Monthly Archives: March 2016

How to Stop Overprescribing Fluoroquinolone Antibiotics

Rx Pad Drugs

Overprescription of Antibiotics

I found this New York Times article, How to Stop Overprescribing Antibiotics, to be really interesting. Doctors know that antibiotic resistance is a serious problem–the word has gotten out sufficiently, but that knowledge hasn’t done much to change antibiotic prescribing patterns. Doctors are still overprescribing antibiotics, despite knowing that antibiotic resistance poses a significant threat to both modern medicine and human health.

I’m not sure what the root of this overprescribing is. It may be from a lack of knowledge of what ailments antibiotics should be prescribed for (many cases of prostatitis, as well as many sinus infections, aren’t bacterial), tradition (it’s the way it has “always” been done), a notion that antibiotics “can’t hurt,” patient pressure on the physician to do something, or if there’s another root to the problem.

Antibiotic overprescription IS a problem though. It’s a problem not only because of bacterial resistance to antibiotics, but also because of the links between antibiotic use and many of the diseases of modernity, and because some popular antibiotics (FLUOROQUINOLONES in particular, but I’ve heard from people who have been devastated by other antibiotics too) are causing multi-symptom, chronic illnesses that are devastating people’s lives.

Overprescription of Fluoroquinolone Antibiotics

How can we get doctors to stop overprescribing fluoroquinolone antibiotics? The NYT article has some good insight and possible courses of action for floxie advocates.

“we asked a group of doctors to place a signed poster in their exam rooms pledging to follow standard guidelines on antibiotic prescription. This tactic, which pressured doctors to act consistently with their own publicly stated commitments, reduced inappropriate prescribing 20 percentage points relative to doctors in a control group who displayed a poster with generic information about antibiotic use.”

A 20% reduction in inappropriate prescribing is pretty good. At the very least, it’s a good place to start.

Guidelines for Prescribing Fluoroquinolones

What should the guidelines for fluoroquinolone (Cipro, Levaquin, Avelox, Floxin, and their generic equivalents) prescriptions be? My suggestions are:

  • Only prescribe fluoroquinolones for verified infections.
  • Only prescribe fluoroquinolones in life-or-death situations.
  • Only prescribe fluoroquinolones if there is no safer antibiotic that can be tried.
  • Review the warning label with the patient.
  • Review the black box warning with the patient. Notify the patient that black box warnings are the most severe warning possible before a drug is removed from the market.
  • Inform the patient that severe musculoskeletal problems have been experienced post-exposure to fluoroquinolones, including, but not limited to, tendon tears that occur months or years after exposure to the drug has stopped.
  • Note that, per the FDA, “A review of the FDA Adverse Event Reporting System (FAERS) was performed to characterize a constellation of symptoms leading to disability that had been observed during FDA monitoring of fluoroquinolone safety reports. This constellation of symptoms will be referred to in this review as ‘fluoroquinolone-associated disability’ (FQAD). While most of the individual AEs that exist within FQAD are currently described in fluoroquinolone labeling, the particular constellation of symptoms across organ systems is not. Individuals with FQAD were defined as U.S. patients who were reported to be previously healthy and prescribed an oral fluoroquinolone antibacterial drug for the treatment of uncomplicated sinusitis, bronchitis, or urinary tract infection (UTI). To qualify, individuals had to have AEs reported in two or more of the following body systems: peripheral nervous system, neuropsychiatric, musculoskeletal, senses, cardiovascular and skin. These body systems were chosen as they had been observed to be frequently involved with the fluoroquinolone reports describing disability. In addition, the AEs had to have been reported to last 30 days or longer after stopping the fluoroquinolone, and had to have a reported outcome of disability.”
  • Fluoroquinolones cause mitochondrial damage and dysfunction, and mitochondrial damage/dysfunction is linked to many diseases, including autoimmune diseases.
  • Fluoroquinolone effects include serious psychiatric problems.
  • Fluoroquinolones are a likely endocrine disruptor.

I suspect that if those guidelines were in every physician’s office, fluoroquinolone prescriptions would decrease significantly.

Present Alternatives to Antibiotics

The NYT article also notes:

“we showed that doctors tended to prescribe less aggressive medications when such options were presented more prominently (one by one, in a vertical column), with more aggressive options presented less prominently (grouped side by side, in a single category). Previous research suggested that listing alternatives individually made them appear more popular — and therefore more appropriate — than when they were grouped together. And indeed, we found that doctors were roughly 12 percent less likely to order more aggressive medications, such as antibiotics, if these options were grouped together, compared with when they were listed individually.”

I think that’s an excellent idea! Give the physician more information and the patient more options. Sounds great!

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Use Social Pressure and Physician Psychology to Achieve Goals

Another approach mentioned in the NYT article is:

“In one approach, doctors received a monthly email informing them of their performance relative to that of their peers. Those with the lowest inappropriate antibiotic prescribing rates were congratulated for being ‘top performers.’ Doctors who were not top performers were told ‘You are not a top performer.’ The email also included a personalized count of unnecessary antibiotic prescriptions and the count for a typical top performer. This ‘peer comparison’ approach almost completely eliminated inappropriate prescribing: from 19.9 percent in the pre-intervention period to 3.7 percent during the post-intervention period — an 81 percent reduction.”

An 81% reduction is impressive and significant!

Peer comparison is powerful because it taps into doctor’s egos. For fluoroquinolones, I think that guilt should be tapped into as well, and with the low-ranking notification should be a story of someone suffering from fluoroquinolone toxicity. These stories may be anecdotal, but they are real stories of people being devastated by these drugs.

Public Accountability

Another approach to curbing antibiotic use mentioned is:

“whenever doctors prescribed an antibiotic that was not clearly called for by the diagnosis, the electronic health record system asked them to provide a short ‘antibiotic justification note.’ The note would be entered into the patient’s medical record and would be visible to others. Introducing this speed bump into the work flow, along with the prospect of social accountability, reduced the inappropriate prescribing rate from 23.2 percent to 5.2 percent — a 77 percent reduction.”

Public accountability is a good thing. This could work well for curbing unnecessary fluoroquinolone prescriptions.

Start Curbing Antibiotic Overprescription by Curbing Fluoroquinolone Overprescription

The article concludes that, “Taken together, our studies suggest that simple and inexpensive tactics, grounded in scientific insights about human behavior, can be extremely effective in addressing public health problems.”

I think that the methods noted above could effectively cut fluoroquinolone use too.

Maybe trying to curb overuse of all antibiotics is too much to take on. Perhaps taking on overuse of one category of antibiotics at a time is an effective thing to do. I suggest that those who are interested in curbing antibiotic overprescription start with fluoroquinolones.

 

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Fluoroquinolone Antibiotics and Oxalate Overload

OXALATE-CRYSTALS

According to the wikipedia entry for oxalobacter formigenes, “Quinolone, a broad-spectrum antibiotic, kills O. formigenes. If a person’s gastrointestinal (GI) tract lacks this bacterium, and therefore lacks the primary source for the oxalyl-CoA decarboxylase enzyme, then the GI tract cannot degrade dietary oxalates which on digestion get absorbed easily and after some vitamin B6-modulated partial metabolical degradation in the body, is excreted in the kidney, where it precipitates with calcium to form calcium oxalate kidney stones.”

Basically, this means that quinolones (and some other antibiotics) kill oxalobacter formigenes, a bacteria in the GI tract that is crucial for breaking down oxalates. When oxalates aren’t broken down properly in the GI tract, they move on to the kidneys where they form calcium oxalate kidney stones.

Kidney stones aren’t the only problems that oxalates cause though. Oxalates cause methylation problems that inhibit detoxification. According to Dr. Rostenberg’s article, OXALATES AND MTHFR: UNDERSTANDING THE GUT-KIDNEY AXIS:

oxalates create biochemical problems that make methylation issues worse. Since oxalate problems cause sulfate problems, the genes most effected will be the SULT and other phase II related pathways. The sulfate molecule is key in order for the liver to perform the daily task of detoxification. If sulfate levels drop, then the body cannot use the SULT pathway to detoxify. Instead it will be forced to use other Phase II pathways which can put greater demand on pathways that are also genetically slowed down. When we consider other slowed Phase II detoxification gene SNPs such as NAT2, ALDH, COMT, GSH, GSS, UGT, and SOUX we can begin to see that a lack of sulfate molecules can have a broad negative impact on all of our detoxification pathways.”

Dr. Rostenberg goes on to say:

As you will soon see, when oxalate levels are high, sulfate levels drop slowing down detoxification. Low sulfate levels put extra stress into the methylation cycle to provide the body with sulfate molecules. In individuals with an impaired methylation cycle this can provoke methylation issues such as high homocysteine, developmental disorders, gallbladder dysfunction, hormone imbalances, excess inflammation, poor growth and to name but a few. So with oxalate issues and the biochemical chaos it creates, a great deal of stress is placed on the methylation cycle.”

In OXALATES AND MTHFR: UNDERSTANDING THE GUT-KIDNEY AXIS Dr. Rostenberg asserts that a poorly functioning gallbladder is a cause of oxalate overload. While I agree that a well-functioning gallbladder and liver are necessary for all aspects of health, I wonder if the decimation of vital gut bacteria, like oxalobacter formigenes, by antibiotics like fluoroquinolones, is what starts oxalate toxicity damage.

Fluoroquinolone Destruction of Vital Gut Microbes

A floxie friend just noted that she got her microbiome mapped by ubiome and, “my Ubiome results tell me I have NO oxalobacter at all.” Additionally, her results showed that, “I also have NO bifidobacterium strains AT ALL.” (According to the wikipedia article for bifidobacterium, “Different species and/or strains of bifidobacteria may exert a range of beneficial health effects, including the regulation of intestinal microbial homeostasis, the inhibition of pathogens and harmful bacteria that colonize and/or infect the gut mucosa, the modulation of local and systemic immune responses, the repression of procarcinogenic enzymatic activities within the microbiota, the production of vitamins, and the bioconversion of a number of dietary compounds into bioactive molecules.”) Both oxalobacter and bifidobacerium are necessary for many aspects of health.

Might the root of fluoroquinolone toxicity, and possibly other chronic diseases of modernity, be the killing off vital microbes like oxalobacter and bifidobacerium?

Oxalate Overload

The depletion of oxalobacter formigenes, and other microbes, doesn’t just affect the gut. As Dr. Rostenberg noted above, oxalate problems (caused by not breaking down oxalates in the gut – caused, in part, by killing oxalobacter formigenes with antibiotics) lead to sulfate problems, which leads to methylation problems, which leads to detoxification problems, which leads to heavy metal overload and toxicity. Additionally, “Sulfate helps us seal our leaky gut and strengthen our body’s bones, ligaments and tendons; and it is required for Phase II detoxification of all kinds of nasty toxins, hormones and heavy metals. In fact, sulfate is so important for our health that it is the 4th most common nutrient in our blood stream!” (source) Sulfate is also necessary for proper hormonal function, “When sulfate levels are low, the body won’t just have disturbed liver function, it will also suffer with all kinds of hormone problems.” (source) As anyone who has experienced hormonal dysfunction will attest, hormonal disorders affect every aspect of health. In “Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection?” it is noted that fluoroquinolones are endocrine disruptors that lead to disruption of thyroid function, and additional information about the effects of fluoroquinolones on the thyroid can be found on http://fluoroquinolonethyroid.com/.

The most thoroughly documented and accepted consequence of oxalate overload is kidney-stones. Kidney-stones are incredibly painful, and they can cause damage to the kidneys. In addition to kidney-stones, it is noted in The Role of Oxalates in Autism and Chronic Disorders that, “Even though oxalate crystals are most common in the kidney, they also can form in virtually any other tissue in the body, including the brain and the blood-brain barrier. Oxalate crystals resembling pieces of glass can form in the heart muscle. As the heart muscle contracts, these pieces of oxalate crystals actually tear into the tissue. If these crystals are deposited in skeletal muscle, normal movement and exercise can be very painful. I’m convinced this is also one of the factors responsible for fibromyalgia. Oxalates may also cause thyroid disease as they react in thyroid tissue.”

In THE DOWN SIDE TO HIGH OXALATES – PROBLEMS WITH SULFATE, B6, GUT, AND METHYLATION, Dr. Rostenberg goes over the connections between oxalates, sulfate depletion (by oxalates), and liver problems, hormonal problems, GI problems including leaky gut, cancer, and autism. Additionally, it’s linked to high homocysteine which is linked to blood clots, strokes, and heart attacks.

Fluoroquinolones and Oxalates

There are literally twenty plausible theories as to how fluoroquinolones cause fluoroquinolone toxicity—a multi-symptom, often chronic, illness that is similar to autoimmune diseases, mysterious diseases like fibromyalgia and CFS/ME, endocrine disruption diseases, and more. Though much of the research into fluoroquinolone toxicity has focused on what fluoroquinolones do to cells (especially mitochondria), as information about the importance of the microbiome emerges, it becomes plausible (and even likely) that the destruction of important microbes by fluoroquinolones is a large contributor to fluoroquinolone toxicity.

In Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues Dr. Martin J. Blaser hypothesizes that the extinction of critical microbes is behind many of the diseases of modernity, from autoimmune diseases to obesity. Dr. Blaser focuses primarily on h. pylori and its connection with both preventing inflammation and causing ulcers, but he acknowledges that many other microbes play important roles in human health and well-being. I wonder if oxalobacter formigenes and other microbial communities are just as interesting, contradictory, and important as h. pylori. I suspect so, and I also suspect that the basic hypothesis that missing microbes (from antibiotic use, glyphosate, and the Western diet) are causing the many diseases of modernity, is, indeed, true.

Fluoroquinolones obliterate the gut, and kill both helpful and harmful bacteria. In wiping out essential species of bacteria in our gut, are they starting the cycle of inflammation and chronic disease in genetically susceptible individuals? It certainly sounds like a reasonably hypothesis to me.

Can the gut be healed?

Can species of bacteria that have been depleted by fluoroquinolone antibiotics be replenished? Do probiotic supplements help? Can changing one’s diet help? What about fecal transplants?

Those are all million dollar questions that many researchers are working on answering. Unfortunately, I don’t know the answers to them. I am certainly hopeful that the gut can be healed, and I know from personal experience that healing after fluoroquinolone antibiotic toxicity can occur. Organizations like The Human Microbiome Project and Ubiome have many smart and capable scientists who are working to answer those questions, and more.

Until those questions can be more thoroughly answered, here are some helpful resources:

Resources for Healing

Trying Low Oxalates Facebook Group – https://www.facebook.com/groups/TryingLowOxalates/

http://www.lowoxalate.info/

Information about a low-oxalate diet can be found on Low Oxalate Info: Hope and Healing on the Low Oxalate Diet.

Dr. Rostenberg’s protocol for reducing oxalates can also be found here – http://www.beyondmthfr.com/high-oxalates/. Additional information from Dr. Rostenberg can be found through the Contact page on http://www.beyondmthfr.com/.

Additional information about MTHFR and other gene mutations, and how they affect health, can be found on https://mthfrsupport.com/.

If you would like to get your microbiome sequenced through Ubiome, here is a 10% off linkhttp://ubiome.refr.cc/VDDLNWP .

ubiome logo

Dr. Rostenberg’s videos on oxalates:

 

 

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Why Athletes Should Never Take Fluoroquinolone Antibiotics

chris-fqwall

No one should take fluorouqinolone antibiotics unless there is no other alternative and one is in a life-or-death situation. Athletes in particular should be aware of the harm that fluoroquinolones can do, and they should avoid them if at all possible. Athletes should know that their athletic abilities, and even their lives, can be taken from them by fluoroquinolone antibiotics.

Please read, and share, this post:

Why Athletes Should Never Take Fluoroquinolone Antibiotics

Thank you!

 

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Tell Your Fluoroquinolone Toxicity Story

we-all-have-stories-to-tell

I encourage every person who has been hurt by fluoroquinolone antibiotics (or any other pharmaceutical) to tell his or her story.

Telling your story of pain caused by fluoroquinolones can be cathartic and relieving. In writing your story, you are saying to yourself and others, “My pain is real. I was hurt by a prescription drug. It happened to me. Listen, because this is important.”

These stories ARE important! Patient stories are important for advocacy, for warning others, for changing minds, and more. The world will be a better, safer, place if physicians and patients alike are aware of the adverse effects of fluoroquinolones and all other drugs. Patient stories help people to understand the severity of adverse drug reactions, so that they understand the real risk associated with each prescription drug. Neither our doctors nor our friends are psychic, and they need to be told about adverse drug reactions in order to understand them. True stories about the effects of fluoroquinolones on individual lives vividly illustrate the risks of these drugs—much more than studies, or data, or warning labels.

Patient stories can also help researchers to understand the real-world effects of pharmaceuticals, and the direction that a researcher chooses to look can be influenced by patient reports and stories.

Because patients reported their symptoms to the FDA, the warning labels for fluoroquinolones have changed to note that peripheral neuropathy is a potentially permanent side-effect of fluoroquinolones. Patient reports and advocacy also led to the November 5, 2015 FDA meeting where the Antimicrobial Drugs Advisory Committee and the Drug Safety and Risk Management Advisory Committee decided that the current warnings on fluoroquinolone labels are not sufficient. We still have a long way to go, but it should be acknowledged that patients, and their stories, are driving the FDA to action, and that is quite special and unusual.

Reporting Fluoroquinolone Toxicity to the FDA

Please, even if you don’t tell your story to anyone else, report your adverse reaction to the FDA. Instructions on how to report your reaction to the FDA can be found here – http://www.fda.gov/Safety/MedWatch/HowToReport/ucm053074.htm.

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Telling Your Story of Fluoroquinolone Toxicity on the Internet

If you would like to tell your story on a web site, there are a few options:

The Fluoroquinolone Effects Study

Please, please, please also tell your story to the researchers who are conducting the Fluoroquinolone Effects Study. The Fluoroquinolone Effects Study is being led by Dr. Beatrice Golomb and it is through UCSD. The Fluoroquinolone Effects Study is a chance to tell your story in your own words to scientists who are studying fluoroquinolone toxicity. More information about the study can be found here – http://www.fqstudy.info/Fluoroquinolone_Effects_Study/Welcome.html.

Media Coverage of Fluoroquinolone Toxicity

Hundreds of people have spoken out to the media about fluoroquinolone toxicity. Thank you to each of you who told your story! I encourage all of you to reach out to the media, because even though many of our stories have been told, many more are needed. Write letters and emails, call your newspaper editors and tv reporters. Please do whatever you can to amplify your voice when telling your story.

People are Listening

People are listening to our screams and our stories. I regularly hear from people who say something along the lines of, “I requested a safer antibiotic because I heard from you that Levaquin is dangerous.” I hear from doctors, nurses, pharmacists, and other medical professionals who are getting information about fluoroquinolone toxicity from Floxie Hope. The number of people in The Fluoroquinolone Toxicity Group on Facebook has increased steadily to almost 5,000 people. Many of those people share information about fluoroquinolone toxicity with their friends. The word is getting out, and that’s a very good thing!

Thank you to all of you who are telling your stories of pain caused by fluoroquinolones! These stories are important, and I even think that it’s healing for you to tell your story.

 

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True Health Made Simple Podcast Featuring Tara

True Health

In episode 31 of the True Health Made Simple podcast, Tara speaks out about her experience with fluoroquinolone toxicity. Please listen and share!

http://truehealthkc.libsyn.com/podcast/031-what-you-need-to-know-abut-the-most-dangerous-class-of-antibioticsfrom-a-patients-perspective

https://itunes.apple.com/us/podcast/true-health-made-simple/id1015211573?mt=2

When Tara sent me the link to the podcast she said, “I just wanted to share – some doctors, like mine – are wanting to get the word out about the dangers of fluoroquinolones so my doctor interviewed me about my story. I let the listeners know to get more info go to floxiehope.com or the QVF website. I think it brings hope to know some doctors really do care.”

It is PHENOMENAL that Tara’s doctors wanted to interview her to spread the word about how fluoroquinolones negatively affected her life, and that Tara was willing to speak out and be interviewed. A HUGE THANK YOU to Tara and her doctors at True Health!

More about Tara can be found on “Tara’s Story – Healing from Levaquin Effects.

Information about True Health can be found on their web site, http://www.truehealthkc.com/, and through their facebook page – https://www.facebook.com/TrueHealthKC.

Thank you for listening and sharing! Great job, Tara!

 

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Antibiotic Brain Fog – Some Possible Solutions

I experienced memory loss, disconnectedness, loss of reading comprehension, and slow-thinking while I was going through fluoroquinolone toxicity. Losing my ability to think, and feeling as if I had lost my ability to do my job (I held onto my job and my employer was kind and patient through the whole ordeal), were truly terrifying. I felt stupid. I was scared that I was stupid, or worse–that I had some sort of permanent brain damage.

Thankfully, those symptoms subsided, and my mind has recovered along with the rest of me. I describe the things I did to heal my brain after fluoroquinolone toxicity in the post, “Healing my Brain After Cipro.” The things that helped my brain to heal are:

  1. Time
  2. Meditation
  3. Sudoku Puzzles
  4. Reading
  5. Writing
  6. Researching

All of those things truly did help me. Each one is a process, not a quick-fix. Being patient and letting the healing hands of time do their magic helped my brain to heal. Meditating every day for a minimum of 20 minutes helped to calm my mind, increase my confidence, give me patience, increase my concentration, and enable me to feel more connected to the world and the people in it. Sudoku puzzles, reading, writing, and researching all helped in that using my brain seemed to make it stronger and more capable.

I wholeheartedly recommend each of those things to everyone who is struggling with brain-fog. They’re helpful, empowering, and they can’t hurt.

I want people to realize that their brains can heal without doing anything drastic, and that with time and use, your floxed mind can heal along with the rest of you.

However, many people look at that list and say, “Those things aren’t going to work for my SEVERE brain fog. I need something more drastic than sudoku puzzles.” Fair enough.

I am risk-averse and, frankly, I’m not a very good biohacker because I’m risk-averse. Therefore, I tend toward gentle, non-invasive, healing methods.

Many of you are willing to take more risks than I am though, and for you, I think that the advice of Dave Asprey (“the world’s most famous biohacker” according to Men’s Fitness Magazine) in his post, “13 Nootropics to Unlock Your True Brain” may be helpful. I highly recommend that each of you read the article because Dave has a lot of excellent insight in it. I’m going to go over some of his recommendations and how they relate to “floxies” in this post.

Dave’s nootropic recommendations:

  1. Modafinil (Provigil), armodafinil (Nuvigil), and adrafinil. I have heard of anyone suffering from antibiotic brain-fog trying these nootropics. If you have something to report about them, please let me know and I’ll add it to this post.
  2. Racetams. Look at the comments on the bottom of the post, “The Mitochondrial Link – Fearless Parent Podcast #81.” The person commenting as “Your Future” gives a lot of interesting information about racetams and mitochondria.
  3. Nicotine. Yes, seriously, nicotine. More information about nicotine can be found HERE. For floxies, it should be noted that fluoroquinolones inhibit CYP1A2 enzymes. Nicotine induces CYP1A2 enzymes. There are significantly safer ways to try nicotine than through smoking or chewing tobacco products and some of those options can be found in “Is Nicotine the Next Big Smart Drug?” It should also be noted that broccoli also induces CYP1A2 enzymes, and it has none of the drawbacks that nicotine has. However, this post is about things that can perk-up your brain, and nicotine can do that while broccoli, unfortunately, can’t.
  4. Amphetamine (Adderall). A floxie friend told me that Adderall helped him immensely. Be careful. Adderall, of course, is not without consequences. Here is the warning label for Adderall – http://www.accessdata.fda.gov/drugsatfda_docs/label/2007/021303s015lbl.pdf. Here are patient reviews of Adderall – http://www.askapatient.com/viewrating.asp?drug=11522&name=ADDERALL+10. I wouldn’t take it, but that’s just my extremely biased opinion.
  5. L-theanine. From Ruth’s recovery story on Floxie Hope, “L-Theanine helps my brain to be a less noisy place—it ‘cuts the chatter’ as Dr. Whitcomb says.” More information about Ruth’s experience with L-theanine can be found in the comments on her story.
  6. Bacopa monnieri. Here are some Floxie Hope comments that note how people dealing with FQ toxicity responded to bacopa monnieri. https://floxiehope.com/comment-page-30/#comment-27587https://floxiehope.com/comment-page-46/#comment-37325https://floxiehope.com/ruths-story-cipro-toxicity/comment-page-6/#comment-35332.
  7. LSD. I haven’t heard from anyone who has tried LSD post-flox. If anyone has anything that they’d like to share with me and/or the Floxie Hope audience, please contact me. I find the stories of healings that occur post hallucinogenic drug use to be interesting. As I said though, I’m risk-averse and not eager to try things like LSD.
  8. Unfair Advantage. Unfair Advantage is a Bulletproof product that contains Bio-identical ActivePQQ™ and CoQ10. It enhances mitochondrial function. There is evidence that fluoroquinolones damage mitochondria, and mitochondrial support supplements such as Unfair Advantage may help floxies in multiple ways. I tried Unfair Advantage just before I was on Bulletproof Radio discussing fluoroquinolone toxicity. I was fully healed at the time that I tried it, so my experience may not be as dramatic as the experience of someone who is recently floxed, but I did find that it improved my energy level and concentration.
  9. Bulletproof Upgraded Aging Formula. I don’t know of any floxies who have tried the Bulletproof Upgraded Aging Formula. If you have an experience with it, please contact me.
  10. Forskolin & artichoke extract. I haven’t heard from anyone who has tried Forskolin & artichoke extract. Please contact me if you have an experience with it. As with all of the things mentioned in this section of this post, more information about them can be found on 13 Nootropics to Unlock Your True Brain. “Forskolin” is a very fun word though. Say it ’til you giggle, ’cause laughter really is good medicine. :p

Please do plenty of independent research before you try any of these. They all have their pros and cons and informed consent really is important.

Things like a healthy diet, getting enough sleep, minimizing anxiety, and healing the gut can also be helpful for getting through fluoroquinolone-induced brain-fog. Those things have no negative side-effects, so concentrating on them is highly recommended.

I hope that the things mentioned in this post help you to get your mental capacity back! Please be patient and kind to yourself as you go through the healing process. Healing takes time, and it may take trying a variety of different things before you find things that heal your mind and body. Patience and kindness toward yourself as you go through the healing process certainly can’t hurt, and they will probably even help.

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Fluoroquinolones and Epigenetic Triggers – Possible Connections with Charcot-Marie-Tooth Disease

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Chromosomes

The post, Do Fluoroquinolone Antibiotics Trigger Charcot-Marie-Tooth and Other Genetic Diseases?, was published on Hormones Matter today (3/7/16).

I hope that you find the connections to be interesting, and not too frightening.

A couple things to note: First, Charcot-Marie-Tooth disease has nothing to do with teeth – Dr. Tooth was one of the people who discovered and named it. Second, though there are potential connections between fluoroquinolone toxicity and several genetic diseases, this is just a hypothesis, so please take it as just that. The connections are interesting, and should be explored. However, I don’t want anyone reading this, or anything else I write, to think that you are doomed.

Many “floxies” have expressed that they feel as if they have aged 20 years in a matter of weeks or months. I wonder if, on a cellular level, they actually have. I wonder if fluoroquinolones age cells and, in doing so, trigger diseases that would have remained dormant until much later in life. I wonder how fluoroquinolones, and other pharmaceuticals, affect gene expression (epigenetics), and if those effects are passed down from one generation to the next. I honestly don’t know the answer to these questions.

IF the damage mechanism for fluoroquinolones is genetic damage, and underlying diseases are triggered, reactions would be different for each person. This could explain the huge variation in fluoroquinolone toxicity reactions. Unfortunately, if this is the case, I think that we’re a long way from proving connections between fluoroquinolones and the triggering of diseases that are thought to be genetic in nature. Epigenetics is a relatively new area of study, and the triggering of epigenetic changes via pharmaceuticals isn’t something that I’ve run across much in my research. I think that it’s a topic that deserves significantly more attention.

Please read and share “Do Fluoroquinolone Antibiotics Trigger Charcot-Marie-Tooth and Other Genetic Diseases?” Thank you!

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The following fascinating article was published under a Creative Commons License, meaning that it can be published freely. It was originally published on www.mosaicscience.com – a great site that I highly recommend you check out. The article is about uncovering some of the genes behind Charcot-Marie-Tooth Disease. It’s also about being your own biggest advocate, and pushing to solve health “mysteries.”

DIY diagnosis: how an extreme athlete uncovered her genetic flaw

When Kim Goodsell discovered that she had two extremely rare genetic diseases, she taught herself genetics to help find out why. Ed Yong tells her story.

Kim Goodsell was running along a mountain trail when her left ankle began turning inward, unbidden. A few weeks later she started having trouble lifting her feet properly near the end of her runs, and her toes would scuff the ground. Her back started to ache, and then her joints too.

This was in 2002, and Kim, then 44 years old, was already an accomplished endurance athlete. She cycled, ran, climbed and skied through the Rockies for hours every day, and was a veteran of Ironman triathlons. She’d always been the strong one in her family. When she was four, she would let her teenage uncles stand on her stomach as a party trick. In high school, she was an accomplished gymnast and an ardent cyclist. By college, she was running the equivalent of a half marathon on most days. It wasn’t that she was much of a competitor, exactly – passing someone in a race felt more deflating than energising. Mostly Kim just wanted to be moving.

So when her limbs started glitching, she did what high-level athletes do, what she had always done: she pushed through. But in the summer of 2010, years of gradually worsening symptoms gave way to weeks of spectacular collapse. Kim was about to head to Lake Superior with her husband, CB. They planned to camp, kayak, and disappear from the world for as long as they could catch enough fish to eat. But in the days before their scheduled departure, she could not grip a pen or a fork, much less a paddle. Kim, a woman for whom extreme sports were everyday pursuits, could no longer cope with everyday pursuits. Instead of a lakeside tent, she found herself at the Mayo Clinic in Rochester, Minnesota.

After four days of tests, Kim’s neurologist told her that she had Charcot–Marie–Tooth disease, a genetic disorder that affects the peripheral neurons carrying signals between the spinal cord and the extremities. It’s rare and carries a varying suite of symptoms, but Kim’s are typical, starting at the feet and heading upward. The neurologist explained that as her neurons died, the surviving cells picked up the slack by sprouting new branches – a workaround that masked the underlying degeneration until the rate of cell death outpaced the rate of compensation. Hence Kim’s crash.

The neurologist told her to come back in a year so he could check how quickly the disease was progressing, but that it would certainly progress. Charcot–Marie–Tooth has no cure.

The Goodsells drove home and Kim, exhausted, slept for two days. When she woke up, she got to work. “My reaction to things that I have no control over is to find out as much as I can about them,” she says. She started by reviewing her clinic notes, and quickly noticed something odd: there was hardly any mention of her heart.

Years before she learned that she had Charcot–Marie–Tooth, Kim discovered that she had another genetic disorder – one that affects the heart, arrhythmogenic right ventricular cardiomyopathy (ARVC). ARVC gradually replaces the heart’s synchronised beating muscle with fat and scar tissue. It nearly killed her once; she still has an internal defibrillator to keep her heart beating. But even though it was there in her medical records, her neurologist hadn’t seen fit to mention it in his report. “It meant nothing to him,” says Kim. “I thought: Wow, that’s really funny.”

It wasn’t the omission per se that bothered her. It was the implicit suggestion that her two life-long diseases – one of the heart, one of the nervous system – were unrelated. That, in the genetic lottery, she was a double-loser. That lightning must have struck her twice.

Surely not, she thought. Surely there must be a connection.

I meet Kim at La Ventana in Baja California, Mexico. She spends winters here, mostly kitesurfing. The sand and water are postcard-quality, but La Ventana has barely any resorts or big hotels. So in the still air of the morning when kites won’t fly, the beach is empty. Kim likes it that way. She has been up since dawn, cycling among the cacti and swimming in the ocean with pelicans and frigatebirds for company. She hauls herself out of the water, dries off, and sits on a small terrace overlooking the ocean. Her face is tanned and wrinkled, and she manifests no obvious signs of her two conditions. That’s partly because she has developed workarounds to mask and control her symptoms. She brushes her teeth on one foot to offset her balance problems. She uses massage balls and spends hours stretching to stop her muscles and joints from seizing up.

“See how I’m sitting?” she says. She has pulled her legs up on the chair to her left, and her back is curving that way too.

“My spine curves this way” – she nods to the right – “so I sit curving to the opposite side. I consciously do the opposite.”

She has a history of that. In 1979 Kim was a mathematically gifted pre-med student at UC San Diego, her hometown college. Her path was clear: graduate, and follow her older brother into medical school. But on a trip to South America – her first time out of San Diego – she ended up hiking for three months instead of working at a clinic as she’d planned. When she returned home, her academic future seemed pale and uninspiring. And then CB – her future husband, at this point a fellow student and regular running partner – started taking her out on wilderness hikes. “He introduced me to the mountains and I thought: this is life,” Kim says.

Within months of graduating Kim dropped out. Her brother, who had been a father figure to her growing up, was furious. “We hardly spoke. CB was his friend and he couldn’t even look at him,” she says. “He said I was being completely irresponsible.” Kim and CB married in 1983, and aside from a brief stint as restaurant owners, they have never had 9-to-5 jobs. They mostly earned a living by buying and remodelling run-down houses and selling them at a profit, and then heading into the wilderness until their supplies ran out. In 1995 they found themselves in La Jolla, California, working on an especially stressful renovation that left Kim drained.

That was when her heart problems began. Kim started having episodes of ventricular tachycardia – the lower chambers of her heart contracted so quickly that they pumped out their contents before they had a chance to fill up, compromising the flow of blood (and therefore oxygen) to the rest of her body. One minute she would be racing down Highway 1 on her bike; the next she would feel like she had been “unplugged”, as if “there was nothing driving anymore”. A cardiologist at Scripps Memorial Hospital told her she’d need an internal defibrillator, but Kim said no – she was worried it’d get in the way of wearing a backpack on a run, and she had faith that she’d be able to deal with the ventricular tachycardia by slowing down and relaxing. “I didn’t want something implanted in me that would limit my opportunities of experiencing life,” she says.

The next week, the Goodsells finished their renovation, packed up and headed into the Sierra Nevada with no return date in sight. It was an unorthodox solution to a life-threatening heart condition: to vanish into the boondocks, far away from any medical care, to do even more exercise.

The thing is, it was the right one. The outdoors rejuvenated her. She was gone for one-and-a-half years, and her heart behaved the whole way through. That unbroken streak only broke when the Goodsells rejoined their old lives in 1997. Back in California, they were once again cycling down Highway 1 when her heart started to beat erratically again. This time, it did not stop.

By the time the paramedics arrived, Kim was slumped against a wall and her chest was shaking. Her tachycardia had lasted for almost an hour and progressed to ventricular fibrillation – that is, her heartbeat was erratic as well as fast. She blacked out in the ambulance, on the cusp of cardiac arrest.

She woke up at Scripps Memorial Hospital. The same cardiologist was there to greet her. Through further tests he discovered that the muscle of her right ventricle was marbled with fat and scar tissue and not contracting properly. These are classic signs of ARVC. It had only been properly described in 1982, back when Kim was regularly signing up for triathlons. ARVC is a major cause of fatal heart attacks in young people, and athletes are especially vulnerable as exercise can accelerate the disease’s progress. And since Kim wouldn’t stop exercising, she finally conceded to the defibrillator. They implanted it the next day.

Kim referred to the implant as her “internal terrorist”. Every shock was debilitating and led to months of anxiety. She had to learn to cope with the device, and it took several years to regain the joy she drew from hardcore exercise. That was when the other symptoms started.

These diseases are rare. In a crowd of a million adults, around 400 will have Charcot–Marie–Tooth and between 200 and 400 will have ARVC. But genetic diseases in general are actually quite common – 8 per cent of people have at least one. This paradoxical combination has fuelled the rise of many online communities where people with rare disorders can find each other. Heidi Rehm, a geneticist at Harvard Medical School, studies a condition called Norrie disease that mostly affects the eyes and ears. She developed a registry for Norrie disease patients to share their experiences, and learned that almost all the men with the disease had erectile dysfunction. “A patient goes to their doctor with blindness and deafness, and erectile dysfunction isn’t the first thing you ask about!” says Rehm. “Patients drove that discovery.” Through communities, families often make connections about their medical problems that their doctors miss.

But Kim was never one for relying on others. She tried a support group when she got her implant, but it did nothing for her. She dipped her toes in patient forums, but was always frustrated by the rampant misinformation. “People just weren’t interpreting things correctly,” Kim says. “I wanted more rigour.”

She started by diving into PubMed – an online search engine for biomedical papers – hunting down everything she could on Charcot–Marie–Tooth. She hoped that her brief fling with a scientific education would carry her through. But with pre-med knowledge that had been gathering dust for 30 years and no formal training in genetics, Kim quickly ran headfirst into a wall of unfamiliar concepts and impenetrable jargon. “It was like reading Chinese,” she says.

But she persisted. She scratched around in Google until she found uploaded PDFs of the articles she wanted. She would read an abstract and Google every word she didn’t understand. When those searches snowballed into even more jargon, she’d Google that too. The expanding tree of gibberish seemed infinite – apoptosis, phenotypic, desmosome – until, one day, it wasn’t. “You get a feeling for what’s being said,” Kim says. “Pretty soon you start to learn the language.”

“Kim has an incredible ability to understand the genetic literature,” says Martha Grogan, a cardiologist from the Mayo Clinic and an old friend of CB’s who now coordinates Kim’s care. “We have a lot of patients who ask great questions but with Kim, it’s like having another research fellow.”

At the time the Goodsells were staying at a friend’s house at Lake Michigan. Kim would sit on the balcony for eight hours a day, listening to the water and teaching herself genetics. Too weak to explore winding hillside trails, she channelled her perseverance and love of isolation towards scientific frontiers and the spiralling helices of her own DNA. “I spent hundreds of hours,” she says. “CB lost me during this process.”

Kim looked at every gene linked to Charcot–Marie–Tooth – there are more than 40 overall, each one imparting a slightly different character to the disease. One leapt out: LMNA, which codes for a group of rope-like proteins that mesh into a tangled network at the centre of our cells. This ‘nuclear lamina’ provides cells with structural support, and interacts with a bunch of other proteins to influence everything from the packaging and activation of genes to the suicide of damaged cells. Given this central role, it makes sense that mutations in LMNA are responsible for at least 15 different diseases, more than any other human gene. These laminopathies comprise a bafflingly diverse group – nerve disorders (like Charcot–Marie–Tooth), wasting diseases of fat and muscle, and even premature ageing.

As Kim read about these conditions and their symptoms, she saw her entire medical history reflected back at her – the contracted muscles in her neck and back, her slightly misaligned hips and the abnormal curve in her spine. She saw her Charcot–Marie–Tooth disease.

She also saw a heart disorder linked to the LMNA gene that wasn’t ARVC but which doctors sometimes mistake for it. “Everything was encapsulated,” she says. “It was like an umbrella over all of my phenotypes. I thought: This has to be the unifying principle.”

Kim was convinced that she had found the cause of her two diseases, but the only way to know for sure was to get the DNA of her LMNA gene sequenced to see if she had a mutation. First, she had to convince scientists that she was right. She started with Grogan, presenting her with the findings of her research. Grogan was impressed, but pragmatic. Even if Kim was right, it would not change her fate. Her implant was keeping her heart problems under control, and her Charcot–Marie–Tooth disease was incurable. She didn’t see a point. But Kim did. “I wanted to know,” she says. “Even if you have a terrible prognosis, the act of knowing assuages anxiety. There’s a sense of empowerment.”

In November 2010 Kim presented her case to Ralitza Gavrilova, a medical geneticist at the Mayo Clinic. She got a frosty reception. Gavrilova told Kim that her odds of being right were slim. “I got this sense that she thought I’d made an unfounded shot in the dark,” says Kim. “That I didn’t understand the complexity of the genome. That I had been reading the internet, and they come up with all sorts of things there.”

Gavrilova pushed Kim towards a different test, which would look at seven genes linked to ARVC. Her insurance would cover that, but if she insisted on sequencing the DNA of her LMNA gene, she would have to foot a $3,000 bill herself. Why waste the money, when it was such an unlikely call? But Kim was insistent. She knew that the known ARVC genes explain only a minority of cases and that none of them was linked to neural problems. In all her searching she had found only one that covered both her heart and nervous problem. Eventually, Gavrilova relented.

Kim, meanwhile, disappeared down to Baja in Mexico. Gavrilova’s scepticism had worn her down and she fully expected that the results would come back negative.

When she returned home in May, there was a letter waiting for her. It was from Gavrilova. She had been trying to call for months. The test had come back positive: on one of her two copies of LMNA Goodsell had a mutation, in a part of the gene that almost never changes. LMNA consists of 57,517 DNA ‘letters’, and in the vast majority of people (and most chimps, monkeys, mice and fish) the 1,044th position is filled by a G (guanine). Kim had a T (thymine). “All evidence suggests that the mutation found in this patient might be disease-causing,” Gavrilova wrote in her report.

In other words, Kim was right.

“I’m beyond impressed,” says Michael Ackerman, a geneticist at the Mayo Clinic. He specialises in inherited heart disorders like ARVC that can cause sudden death at any time. Such diseases make for people who do their homework, but Ackerman describes most as “Google-and-go” patients who check their diagnosis online, or read up about treatment options. Kim had written up her research as a white paper – 36 pages of research and analysis. “Kim’s the only one who handed me her own thesis,” he says. “Of all the 1,000-plus patients I’ve taken care of, none have done extensive detective work and told physicians which genetic test to order.”

He thinks she nailed it too. It is unlikely to be the whole story – Kim almost certainly has other mutations that are affecting the course of her disease – but LMNA “is certainly the leading contender for a unifying explanation, without there being a close second,” he says. “The evidence is pretty good for this being a smoking gun.”

The test had vindicated her hypothesis, but it also raised some confusing questions. Heart problems are a common feature of laminopathies, but those mutations had never been linked to ARVC, Kim’s specific heart malfunction. Had she been misdiagnosed? A few months later, Kim stumbled across a new paper by a team of British researchers who had studied 108 people with ARVC and found that four had LMNA mutations (and none of the standard ones). “To the best of our knowledge, this is the first report of ARVC caused by mutations in LMNA,” they wrote. They didn’t know about Kim’s work – they couldn’t have, of course. But she knew. Kim had beaten them to it. “I was so excited, I was running up and down the beach,” she says.

When patients get solutions to their own genetic puzzle, it’s always professional geneticists who do the solving. Take James Lupski. He has been studying Charcot–Marie–Tooth for decades, and discovered the first gene linked to the condition. He also has it himself. In 2010 he sequenced his own genome and discovered a previously unidentified mutation responsible for the disease. In other cases anxious parents have been instrumental in uncovering the causes of their kids’ mysterious genetic disorders after long diagnostic odysseys, but only by bringing their cases in front of the right scientists.

Kim, however, was an amateur. And to her, sequencing was not a Hail Mary pass that would – maybe, somehow – offer her answers; it was a way of confirming a carefully researched hypothesis.

“People have been talking about empowering consumers since there was an internet,” says Eric Topol, a geneticist at the Scripps Clinic. “But finally, we’ve reached a point where someone can delve into their condition beyond what the top physicians at the Mayo Clinic could. They couldn’t connect the dots. She did.”

Topol, a self-described “digital medicine aficionado”, argues that Kim is a harbinger of things to come. In his book The Creative Destruction of Medicine, Topol foretells a future where doctors are no longer the gatekeepers of medical information. Advances like personal genetic testing or sensors that measure molecules in the blood will give patients the power to better understand themselves and to exercise more control over their healthcare. Medicine is becoming more democratic.

Kim is a vanguard of that change. She lacked academic knowledge, but she had several advantages over her physicians and other researchers in the field. She had detailed first-hand knowledge of her own symptoms, allowing her to spot connections in the scientific literature that others had missed. She could devote hours to learning everything about her niche disorders – time and focus that no clinician could reasonably spend on a single case. And she had unparalleled motivation: “There’s nothing that engages your curiosity more than being confronted by your death,” she says.

It is also becoming ever easier for that curiosity to lead to discovery. In the past geneticists would try to diagnose patients by looking at their medical history and deciding which genes might be worth sequencing, as Gavrilova tried to do for Kim. The approach makes sense, but it only ever confirms known links between genes and diseases.

One way of finding new links is to sequence a patient’s exome – the 1 per cent of their genome that contains protein-coding genes. It’s cheaper than sequencing a full genome, but allows researchers to hunt for disease-related genes by interrogating every possible suspect simultaneously, without having to whittle down the list first. “Suddenly, we’re finding patients presenting with Disease X who have mutations in genes never previously associated with that disease,” says Daniel MacArthur, a geneticist at Massachusetts General Hospital. “That’s happening in nearly every disease field right now.”

Exome sequencing is now barely more expensive than sequencing much narrower gene panels. MacArthur says that the cost has already fallen below $1,000 and may halve again this year. And once patients have that information, they could use it to find others with the same mutations and check if they have the same symptoms.

Currently, the results from DNA sequencing studies are largely squirrelled away in boutique databases that collate mutations for specific diseases or genes. The ironically named Universal Mutation Database covers mutations in only 34 genes, including LMNA. Broader ones exist, but for decades they have been incomplete, rife with mistakes, or inaccessible, even to other researchers – a sad state of affairs that MacArthur laments as the “single greatest failure in human genetics”. Now, though, the National Institutes of Health are developing an open database called ClinVar that covers all disease mutations. “A lot of us are putting our hopes on this,” says MacArthur. “We need to come up with resources that empower people to make surprising links, which is hard to do if the data are broken up by disease or gene.”

But for every Kim, there are others who research their own conditions and come up with wrong answers. In one study four non-specialist volunteers tried to diagnose 26 cases from the New England Journal of Medicine by Googling the symptoms. They got less than a quarter right. Genetic diseases arguably lend themselves to confusion and misinformation. They are often both debilitating and enigmatic, and getting sequenced can offer little comfort beyond a diagnosis. If mainstream science has no easy answers to offer, many patients will follow any lead, no matter how weak. “There’s a tendency for people to spin very convoluted stories on tenuous threads of evidence. Even scientists do that,” says MacArthur. “I have heard of a lot of rare-disease patients who come up with hypotheses about their disease, and very few turn out to be correct.”

Even Kim’s tale could have taken a different turn. Last year, a team from the Baylor College of Medicine sequenced the exomes of 250 people with suspected genetic disorders, and found that four of them had two diseases caused by mutations in different genes. In other words, Kim’s hunch about her two diseases sharing a common root could well have been wrong. Lightning does occasionally strike twice.

“We almost always have to spend time with patients decoding and recoding the impression that they’ve acquired about their disease from their own homework,” says Ackerman. Kim was an exception, he says, and her other physicians echo that view. She is unique. She is one-of-a-kind. She is extraordinary. High praise, but it conceals the implicit suggestion that she is an outlier and will continue to be.

“Bullshit,” says Kim. “I hear this all the time: that I’m an exception. That the patient of the future is not going to do what I did.” She bristles at the very suggestion. “I almost take offence when I hear that what I’ve done is exceptional.”

We are talking over coffee at La Ventana. This is her fifth winter here, and she and CB have just celebrated their 30th wedding anniversary. CB leans back against a wall, quiet and contemplative. Kim sits forward, animated and effusive. She’s drinking decaf because of her heart, but it’s not like she needs the caffeine. “Take Rodney Mullen. He’s a real genius,” she says. Mullen is not a figure from science or medicine. He is, in fact, a legendary skateboarder, famous for inventing mind-blowing tricks that previously seemed impossible. One of them is actually called the ‘impossible’. “He executes these movements that defy reason, films them and publishes them on YouTube,” Kim says. “And inevitably, within a few weeks, someone will send him a clip saying: This kid can do it better than you. He gave that trick everything he had, he’s pulling from all of his experience, and here’s this kid who picks it up in a matter of weeks. Because he learned that it’s possible to do that. Rodney just acts as a conduit. He breaks barriers of disbelief.”

Her protestations aside, Kim is unique. Throughout her life she had built up a constellation of values and impulses – endurance, single-mindedness, self-reliance and opposition to authority – that all clicked in when she was confronted with her twin diagnoses. She was predisposed to win. Not everyone is. But as genetic information becomes cheaper, more accessible and more organised, that barrier may lower. People may not have to be like Kim to do what she did.

Kim isn’t cured. Her LMNA discovery offered her peace of mind but it did not suggest any obvious treatments. Still, she has made a suite of dietary changes, again based on her own research, which she feels have helped to bring her nervous symptoms under control. Some are generic, without much hard science behind them: she eats mostly organic fruit, vegetables, nuts and seeds, and avoids processed food. Others are more tailored. She drinks ginger tea because it thins the blood – she says that many people with laminopathies have problems with clots. Whether her choices are directly slowing the progress of her diseases or triggering a placebo effect, she is fit and happy. Her defibrillator hasn’t shocked her in months. And, of course, she still exercises constantly.

Up the hill from the beach we can see the little yellow house where she wrote the 36-page booklet that put together all her research. It convinced her doctors, yes, but it did even more. She showed it to her brother, now an anaesthesiologist, and it allowed them to reconcile. “It’s like I’ve finally done something worthy with my life,” Kim says. “He told me I’d done some really good research and that I’d missed my calling as a medical researcher. I told him I think I’ve been doing exactly what I needed to do.”

This article first appeared on Mosaic and is republished here under a Creative Commons licence.

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