When I was a kid food was different.  We didn’t have much packaged food.  We were 6 in my family so meals had to be affordable.  My Mom mostly made soups and stews or meat and vegetables.  We were rarely allowed sugary foods – only on birthdays. That included soda.  My Mom had a craving for salt so she would order Charles Chips by the container and sometimes their pretzels. (But those were mostly for her and she kept them hidden for special treats.)  Fruit was our snack.  Nobody in our family was overweight.  Thank you Mom!

Recently (the last decade) I’ve had the amazing opportunity to study lifestyle genetics.  I find I have all the carb sensitivity gene mutations (proven with clinical studies) and many of the fat sensitivity gene mutations.  I have blood sugar mutations.  I have a profile that would set me up to be overweight if all of those genes expressed but because my Mom had us on a low glycemic eating program, they did not express.

When I went to college I went “hog wild” and ate packaged crumb cakes, cookies, all kinds of carbs and drank soda.  No surprise I gained 25 pounds.  I managed to lose it all by taking up racquetball and for 30 years I maintained my weight with exercise.

Last year my Mom died. She had just turned 88 and had blocked arteries. Her first symptom was extreme pain. She was told she had shingles. I suggested she have a stress test.  They found the blockages.

She was recommended open heart surgery.  I work with many kinds of health professionals.  Not one of them thought that was a good idea.  If she did not have the surgery she would die.  But we (the health professionals and myself) all felt if she did have the surgery, she would not recover and the end would be beyond miserable.  My siblings encouraged her to have the surgery, I believe out of their own desire to keep her alive but also because the hospital MDs said she could make it.  They likely knew she could not survive this surgery.  They also most likely knew what her end would be like.

So why would they do that?

That is what my best friend calls a “walletectomy.”  I don’t blame MDs.  They have to follow hospital protocols or they can get sued.

So why is it the hospital protocol?

That brings us to the United States medical system.  You can’t avoid politics if you are talking about health.  The U.S is the only western country that doesn’t take care of its citizens’ health.  Right now they want to downgrade the little care they do offer.  Why?  Because the current administration values the support of business more than they value the quality of life of their citizens regardless of the spin they constantly put out.  And BTW, the alternative to truth is falsehood.

But, I digress….

After my Mom’s surgery she told me she was being “blamed” for not trying to do the exercises and recovery routines they recommended.  During this time her organs were all struggling to recover.

I’m pretty sure my Mom continued her low glycemic style of eating most of her life but I learned eventually she was an alcoholic – the secret kind.  It’s always a clue when someone BRINGS alcohol with them to visit you.  Just in case…

The point of my story is I BELIEVE in low glycemic lifestyle. Alcohol is not part of it. Alcohol will make you fat and it will contribute to heart disease.  It also puts you at a higher risk for cancer.

Once in a while is a good rule for most things.  I have a glass of red wine maybe 3 times per year and I can only drink about an inch of it because I have liver detox mutations and a whole glass will give me a hangover. Yuk.  What is once in a while for you?

I’d suggest once/week.

If you can’t do that, I’d suggest you ask yourself why.

I’m a super enthusiastic proponent of the TLS system for weight management and healthy cardiovascular system.  I highly recommend you watch this video and then do the quiz.  Does it cost money?  Yes.  Is it worth it?  YES YES YES!!!!  I will personally help you to be accountable on a daily basis, no fee.  This will be the last program you will every need to get fit. I’ll add one caveat – IF YOU ARE READY to stop yo yo-ing.

It would be my pleasure to speak to you.

If you are a health professional who would like to be the health leader you know you can be, implement epigenetics, weight management, prevention, etc. ….

It would be my pleasure to offer a complementary proposal and the support you deserve.

Kathy@criticalhealth.org, 617.515.7559.

Below is more information on cardiovascular support and weight management for the science minded, clinically trained.  This infographic is also for women. Women can commit domestic violence, assault, be aggressive, etc.

An article by Dr. David Brownstein, (MD),03/18/17 about using cholesterol to diagnose heart disease

In an on-line article in The New York Times today (3.17.17), the headline states, “Cholesterol-Slashing Drug Can Protect High-Risk Heart Patients, Study Finds.”  The article describes the first test of the new cholesterol-lowering medication—Repatha.  Repatha is part of the PCSK9 inhibiter family that works by lowering LDL-cholesterol levels through poisoning an enzyme—PCSK9–thereby allowing LDL receptors to remain in circulation.  LDL receptors can bind LDL-cholesterol, thus more LDL receptors will result in lowered LDL-cholesterol levels.


I have written about PCSK9 inhibitors before.  In my book, The Statin Disaster, I wrote, “I do not think PCSK9 inhibitors will be an effective treatment for heart disease as it will disrupt a normal physiologic process in the body: the binding of LDL to its receptor.” (1) So, let’s look at the first study which was published in the New England Journal of Medicine, March 17, 2017. This was a randomized, double-blind, placebo controlled trial involving 27,564 subjects with heart disease and LDL-cholesterol of 70 mg/dl or higher who were receiving statin therapy.

The primary endpoint was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization.  Keep in mind that hospitalization for angina and coronary revascularization (i.e., coronary artery bypass graft surgery or stent placement) are considered soft endpoints since the decision to hospitalize or place a stent is a subjective decision by the physician.  The ultimate success of any cardiac medication should be based on hard endpoints such as death, heart attacks, or stroke.

After 48 weeks of Repatha therapy or placebo, the authors reported that, compared to placebo, the Repatha group significantly reduced the risk of the primary end point by 15% (9.8% in the treatment group vs. 11.3% in the placebo group.)  However, as I have pointed out to you before, the 15% reduction is actually a relative risk reduction.  The relative risk is a statistical term that has no meaning when considering whether to recommend or not recommend a therapy to a patient.  A more accurate assessment is the absolute risk difference.  In this case, the absolute risk difference between the two groups is 1.5%.  A more accurate description of the results should state: as compared to placebo, taking Repatha for two years’ results in a 1.5% decline in a combination of outcomes including death, stroke, myocardial infarction, hospitalization for angina and coronary revascularization.  Another way to look at the data is that the drug failed 98.5% who took it as they received no benefit.  And, if you take out the soft endpoints, the 1.5% decline disappears.

I called Specialty Pharmacy to find out how much Repatha costs.  I was told Repatha costs $2,351.05 per month for a total of $28,212.60/year). So, a two-year course of the medication costs $56,425.20.  (Note; The NYT article states the drug costs $14,523 per year.)

For the physicians, out there, I have a question for you:  Who the heck would prescribe an expensive drug, associated with serious adverse effects, that fails 98.5% who take it?

For the patients, out there I have a question for you:  Who the heck would spend $28,212.60/year for a drug that is associated serious side effects and fails 98.5% who take it?  In this study 25% of those that received Repatha reported serious adverse effects.     What were the serious adverse effects?  I don’t know—they weren’t listed individually.

Repatha is another example about what is wrong with conventional medicine. President Trump just released his first budget.  I would advise him to start tweeting about the failure of Repatha and why it should not be allowed in the market place.  There are far too many ineffective, expensive drugs right now.  We don’t need another one.  Statins are a great example of ineffective drugs that fail nearly 99% who take them.  Now we can add PCSK9 inhibitors to the pile of poorly-performing drugs.

More information about cholesterol lowering medications can be found in my book, The Statin Disaster.

Repatha for heart disease?  Fugetaboutit!

The Triglyceride/HDL Cholesterol Ratio. What Is Ideal?

Many studies have found that the triglyceride/HDL cholesterol ratio (TG/HDL-C ratio) correlates strongly with the incidence and extent of coronary artery disease. This relationship is true both for men and women.

One study found that a TG/HDL-C ratio above 4 was the most powerful independent predictor of developing coronary artery disease.

With the increasing prevalence of overweight, obesity, and the metabolic syndrome this ratio may become even more important because high TG and low HDL-C is often associated with these disorders.

The TG/HDL-C ratio can easily be calculated from the standard lipid profile. Just divide your TG by your HDL-C.

However, when looking at the ideal ratio, you have to check if your lipid values are provided in mg/dl like in the US or mmol/L like in Australia, Canada, and most European countries.

If lipid values are expressed as mg/dl (like in the US);

TG/HDL-C ratio less than 2 is ideal

TG/HDL-C ratio above 4 is too high

TG/HDL-C ratio above 6 is much too high

If you live outside the US or are using mmol/L, you have to multiply this ratio by 0.4366 to attain the correct reference values. You can also multiply your ratio by 2.3 and use the reference values above.

If lipid values are expressed as mmol/L (like in Australia, Canada, and Europe);

TG/HDL-C ratio less than 0.87 is ideal

TG/HDL-C ratio above 1.74 is too high

TG/HDL-C ratio above 2.62 is much too high

My lifestyle genetics

My good friend Nancy Miller-Ilhi, PhD

NIH clinical study LeptiCore

Training, Competition and Genetics


The regular demands of training and competition make professional, collegiate, and recreational athletes highly susceptible to injury.

Genetics have a large influence over strength, muscle size and muscle fiber composition (fast or slow twitch), anaerobic threshold (AT), lung capacity, flexibility, power and endurance.

Injury is a fact of life for most athletes, but some professionals—and some weekend warriors —just seem more injury-prone than others. But what is it about their bodies that makes the bones, tendons, and ligaments so much more likely to tear or strain—bad luck, or just poor preparation?

A growing body of research suggests another answer: that genetic makeup may play an important role in injury risk.

Recreational distance running causes high numbers of injuries, with incidence rates estimated between 30% and 75% per person per year.

Treatment of sports injuries costs at least $160 billion per year in the U.S. and Major League Baseball lost $1.6 billion in payroll between 2008 and 2013 because of injuries to players. Avoiding injuries and remaining healthy is key to the success of a team or an individual athlete.

The potential to use genetic testing to reduce sports injuries



The COL1A1 gene, for example, encodes the alpha chain of type I collagen, the major protein component of all tendons and ligaments.  It’s associated with vasodilation, blood pressure control, efficiency of muscular contraction and cell hydration.

The GT alleles have a moderately raised risk of tendon and ligament injuries in sport. They need to undertake pre-habilitative exercises relevant to the sports they participate in and consider nutritional support for connective tissue.  They will have reduced response to endurance training and should make sure they stay sufficiently hydrated during endurance activities.

The GG will have an increased risk for tendon and ligament injuries and ruptures and or shoulder dislocations especially related to sports participation. They should also undertake pre-habilitative exercises relevant to the sports they participate in and consider nutritional support for connective tissue. They will have reduced response to endurance training and should make sure they stay sufficiently hydrated during endurance activities.

The TT variants contribute to positive response to endurance training.  They are positive for increased muscle efficiency especially in conjunction with ACE I-allele.  The T allele leads to increased expression of type I collagen alpha polypeptides compared with the G nucleotide, which may increase the tensile strength of tendons and ligaments. About 4% of athletes carry 2 copies of the T allele.

(90% of people who have brittle bone disease have mutations in COL1A1 and COL1A2.  I’m sure these folks would have liked to know early on so they could have taken preventive measures.)

Besides polymorphisms in COL1A1, there are additional DNA variants associated not only with ACL rupture and Achilles tendinopathy but also with other athletic injuries (shoulder dislocations and muscle strain severity).  It is important to note here that there are antibiotics that can flox genes and cause serious injuries, ruptures of the Achilles tendons and other tendons and even disability.  To learn more about fluoroquinolones like Cipro and Levaquin click here.  (Pharmacogenetic screenings can identify contraindication with prescription medications.)

The gene COL5A1 encodes the protein collagen alpha-1(V) chain. It is a minor connective tissue component but of ubiquitous distribution.  Type V collagen binds to DNA, heparin sulfate, thrombospondin, heparin, and insulin.  Defects in COL5A1 are a cause of Ehlers-Danlos syndrome (EDS1).


A functional skeletal system requires the coordinated development of many different tissue types, including cartilage, bones, joints, and tendons. Members of the Bone morphogenetic protein (BMP) family of secreted signaling molecules have been implicated as endogenous regulators of skeletal development. This is based on their expression during bone and joint formation, their ability to induce ectopic bone and cartilage, and the skeletal abnormalities present in animals with mutations in BMP family members. One member of this family, Growth/differentiation factor 5 (GDF5).



IL-6 mutations can be involved with other mutations like CRP and TNF in autoimmune disorders like Epstein Barr if the athlete has the mutation and is overtraining.

IL-6R is associated with immune response and cell growth. Dysregulated production of IL6 and this receptor are implicated in the pathogenesis of many diseases, such as multiple myeloma, autoimmune diseases and prostate cancer.


C-Reactive protein (CRP) is associated with acute phase protein and rises in response to inflammation in the body.  Elevation in CRP concentration will aid in determining the severity of acute tissue injury.


The genetic variant Tumor Necrosis Factor (TNF) causes over-inflammation. There is data suggesting that TNF may exacerbate neurobehavioral deficits and tissue damage.  If an athlete is over-training it could be involved in autoimmune disease.

Acute traumatic joint injury increases the risk of developing osteoarthritis.  Elevated levels of TNF and IL-6 have been detected in joint injuries.

There are separate studies concerning genetic polymorphisms associated with athletic performance, such as muscle contractility and V̇O2 max. Genetic information of this sort has recently been used to prevent injuries and maximize athletic performance. A professional soccer team in the English Premier League, for example, tested athletes for genetic loci associated with sports performance, and the English Institute of Sport expressed interest in providing genetic testing to Britain’s Olympic athletes in 2012.

The future holds promise for everyone. Someone with limited genetic potential can find ways to compensate and become a solid performer and athletes who are lucky to have exceptional genetics can optimize them.

Trainers and professionals can use this information to help optimize their clients and patients.

I think this is the best genetic lifestyle screening on the market because of the genetic scientist behind it, Dr. Keith Grimaldi.  I know his integrity and ethics.  He will not put genes in his screening that haven’t been tested with 3 independent clinical placebo studies proving a change in genetic expression influenced by a change in lifestyle.

If you would like to integrate this screening into your practice to improve patient outcomes, I’d be happy to offer you a complementary proposal.  Contact me at Kathy@CriticalHealth.org or 617.515.7559.

If you would like to use this screening to develop an action plan for your own optimal health, I’d be happy to offer it to you with my complementary services for a review of results.  Contact me at Kathy@CriticalHealth.org or 617.515.7559.


Why Genetic Lifestyle Screening Can Make a Difference

General Timeline of Genetic Training in Sports

1966 – 1991 Y-chromosomal testing as part of official sex segregation.
2001 Policy of the International Association of Athletics Federations and of the International Olympic Committee, respectively.
2001 Professional Boxing and Martial Arts Board of Victoria considers compulsory genetic screening for APOE4 variant in boxers.
2003 World Anti-doping Agency prohibits methods of gene doping.
2005 Eighteen Australian male rugby players were tested and analyzed for 11 genes.

The Chicago Bulls attempt genetic testing of free agent, Eddy Curry, for the purpose of ruling out hypertrophic cardiomyopathy.

2009 23andMe analyzes DNA samples from 100 current and former NFL linemen.

Major League Baseball begins using genetic testing with prospective players from the Dominican Republic and other Latin American Countries.

2010 The National Collegiate Athletic Association implements mandatory sickle cell trait screening.
2011 An English Premier League soccer team analyzes players’ DNA samples at 100 genetic loci.

The National Football League screens for genetic conditions sickle cell trait and G6PD under the 2011 NFL collective bargaining agreement.

2012 2012 English Institute of Sport expresses interest in the integration of genetic technologies to “tailor the training, conditioning, and preparation” of Britain’s Olympic and Paralympic athletes.
2014 Two Barclay’s Premier League soccer teams commission tests of their players’ DNA for 45 variants.












Fluoroquinolones and What Might Help

Six years ago I dated a man who worked for a pharmaceutical company.  I only went on two dates with him but I remember he was a runner and he was complaining about digestive problems that he had been having for three years after taking one of his company’s antibiotics, Levaquin.  He said while he was taking it he was out running and could feel something strange happening to his heals.

He stopped running and called a nurse at his company and asked her to look up side effects.  She told him, “Stop running right now. One of the side effects is spontaneous rupture of the Achilles Tendon.”

I warned PTs that I work with and they all responded that they’d already treated multiple patients with the Achilles tendon issue related to the antibiotic.

Three years ago I was hospitalized with an infection.  The night I went to the emergency room I had a white cell count in the fatal area.  The reason all patients need an advocate when they are in the hospital is that the patient can’t be expected to advocate for themselves when they are literally “dying.”

Cipro and Levaquin saved my life.  However, I have MTHFR (and other genetic polymorphisms that are listed in pharmacogenetics screenings as contraindicated with some pharmaceuticals). I have had infections a number of times (a symptom of MTHFR) and was treated with antibiotics that did not have the serious side effects of fluoroquinolones.

I was treated with FQs in March, 2013.  The first side effect I noticed was blurry eyes.  I was 64 and had not needed glasses previously.  When I saw an eye doctor she told me that the cocktail of fluoroquinolones I was given causes eye damage.  Blurry vision and trouble switching from close up to distance is what I’ve noticed.  Studies in Pubmed indicate fluoroquinolones inhibit corneal cell growth and repair.  (Ironically, they are in eye drops.)

I may have also received them after my daughter’s birth when I became septic in 1988.  Shortly after that I started having tendon problems in my wrists, shoulder and ankle.  I didn’t connect those to my treatment.

Some people are saying they experience a cycle of pain.  I’ve noticed 3-4 months I have pain for up to 3 days, then it mostly stops except for the gluteal tendon which has been constant.  I’ve literally had a pain in the ass for years. (I’m 67 years old.) People who experience the cycles of pain are calling it floxing.

Some people say they are in pain all the time.  There is a documentary about fluoroquinolones here.

Icing affected tendons helps me. I’ve noticed tendons and ligaments that experience repetitive use or have been damaged previously might be affected more by side effects. Hormones like Cortisol and lack of sleep might increase side effects.

Microcore ice packs have helped me.

I put them in a pad called Better Back to sit on to numb the discomfort from gluteal tendinopathy.  I use a bandage to wrap them around my wrists and ankles.

There is a support group on FB and www.floxiehope.com

There is a note by an MD to give your MD at the bottom of this blog along with the links I have found inside PubMed.  (Double Blind, Clinical studies on fluoroquinolones.)

What might help?

 Avoid all fluoroquinolones in the future. Be tested for genetic contraindications.

Polytrim can be substituted for antibacterial eye drops.        

BluTek lenses in glasses to deflect further damage to eyes from digital blue light.

My eye doctor told me my eyesight would not improve.  However my eyes did improve with patented lutein, zeaxanthin, astaxanthin, pycnogenol, resveratrol and other antioxidants including OPCs and Omega III fish oils. If I stop taking the protocol, they worsen.  I have since found clinical studies in PubMed indicating resveratrol protects the endothelial cells of the cornea.  I had been taking resveratrol for over a decade so it may have had some protective effect.

When working with health professionals ask if they know about MTHFR, genetic lifestyle screenings

and pharmacogenetics screenings.  Find the ones who know.

Eat a lot of green leafy vegetables (organic if possible).  Fluoroquinolones cause mitochondrial damage.  Dr. Terry Wahls did a TED Talk called Mind Your Mitochondria.   She talks about how she cured herself from MS, a disease that impacts mitochondria.


 For years I’ve heard health professionals and experts say food alone is all that is necessary for health.  That might have been true decades ago but it is not true now.

Industrialized farming and food practices in the US as of 2015 leave soils severely depleted of minerals – more than 85%.

Food is harvested much too soon for full maturation of the plant therefore it will be lacking in nutrients and enzymes.  Have you noticed fruits or vegetables that are hard as rocks in the grocery store?

You can watch a presentation I did for doctors on the topic here, GMO, glyphosate and surfactants, BT toxin.

You would have to eat an excess of 12 servings of organic vegetables per day to get the minimum nutrients if you have no health issues.

The MDs and other health professionals I work with who pay attention to environment and epigenetics say the environment is much more toxic now.

They say it is nearly impossible to get the nutrients you need from food in the US if you have no health conditions.

Fluoroquinolones deplete iron (and other minerals as well as magnesium, calcium and antioxidants).  Iron is already depleted in food.  The two diagrams below only go to the late 1990s.







Humans can’t make some essential nutrients.  If you can’t make them and you can’t get them from your food, and they are depleted by prescriptions, you need to supplement.  Nutrients need co-factors and enzymes and other nutrients.  Working with an expert who knows about this and ingredients that are patented and bioavailable will help.

Depending on severity of symptoms, digestive issues, etc. IV or Isotonic  antioxidants including OPCs (cross the blood brain barrier) and Glutathione, magnesium, calcium, iron, vitamin D, activated B-Complex with 5-MTHF (Quadrafolic), amino acids for collagen synthesis and repair of tendons can be put into a custom cocktail.

I bolded nutrients mentioned in clinical studies as being depleted.

Bromelain is the enemy of protein and cytokines are proteins that may be created in excess related to inflammation.  Genetic Polymorphisms like TNF and IL6 may put that person at risk for over-inflammation.

I have found digestive enzymes, probiotics and pharmaceutical grade aloe juice might heal the gut and address the depletion of good bacteria.

(Commercial brands of aloe that are carried in stores like Whole Foods are mostly water and are not pharmaceutical grade. A good aloe should say 150% concentrated aloe, should have the more toxic part of the plants removed and should have the Aloe Association Seal.)

*AVOID ALL SYNTHETIC FOLIC ACID if you have MTHFR polymorphism.

Why Intermittent Fasting May Help Pain and Fatigue

Learn more about Intermittent Fasting here.

Some of you may balk at the idea of calorie restriction when dealing with chronic fatigue, but there’s actually compelling evidence showing it can play a significant role in correcting mitochondrial function. As noted earlier, when excessive electrons are produced in the mitochondria they create highly destructive free radicals. The best way to address this is to limit excessive electron production, as if there are fewer free electrons, they’re less likely to leak out.

So how do you limit free electrons?

One of the most effective ways to do this is through calorie restriction, which in fact is a proven method to increase lifespan in mammals. Resveratrol has also been shown to activate the SIRT1 gene which is the genetic mechanism that caloric restriction is activating.

The drawback of calorie restriction is that it is enormously difficult to maintain over extended periods of time. Fortunately, research has shown that intermittent fasting effectively mimics calorie restriction, and it’s far easier to comply with, especially if you do it daily, restricting your eating to a window of about six to eight hours, where your last meal is taken at least three hours before bedtime. Ideally, aim for as much as six hours between your last meal and your scheduled bedtime.

Note on Environment

 The U.S. is still addicted to fossil fuels.  The by-product of burning coal is methyl-mercury. It is in the air, water and ground.

Senator Whitehouse of R.I. said a whale that beaches on R.I. shores is considered toxic waste.  The cod industry in New England has collapsed.  The oyster industry in Mid-Atlantic has collapsed.

Pesticides are spread like water. Bees are dying.  No bees, no food.

This topic is another book but it impacts quality of food, air and water.

 *Synthetic folic acid UMFA (unmetabolized folic acid) is being associated with MTHFR polymorphism.  People with MTHFR, 50%+ of the population should avoid UMFA.  Linked to interfering with T cells (vulnerability to cancer) and neurological problems.  The only folate that does not mask a B-12 deficiency is 5-MTHF. (Quadrafolic) Synthetic folic acid is in most fortified foods as of 11/8/2015 in the U.S.

When looking at nutraceuticals, patented, science based protocols are advised.  The manufacturer has spent millions to prove the effectiveness of their product.  Many companies use the patented clinical studies but they do not have the patented ingredient.

Problems related to fluoroquinolones were reported as early as 1980s from Europe.

The Freedom of Information Act has obtained data showing more than 50,000 reported adverse reactions and 3,000 deaths.  We know that most doctors don’t report the side effects and because of the “constellation of symptoms” most patients don’t connect the dots so the figure for adverse side effects could be in the millions.

Examples of well known fluoroquinolones are Avelox, Cipro (Bayer), and Levaquin (Johnson and Johnson).  These are not the only ones.  You have to ask.

Letter for an MD by an MD:

Dear Doctor,

As you are probably aware, the fluoroquinolone class of antibiotics is useful for certain serious infections. Unfortunately, fluoroquinolones also have a long history of serious adverse drug reactions, many of them long term . (1) As a consequence of these reactions, several of these drugs have been removed from clinical practice or their use severely restricted. Besides the severe life threatening immediate reactions, those of a more chronic nature may occur.

The spectrum of these adverse reactions is extremely broad. Patients suffering from these reactions are often misdiagnosed, referred for a psychiatric consult or even unfairly labeled as “difficult patients.”

Many physicians have not been properly educated about the severe nature of these chronic adverse reactions, some of which result in life-long disabilities. Post-marketing studies of several flouroquinolones have shown an incidence of adverse reactions much higher than were originally reported in pre-clinical studies. (1,2,3)

You are probably aware that the fluoroquinolones are eukaryotic DNA gyrase and topoisomerase inhibitors very similar to many antineoplastic agents. Because of their similar mechanisms of action, it’s no surprise that fluoroquinolones and many antineoplastic agents share similar toxicity profiles. Studies have even been conducted using fluoroquinolones to inhibit neoplastic chondrocyte growth in chondrosarcoma. (4)

There are many patients who have a syndrome of associated symptoms that include, but are not limited to: CNS agitation, depression, insomnia, new-onset anxiety and panic attacks, and even elevated intracranial pressure and visual abnormalities. They may also present with peripheral neuropathy usually of the small fiber type with temperature and pain sensory aberrations, but also often involving larger sensory and motor nerves. Spontaneous muscle activity with fasciculations, myokymia and myoclonic jerks may also occur. Many have musculoskeletal damage with degeneration of cartilage and tendons often leading to tendon rupture and severe ongoing musculoskeletal pain long after therapy has been discontinued. (1,2,3,4,5,6,7,8)

This complex symptomatology does not usually resolve after discontinuation of the inducing fluoroquinolone and may in fact worsen. Many patients go on to have disability that may persist for years. (1) Unfortunately, such patients are often seen by many physicians from multiple specialties who, given the complex symptomatology, fail to recognize a unifying diagnosis.

The mechanism of injury is not fully apparent, but several studies have been conducted and researchers have implicated the following possible mechanisms:

  1. Inhibition or disruption of the CNS GABA receptor. (9)
  2. Depletion of magnesium and disruption of cellular enzymatic function. (10)
  3. Disruption of mitochondrial function and energy production. (11,12)
  4. Oxidative injury and cellular death. (14)

This seems to be a functional disorder and structural abnormalities are not usually seen on radiological studies. (13) Patients may have abnormal EMG/NCV studies, abnormal skin punch neurologic density and morphology, abnormal vasomotor and sudomotor function on autonomic testing, and abnormal degeneration of tendons and cartilage on MRI. (13)

There may be a large number of these patients with coexisting endocrine abnormalities including: antithyroid antibodies and abnormal thyroid function, abnormal adrenal function with either hyper or hypocortisolism, hypogonadism, hypo or hyperglycemia and possibly impaired pituitary function. (13)

Most patients suffering from these side effects have a very clear onset of symptoms temporally related to a course of fluoroquinolone antibiotic. (13) They were often given the fluoroquinolone in conjunction with a corticosteroid or NSAID. Both of these classes of medications are associated with an increased incidence of adverse drug reaction from fluoroquinolones. (10,13)

As of yet no scientifically proven effective treatment is known, however patients will definitely benefit from your caring support and appropriate informed care. Of course, other diseases with similar symptoms need to be carefully ruled out.

There exists a large community of these patients who share information on the World Wide Web. Their numbers grow as the prescription of fluoroquinolones increases. Many of these patients are professionals like myself who have been affected by these drugs. Thank you for your time and consideration.

Todd R. Plumb MD


  1. Cohen JS; Peripheral Neuropathy Associated With Fluoroquinolones
    Annals of Pharmacotherapy. 2001;35(12):1540-1547
  2. Francesca Lunzer Kritz; New Cipro, Same Side Effects, Washington Post, December 24, 2002.
  3. Shepard CW et al; Antimicrobial Postexposure Prophylaxis for Anthrax: Adverse Events and Adherence Emerging Infectious Diseases ¡E Vol. 8, No. 10, October 2002
  4. Fox EJ et al; The effects of ciprofloxacin and paclitaxel on metastatic and recurrent chondrosarcoma COMMUNITY ONCOLOGY ¡½ November/December 2005
  5. Physisicans Desk Referfence 2006
  6. de Bazignan DA etal; Psychiatric adverse effects of fluoroquinolone: review of cases from the French pharmacologic surveillance database[Article in French] Rev Med Interne. 2006 Jun;27(6):448-52. Epub 2006 Mar 9
  7. FDA Medical Bulletin * October 1996 * Volume 26 Number 3
  8. Saint F. etal; Tendinopathy associated with fluoroquinolones: individuals at risk, incriminated physiopathologic mechanisms, therapeutic management [Article in French]
    Prog Urol. 2001 Dec;11(6):1331-4.

  9. De Sano A. etal; Adverse Reactions to Fluoroquinolones. An Overview on Mechanistic Aspects Current Medicinal Chemistry 2001, 8, 371-384 371
  10. Stahlmann R. etal; Effects of magnesium deficiency on joint cartilage in immature Beagle dogsimmunohistochemistry, electron microscopy, and mineral concentrations, Archives of Toxicology. Jan. 2000 73(11,12)
  11. Hayem G. Cytofluorometric analysis of chondrotoxicity of fluoroquinolone antimicrobial agents. Antimicrob Agents Chemother. 1994 Feb;38(2):243- 7.
  12. Kozie[lstrok]; Ciprofloxacin reduces mitochondrial potential and inhibits calcium entry into Jurkat cells
    R European Journal of Biochemistry 2003; 1 Supplement 1 July: Abstract number: P4.8-33., Zab[lstrok]ocki K., Szczepanowska
  13. http://health.groups.yahoo.com/group/quinolones/
  14. Simonin MA etal. Pefloxacin-Induced Achilles Tendon Toxicity in Rodents: Biochemical Changes in Proteoglycan Synthesis and Oxidative Damage to CollagenAntimicrobial Agents and Chemotherapy, April 2000, p. 867-872, Vol. 44, No. 4

Note to readers: The purpose of this E-Letter is solely informational and educational. The information herein should not be considered to be a substitute for the direct medical advice of your doctor, nor is it meant to encourage the diagnosis or treatment of any illness, disease, or other medical problem by laypersons. If you are under a physician’s care for any condition, he or she can advise you whether the information in this E-Letter is suitable for you. Readers should not make any changes in drugs, doses, or any other aspects of their medical treatment unless specifically directed to do so by their own doctors.

There are more updated links like the ones below here.

FDA November 4th, 2015

Suzy Cohen


Musculoskeletal problems

​​Mitochondrial Dysfunction

Increased Oxidative Stress

NY Times


DNA Adduction

2015  Fluoroquinolones, serious side effects

2015  Fluoroquinolones in drinking water

2015  Fluoroquinolones ubiquitous surface waters, waste waters

2015  FQs Ecotoxilogical effects aquatic organisms

2015  Fluoroquinolones and Corneal Fibroblast Motility

2015  Cipro and gluteal tendinopathy

2015  FQs and Neurological Toxicity

2015  FQs Increased Oxidative Stress

Kathy O’Donnell Kaufman put some documents together and continues to update.

 Some of the links are from www.pubmed.com. The FDA has not evaluated any of the information I put together. I, alone, am solely responsible for it.  Kathy.od (skype) kathy@criticalhealth.org.  It is as science based as I can make it with the assistance of scientists and health professionals.

I am in the U.S. where the environment is worse therefore more toxic and epigenetics are affected. Many MDs I know agree the most dangerous thing in America is an empty hospital bed.

How We Can Halt the Cipro_Levaquin Catastrophe