding a stationary bike – to focus on different parts of the body.

 

In general, avoiding physical and mental routine can reinforce brain and overall health. This has led me to practice “neurobics,” a word that combines words “neurons” and “aerobics.” Such brain workouts can include something as simple as engaging with interesting people or taking a different route every time I walk. Neurobics can increase levels of the critical brain nutrient BDNF, brain derived neurotrophic factor. (Click here to read more.)

 

After the start of the pandemic, we noted the extensive TV advertising for Peloton (which even became the subject of a recent Saturday Night Live skit poking fun at the motivational online workouts).

 

The Peloton bike and other online exercise apps that feature live and recorded exercise classes are an innovative, neurobic way of connecting with coaches and others. Users can expand their physical and mental horizons with the wide variety of online cycling classes, strength exercises, stretch classes, yoga, and other activities.

 

 

Gene Veritas riding the Peloton Bike+ (photo by Regina Serbin)

 

We have found the Peloton Bike+ and the app to be far superior to our previous exercise bike, which had begun to deteriorate. A spin bike, the Peloton allows for a more versatile workout.

 

In the psychologically devastating social isolation of the pandemic, the Peloton is also allowing us to thrive indoors. Despite a significant sticker price, the bike makes sense budget-wise, since the money from Regina’s cancelled gym membership goes to a monthly payment plan.

 

Subtle impairments predate onset

 

On February 16, I received a stark reminder of how Huntington’s disease can impair gene carriers, however slightly, in the years leading up to an actual clinical diagnosis.

 

I attended an online presentation by Paul Gilbert, Ph.D., a professor and the chair in the Department of Psychology at San Diego State University, to the University of San Diego Neuro and Psych Research Club. Titled “Neuropsychological Changes in the Premanifest and Manifest Stages of Huntington’s Disease,” Dr. Gilbert’s talk highlighted some of the key findings in his ongoing research on this topic, including data from a 2020 article by his team in the journal Cognitive and Behavioral Neurology.

 

Premanifest HD involves the period before a neurologist can actually observe a gene carrier as having experienced the onset of the disorder’s typical motor, cognitive, and/or behavioral symptoms, stated Dr. Gilbert. In the past, physicians only saw the motor symptoms – involuntary movements and unstable gait, for example – as signs of the malady

 

Using verbal learning and memory tests, the research has demonstrated that these individuals can develop subtle cognitive symptoms – in particular, memory loss – ten to fifteen years before the formal diagnosis, Dr. Gilbert explained. The memory deficits increase dramatically after HD onset, he added.

 

“It really argues that we as clinicians need to be looking at not just the motor symptoms to make a diagnosis of Huntington's disease, but really starting to look at cognitive symptoms,” Dr. Gilbert asserted.

 

That position echoes the general trend towards a view of Huntington’s as a multi-symptom disease over the past several decades.

 

Statistical versus clinical signs

 

As a regular participant in research studies, I have performed a number of the tests that Dr. Gilbert described.

 

During the Q&A, noting that gene carriers like me worry about where we stand on the road to onset, I asked Dr. Gilbert whether the premanifest impairments hamper “actual functioning,” for example, daily activities such as driving, balancing a checkbook, and communicating with others.

 

“They’re statistically impaired, but they’re not clinically impaired,” Dr. Gilbert observed about the gene carriers in the research studies. The deficits are “very subtle” and can only be picked up on testing, he added.

 

Nevertheless, he added that his research has also determined that subtle memory impairment does have a “measurable but quite mild” impact on activities like handling finances or taking medications, but that only after onset does the disease seriously interfere with daily living.

 

(Dr. Gilbert’s work also echoes the recent landmark study of young HD gene carriers, ranging in age from 18-40 and illustrating no significant cognitive of psychiatric decline. Click here to watch Dr. Gilbert’s 2018 presentation on HD to University of San Diego students.)

 

Anticipating a brighter future

 

With the pandemic and the worst economic crisis since the Great Depression, I am very fortunate to have a job and work remotely.

 

Because an estimated 20 percent of HD onset results from non-genetic factors, my imminent protection from COVID-19 and anticipation of new neurobic adventures with the Peloton can help me maintain stable health.

 

They certainly have helped me to feel optimistic about the future – for the first time in a year. I am also looking forward to news on the key HD clinical trials in progress.

 

Although we recognize the long-term social impact of the pandemic, Regina and I are especially looking forward to a healthier and happier 2022 for all, and the chance to travel: we hope to attend my 40th college reunion, celebrate our 30th wedding anniversary, and watch our HD-free daughter Bianca graduate from college.

 

We are thankful for every moment of life.

What’s in a name? How Huntington’s disease gene carriers are seen by themselves and by others

In 1999 I received the results of a genetic test that showed I had 40 CAG repeats on the huntingtin gene inherited from my mother, who died of Huntington’s disease in 2006 after a two-decade struggle with the disorder.

Everybody has this gene, which first appeared 800 million years ago in a species of amoebae. Huntingtin helps our cells function properly.

The gene’s CAG repeats refer to the sequence of three nucleotide bases – cytosine, adenine, and guanine, all building blocks of DNA – on the DNA molecule. Most people have 27 or fewer repeats. The gene I inherited from my father had fewer than 20.

My mother’s high CAG count caused her to start experiencing HD symptoms – typically manifested as emotional distress, cognitive loss, and involuntary movements – in her late forties.

The term “CAG repeats” and my mother’s count of 40 were two of the very first facts I learned about HD after receiving news of her diagnosis in late 1995.

The geneticist used the same terminology when he revealed my test results.

However, as he told me and many other recipients of HD test results, “a positive test result is not a diagnosis.” While everybody with 40 or more repeats will develop HD in his or her lifetime, scientists cannot yet predict the exact moment and type of disease onset.

According to John Warner, Ph.D., the director of biostatistics for CHDI Management, Inc., which carries out the day-to-day mission of the non-profit, HD drug-discovery biotech CHDI Foundation, Inc., 95 percent of those individuals with 40 CAG repeats will experience disease onset between the ages of 50 and 74. (A future article will explore the statistical meaning of the CAG count in greater detail.)

With an ominous test result at age 39 but no symptoms, I needed to construct a definition of my genetic predicament for both myself and for others.

As I said recently in an interview, unlike treatments for certain kinds of cancer, I cannot irradiate my defective huntingtin gene to destroy it. It’s part of me, literally residing in every cell.

Because of its genetic nature, HD also requires a far more nuanced kind of diagnosis. Subtle symptoms can exist for years before the more noticeable symptoms commence.

'Gene-positive'

For many years, I referred to myself as “gene-positive for Huntington’s disease,” a term I heard often in HD family and scientific circles. I also used phrases such as “tested positive for HD.”

“Gene-positive” echoed the term “HIV-positive” used by the AIDS community. It meant not only that I had tested positive for a condition, but that I inevitably faced its dire consequences.

Thus, “gene-positive” resonated with the deep stigma, discrimination, and alienation suffered by members of both the AIDS and HD communities.

“Gene-positive” further implied an activist stance. As with the early years of the fight against AIDS, we in the HD community needed to tell the world we needed treatments and the resources to find them.

I experienced all of these feelings in the late 1990s and early 2000s, as I immersed myself in advocacy work for the Huntington’s Disease Society of America.

They remain with me today as we still await the discovery of an effective treatment.

Changing perceptions

As my knowledge about HD increased, and as I came into ever closer contact with HD researchers in labs and at events such as the annual CHDI-sponsored HD Therapeutics Conference, both my perceptions of HD and the terms I used to describe my situation changed.

As I learned to my first visit to CHDI in 2009, many scientists see gene-positive individuals as genetically and, at least at the cellular level, even functionally compromised from birth.

I started to hear scientists used the word “premanifest” to describe asymptomatic, gene-positive individuals.

Soon I would be introduced to “prodrome” and “prodromal”. A precursor or forerunner to the disease, prodrome refers to the period before onset.

However, I could never imagine using such a technical term to describe myself to others.

Scientists and physicians also used “asymptomatic” and especially “presymptomatic” to describe people like me. I have frequently used the former to indicate to people that I face the danger of HD but am fine for now.

Other phrases I have used or heard include: HD gene carrier; HD gene mutation carrier; asymptomatic HD gene carrier; disease-gene carrier; tested positive for the genetic defect that causes Huntington’s disease; and carry the gene for Huntington’s disease.

Living with the ‘phantom gene’

At the World Congress on Huntington’s Disease in Rio de Janeiro last September, HD activist, historian, and author Alice Wexler, Ph.D., noted that much recent scientific discussion has focused on defining when HD actually begins.

During a panel on coping with HD, Dr. Wexler asked how global HD advocate Charles Sabine and I – both gene-positive but asymptomatic – viewed ourselves as individuals living with the “phantom gene” and in what circumstances would consider ourselves as having HD.

“It changes for me depending on where I am,” I replied. “If I’m at a conference like this: ‘Oh, my God! I have HD.’ Because I see all these studies and brain scans and searches for biomarkers … and references to me as prodromal…. There’s a tendency of the scientific community to see gene carriers as diseased from Day One.”

In settings such as my doctor’s office, I felt different, I said. “My doctor’s telling me: this time you got a clean bill of health.”

Charles, agreeing with my outlook and saying that he “treasured” his current good health, answered the question in a “wider, more metaphysical sense.”

“We are not just someone who’s had a bit of bad luck,” Charles said about having inherited the HD mutation. “We are a part of history. I have absolutely not a single shred of doubt in my mind that, whether it’s 20, 50, or a 100 years [off], that this disease will be managed just like HIV-AIDS can be now.”

You can watch the entire exchange in the video below.

Living with a 'Phantom Gene': Two Huntington's Disease Gene Carriers Discuss Their Perceptions from Gene Veritas on Vimeo.

A new shorthand

The latest conception emerged at the CHDI-sponsored HD therapeutics conference in Palm Springs, CA, last month, where Andrea Varrone, M.D., Ph.D., of the Karolinska Institutet (Sweden) gave a presentation whose title included the phrase “Huntington’s disease gene expansion carriers.”

That phrase very accurately describes someone like me, because it specifically identifies the cause of the disease: an expansion of the huntingtin gene. However, the term does not by itself identify whether a person is symptomatic or asymptomatic.

Nevertheless, it’s good shorthand for the concept of expanded CAG repeats.

However, both the phrase and its acronym, HDGEC, are a mouthful! They might not resonate with the community, and even less so with the general public, which is more familiar with the idea of a “mutated gene” than with the term “expanded gene.”

‘You don’t look like an HD person’

The abundance of terms to describe asymptomatic HD gene carriers reminds me that those of us in this predicament are undergoing “the new and harrowing human experience of living in the gray zone between a genetic test result and the onset of a disease foretold.”

Scientists have demonstrated that changes in the brain occur ten and even 20 years before onset – meaning that my brain may already be seriously compromised, even though I function just fine.

Inexorably, perniciously, but silently, HD attacks the brain.

However, it’s not discernible from the outside.

“You don’t look like a person who has Huntington’s disease,” a health professional told me recently as I contemplated him writhing with pain and discomfort from a knee operation that forced him to wear a brace and use crutches.

There is no particular way for a premanifest person to look! Moreover, no “crutch” yet exists to help the presymptomatic HD brain recover from the initial assault on the cells.

As an HD gene carrier and advocate for this orphan neurological disorder, I continually face the challenge of explaining the seriousness of the disease and its many social implications.

Along with other neurological disease communities, we in the HD community are still searching for the right formula to project the urgency and significance of our predicament.

A temporary escape

Often those of us in the gray zone prefer not to deal with HD. Unlike others in the community, we don’t yet face the minute-by-minute struggle with symptoms.

At the local HD support group meeting this week, I was the only at-risk individual to appear. Even so, the facilitator and her replacement-in-training for the at-risk section (which normally includes both tested and untested asymptomatic individuals) held a session with me. I wanted to help bring the new person up to speed on the history of the support group and the needs of the at-risk section.

We noted that the support group’s caregiver section is usually the largest of the three subdivisions, followed by the section for those already affected.

The at-risk is usually the smallest – even though at-risk individuals outnumber affected individuals nationally by a ratio of at least five to one.

I sympathize completely with the occasional need to “escape” from HD, so I understand why other at-risk people didn’t attend the meeting. However, I am hyper-aware of the need for more individuals to participate in research studies and clinical trials to create effective treatments.

The transition to patient status

The facilitators and I also discussed the difficult choice individuals and facilitators must make in transitioning newly affected individuals out of the at-risk section and into the affected section.

I’ve witnessed this transition for a number of people. I can’t imagine how hard it is.

Once the symptoms begin, the terminological ambiguity ends. They are now “affected” or “symptomatic” individuals. They are “HD patients.”

I anxiously await the moment when an effective treatment would not only ameliorate these and other patients’ symptoms, but also prevent onset in asymptomatic gene carriers.

To take, or not to take, unproven supplements in the fight against Huntington’s disease

Should people facing Huntington’s disease take creatine and other supplements to relieve or prevent symptoms?

I do.

I saw HD inexorably destroy my mother’s ability to walk, talk, and care for herself. She died eight years ago this month. I tested positive for HD in 1999 and since then have worried daily about when it will strike.

There is no treatment to slow HD’s devastation of the brain. So I’ve been open to taking supplements that might help.

In early 1996, just shortly after learning of my mother’s diagnosis, I started taking coenzyme Q-10 (Co-Q), a vitamin-like substance found throughout our bodies and seen by researchers as a possible way to help remedy the energy deficits suffered in HD.

In 2004, when Dr. LaVonne Goodman introduced a “treatment now” regimen and clinical trial of safe supplements that had shown promising results in animal testing, I jumped at the chance to participate. I was the only presymptomatic individual in the small, three-year study, run under the auspices of Dr. Goodman’s Huntington’s Disease Drug Works (HDDW).

Starting in 2005, I introduced the supplements into my diet in steps. I worked up to a daily routine in which I took 75 grams of trehalose, a sugar that seems to help the brain clear cellular debris; 600 mg of medical-grade Co-Q; two g of omega-3 oil; two g of blueberry extract; and ten g of medical-grade creatine. The trial paid for and delivered the supplements.

The trial did not show significant improvement for any of the symptomatic participants. “The only thing that appeared to be helpful was trehalose,” Dr. Goodman said in a February 9 phone interview. Today, almost a decade later, the supplements remain medically unproven to affect HD.

Nevertheless, scientists still think that trehalose, Co-Q, and creatine might still provide help in treating HD. Since the end of the HDDW, I have continued to take all of the supplements, spending about $2,000 per year. In fact, several years ago, relying on medical advice, I roughly doubled my daily intake of creatine to about 20 g.

I get semi-annual blood tests to monitor potential kidney damage, which creatine can cause. I also drink plenty of water throughout the day to prevent dehydration, which can occur at doses higher than 10 g. Creatine also can cause weight gain.

Am I wasting money and endangering my health?

I don’t think so. A few years ago, one of the doctors at the local Huntington’s disease clinic told me to stay on the supplements, observing that the combination of substances might be helping to delay my HD onset. I inherited the same degree of mutation as my mother, but, at 54, have passed the age of her onset.

The yin-yang of supplements

Whether others in the HD community should take creatine and other supplements is an individual choice ideally made in consultation with a doctor.

During our interview, the Seattle-based Dr. Goodman reviewed the pros and cons of taking creatine.

She cautioned against taking high doses of the substance, because more serious side effects occur at higher dosage, and urged people to consult a physician before starting any supplement.

She stressed that people need to understand the “yin-yang” involved in the decision to take supplements.

“Yes, you want to take care of yourself,” Dr. Goodman said. If they do nothing else, supplements can at least furnish a “very important” placebo effect and the prospect of hope, she said.

Dr. LaVonne Goodman (photo by Gene Veritas)

The placebo effect is a “real” phenomenon, she observed. “If you could bottle it, it would be great.”

However, taking supplements also reminds asymptomatic gene carriers of their risk, she added.

More importantly, people’s use of supplements could also obstruct the path to other, potentially far more promising treatments, she said.

The benefits of supplements “need to be counterbalanced with the need to test promising new drugs, or we will never have better treatments for Huntington’s,” she explained.

Interfering with clinical trials?

“There are so many competing interests here,” Dr. Goodman continued. “We all want to believe that (creatine) is helpful, because it’s available, and we can take it, so why not do it, we say. This is what I said with HDDW trials. Well, yes, but it needs to be measured. Otherwise, we’re going to know nothing more than we did.”

“It is important for people to know that if they take these things, they can’t be in clinical trials at the same time. We deplete our clinical trial participant base, which is going to impede progress for finding better treatments. There’s the yin-yang. And people need to hear both.”

However, Dr. Goodman noted that individuals could do both: to become eligible for a clinical trial, individuals could clear the supplements out of their system so that they don’t interfere with the measurement of the tested drug’s effects, then resume the supplements after completing the trial.

I would stop taking my supplements in order to qualify for a trial, although until the most recent creatine trial (see below), practically every trial has targeted only symptomatic individuals.

Dr. Goodman underscored the need to treat creatine and all other supplements as “medicines.” Supplements should meet USP (U.S. Pharmacopeial Convention) standards, she added. The HDDW website contains information on supplement safety. Further information on supplements is available at Huntington’s Disease Lighthouse Families.

(I buy my creatine from my local GNC outlet but plan to search for a better grade of the product.)

All drugs, including FDA-approved ones, produce side effects and can affect individuals differently, Dr. Goodman noted.

Regarding creatine, she concluded: “If it’s not watched closely, it may cause more harm than good.”

A historic trial

People in the HD community became excited about creatine as a potential treatment after Harvard University’s online news service on February 7 published an article titled “Nutritional supplement slows onset of Huntington’s.”

According to the article, a team of researchers based at the Harvard-affiliated Massachusetts General Hospital had finished a historic Phase II clinical trial that produced MRI scans showing evidence of the slowing of brain atrophy (shrinkage) in HD gene carriers who have yet to manifest the classic symptoms of the disorder. Sixty-four people took part.

Participants took up to 30 g of creatine per day.

According to Steven Hersch, M.D., Ph.D., the trial, called PRECREST (Creatine Safety and Tolerability in Premanifest HD), was a “huge step” for three reasons – including its impact on a separate creatine trial for symptomatic patients called CREST-E (Creatine Safety, Tolerability, and Efficacy in Huntington’s Disease)

“One, it’s the first therapeutic trial that has tried doing prevention,” Dr. Hersch, the study’s senior author and a long-time HD researcher, said in a February 11 phone interview. “Two, because we created a design that let anybody participate who’s at 50% risk, as well as those who have tested positive. And three, the imaging finding increases the probability that CREST-E will show a clinical benefit.”

Dr. Steven Hersch (photo from HDSA website)

Currently in progress and still recruiting participants, CREST-E is a phase III trial – the final step before drug approval (click here to learn how to enroll).

The PRECREST administrators recruited untested at-risk individuals who were then tested for the purposes of the trial as well as individuals who already knew that they have the HD mutation. However, those who entered the study untested did not receive their results, which were only known to the statistician. Thus, they avoided the potentially traumatic psychological aftermath and remained protected from genetic discrimination.

“The ethical challenges for those recruiting and conducting trials include how to accommodate nontested at-risk individuals while preserving a noncoercive choice regarding genetic testing,” states an editorial about PRECREST in the March 2014 issue of the prestigious journal Neurology, adding that “unequivocal changes” occur in the brain of presymptomatic individuals “15 to 20 years before conventional clinic-based diagnosis.” An article on PRECREST by Dr. Hersch, lead author Herminia D. Rosas, M.D., and nine other collaborators appears in the same issue.

For these and other reasons, 90 percent of at-risk individuals choose not to test, Dr. Hersch explained.

The MRI changes and other data from PRECREST will eventually be assessed in CREST-E, Dr. Hersch explained. CREST-E is also doing MRI imaging. With nearly 600 participants so far, it will be large enough to show whether the benefits shown in PRECREST images correspond to a significant slowing of HD.

Avoiding false hopes

As with many news articles about clinical trials and other scientific experiments, the Harvard report’s headline, which claimed the supplement slowed the onset of HD, inaccurately reflected the researchers’ results as reported in the actual scientific article.

“While slowed atrophy suggests that creatine could slow preclinical progression, the potential clinical impact of these findings on delaying the onset of HD is unknown and must be defined by an efficacy study designed to measure it,” the Neurology article states.

Nor can the public buy the high-quality creatine used in the study, as it’s prepared specially for clinical trials.

“I don’t want people to take from this study that they ought to go running out and take a bunch of creatine or take it at these doses,” said Dr. Hersch. “Even though the imaging benefit is very exciting, we don’t know what it means clinically. It doesn’t provide the evidence that would lead me to recommend that people take it. The high doses that we used should also not be used without medical supervision.”

As noted in the Neurology article, some PRECREST participants suffered stomach upset and diarrhea caused by the creatine. About a dozen people had to drop out of the study.

Regarding the study’s clinical significance, Dr. Goodman offered an assessment similar to that of Dr. Hersch.

The widely read HD research website HDBuzz.net also weighed in.

“How much hope and how my hype?” an HDBuzz article asked. While recognizing the importance of the study, it pointed out that the causes and effects of the slowed shrinkage in the brains of the PRECREST participants need further study.

“It’s possible that creatine causes HD brain cells to bulge or swell without making them healthier,” it states. “Swelling like that could produce false optimism and might even be harmful. That’s not something this trial can tell us either way, because the patients weren’t followed long enough to see whether creatine treatment delayed the onset of symptoms.”

“The participants in PRECREST who took creatine but did not have the HD mutation did not experience any brain swelling, so this is an unlikely explanation for our findings,” said Dr. Hersch. “Including and treating these subjects was very unusual. However, we did so to allow us to answer questions like this.”

Awaiting the Holy Grail

“HD researchers face a major challenge in finding a treatment for the pre-manifest,” I wrote in 2011. “It’s really the Holy Grail not only for HD, but also for other neurological diseases such as Alzheimer’s in which brain damage occurs many years before symptoms appear. Ideally, researchers want to design medications that will completely prevent these diseases.”

The Neurology editorial used the term “Holy Grail,” too, in noting how the PRESCREST study “investigates a potentially neuroprotective agent designed to delay disease onset.”

The word “potentially” is key.

As Dr. Hersch explained, the PRECREST findings about slower shrinkage “suggest” that creatine provides a benefit, but they don’t permit researchers to say anything about delayed onset of symptoms in presymptomatic individuals or a longer lifespan for patients.

It remains for the CREST-E Phase III trial to produce similar brain scan results – and an actual effect on symptoms.

“If CREST-E shows efficacy in slowing down the disease in people who are symptomatic, I would think that most people would think that you may be slowing down the disease in people who aren’t symptomatic yet as well,” he said.

Until treatments become available, presymptomatic gene carriers like me will continue to face the extremely difficult decision about whether to take supplements.

I’m grasping at creatine and other supplements in the hopes of delaying onset until researchers succeed.