What are the risk factors for type 2 diabetes? Obesity and a high-sugar diet, right? Those are the most highly publicized factors that can lead to an onset of type 2 diabetes – but they’re not the whole picture.
Numerous studies have linked magnesium deficiency to type 2 diabetes. While the magnesium levels in one’s diet are a large factor in determining cellular magnesium content, there are things other than not eating magnesium-rich foods that can lead to depleted cellular magnesium. Namely, many pharmaceuticals and environmental toxins (especially glyphosate) have been shown to deplete magnesium from cells, leading to intracellular magnesium depletion and, potentially, diabetes and other diseases related to magnesium deficiency.
Fluoroquinolones are Linked to Diabetes – By Way of Magnesium Depletion
In an article published in the journal Medical Hypothesis entitled “Fluoroquinolone Antibiotics and Type 2 diabetes Mellitus,” it was found, through statistical analysis of the rates for both diabetes diagnosis and fluoroquinolone antibiotic (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/Ofloxacin and a few others) prescriptions, that “the probability of developing diabetes following a fluoroquinolone prescription is thus estimated at 3.5 percent.”
3.5 percent. Who would think that a commonly prescribed class of ANTIBIOTICS could affect diabetes rates?
Fluoroquinolone antibiotic use is a completely unrecognized risk factor for future development of type 2 diabetes. In taking Cipro, Levaquin, Avelox or another fluoroquinolone to treat a sinus infection, urinary tract infection, prostatitis, etc., patients are increasing their risk of developing type 2 diabetes significantly. It is postulated in “Fluoroquinolone Antibiotics and Type 2 diabetes Mellitus” that fluoroquinolones are “responsible for much of the increase in the prevalence of type 2 diabetes in the United States from 1990 to the present day.” (The article was published in May, 2014.)
Fluoroquinolone antibiotics increase the risk of diabetes because they “can penetrate cell membranes inducing an intracellular magnesium deficiency that increases the probability of insulin resistance. This can lead (when accompanied by other risk factors) to type 2 diabetes.”
Cellular magnesium deficiency, brought on by fluoroquinolone antibiotics – antibiotics used to treat common infections – can lead to type 2 diabetes.
To support the hypothesis that much of the increase in prevalence of type 2 diabetes in the United States since 1990 is due to the use of fluoroquinolones, the study notes that the correlation between the rates of type 2 diabetes and fluoroquinolone prescriptions is strong.
While the tracking of the dramatic increase in type-2 diabetes rates (from 3.5/1000 in 1991 to 9/1000 in 2009) with increasing fluoroquinolone prescription rates is alarming, the more interesting correlation is the downturn in type-2 diabetes rates that corresponds to the decrease in fluoroquinolone prescriptions after a black-box warning of tendon ruptures was added to the warning label for all fluoroquinolones in 2008. (Though correlation does not mean causation, statistical tools and analysis were utilized in the study to analyze the data and remove some of the cross-correlations. The R-squared for the correlations are high – indicating that the correlation is strong and that the data fits well.)
History of Dysglycemia with Fluoroquinolones
The link between fluoroquinolones and type 2 diabetes should not come as a surprise to the FDA or anyone who has studied fluoroquinolones. Gatifloxacin, a fourth generation fluoroquinolone sold under the brand name Tequin, “was withdrawn from clinical use after reports of drug-induced hyperglycemia.” Additionally, “other fluoroquinolones have been reported to interfere with glucose homeostasis.” Severe dysglycemia has been induced in already diabetic patients when they have been exposed to fluoroquinolones.
Despite the fact that Tequin/gatifloxacin was removed from the market because it caused severe dysglycemia, and that fluoroquinolones have been shown to adversely affect glycemic indicators at rates much higher than those of other antibiotics, more than 26 million prescriptions for fluoroquinolones were given out to the American public in 2011 alone. And though both hyper and hypo-glycemia are noted as adverse reactions on the Cipro/ciprofloxacin warning label, there is nothing on the label that warns of increasing the risk of type 2 diabetes.
Repairing the Damage
Multiple studies have shown that a high-magnesium diet and high intracellular magnesium levels are protective against both diabetes and fluoroquinolone toxicity, but clinical experiments where magnesium is supplemented in order to treat diabetes shows mixed results. Although magnesium is protective, once it is depleted, it takes more than supplementation and eating leafy greens to repair the damage. Additional research shows that thiamine, which works in conjunction with magnesium, improves mitochondrial function and diabetic outcomes.
Cells that are depleted of magnesium enter cycles of self-perpetuating damage and further magnesium depletion. ATP, the enzymatic process of cellular energy production, is dependent on magnesium. It has been suggested that insufficient magnesium, because of depletion by pharmaceuticals (especially fluoroquinolones), environmental toxins, or a deficient diet, cells do not have enough energy to renormalize their magnesium levels, and the deficiency becomes chronic.
When magnesium is depleted, other cellular mineral balances are also disturbed. In “Magnesium: the Forgotten Electrolyte,” it is noted that “Magnesium is needed for the proper functioning of the Na+/K+—ATPase pump, so a deficiency causes an increase in intracellular sodium and allows potassium to leak out of cells.” Intracellular magnesium deficiency also disrupts intracellular calcium homeostasis. The proper balance of magnesium, sodium, potassium, calcium and other minerals within cells is quite important, and restoring the balance of these vital minerals is difficult.
Magnesium Depletion and Chronic Diseases of Modernity
When are the connections between magnesium depleting pharmaceuticals and the “diseases of modernity” (such as diabetes, autoimmune diseases, and others) going to be realized? Depletion of intracellular magnesium can lead to a spiral of ill-health effects. After all, magnesium is necessary for more than 300 enzymatic reactions. Without proper levels of intracellular magnesium, ATP doesn’t work properly and mitochondrial dysfunction can result. Mitochondrial dysfunction leads to an over-production of reactive oxygen species (ROS) / oxidative stress. An over-production of ROS has been linked to almost every chronic disease there is, from Gulf War Syndrome to Autism. Liver enzymes are dependent on magnesium and when magnesium is depleted, the liver’s detoxification processes malfunction. This leads to toxic metabolites circulating through the body, which is connected with autoimmune diseases and many other chronic illnesses. Sufficient levels of magnesium are necessary for the proper metabolism of many vitamins and nutrients, including the B vitamins. Taking fluoroquinolone antibiotics or other magnesium depleting pharmaceuticals can lead to a spiral of ill-health and disease.
The correlation between fluoroquinolone prescriptions and diabetes is clear, however, longitudinal studies would be necessary to show causation. Similar studies should be done for all of the diseases of modernity that have been on the rise since fluoroquinolones were introduced. Though fluoroquinolones aren’t the only toxic chemicals that can deplete cellular magnesium, they are common and frivolously over-used. Fluoroquinolones (chemotherapeutic agents masquerading as simple antibiotics) cause magnesium depletion and mitochondrial damage, which in turn lead to massive, progressive, sometimes irreversible, cellular damage and many chronic, poorly understood diseases.
Type 2 diabetes is a serious, debilitating, and sometimes fatal disease. It is unconscionable to give patients a drug that increases their chances of developing type 2 diabetes when there are other, safer drugs available.
Recognition of the connection between fluoroquinolone antibiotic use and the onset of type 2 diabetes requires a re-examination of the prevalent assumptions about the causes of diabetes. The findings in “Fluoroquinolone Antibiotics and Type 2 Diabetes Mellitus” may revolutionize our paradigms.
Credit for the graphical image: Fluoroquinolone antibiotics and type 2 diabetes mellitus; Telfer, Stephen J., Medical Hypotheses, Volume 83, Issue 3, 263 – 269. The graphic was used with the author’s permission.
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.
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I’ve been taking Cipro 500mg twice a day for 20 years. 7 years ago I was diagnosed with diabetes type 2. I recently found this article and while my blood work seems to say other wise I still believe Cipro may have a connection to my diabetes. Diabetes doesn’t run in my family and I’m not over weight. I would appreciate access to any new information you have
I am a diabetic patient. I took Ciprofolxacin 40 tablet My chest is shaking continously and making chest heaviness palpitation, halucination, panic, body burning etc I stopped 15 days ago. But still I am shaking. I feel heavy more papitation while walking
Can any body help me
Great post (as usual), Lisa! I’ve become “borderline” diabetic since my floxing 5 yrs ago. My diet: vegan (with some fish) and very little sugar/desserts (less than 1 small dessert/week, no sodas, etc.). I also am fortunate that I’m able to do about 30 min of cardio/day (recumbent bicycle). I even only have whole wheat pasta and bread. Basically, no one following this diet/lifestyle should be getting type-2 diabetes, but I’m on the way… thanks to Cipro, the gift that keeps on giving!
has it improved? are your diet back to normal?
Lisa, as always you have delivered a well-researched, informative, and relevant piece. I was floxed (disabled by Levaquin) in November 2012. I instantly became hypoglycemic and often experienced terrible reactive hypoglycemia after eating. This remained for a year until I suffered several bouts of strep, had a flu shot, and took amoxicillin. Suddenly, my blood sugar began to flip-flop. For the first year of floxing my morning blood sugars were 70-80 and never went above 90 even after eating a meal or sugary snack. Now my morning blood sugars range from 110-125 most mornings, but my 2 hour post meal sugars are normal. All along I have had severe neuropathy since taking the Levaquin. I did discover that when I ate foods high in advanced glycation end products (AGEs), my neuropathy flared. You see, foods high in AGEs (mostly meats cooked at high temperatures, grilled, broiled, etc., also pasteurized cheeses, and baked goods) are linked to the worsening of diabetes and diabetic symptoms in both Type I and Type II diabetic patients. Hmmm. So there is a connection here though my endocrinologist insists I am fine. Since my A1C and post meal blood sugar numbers are perfect I am deemed ok. However, I know something isn’t right and I am suffering from dysglycemia. It is just so frustrating that my endocrinologist and neurologist dismiss me and don’t outright acknowledge the connection of my symptoms to the fluoroquinolones even with all of the documented research out there. All I can do is boil my meat, and eat an AGE-reduced diet and try to limit sugars, starches, and other carbs. I just pray this resolves and doesn’t turn into diabetes. If so, I will have Levaquin to thank!