April 2014

Cipro, Levaquin and Avelox are Chemo Drugs

Published on
21141 views
Lisa Bloomquist

When I first heard people referring to fluoroquinolone antibiotics (Cipro, Levaquin, Avelox, Floxin and a few others) as “chemotherapy drugs,” I thought that they were exaggerating or incorrect.  After all, fluoroquinolones are used to treat urinary tract infections, traveler’s diarrhea, anthrax, and other bacterial infections, not cancer. But then I started to do some research into how fluoroquinolones work and I discovered that they cause mitochondrial damage, which leads to oxidative stress and cell death (1, 2), they interfere with the DNA replication process of mitochondria (3), they disrupt tubulin assembly (4) and that they are being investigated for their tumor killing abilities (5, 6).  I also found that all other drugs that have the same mechanism for action as fluoroquinolones – topoisomerase interrupters (FDA warning label, 7) (topoisomerases are necessary for proper DNA replication) – are used as chemotherapy drugs – topotecan, amsacrine, etoposide, etc.  Fluoroquinolones are, truly, chemotherapy drugs – they just happen to be used as popular antibiotics. They can kill cancerous tumor cells because, in addition to killing bacterial cells, they also kill eukaryotic cells (8, 9).

Use of Fluoroquinolones for Cancer Treatment is Appropriate

There are almost certainly some legitimate and reasonable uses for fluoroquinolones as chemotherapy drugs (10).  As tumor killing agents, they may save lives of those with cancer.  Unfortunately, they’re not as targeted as the chemotherapy drugs that are currently in use.  Many chemotherapy drugs on the market specifically target quickly dividing cells – like tumor and hair cells; so they kill the cancer cells while leaving most other cells intact. Fluoroquinolones aren’t that precise. They indiscriminately kill cells throughout the body – including neurons and lymphocytes (11) (immune system cells).  The mitochondrial DNA (mtDNA) replication process is disrupted by fluoroquinolones (3), and the disruption of that process leads to mitochondrial damage, oxidative stress and cell death (12).  Fluoroquinolones are effective cell killers, but because they are indiscriminate cell killers, they are a step backward in chemotherapy drug technology.

Lousy Chemo Drugs?  Let’s Use Them as Antibiotics for Everyone!

Because they are not particularly good chemotherapy drugs, fluoroquinolones are rarely used for the purpose of killing cancer cells.  Instead, they are used as antibiotics. They are prescribed to treat sinus infections, bladder infections, strep throat, and they are even prescribed prophylactically (typically for future treatment of travelers’ diarrhea) when no infection is present. They kill bacteria, and are effective antibiotics, but they also damage mitochondria and destroy cells and therefore have many of the same side-effects as chemotherapy drugs, because, as noted above, they are chemotherapy drugs.

Side-Effects of Fluoroquinolones, and Other Chemotherapy Drugs

Some of the side-effects that fluoroquinolones share with chemotherapy drugs are (13, 14, 15, 16 and the FDA warning label for Ciprofloxacin – the warning labels for Levofloxacin and the other fluoroquinolones are similar):

  • Exhaustion / Loss of energy / Fatigue
  • Brain-fog / Loss of cognitive abilities
  • Anemia
  • Muscle Loss / Wasting
  • Neuropathy / Peripheral Neuropathy / Fibromyalgia

Additionally, Fluoroquinolones destroy connective tissue, especially tendons.  (17, 18, 19)

When one thinks of fluoroquinolones as chemotherapy drugs as opposed to antibiotics (yes, they do kill bacteria, but they should not be thought of in the same terms as benign drugs like penicillin and cephalosporins), many aspects of adverse reactions to fluoroquinolones make sense. Like several other chemotherapy drugs, there is a tolerance threshold (and/or lifetime limit) for fluoroquinolones (20, 21). Many people don’t react to their first dose of a fluoroquinolone. Rather, they tolerate the drugs up to a point – then they can no longer tolerate them and Fluoroquinolone Toxicity results. For fluoroquinolones, and possibly for other chemotherapy drugs, this tolerance threshold issue is because mitochondria are able to withstand a certain amount of damage before a disease state ensues. It is only after the tolerance threshold for damage is crossed that mitochondria stop adapting to harmful stimuli and a disease state ensues. (22)

Cellular Damage from Chemo Drugs can Lead to Cancer – Isn’t that Ironic?

Destruction of mitochondrial DNA can result in mitochondrial dysfunction and oxidative stress – which lead to apoptosis and necrosis of cells (23). When this occurs, a multi-symptom, chronic, autoimmune-disease-like reactions can occur (24, 25). However, if cell damage occurs but the cell does not die, but rather replicates the DNA errors, cancer can result (26, 27, 12).

Additionally, drugs that inhibit CYP450 liver enzymes [Cytochrome P450 enzymes metabolize xenobiotics and foreign chemicals from the body. (28)] leave people more susceptible to cancer-causing pathogens (29). Fluoroquinolones inhibit multiple CYP450 enzymes (30, FDA warning label). How ironic, isn’t it? Cancer can result from chemotherapy drugs. And when it is understood that fluoroquinolones are chemotherapy drugs that damage mtDNA and cause oxidative stress and apoptosis/necrosis, the irony of chemotherapeutic drugs causing cancer becomes horrifying, as opposed to thought-provoking.

Cellular Harm Results from Willful Ignorance About the Effects of Fluoroquinolones

There are articles that say that fluoroquinolones have an excellent safety record. (31)  None of those articles look at the effects of these drugs on the mitochondria – the depletion of mtDNA, the oxidative stress that results from damaged mitochondria, the DNA damage that is caused by the oxidative stress, etc.  In not looking at mitochondria, those articles are looking at the wrong things and they in no way negate the findings of the articles that note the deleterious effects of fluoroquinolones on human cells.

While it may be appropriate to give drugs that disrupt the process of mitochondrial DNA replication, have horrific side-effects and cause indiscriminate cell death, to people who are have cancer, it is absurd to give them to people who are healthy other than a minor infection. Even for major, difficult to treat infections, fluoroquinolones should be the drugs of last resort because of their effects on mitochondria. (1, 32)  Chemotherapy drugs should be used exclusively in life-or-death situations. They should not be used frivolously or without true informed consent of the patient, or without awareness of the consequences of the drug on the part of both the physician and the patient. Protocols should be in place for ensuring that they are used appropriately and that all parties are aware of the consequences of the drugs.

Sadly, appropriate informed consent around fluoroquinolones involves a complete shift in how physicians and patients alike think about them. In order for the risks of taking fluoroquinolones to be properly acknowledged, all parties involved need to see, and acknowledge, that fluoroquinolones are chemotherapeutic drugs that cause mitochondrial destruction and cell death, and that they should not be used lightly. But because fluoroquinolones have been given out frivolously – 26.9 million prescriptions for oral and IV fluoroquinolones were given out in 2011 alone (33) for simple infections, I don’t foresee the shift in how they are perceived as an easy one. It must involve many doctors admitting that they have been prescribing these drugs incorrectly for decades, that they have been wrong about the severity of adverse effects, and that they have been misled about the risks of fluoroquinolones.

The Effects of Drugs on Mitochondria are Systematically Disregarded

It should also be noted that the effects of drugs on mitochondria are systematically disregarded. Mitochondrial function, and drug-induced dysfunction, is important to all areas of human health.  An article published in Molecular Nutrition and Food Research entitled “Medication Induced Mitochondrial Damage and Disease” noted that the effects of drugs on mitochondria are ignored by both the drug companies and the FDA when reviewing drug safety. Because of this omission in review and oversight, human mitochondrial DNA have been repeatedly damaged by fluoroquinolones and other pharmaceuticals. The consequences of this are, as of yet, unknown. (Though it should be noted that mitochondria and the signals that they produce influence gene expression (35) and that an article published in Nature in July, 2013 entitled “Topoisomerases Facilitate Transcription of Long Genes Linked to Autism” showed that topoisomerase interrupting chemotherapy drugs effect the expression of genes linked to Autism.) We can only hope that the FDA’s failure to force drug reviewers to look at the effects of drugs on mitochondrial DNA isn’t horribly consequential.

Sources:

  1. Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells”
  2. British Journal of Cancer, “Ciprofloxacin Induces Apoptosis and Inhibits Proliferation of Human Colorectal Carcinoma Cells”
  3. Molecular Pharmacology, “Delayed Cytotoxicity and Cleavage of Mitochondrial DNA in Ciprofloxacin Treated Mammalian Cells”
  4. Current Medicinal Chemistry, “Recent Advances in the Discovery and Development of Quinolones and Analogs as Antitumor Agents”
  5. Inorganic Chemistry, “New uses for old drugs: attempts to convert quinolone antibacterials into potential anticancer agents containing ruthenium”
  6. Asian Pacific Journal of Cancer Prevention, “Comparative Evaluation of Antiproliferative Activity and Induction of Apoptosis by some Fluoroquinolones with a Human Non-small Cell Lung Cancer Cell Line in Culture”
  7. Mutation Research, “Ciprofloxacin:  Mammalian DNA Topoisomerase Type II Poison In Vivo”
  8. The Journal of Biological Chemistry, “Cytotoxicity of Quinolones toward Eukaryotic Cells:  Identification of Topoisomerase II as the Primary Cellular Target for the Quinolone CP-115,953 in Yeast”
  9. Antimicrobial Agents and Chemotherapy, “Effects of Novel Fluoroquinolones on the Catalytic Activities of Eukaryotic Topoisomerase II:  Influence of the C-8 Fluorine Group”
  10. Urology, “Quinolone antibiotics: a potential adjunct to intravesical chemotherapy for bladder cancer”
  11. Nepal Medical College Journal, “Genotoxic and cytotoxic effects of antibacterial drug, ciprofloxacin, on human lymphocytes in vitro”
  12. Toxicology and Applied Pharmacology, “Mitochondrial abnormalities–a link to idiosyncratic drug hepatotoxicity?”
  13. National Cancer Institute, “Chemotherapy Side Effects Sheets”
  14. The Annals of Pharmacotherapy, “Peripheral Neuropathy Associated with Fluoroquinolones”
  15. Indian Journal of Psychiatry, “Levofloxacin Induced Acute Psychosis”
  16. Journal of Antimicrobial Chemotherapy, “Peripheral Sensory Disturbances Related to Treatment with Fluoroquinolones”
  17. The American Journal of Sports Medicine, “The Effect of Ciprofloxacin on Tendon, Paratenon, and Capsular Fibroblast Metabolism”
  18. Physical Medicine and Rehabilitation (PM & R) “Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population”
  19. Laboratorie de Toxicologie, “In Vitro Discrimination of Fluoroquinolones Toxicity on Tendon Cells:  Involvement of Oxidative Stress”
  20. Carcinogenesis, “Mechanisms of tolerance to DNA damaging therapeutic drugs”
  21. Non-Hodgekin’s Lymphoma Cyberfamily
  22. Molecular Interventions, “Mechanisms of Pathogenesis in Drug Hepatoxicity Putting the Stress on Mitochondria”
  23. Toxicology and Applied Pharmacology, “Mitochondrial abnormalities–a link to idiosyncratic drug hepatotoxicity?”
  24. Cleveland Clinic Journal of Medicine, “Mitochondrial cytopathy in adults: What we know so far”
  25. Antimicrobial Agents and Chemotherapy, “Ciprofloxacin Induces an Immunomodulatory Stress Response in Human T Lymphocytes”
  26. Scitable by Nature Education, “DNA Replication and Causes of Mutation”
  27. British Journal of Haematology, “Topoisomerase II Inhibitor Related Acute Myeloid Leukaemia”
  28. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, “Role of cytochromes P450 in chemical toxicity and oxidative stress: studies with CYP2E1”
  29. Europe Pubmed Central, “Role of cytochromes P450 in drug metabolism and hepatotoxicity.”
  30. Pharmacy Times, “Get to Know an Enzyme: CYP1A2”
  31. Expert Reviews, “Levofloxacin: update and perspectives on one of the original ‘respiratory quinolones’”
  32. Journal of Young Pharmacists, “Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients”
  33. FDA Drug Safety Communications, “FDA Drug Safety Communication: FDA requires label changes to warn of risk for possibly permanent nerve damage from antibacterial fluoroquinolone drugs taken by mouth or by injection”
  34. Molecular Nutrition and Food Research, “Medication Induced Mitochondrial Damage and Disease”
  35. BBA, “Mitochondrial DNA Damage and its Consequences for Mitochondrial Gene Expression”
  36. Nature, “Topoisomerases Facilitate Transcription of Long Genes Linked to Autism”

 

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us – Buy an Unsubscription.

Related posts:

Cipro flagyl toxicity jiu jitsu athleteCipro and Flagyl Neurotoxicity in Brazilian Jiu Jitsu Athlete beyond the ER with FQWhen Investigating Fluoroquinolone Reactions, Move Beyond the ER

You might be interested in

Pap Smears Saved my Life: Cervical Cancer After Gardasil

Published on
5709 views
pap smears saved my life

I went to the doctor in early January 2008 and during the consultation was asked if I’d had my Gardasil shot. There was no discussion about possible side effects and I was urged to have it while it was still free. So I had the first shot then, just before my 26th birthday. I had the second shot at the end of February.

I was healthy, fit and enjoying life.  I was working in retail and there was talk of promotion and management training.  My long term plans included a career change so I was training at the gym regularly to get my fitness level up. I passed a thorough preliminary medical examination in early May.

A Delayed Reaction to Gardasil?

In mid-May, I broke out in a rash. Originally I thought it might have been bed bugs or a reaction to laundry powder but it persisted and the doctor thought it was an allergy of some sort. I was put on antihistamines but the rash continued. One day my eyelid was swollen. Another day my lip swelled up. It seemed random and puzzling.

In June, I had my third Gardasil shot and then things really started to rev up with the symptoms escalating in frequency and severity.

It was then, that I started keeping a health diary to track what I was eating, what medication I was on, and what symptoms I was experiencing. After a few weeks I realised that it was not related to what I was eating, so just recorded medication and symptoms being experienced.

By July, the rash was all over my torso, legs, and arms and my face. It would sometimes come up in great welts. One night my thighs were blood red and so itchy I thought I’d go mad. One day I woke up and my entire face was so swollen, I looked like I’d been beaten up and I could barely recognise myself. My hands and feet would swell up and be so painful I could barely walk. My wrists and ankles ached and I had trouble sleeping because every time I moved I was in pain. I had strange bald patches on my tongue.

A Post Gardasil Inflammatory Condition

I had so many blood tests I felt like a pin cushion. In early July the doctor rang back to say my recent blood tests showed elevated CRP levels (an inflammatory indicator). I went back for weekly blood test, and the CRP levels continued to be elevated and rising higher each week. Up until then I had been seeing different doctors at different clinics so my mum suggested I see her doctor, Dr R, so there was some overview perspective.

By this stage I had taken so much time off work that I ran out of sick leave and went onto sickness benefits.

Dr R tried to get me an appointment with an Allergist but the waiting time was 10-12 weeks, and I was put on the cancellation list. In the mean time I went gluten-free and cut down on processed foods. Nothing worked.

Idiopathic Urticaria and Angioedema

On the 24th July my tongue started to swell. My mum drove me to the Emergency Department of The Alfred Hospital. I thought it will be just like on ‘House’ or ‘All Saints’ and the doctors will solve the riddle, provide a diagnosis and cure me. But no such luck.  I was told I had “idiopathic urticaria / angioedema”.  They couldn’t say what caused it and all they could do was try to control the symptoms. After spending hours there I was eventually sent home with a script for high dosage antihistamines – I was on 2 x 24 hr strength tablets twice a day.  One thing I learnt was that I was meant to be taking 2 different types of antihistamine, R1 and R2, for the urticaria.

The doctors assured me this would control my symptoms. It didn’t.

Connective Tissue Involvement

I managed to get an appointment at short notice – there had been a cancellation- to see Dr S, a Specialist Physician (specialising in diagnosis), on 25th July. He took thorough notes of my history and symptoms. He said clinically it looked like connective tissue involvement suggestive of rheumatoid arthritis or a lupus-type condition. He ordered more blood tests, including a specific one for lupus. He also said not to worry too much as clinicians had recently being seeing patients presenting with what they were calling ‘pseudo lupus syndrome’.  Could these pseudo lupus syndromes be related to the Gardasil vaccine or other medication reactions? I wonder.

Swollen Tongue

On 14th August, exactly three weeks after my previous visit, I was back at the Alfred Hospital Emergency Department. Three weeks of the treatment had not controlled the symptoms, but had left me physically weaker – I was nauseous, tired from lack of sleep and in pain. I went to the Emergency Department at 10.15 pm as the back of my tongue was swollen and there was a strange feeling in my throat. I felt like I had a large bubble in my throat and it was difficult to swallow. The Alfred Hospital staff were spectacularly unhelpful – I was told to report back to the desk if unable to breathe. Over the next hours the swelling seemed to stabilise in that it wasn’t getting worse. I left The Alfred at 12.30am having not been seen and I got home at 2.30am.  At about 6.30am the swelling suddenly started to increase and I had difficulty in swallowing. My mum came and collected me and we went straight to see Dr R. She said in over 30 years of practice she had never seen or heard of anything like it. I was put back onto cortisone.

On 20th August I had my revisit with Dr S. The blood test for Lupus was negative, so I was one of the ‘pseudo lupus syndrome’ patients. He recommended I see a Rheumatologist rather than an Allergist or Dermatologist. He said that, in Melbourne, Immunologists tended to be research rather than clinical, and that Rheumatologists were the autoimmune specialists. So, onto another waiting list to see a yet another specialist – an appointment was made with Dr A for 9th September.

On the 2nd September I finally got to see an Allergist. He recommended a very restricted “elimination diet” which, by that stage, I didn’t have the energy or inclination to follow.  I had worked out weeks earlier that the swellings were not related to what I was eating. However, I did buy some allergy free soap, toothpaste and shampoo. And he provided a list of foods/drinks to avoid because of preservatives.

A Heart Murmur

On the 9th September I saw the Rheumatologist Dr A. Like Dr S she took a comprehensive history. She ordered an extensive battery of blood tests – for HIV, Barmah forest virus, Ross river virus etc. On examining me she detected a heart murmur and ordered a chest CT scan and echo cardiogram. One thing I was sure about was that I had no heart murmur when I passed the comprehensive medical back in May.

Still No Answers

It was the same old story: Dr. A as a Rheumatologist was a connective tissue specialist, not an autoimmune specialist. She suggested seeing a clinical Immunologist, Professor H, and appointment was arranged for 13th October.

So I spent months on high-dose antihistamines and intermittent short courses of cortisone. The cortisone initially controlled the rash, but as soon as I stopped the treatment the rash came back. Eventually the rash appeared even when I was on cortisone. So the recommended treatment didn’t work.  What was worse was that the doctors seemed mystified and perplexed by my multitude of symptoms.

By this stage, based on my diary, I was seeing some emerging patterns: The symptoms appeared more severe around the time I got my period; and also after exercise, if I went to the gym or personal training.  I also had the feeling that the antihistamines may have been actually exacerbating the symptoms, particularly the swellings. The most striking instance occurred on the evening of 14th August within 15 minutes of taking the histamines, my lip suddenly started swelling up and then the swelling progressed to my tongue and throat.

Unstable Mast Cells

A breakthrough of sorts came when a colleague gave Dr R an information sheet about Ketotifen – a mast cell stabiliser – that seemed to explain and (hopefully) treat my symptoms.

Apparently people with chronic urticaria and angioedema do not suffer from specific allergies, but rather an unstable mast cell system. According to the fact sheet, the unstable mast cells leak histamine, prostaglandins and leukotrienes, which result in other associated symptoms, such as headaches, tiredness, lethargy, irritability and difficulty in concentration. It can also affect the gastrointestinal tract causing cramping, bloating, indigestion, regurgitation, flatulence, intermittent diarrhoea and constipation. Many patients suffer from joint pains and muscle pain. These symptoms are due to the inflammatory properties of leaked histamines, prostaglandins and leukotrienes. I was unable to see the doctor who wrote the information sheet, as he only saw asthma patients.

Also, Ketotifen was not available in tablet form in Australia and we had to send to New Zealand for it. Ketotifen is only available in Australia as eye drops. A friend sent me an advertising leaflet for Zaditen “the only triple action, anti-allergy eye drops for symptomatic short term treatment of seasonal allergic conjunctivitis available over the counter without prescription.”  Strangely, it was titled Zoe’s Dilemma and featured a cartoon of teary-eyed Zoe “I’ve got minutes to pull myself together!” being ZAPPED with Zaditen by a handsome young white-coated healthcare professional, saying “Only I can give you a quick solution”.

By the time we sent to New Zealand, received the tablets and found a doctor willing to oversee it, I didn’t start the Ketotifen until September. Gradually the swellings became less frequent. The rash remained but became more “normal”.

Back to Urticaria

When I saw the Clinical Immunologist, Professor H, on 13th  October he was the first health professional I’d seen that wasn’t mystified by my many and varied symptoms. He diagnosed severe chronic urticaria and, when shown my photos, said they were classic of severe urticaria. In terms of severity, my condition was in the top 5% he had seen.

He went on to explain that an unstable mast cell system was the basis of all autoimmune conditions. Researchers were just starting to unravel how the immune system works, particularly autoimmunity. He said that researchers had recently discovered that unstable mast cells leaked many chemicals, much more than previously thought (i.e. many more than mentioned in the Ketotifen information sheet). He was currently supervising a PhD student researching this topic.

I queried how it was strange I should, within a two month period, be so badly affected -particularly as I had been so fit before. Professor H said that, for some reason, the fittest people were often the most severely affected by autoimmune disease. It was as if their immune systems were also super fit, and turned in on the body with extra zeal. He also said that there was evidence in support of my intuitions – that symptoms were often worse after exercise; and, for women, worse around the time of menstruation.

The only recommended treatment was a long-term course of high dose cortisone. He explained that long-term cortisone use had some nasty side effects. Although he couldn’t guarantee it, he was confident  that the treatment would get rid of the rash. He couldn’t say how long I would have to stay on cortisone. I was to think about the pros and cons of this, and decide whether to start the cortisone when I came to my next appointment in December.

Alternative Therapies

On 28th November I consulted a Traditional Chinese Medicine practitioner, Dr Z. He was the first health practitioner I had seen who was confident that the rash could be treated successfully. He said there were acupuncture and Chinese herbs specifically for it. I had the treatment and the rash disappeared.

I don’t know whether it was the acupuncture or a combination of acupuncture and the Ketotifen, but something finally worked. I was still having intermittent swellings, but at least the rash was gone.

When I revisited Professor H on 2nd December, the rash was gone. I decided to stick with the Ketotifen for another 4 months as recommended on the information sheet.

I did remain rash free taking just the Ketotifen, and then remained rash free when I stopped it in March 2009.

The whole experience left me exhausted, I felt as if my life had been put on hold for months. I had to take time off work and could only work part time after that. Not only did it cost me a lot financially in terms of being off work, I had to spend a fortune on antihistamines, Ketotifen, painkillers, indigestion tablets, and assorted other drugs.

In March 2009, just after finishing the Ketotifen and possibly as a result of all I’d been through, I experience for the first time ever an episode of acute anxiety and panic attacks for which I had treatment and counseling.

And Now Cervical Cancer

The biggest shock occurred in March 2011 when I went for my regular pap smear and was diagnosed and treated for cervical adenocarcinoma in situ (AIS). This was 17 months after my previously normal Pap smear, and three years after the first Gardasil shot. All of my previous pap smears had been clean.

I went for my regular pap smear with Dr P. early March 2011. A week later he rang me to say the report was showing glandular-cell abnormalities and I was to come in the following Tuesday for an assessment. [There are two main types of cervical cancer: the more common squamous-cell abnormalities and cancer (squamous carcinoma); and the rare but more aggressive glandular-cell abnormalities and cancer (adenocarcinoma)].

The following Friday I was in surgery and had a cold knife cone biopsy. The results came through the following Wednesday that the margins of the cone biopsy were clear.

I am very aware that I was fortunate – having my screening with a specialist colposcopist and having the surgical procedure within 10 days of the results being received. As a result of this, the cancer was detected early, at the in situ stage.

I have to have a follow-up screening every 6 months to make sure the cancer doesn’t return, and so far so good. I’m reassured that I’m having reliable and expert follow-up

So not only did I experience severe adverse reactions to the vaccine, it is obvious that Gardasil does not even protect against the serious cervical cancer: glandular cell cervical cancer. As AIS is thought to be caused by HPV 16 and 18, the exact viruses the Gardasil vaccine is supposed to protect against. Since I didn’t have the either HPV or cancer a mere 17 months prior to my vaccination, I have to wonder whether the Gardasil vaccine introduced the virus and the cancer into my system.

Recurrence of Urticaria and Angioedema

In June 2011, maybe as a result of stress, I had a recurrence of the urticaria/angioedema, including swelling of my tongue and throat. This time I was touring around Cornwell, UK so it was a little scary not knowing where to locate the local doctor or hospital.

When I saw Professor H a couple of months later, he said researchers in Australia had now developed a new version of the mast-cell stabiliser. It was being trialled with impressive results and they were trying to get the government to approve its use in Australia.  He suggested that, as the Ketotifen had worked for me before, I go back onto it. When I eventually got the capsules for New Zealand and started taking them, the symptoms gradually subsided.

When I was telling Professor H. about being in Cornwell at the time of the recurrence, he said “Just as well your tongue didn’t start to swell.” On hearing that I’d had episodes of my tongue and throat swelling both recently and in 2008, he immediately wrote out a script for an epi-pen and told me to carry it at all times. As my mum later commented, it would have been helpful to know this three years earlier in 2008.

Six Years Post Gardasil

So how am I, six years on? I am still struggling with the aftermaths of Gardasil.

Although the urticaria / angioedema haven’t reoccurred for 3 years, I am struggling with an “invisible” legacy of insomnia and fatigue.

My sleep pattern is extremely disrupted. I have had a problem with insomnia since a teenager but, post-Gardasil, this became much more severe. I have been experiencing the strange situation of having no energy, being extremely fatigued, and yet I can’t get to sleep.

In 2010, I made the decision to return to study and relocated to Geelong (about an hour away from Melbourne) to attend Deakin University.  Distance, work and university commitments made it impossible to have consistent follow-up treatment with Dr Z.  TCM seems the best prospect to help with my sleep/energy problems, but unfortunately wasn’t an option for me at the time. I didn’t have the energy to go another round of finding local doctors, explaining symptoms, having more blood test, etc. So I battled on as best I could – herbal tea, Valerian, prescription sleeping tablets – nothing worked.

After the 2011, recurrence of symptoms my sleep patterns were even more disrupted. Early in 2012, I saw Dr M., a sleep specialist, and did a sleep test. I was awake all night and was officially diagnosed with sleep narcolepsy – falling asleep during the day due to exhaustion from insomnia.

A more visible legacy of Gardasil has been with my skin. Post-Gardasil my skin has been shocking with acne much worse than I’ve ever experienced, even when I was a teenager.

On reading Gabriella’s story I realise that maybe I can finally find some answers to regaining my health… it’s just a matter of knowing where to start and who to see.

However, the main message I want to get out to other Gardasil women – and all young women – is the need for annual pap smears. Dr P, who diagnosed and treated me for cervical adenocarcinoma, says there has been an increase in the number of young women developing this type of cancer, and that annual Pap smears are essential to monitor for it. Again, I have to wonder if the Gardasil vaccine and the increase in cervical cancers in young women are connected.

Pap smears saved my life, not bloody Gardasil.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by manseok Kim from Pixabay

Related posts:

My Decade of 24/7 Depression Metronidazole toxicity and doctor denialMetronidazole Toxicity and Doctor Denial hormones gut bacteriaHormones, Gut Bacteria, and Autoimmune Disease

You might be interested in

Testing for Cerebral Mitochondrial Dysfunction Post Medication or Vaccine Induced Damage

Published on
3772 views
Chander Marrs

Over the last several weeks I have been the beneficiary of a fair amount of synchronicity; seemingly random introductions to interesting people and research connections from disparate sources. Not the least of which was a recent introduction to the concept of lactate doublets. What the heck are lactate doublets?  I had no idea and I am certain most of you reading this do not know either. Well, it turns out lactate doublets may be a missing piece in the diagnostic puzzles that present post medication and vaccine adverse reactions. Let me explain, but first a bit of background.

Mitochondrial Dysfunction

If you’ve followed Hormones Matter for any length of time, you know that we cover complicated diseases and medication and vaccine reactions. Inevitably, these reactions include neurological and neuromuscular symptoms that, almost to tee, fail to show up on standard diagnostic testing. This is particularly troubling when the symptoms include seizures, migraines, tremors, ataxias, neuropathies, dysautonomias and other obvious signs of nervous system damage.

We’ve attributed many of these cases to mitochondrial damage and subsequent dysfunction but testing for damage has proved problematic in most cases. While genetic disorders of mitochondrial dysfunction are reasonably well documented, the more dynamic, environmental and even epigenetic functional changes suspected in toxin, medication or vaccine induced mitochondrial disease are neither well documented nor easily recognized. With no easy testing, folks whose mitochondria are functionally or operational deficient, suffer needlessly and chronically. So when I read the report about lactate doublets as evidence of mitochondrial dysfunction in autism, I was intrigued. And, since I had just attended a talk on the mechanics of measuring basal metabolic rate as indicator of mitochondrial respiration e.g. mitochondrial functioning, I was doubly intrigued.  Could we use these measures as pre-screening tools for mitochondrial damage in health and disease? After all, what could be more fundamental to overall health and cellular energetics than aerobic and anaerobic metabolism? Identify problems with energy metabolism and there’s a good chance something is hinky in mitochondria land.

The Wonders of Lactate

For those of you who are athletes, lactic acid and lactate are familiar topics. For those who are not athletes, consider the last time you exercised rigorously and that point at which the demand for oxygen and fuel for your muscles out-paced your body’s ability to adapt and provide that fuel. What happened? Your muscles began to fatigue, you slowed down, you may have begun to hyperventilate and eventually you hit the wall, exhausted.

If you’re an athlete, a large part of your training involves moving that exhaustion threshold, that wall, further and further away. You train to increase muscle strength – anaerobic capacity, cardiopulmonary functioning- aerobic capacity and the tolerance for pain. Lactate production and utilization is the key to training and athletic success. In the common vernacular, lactate is incorrectly referred to as lactic acid. They are two different molecules. Lactic acid is precursor to lactate and lactate is both a substrate and a product of anaerobic metabolism. Lactate is currency for energy metabolism between cells, tissues and organs. The point at which lactate production outstrips its utilization as fuel or energy is one of the first steps of fatigue in healthy, athletic individuals. In not so healthy individuals and many disease processes, excess lactate can be a marker for mitochondrial dysfunction. In not so healthy individuals where the mitochondria are functioning sub-optimally, that feeling of hitting the exercise wall, is continuous with normal activity.

Lactate and Mitochondria

Over the last several months we’ve discussed mitochondrial ATP production on a number of occasions, mostly in relation to the aerobic process of the energy production that converts glucose (sugars) to adenosine triphosphate (ATP), the cellular energy that fuels our existence. This process requires large amounts of oxygen and numerous chemical co-factors, thiamine being one of the more major among them. Diminish oxygen levels or one of the necessary co-factors and energy/ATP production is reduced.

Not to worry yet, we have a backup or secondary ATP production cycle involving lactate. Here glucose is converted to compound called pyruvate which then is either shuttled into the mitochondria to produce ATP or it remains in either the extracellular or  intracellular cytosolic (cell fluid) space and is converted to lactic acid and then to lactate. The pyruvate>lactate path is anaerobic. That is, it does not require oxygen. The heart, kidneys and liver prefer lactate for fuel and rely heavily on anaerobic metabolism. In our exercise model, anaerobic metabolism and increasing lactate production parallel increasing exercise intensity, though it is less efficient. In comparison to aerobic metabolism that produces 38 mol of ATP, the anaerobic pyruvate>lactate path produces only 2 mol ATP.

The connection between lactate and mitochondrial functioning was only recently discovered and remains hotly debated. For a long time, it was believed that lactate remained outside the mitochondrion. Now, evidence suggests that mitochondria can convert lactate to ATP and that lactate is shuttled in and out of mitochondria to be used when needed. Based upon this possibility, measuring lactate either alone or in combination with respirometry measures may provide an indirect marker of mitochondrial functioning. Here’s where it gets interesting.

Body and Brain Lactate

Lactate is a fuel used readily in the body. Lactate levels change relative to metabolic needs (exertion and stressors) and efficiencies (oxygen usage, co-factor availability). Exercise physiologist have been measuring lactate and other indicators of metabolic functioning and path (aerobic versus anaerobic) for decades using a variety of respirometry tools, from breathing apparatus to blood tests and tissue biopsies. In a grossly oversimplified manner, the extent to which one produces and utilizes lactate during training indicates one’s overall fitness. Could we use some of those same tools, the less invasive ones, to provide a broad indicator of mitochondrial health?  Yes, we can.

Indeed, those same aerobic/anaerobic processes that occur in our body occur in the brain. Even though the brain is a huge consumer of glucose as its preferred fuel, recent evidence suggests that it also produces and consumes lactate in parallel to the body during exercise and other stressors. Beyond just the production of lactate in brain trauma, where oxygen and glucose are depleted rapidly and chronically, brain lactate levels appear to correspond with shifts in aerobic/anaerobic metabolism.

My thought, and what began this entire adventure, couldn’t measures of aerobic/anaerobic metabolism be adapted to compare healthy mitochondrial functioning versus non-healthy mitochondrial functioning? Wouldn’t a skew towards anaerobic metabolism and excess lactate, especially during rest and low exertion, indicate, at least broadly, mitochondrial damage?  The answer is yes; measures of respirometry, along with body and brain lactate could broadly indicate mitochondrial functioning.

But wait, there’s more. Instead of tissue biopsies, and perhaps even instead of the blood tests, researchers have figured out how to image lactate metabolism within the brain and presumably the body. Enter the lactate doublet.

Imaging Lactate with Magnetic Resonance Spectroscopy

Magnetic resonance spectroscopy (MRS) is like a magnetic resonance imaging (MRI) except that instead of simply taking pictures of the tissue, through a myriad of complicated calculations, the MRS measures the relative concentrations of specific metabolites in the brain and other tissues. The MRS can measure lactate metabolism in the brain and researchers around the world have begun to look at brain lactate as markers of different disease process, like autism, aging and brain injury. It is not without technical difficulties (machine calibration is complicated) and controversy, especially around the clinical interpretation, but I surmise it will open up a whole new area of diagnostic possibilities once the early glitches are worked out.

What is a Lactate Doublet?

The lactate molecule has two, weakly coupled, signals or resonances. When viewed on the MRS the lactate doublet presents as a double peak in the signal algorithm.

Lactate Doublets in Cerebral Mitochondrial Dysfunction

The presence of lactate can be diagnostic of specific types of brain tumor or stroke. Since lactate is elevated in mitochondrial disease, evidence of lactate doublets from MRS, even when MRI imaging shows no irregularities, can point to cerebral mitochondrial dysfunction. More specifically, in patients with genetic mitochondriopathies researchers have been able to delineate the regional differences in brain lactate corresponding to the neurological and clinical symptomotology associated with each mitochondriopathy. As was indicated previously, lactate doublets have been recognized in autism, aging (although mechanisms remain contended) and other mitochondrial disease processes.

Using MRS and Respirometry to Detect Post Medication or Vaccine Induces Mitochondrial Damage

Dynamic and functional changes to mitochondria are emerging as culprits in the more complicated adverse reactions we observe post medication and post vaccine. Recognizing the potential for mitochondrial damage post reaction is difficult, especially those impacting the nervous system. Conventional MRI’s and other imaging tests rarely detect visible lesions that can be attributable to clinical symptoms and standard blood tests are often normal, leaving the doctor and the patient without recourse. In advance of genetic testing and the measurement of each co-factor required for proper mitochondrial functioning, respirometry and MRS could be used to identify potential deficits in mitochondrial functioning. Measuring respiratory efficiency and lactate production and usage efficiency could be an easily detectable marker to rule in or out mitochondrial dysfunction. Those results could then be used to determine the need for additional testing that would identify more specific causes of mitochondrial dysfunction.

 

Related posts:

COVID notes drug induced mitochondrial damageCOVID Notes: Considering Drug Induced Mitochondrial Damage hair loss, mitochondria and thyroidThyroid Hormones, Mitochondrial Functioning, and Hair Loss orexin hypocretin neurons brain energyMedication and Vaccine Adverse Reactions and the Orexin – Hypocretin Neurons

You might be interested in

Could Autism be Linked to Mitochondrial Dysfunction?

Published on
3429 views
Lisa Bloomquist

I started thinking about the relationship between autism and mitochondrial dysfunction in the opposite direction from most people. I began studying mitochondrial dysfunction before I did much research into autism. Most people who look deeply enough into the causes and symptoms of autism to note the relationship between mitochondrial health and autism are trying to find a cause/cure for autism; not to formulate an overarching theory about mitochondrial dysfunction and various diseases. I came about it from the mito side – I’m strange like that. No matter how you come to it, there is quite a bit of evidence that mitochondrial dysfunction is related to autism. Perhaps it’s presumptive of me to say this – but of course there are links between mitochondrial dysfunction and autism! Autism is a multi-symptom chronic disease that primarily affects the brain. All mitochondrial dysfunction related diseases are chronic multi-symptom illnesses, and brain cells are dense with mitochondria, so mitochondrial dysfunction should be at the top of the list of possible causes. Apparently, though, it is not.

A new study, “Mitochondrial Dysfunction as a Neurobiological Subtype of Autism Spectrum Disorder,” published in JAMA Psychiatry in April, 2014, claims:

“This is the first study, to our knowledge, to demonstrate evidence for mitochondrial dysfunction in vivo in the brains of individuals with ASD.”

Connections between autism and mitochondrial dysfunction have been made in earlier studies (links below), so claims that this is the first study to show that are a bit of an exageration.  But all the research on mitochondrial health and autism is recent and the fact remains, the relationship is not as well-established as it seems it should be – given the important role of mitochondria as the energy centers of our cells and the similarities between autism and recognized mitochondrial disorders.

Study Basics: A New Measure of Mitochondrial Dysfunction

In the study, researchers assessed brain lactate levels via MRI in 75 children and adults along the autism spectrum and compared them to the same measures taken from healthy, non-autistic, age-matched, children and adults. Brain lactate is emerging as a possible non-invasive measure of mitochondrial damage. Lactate is not supposed to be in the brain, and when it is, that is evidence of damage. In this case, researchers used an MRI to detect what are called lactate doublets, a specific pattern of signal, thought to be indicative of mitochondrial damage and oxidative stress. Other methods of testing mitochondrial function are much more invasive – tissue biopsies – so it’s interesting (and awesome) that they were able to use a non-invasive technique like a MRI to show mitochondrial damage.

Even though MRIs are not nearly as invasive as tissue biopsies, MRI based research still limits the types of participants that can be assessed to those that are able to remain still without sedation for the length of time required for imaging. The study also excluded patients with genetic or metabolic abnormalities (so those with known mitochondrial diseases were not included in the study), a history of neurological injury or uncontrolled seizures. Such exclusions necessarily bias the study toward participants that are higher-functioning individuals. Individuals with more severe ASD were not studied.

Nevertheless, even with these exclusions, the researchers were able to identify differences between the patients and the control group. The researchers report:

“Lactate doublets were present at a significantly higher rate in participants with ASD (13%) than controls (1%) (P=.001), providing in vivo evidence for the presence of mitochondrial dysfunction in the brains of individuals with ASD (Table 1). Elevated lactate correlated significantly with age (P=.004) and was detected more often in adults (20%) than in children (6%). Its presence did not correlate, however, with sex, ASD subtype, intellectual ability, Autism Diagnostic Observation Schedule total score or subscores, or presence of comorbid neurological or psychiatric diagnoses.”

The researchers go on to note that this was the first study to present in vivo evidence for mitochondrial dysfunction in the brains of individuals with ASD – the conclusion boggled my mind as to why it took this so long to reach.

Mitochondria and Disease

It should be noted that little is known about how mitochondria work, or how they relate to the chronic diseases of modernity generally, or autism specifically (they’re just the energy centers of our cells – but they have been treated as if they are nothing to bother looking at). Also, limiting discovery of connections between mitochondrial dysfunction and disease are the testing methods. In vivo testing of mitochondrial function has historically been invasive. Brain biopsies are not exactly an easy, or ethical, option for testing the hypothesis that neurological mitochondrial damage is part of ASD (or any other disease).

Making matters even more complicated, if mitochondrial damage was noted as a cause/effect (it’s probably both – damaged mitochondria produce excess ROS which further damage mitochondria and there is a vicious cycle of damage) of ASD, the question of how mitochondria get damaged would have to be asked. The answer is complicated and not one that anyone in the medical system wants to admit – pharmaceuticals and environmental toxins cause mitochondrial damage. It is easier to say that the problem doesn’t exist, or to look elsewhere, than it is to look into mitochondrial damaging chemicals as the culprits.

Even though, in my mind the link between mitochondrial damage/dysfunction and autism is well established, it is not well established for the general population, so studies like “Mitochondrial Dysfunction as a Neurobiological Subtype of Autism Spectrum Disorder,” are very much necessary and appreciated.  This is one more piece of evidence that mitochondria are important, and that ignoring them is madness. Significantly more research needs to be done. There is some research, however. Take for example the following articles:

For a disease that has been in the public consciousness for at least the last 25 years and is affecting the lives of 1 in 68 children, along with their loved ones, the research connecting mitochondrial dysfunction to autism is woefully lacking. As someone who is coming to this debate from the side of mito disease first, what I am learning is that regardless of the disease processes that mitochondrial dysfunction are thought to elicit, those diseases are complicated, testing is often insufficient and many researchers and physicians have a difficult time understanding or attributing the seemingly diverse conditions to the mitochondrial dysfunction or damage. This is but one more piece of evidence suggesting that a model of disease that looks at mitochondria is in order.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us.

Related posts:

picky eaterFood Aversions in Children with Autism

You might be interested in

Beyond Sex as a Zero Sum Activity

Published on
3748 views
Sex - A Zero Sum Game

After another series of posts on Hormones Matter focused on sex and libido, I realized how rarely we speak of sex and libido in a positive light. Certainly, our audience and topics are skewed towards negative medication and surgical outcomes, but across the internet (and history), it is difficult to find thoughtful discussions about sex and libido that aren’t in some way dominated by shouldn’t, wouldn’t, or couldn’t. I find that troubling, if not a little disturbing. Where are the conversations about sex and libido that include the positive, the pleasurable, or the passionate? I am serious, I couldn’t find any.

So, sorry mom, kids, I am writing about sex again. I’m not sure why I should have to apologize or why such topics are so taboo that one cannot speak openly about them, but they are and we cannot. And perhaps, that is the root of the problem.

Talking about Sex is Taboo, Unless…

I write about sex periodically and almost to a tee my mother chimes in, ‘you shouldn’t be writing about such topics, you’re too smart’ as if having a brain disqualifies one from writing or even thinking about sex. Apparently though, it does. This is perhaps even truer for women, where the topic of sex is veiled in cultural and political taboos so opaque that navigating them can be perilous to one’s career, if not one’s sanity and one’s health. That is, unless of course, the topic is framed in some feminist conception of power structures, patriarchy, or other implements of victimhood. Then discussing sex is alright because it is so far afield from the actual act and so cloaked in theory, and often violence, that it bears little resemblance to sex and no one but others of similar leanings pay much heed. This is not to say that discussions of sexual violence, sexual victims and the like are not important, they are, but what about the rest of it? Certainly, not all sex is framed within a power struggle of cultural, political and violent tendencies. Certainly, there is a space beyond theory, beyond advertising, beyond politics or religion, where a man is just a man, a woman is just a woman and sex is just sex.

If there is such a space, no one seems to write about it. Our entire conversation about sex involves intruding contexts delineating what we should and should not think about sex. Advertisers use sexiness to sell products. Politicians and religious leaders use sex to coalesce and manage followers, while theorists and power mongers of every ilk, use sex to realign power structures. Sex in these contexts is always a tool to be wielded and in many cases manipulated and controlled. Sex is never just sex. It is always about something else or for something else. What happened to sex as a pleasurable activity, in and of itself, absent all other contexts? Was sex ever just for pleasure? It is a legitimate question to which I have no answer.

Sex as a Zero Sum Game

What I do know is that sex today is portrayed as zero sum game of sorts and that framework has done more to erase any notion of pleasure from sex than perhaps any other in history. In a zero sum game there are always victors and losers, oppressors and the oppressed. It is a model built on old industrial economies of scarcity and fear where heat, read passion, means friction, an inefficiency to be controlled at all cost. It is a model where when the debts are tallied, the more I have, the more I win and dominate, the less you have, the better. In a zero sum game, there is an assumption of equal proportionality between the winners and losers, wins and losses, dominators and dominated. To the degree I become more powerful, you lose power and vice versa. There is no room for abundance, synergies, shared responsibilities or even just winners and losers. And there little room for pleasure or passion except perhaps as tokens of victory to demonstrate success, but more frequently as vices, impurities and inefficiencies to be controlled.

What a totally sad state of affairs.

One has to wonder if, at least in the space where sex and sexuality lie, there isn’t a better way to conceptualize, talk about, and perhaps even, experience sex. Aren’t there overlapping interests here? What would happen if we re-framed the conversation away from this zero sum illusion towards a more equanimous perspective where passion and pleasure for all parties took center stage? What would those conversations look like?

Are we even capable of talking about sexual pleasure openly and frankly, not as a means to an end, not as something to be controlled or protected from, not within the context of a power structure, but simply as it is?

If we talked about pleasure, if we aspired towards giving and receiving pleasure and understanding pleasure, if we didn’t shy away from it as we do now, wouldn’t we also totally change the conversations we have about sexual violence, sexual inequality, heck, even economic inequalities?  Wishful thinking perhaps, but when one considers the pendulum of history and the power of discourse, how the conversation is framed is as important as what is said. In the case of sex, we need to talk more about pleasure and a lot less about everything else.

Alas, that is easier to think about than said or done.

Related posts:

proteins, protein folding and enzymesProtein, Protein Folding, and Enzyme Activity reframing maternal healthReframing Maternal Health: How Do We Know What We Think We Know?

You might be interested in

Post Fluoroquinolone Sex and Libido

Published on
8135 views
Lisa Bloomquist

One of my symptoms of getting “floxed” (a short-hand term for fluoroquinolone toxicity – an adverse reaction to a fluoroquinolone antibiotic including Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin, and Floxin/Ofloxacin) was losing my “give-a-damn.”  I stopped caring about many aspects of my life – my job, my relationships, my aspirations, and many other things that used to give me pleasure; including three things that were previously on my list of favorite things in the world – food, sex and alcohol.  My desire for those things, things that used to bring me pleasure and excitement, was simply gone – over night – as my body went from being healthy and strong to being fatigued, in pain and unable to move much at all.

To lose the desire for sex, at the age of 32, was bizarre and disquieting. At 32 I was supposed to be at my sexual peak, but instead I found myself not caring at all about my former favorite recreational activity. As I went through sexual relationships I was able to muster up the energy to participate, and enjoy, sex. But it was different after I got “floxed.”  My way of thinking and feeling about sex was just… different.  I no longer cared about sex and I no longer desired it. It moved from the top of my priority list to the bottom. My libido was a faint shadow of its former self.

As I’ve recovered (it took a couple of years to recover from the toxic reaction that I had to an antibiotic that I took to treat a urinary tract infection brought on, ironically, by sex), my sex drive has come back, and I have started to feel like myself again – with the desires and appetites that make me feel like me. It’s nice to be recovering, and to be getting my “give-a-damn” back.

Because I was able to “fake it till you make it” as they say, my story of losing my sex drive is not the most compelling.  It was not the biggest loss that I suffered from, and, well, there are worse things in the world than what my vagina went through. But some of the other sexual side-effects that other people have suffered through as a result of fluoroquinolone toxicity, are far worse, and they are nothing to be dismissed or disregarded.

My fellow “floxie” friends have been through more sexual adverse effects of fluoroquinolones than I have. Here are a few snippets of their stories:

  • A woman in her mid-20s is unable to orgasm
  • A man in his 40s feels like he is being kicked in the groin when he orgasms
  • A man in his 50s does not respond to any erectile dysfunction medications – including a shot that “works every time” according to his doctor
  • A woman in her 50s experiences nerves that are so over-stimulated that she has a continuous, painful orgasm that lasts for hours
  • A woman in her 30s with extreme vaginal dryness
  • A man in his 30s with erectile dysfunction
  • People of all ages and both sexes who have not had sex for years

I hope that some of my “floxie” friends come forward with their stories about what it feels like to go through the loss of sexual function and sexuality described above.  It affects every aspect of a person’s life and it even rocks their identity. It is wrong for a drug to take away such an important part of being human as one’s sexuality.

Fixing a person’s sexual dysfunction, or lack of desire, isn’t as easy as taking a pill – though the people who advertise Viagra and Cialis would like for us to think that it is.  The people who are suffering from fluoroquinolone induced sexual side-effects are, unfortunately, not helped by any pharmaceutical “cures.”

Sexual dysfunction is real, it is serious and it is life altering.  To take away a person’s ability to be sexual with an unnecessarily strong antibiotic that damages a patient’s central, peripheral and autonomic nervous systems, is wrong.

Please consider the possibility of losing your ability and desire to have sex before you take Cipro, Levaquin, Avelox or Floxin.  If there are alternative antibiotics available, please use those; because your sexuality is really quite important and fixing it once it’s broken isn’t easy.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us.

Related posts:

cipro vision problemsA Fluoroquinolone Reaction After Just One Pill beyond the ER with FQWhen Investigating Fluoroquinolone Reactions, Move Beyond the ER floxed earth fluoroquinolones environmentThe Earth is Floxed adverse drug reactionsAdverse Drug Reactions (ADRs): We’re ALL at Risk

You might be interested in

A Kiss Is Just a Kiss or Is It?

Published on
11180 views
kissing

The mind-body connection makes us unique in our sexuality and preferences. As a women’s sexual wellness expert, I work with women on a large variety of issues from frequency disparity, pre-menopausal dryness and communication to understanding how antidepressants affect their libido, finding complementary therapies and understanding erectile dysfunction. While most of my time is spent educating and sharing information about how the mind affects the body (after all the brain is our largest sex organ); sometimes it is just as important to step back and let our bodies inspire us intellectually.

Physiologically we are sexual beings. How else can you explain the clitoris? With 8,000 nerve endings, its sole purpose is pleasure. No wonder 70% of women experience orgasm through clitoral stimulation. However, clitoral stimulation involves feeling aroused because it usually doesn’t happen until right before penetration if it is stimulation from a partner. Here lies the problem for so many women.  Equal rights, the pill and the sexual revolution came as part of a package that added all kinds of other stress along with the benefits. Unfortunately, for some women the revolution added no real revolutionary thinking when it came to their sexuality.

When I am out sharing the good news about sexual wellness, one of the saddest things I hear from the baby boomer generation is the woman who says “Oh, I don’t need any of THAT. THAT is all out of commission.”  My heart goes out to her immediately. In my mind I wonder who could have reduced her to just a reproductive machine, whether she was abused and associates her femininity with the source of the abuse or maybe even that she must tragically still be recovering from the loss of the love of her life. Certainly, it would have to be something so severe as one of these circumstances for someone to believe that sexual health is not important to overall health or to limit their sexuality to only their reproductive capabilities. Sadly, that is not the case. While there are many reasons why a woman may make such a statement; in many cases it is because a woman doesn’t know the benefits of an orgasm or how pelvic floor health can impact other bodily functions. These are important facts that have long been either unknown or not discussed.

The Kissing Connection

As I mentioned earlier while the brain is the largest sex organ in the body; sometimes it doesn’t hurt to not listen to our head and just dive into something that we know works for us physically. While the clitoris has 8,000 nerve endings, the lips (both male and female) have somewhere around 10,000. This makes the lips quite the erogenous zone in their own right and kissing would be the ideal way to stimulate them. I am often singing the praises of products that are made with mint as a means of encouraging blood flow. I usually talk about kissing when I am explaining why we all seem to lose our head during the throws of puberty. All those new and unfamiliar hormones are stirring and then we add the stimulation of lips against lips and lose sight of everything but the physical. I recently saw a video of an ad on social media that captured total strangers kissing for the first time. The ad went viral because so many people were enthralled with the idea that a first kiss can lead to love. Ultimately everything we do is motivated from love or fear and 95% of everything we do is done by the subconscious.  So for those who are struggling with their libido or just can’t seem to get there mentally a little oral exercise such as a passionate kiss can be a magic bullet. The thing about kissing is it can start slow and build momentum. So even if you aren’t feeling sexual, the stimulation with your significant other or your partner of choice can start with a little effort and go a long way.

Kissing Stimulates Blood Flow

Blood flow is the key to arousal and lubrication. Kissing stimulates nerve endings which in turn increase blood flow.  Once this cycle begins, the body begins a natural responsiveness and triggers emotional responsiveness in the mind.  The mind-body connection is a two way street and while the mind may be the dominant force it is important to never underestimate the physical contributions. A question I find myself asking women who are struggling with a lack of desire and determined to save their relationships is “When was the last time you made out on the couch?” and the question is generally followed by a quiet response of something to do with a lack of time or a repeat of their lack of desire.  Time is the great equalizer. We all have the same amount each day in our account. I am amazed how there is time for everything else, but not for something as good for us as sex. My next step is to challenge them. The next time they feel insecure about their relationship, because of their lack of desire for sex; their challenge is to “make out” for at least fifteen minutes. I coach them about starting slow and innocent and building until they are out of breath.  (Keep in mind I am not a doctor. These conversations come after I know whether this person is on medications under a doctor’s care, or am assured we shouldn’t be looking for medical assistance or if there is a need for a therapist.) Of course after the challenge, I work on helping them understand why this exercise can help them and some of the biological reasons behind it. The challenge itself is met with a wide variety of responses. I hear everything from an insecure laugh to outright refusal. Of course the receptiveness determines the next course of action and everyone is slightly unique in how we proceed; because we are all unique.

Sealed with a Kiss

What is important to remember is emotional fulfillment is one of the three reasons we have sex. Kissing inspires some of those emotions that we are looking to fulfill such as passion, intimacy, sensuality and desire. Kissing also allows us to warm up to the idea and if for some reason after kissing for a while one doesn’t feel sexual arousal there is still the ability to decline further sexual activity. This is very important for women who are struggling with a lack of sexual desire. It is not as easy to change course if you start out initiating sex and then change your mind and decline. Since kissing can stand as an activity all on its own; if it goes no further than an oral exchange there is no harm. From the feedback I receive, it is often successful in leading to more. One of the things I hear from men who are in relationships with women struggling in this area is the negative impact obligatory sex has on their self image. No one wants to feel as if sex is an obligation. Of course communication is key in all relationships; however there is a lot to be said for learning to effectively use body language. When trying to overcome issues with libido, what better way to communicate to your partner than with your lips?

About the author: Patricia Mooneyham is a Jersey girl on  global mission to help women be happier. She is a practitioner of complementary therapies and is passionate about helping women find happiness by defining their own sexuality. For the last several years she hosted the I’ll Have What She’s Having Online Radio Show. Her website: PatriciaMooneyham.com.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Photo by zelle duda on Unsplash.

Related posts:

Birth control breast cancerBirth Control’s Breast Cancer Curveball Thirty Years of Painful Sex Resolved With Pelvic Therapy – An Interview drinking water, hydrationHydration, Thirst, and Drinking Water proof pudding depo proveraProof, Pudding, and Depo Birth Control

You might be interested in

female sexual dysfunction

Resolving Anorgasmia

A 76-year-old woman was referred to me by her daughter for health and wellness. After a consultation about arthritis, a

Osteoporosis in Young Women: The Perils of Common Medications

Published on
6492 views
Osteoporosis in young women

Recently, while discussing loss of ovaries and the use of some drugs for treatment of endometriosis, I was surprised to learn how many women had not been advised about the use of Calcium and/or Vitamin D.  Vitamin D deficiency is becoming more common. For women who have undergone medical treatments using GnRH agonists such as Danocrine, Danazol and Lupron (leuprolide), the risk osteoporosis, even at a younger age, increases. These drugs carry with them some risk of spinal and hip bone loss. Since spinal fractures and hip fractures are likely to cause immobility, they too can cause significant risks to the quality of our lives.

Medications that Cause Osteoporosis in Young Women

Bone density loss and osteoporosis are often considered a disease of older individuals and so may be missed in younger women, especially those who have undergone courses of Lupron, Danocrine or Danazol and other menopause inducing treatments for endometriosis. In premenopausal women, Lupron treatment causes a rapid decline in bone density within 6-12 months. Similarly, depot medoxyprogesterone acetate (DMPA), an injectable contraceptive used millions of young women, decreases bone mass and can increase the risk of fracture; ditto for long term steroid treatment for inflammatory conditions such as rheumatoid arthritis.

Osteoporosis and Fractures

According to experts, hip fractures are “considered to be the most devastating outcome of osteoporosis”.  Part of the reason is once fractured, the hip often needs to be replaced or pinned but can only be done if the bone is healthy enough to accept the repair.  When the bone will not tolerate the artificial hip or the pinning, then confinement to bed or chair becomes permanent.  Confinement leads to a plethora of complications including blood clots, pneumonia, infection, cardiovascular disease as well as other fractures from further bone loss related to inactivity.  A second concern is compression fractures of the spine which can occur with simply standing or lifting of items.  Either of these conditions can be painful as well as confining.  I saw a case a couple years ago where a lady was preparing an eight pound turkey for dinner, and simply turned it over in the sink, and felt a compression fracture in her spine occur.  It was later confirmed on xray.

Identify Your Risk for Osteoporosis

There is no cure for osteoporosis, but there are things that can be done before bone loss becomes serious.  First and foremost should be a consultation with your primary care physician or gynecologist to determine your risk.  If you have been on any of the drugs listed above, are inactive, have a history of low calcium intake, been hysterectomized at a young age, or have an eating disorder, this may increase your risk and discussion of a dexascan to determine your current status would seem wise. You may find that some do not believe the risk of bone loss with the various drugs is an issue, but most reports do indicate it is a serious potential. You should also have your physician test your calcium and vitamin D levels. Many men and women are vitamin D deficient and do not even know it.

Low Vitamin D and Osteopenia or Osteoporosis

Once your bone status, calcium and vitamin D levels are known, then calcium and vitamin D should be discussed and prescribed as necessary.  In the Northern Hemisphere of the world, many people are Vitamin D deficient, perhaps further increasing the risk.  So assessment of your Vitamin D level would seem wise and can be done with a simple blood test.  Adequate Vitamin D must be present for calcium to be properly utilized.

Weight Bearing Exercised and Vitamin D for Building Bones

If you fall in the low bone density category, (osteopenia) then diet, supplements and weight bearing exercise will become critical to stop or reverse the low bone density.  It would appear that consistency is important if you are to stem this problem. Once you know what your doctor wants in the way of Vitamin D and Calcium, a pill minder kept where you eat or where you brush your teeth, can help avoid missing doses. The minder gets filled once a week or every two weeks depending on size. Finding ways to bear weight every day is also as important as the supplements. Walking or stair climbing are probably the safest weight bearing exercise, as there is less risk of a fall and potential injury.  A nutritional consult may also be a good idea to review and improve dietary sources of calcium and Vitamin D.

For More Severe Osteoporosis

If you fall into the greater bone loss category (osteoporosis), then you are likely to see recommendations for one of the many osteoporosis medications. They are not perfect by any means and each has its own associated risks and side effects. Before taking anything, be sure to do your research, perhaps discuss with both your doctor and the pharmacist as to the safest ones to consider. To do nothing has even greater risks. Some newer drugs are on the horizon which may have fewer side effect issues.

Once you have actually been diagnosed with osteoporosis, it is important to follow scanning every couple years to be certain you are not continuing to lose ground so that adjustments in your treatment can be made.

Final Thoughts

When we are young we don’t think much about aging or the impact of diet and drugs on our bones now.  Since many of the medications for osteoporosis are fraught with issues themselves, leading to spiral fractures of long bone, and other systemic side effects, so it is far better to prevent loss or reverse it before it becomes pathological.

For women with endometriosis particularly, several of the drugs commonly used in the past, and some still used today, have bone loss risks not fully apparent in the literature. Women with endometriosis have to be extra vigilant in caring for our bones. The same holds true for women who have had complete hysterectomies at a young age. Loss of the estrogens may accelerate bone loss and estrogen replacement may not be fully protective. So it becomes critical to be sure diet and supplements cover the calcium and Vitamin D issues and that weight bearing exercise such as walking and or stair climbing are in your daily activity.

Related posts:

Breast cancer micro-calcificationsDying Too Young: Oxalate and Breast Cancer Male athlete with mitochondrial malnutritionLongstanding Mitochondrial Malnutrition in a Young Male Athlete
1 2