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Stop the Metformin Madness

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Chandler Marrs

I have never been a fan of Metformin. It seemed too good to be true. Many years ago I had a conversation with a researcher about all of its possible therapeutic indications. His lab was actively pursuing the anti-cancer angle. That should have been a clue that Metformin might be causing more damage than we recognized, but it wasn’t. At that point, I was still enamored with the wonders of pharmacology and hadn’t yet begun my path toward understanding medication adverse reactions. Indeed, it wasn’t until very recently, when a family member began suffering from one of these reactions, that I began my investigation in full. This is what I learned.

Type 2 Diabetes is Big Business

The global profits from Type 2 diabetes medications rested at a paltry 23 billion dollars in 2011 but are expected to grow to over $45 billion annually by 2020. The market growth is bolstered in large part by the ever-expanding demand for therapeutics like Metformin or Glucophage. Metformin is the first line of treatment and standard of care for insulin resistance across all populations of Type 2 diabetics with over 49 million Americans on Metformin in 2011-2012. It is particularly popular in women’s health with an increasing reliance on Metformin for the metabolic dysfunction observed in women with PCOS, PCOS-related infertility, and even gestational diabetes. Metformin is prescribed so frequently and considered so innocuous that it is sometimes euphemistically referred to as vitamin M.

If we quickly scan the safety research for metformin, there is little immediate evidence suggesting any side effects whatsoever. In fact, in addition to controlling blood sugar by blocking the hepatic glucose dump, this drug is suggested to promote weight loss, increase ovulation in women, (thereby helping achieve pregnancy), and prevent an array of pregnancy complications (everything from miscarriage to gestational diabetes, pre-eclampsia and preterm birth). Metformin is argued to prevent cancer and the neurocognitive declines associated with aging, even aging itself. By all accounts, Metformin is a wonder drug. Why isn’t everyone on Metformin prophylactically? Increasingly, we are.

With the increasing rates of obesity and associated metabolic disturbances, drugs that purportedly reduce those indicators are primed for growth. Like the push to expand statin prescription rates from 1 in 4 Americans to perhaps 1 in 3, millions have been spent increasing the therapeutic indications and reach for this medication. Amid all the excitement over this drug, one has to wonder if it isn’t too good to be true. In our exuberance to get something for nothing, to have cake, if you will, have we overlooked the very real risks and side effects associated with Metformin?  I think we have.

Metformin and Vitamin B12 Deficiency

As we’ve reported previously, Metformin leaches vitamin B12 and to a lesser degree B9 (folate) from the body. One study found almost 30% of Metformin users are vitamin B12 deficient. For the US alone, that’s almost 15 million people who could be vitamin B12 deficient and likely do not know that they are deficient. What happens when one is vitamin B12 deficient?

Firstly, inflammation increases, along with homocysteine concentrations, which is a very strong and independent risk factor for heart disease (the very same disease Metformin is promoted to prevent).  And that is the tip of the iceberg.

Vitamin B12 is involved with a staggering number of physiological functions including DNA, RNA, hormone, lipid, and protein synthesis. Deplete vitamin B12 and a whole host of problems emerge, mostly neurological.

Vitamin B12 is critical for the synthesis of the myelin sheaths around nerve fibers. There is a growing relationship between multiple sclerosis, which involves the disintegration of myelin and brain white matter, and vitamin B12 deficiency.  Often the first signs of B12 deficiency are nervous system-related with cognitive disturbances and peripheral neuropathy among the most common.

Additionally, many women have dysregulated hormones connected to vitamin B12 deficiency. In light of the Metformin-mediated vitamin B12 deficiency, one has to wonder if some of the chronic health issues plaguing modern culture are not simply iatrogenic or medication-induced.

Metformin, Pregnancy and Maternal and Fetal Complications

Considering that half the population is female, many of whom are on Metformin and may become pregnant, we must consider the potential effects of Metformin-induced vitamin B12 deficiency during pregnancy. As troubling as the effects of B12 deficiency are on non-pregnant individuals, during pregnancy they can be devastating. Vitamin B12 deficiency during pregnancy leads to an increased incidence of neural tube defects and anencephaly (the neural tube fails to close during gestation). Once thought to be solely related to folate deficiency (vitamin B9) which Metformin also induces, researchers are now finding that B12 has a role in neural tube defects as well.

Scan the internet for Metformin and infertility and you’ll see long lists of fertility centers boasting the benefits of this drug. During pregnancy, the exuberance for vitamin M is palpable, although entirely misplaced. Early reports suggested Metformin would reduce an array of pregnancy complications including gestational diabetes. The data supporting these practices were mixed at best. At worst, however, they were downright incorrect. Metformin, it appears, may evoke the very conditions it was promoted to prevent during pregnancy and then some. Additionally, recent research suggests Metformin alters fetal development and induces long-term metabolic changes in the offspring, likely predisposing the children to Type 2 Diabetes, an epigenetic effect perhaps.

Metformin Inhibits Exercise-Induced Insulin Sensitivity

As if those side effects were not enough to question mass Metformin prescribing practices, it appears that Metformin reduces any gains in insulin sensitivity that normally would be achieved from exercise. I cannot help but wonder if Metformin impairs insulin signaling in general. Cancer research suggests that it might.

According to one study, physical exercise can increase insulin sensitivity by up to 54% in insulin-resistant individuals, unless of course, they are taking Metformin. Metformin abolishes any increased insulin sensitivity gained by exercise. Metformin also reduces peak aerobic capacity, reducing performance and making exercise more difficult. Moreover, despite claims to the contrary, Metformin does not appear to be an especially effective tool for weight loss, netting a reduction of only 5-10 pounds over 4-8 months. Regular exercise and a healthy diet net on average a loss of 5-10 pounds per month for most people and are significantly more effective at reducing diabetes and associated health complications without the potential side effects.

Metformin and Mitochondrial Damage

Perhaps most troubling amongst the Metformin side effects is its ability to severely impair mitochondrial functioning.

Recall from high school biology, the mitochondria are those bean-shaped organelles inside cells that are responsible for cellular respiration or energy production. Through a variety of pathways, the mitochondria provide fuel for cell survival. In addition to cellular energy production, mitochondria control cell apoptosis (death), calcium, copper, and iron homeostasis, and steroidogenesis. In essence, mitochondria perform the key tasks associated with cell survival, and indeed, human survival. Damage the mitochondria and cellular dysfunction or death will occur. Damage sufficient numbers of mitochondrion and chronic, multi-symptom illness arises.

As we have come to learn, many pharmaceuticals, environmental toxicants, and even dietary deficiencies can impair mitochondrial functioning and induce disease processes that are often difficult to diagnose and treat. Metformin is no different. Metformin impairs mitochondrial functioning quite significantly by several mechanisms and, in doing so, sets off a cascading sequence of ill effects.

At the center of metformin’s mitochondrial damage is its effect on the most basic of mitochondrial functions – ATP (cellular energy) production. Metformin reduces mitochondrial ATP production in skeletal muscle by as much as 48%. Sit with that one for a moment, a 48% reduction in cell fuel. Imagine functioning at only half capacity. This would make basic activities difficult at best and exercising to lose weight a very unlikely proposition. Imagine similar reductions in ATP production were observed in the brain or the heart or the GI tract (which, when on Metformin are likely), the types of disturbances we might see become quite clear: neurocognitive decline, psychiatric instability, neuropathy, heart rate, rhythm and blood pressure abnormalities, along with gastrointestinal distress to name but a few. Underlying all of these symptoms, and indeed, all mitochondrial dysfunction is an overwhelming sense of fatigue and malaise.

Metformin Alters Immune Reactivity via the Mitochondria

As I wrote in a previous post:

Some researchers argue that the mitochondria are the danger sensors for host organisms; having evolved over two billion years to identify and communicate signs of danger to the cells within which they reside. The signaling is simple and yet highly refined, involving a series of switches that control cellular energy, and thus, cellular life or death. When danger is present, energy resources are conserved and the immune system fighters are unleashed. When danger is resolved, normal functioning can resume.

If the danger is not resolved and the immune battles must rage on, the mitochondria begin the complicated process of reallocating resources until the battle is won or the decision is made to institute what can only be described as suicide – cell death. Cell death is a normal occurrence in the cell cycle of life. Cells are born and die for all manner of reasons. But when cell death occurs from mitochondrial injury, it is messy, and evokes even broader immune responses, setting a cascade in motion that is difficult to arrest.

Metformin alters this process, first by damaging the mitochondrial ATP factory and reducing energy production capacity and then by inhibiting the signaling cascades that would normally respond to the danger signals. The double hit fundamentally alters immune function and I would suspect predisposes those who take Metformin to more infections and an array of inflammation-based disease processes. More details on this in a subsequent post.

Metformin and the Statins: Beware

The mechanisms through which Metformin derails mitochondrial functioning are complex but likely related to depletion of coQ10, an enzyme involved in what is called the electron transport chain within the mitochondria. CoQ10 also referred to as ubiquinol and ubiquinone, is critical for mitochondrial functioning. Recall from a previous post, that statins, like Lipitor, Crestor and others also deplete coQ10 and from a pharmacological perspective these mechanisms are implicated in the development of atherosclerosis and heart failure.

“statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation.”

CoQ10 depletion is also implicated in the more common statin-induced side effects like muscle pain and weakness and in severe cases, rhabdomyolysis. Since Metformin and statins are regularly co-prescribed, the potential for severely depleted mitochondria and significant side effects is very high. Consider muscle pain and weakness among the first signs of problems.

My Two Cents

When we contrast the reduction in glucose mediated by Metformin with the damage this medication does to the mitochondria and immune signaling, along with its ability to leach vitamin B12, block insulin sensitivity and reduce aerobic capacity, one cannot help but wonder if we are causing more harm than good. Admittedly, obesity and hyperglycemia are growing problems in Western cultures. As we are coming to learn, however, obesity itself is not linked to the diseases processes for which many drugs like statins and Metformin are promoted to protect against – the obesity paradox. Growing evidence suggests that obesity is indicative of mitochondrial dysfunction and chemical exposures which then may provoke impaired insulin sensitivity and hyperglycemia and continued fat storage versus metabolism. If this is true, simply reducing circulating glucose concentrations, in an effort to reduce obesity and the purported health problems associated with obesity, will do nothing to treat the underlying problem.

Insulin resistance and the associated hyperglycemia are environmental and lifestyle-mediated problems that should be reversible with environmental and lifestyle changes. Having said that, those lifestyle and dietary changes will fail unless we consider the underlying mitochondrial damage initiated by dietary choices, pharmaceuticals, and other environmental exposures. For that, we must dig deeper into mitochondrial functioning and correct what we can.

I believe obesity and hyperglycemia are symptoms of damaged and dysfunctional mitochondria, partly mediated by lifestyle, partly iatrogenic (pharmaceutically induced), and likely epigenetic. If we are to solve the ‘obesity’ problem and prevent the damage mediated by hyperglycemia, we have to address these variables. Failing to do so serves no one except those who profit from our continued ill-health.

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Sweet Death by Sugar

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Angela A Stanton,Ph.D.

We all know that sugar is bad for us but we cannot resist it. Why not? Expert Robert Lustig MD, reasoned on 60-Minutes that for humans in nature all sweet tasting things are edible and not poisonous. There are no toxins in nature that taste sweet, and thus, evolutionarily speaking, favoring sweet things is predetermined in our genes; we are born liking sweets. All of this is true with one major exception: sugar, the natural substance, can become poisonous when modified.

Sugar and Ethanol

Consider the simple modification of squeezing a fruit for its juice. The modification is not chemical: we merely separated the sugary liquid from the insoluble fiber in the fruit–some soluble fibers may remain. This little change makes no difference for most fruits or our taste buds, but it modifies how our body metabolizes sugar in it. According to Lustig’s book Fat Chance (a must read!), when we eat the fruit with insoluble fiber attached (typically the skin), the fructose in the fruit (most sugar in fruit is fructose) bypasses our metabolic digestive process (insoluble fibers are not digestible) and heads straight to the gut where the good bacteria digest the fructose as their food from the fibers, thereby producing more nutrients for us. But if we drink the juice alone without any insoluble fiber, the same amount of fructose now gets into the metabolic cycle and by a complicated process turns into ethanol and gets stuck in the liver. Ethanol is a toxin. Ethanol is an alcohol we also use to improve car mileage. Ethanol causes non-alcoholic “alcoholic” liver disease. In fact, ethanol is alcohol and those drinking apple juice (thinking of kids now) are in fact drinking alcohol in terms of the likely outcome of the metabolic process, as per Dr. Lustig.

So we all thought that feeding our kids fresh fruit juices is a good thing but we also knew that they should not be getting too much sugar because their behavior changes from it. Now it is clear why their behavior changes: the part of sugar that turns into ethanol is alcohol. The other parts of the fruit juice that do turn into digestible sugars (glucose and sucrose) do something else to the body.

What is Glucose?

Glucose is “blood sugar” meaning the sugar our body can use. Sucrose converts to glucose as well. What happens to the glucose?

Some stores sell glucose in a liquid gooey form—thicker than honey—that I recommend you taste. Take a small teaspoon, fill it with glucose and swallow. The first thing you will notice (yes, I did the tasting test) is that it is not that sweet. The second thing you will notice is that the moment you swallow it, you cannot count till 5 and you are hot. So you take your sweater off. Then you have the urge to do something—paint the house? Mow the grass? If you are a kid: bounce off the walls and drive the people around you nuts. This is normal. This is what glucose feels like.

Note, however, that when you eat a teaspoon of table sugar, you will neither feel so hot, nor will you have so much energy. What is the difference? What happens when you drink a diet drink or eat sugar substitutes? You will neither be hot nor have any energy. The difference in feeling hot and having energy versus not feeling hot and not having energy represents the difference in the metabolism of glucose versus fructose and the fake sugar stuff.

The Metabolism of Glucose versus Fructose

I will not get into deep chemical equations or models; for that please watch the video below by Dr. Lustig. Rather, I will reduce all complexity and simply tell you the end of the story with as minimal of the underlying process as possible.

When food arrives into the body, insulin is released to convert the food into fat and deposit it for later use as glucose. Glucose is used by our brain and muscles for energy. After insulin has done its conversion, all insulin is used up. When the brain is hungry, it fetches the hormone leptin to get some energy. Thus, leptin grabs a hold of the available glucose and serves it to the brain (this is highly simplified!). The brain is happy and full of energy.

Now consider the situation when the only food we eat is glucose. Insulin is released but it has nothing to convert. It is already in the final form (glucose for the brain) and so the glucose goes straight to the brain, the kids are popping off the wall, and you suddenly find yourself painting the house. Note, however, that the insulin is in the blood and it is waiting for the food to arrive so it can work and convert it to fat. But there is no food; we only ate glucose and it is already being used by the brain! So what is insulin in the blood to do? Insulin stays in the blood, circles around looking for food. It finds none. By staying in the blood, over time this is a “cry wolf” scenario and the body starts ignoring insulin announcing the arrival of food that isn’t there. This is how insulin resistance starts.

Now consider that instead of glucose, you drink a glass of apple juice. It has natural sugar in it, some vitamins (very little), no fiber, no protein. The sugar of fruit is mostly fructose but a small part of it is also sucrose. So insulin releases again to match the size of the apple juice drink we just had, but again, it faces a problem. While sucrose becomes glucose in our body and can be converted and stored as fat, fructose is not seen as sugar. So once again, insulin is looking for food but finds none; it keeps on circling in our blood looking for food. It is ignored and insulin resistance begins.

The Metabolism of Glucose versus Sugar Substitutes & “Natural” Sugars like Stevia

Now consider you eat a diet something—by diet I mean sugar substitutes with reduced or zero calories. It certainly tastes sweet (very sweet indeed) but again, there is no glucose or sucrose in it and while it does not become alcohol in the liver, it certainly makes insulin run around in circles looking for food to convert to fat and deposit. Cry wolf again and the insulin is ignored. Insulin resistance begins. Why is this important? Because insulin resistance is type II diabetes!

The Famine

Now let’s continue about the peril of our non-toxic sweets. The fact that insulin is out looking for glucose also signals leptin that energy is incoming! Leptin is a hormone that is in charge of messaging the brain that glucose is available. In the case when insulin is running around in our blood in search of food it can convert to fat for later use as glucose but there is no food to be found, leptin finds no glucose. Thus, leptin tells the brain that famine is here.

Famine for the Brain is Obesity for Your Body!

The famine message to the brain means one thing: conserve energy. It reduces all non-essential activities, and literally, will not let you get up from that couch! This is highly simplified of course, but pay attention to the outcome. You are actually eating and drinking and at the same time your brain is getting the message of famine. What will that lead to? When the brain thinks it is famine time, it is famine time. The fact that you are eating and drinking sugar or sugar substitutes with lots of calories is not noticed by the brain. As far as it is concerned, there is no glucose available so it must slow your metabolism. A slow metabolism leads to obesity.

Sugar Anyone?

So, while there are many people who think nothing of having sweets or a soda, consider what it does to your body! Consider that it slows down your activity and forces you into famine state even though you are well fed! Consider that it makes you obese and sets you up for type 2 diabetes.

Now tell me if you still think that sweets are not toxic poisons for us! They are. And there is one more thing to add to the story that no one talks about. I mention this because I deal with a group of migraineurs—I was one of them until I figured things out and wrote a book about it and several articles about it on Hormones Matter.

Consider this quote from the Harrison’s Manual of Medicine:

…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells. (page 4)

Na+ is sodium ion. Sodium is part of sodium-chloride, which is salt. Glucose-induced H2O efflux from cells represents water exiting the cells as a result of an increase of glucose. Why is that, you may ask? The answer is very simple: sugar is an amazing water soak-up device. It pulls water from everywhere it can. It holds onto water like its life depended upon it. Unfortunately for the body, sugar pulls the water from the cells leaving the cells empty on the inside and a lot of fluid tied to sugar on the outside. As long as that sugar is there, the cells are not able to hydrate in any fashion until the level of Na+ is increased beyond a threshold level where Na+ can take water away from the glucose. Na+ also attracts water. In fact, all saline electrolyte liquids provided by IV or for drinking in hospitals are Na+ heavy to rehydrate the cells.

Thus, sugar not only starts and enhances diabetes II and obesity; it also shuts down cell hydration. This may cause headaches or migraines depending on your propensity.

In conclusion, if someone asks you if you would prefer to eat a teaspoon of sugar or a teaspoon of salt, while your taste buds will undoubtedly scream for sugar, you should know better!

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. 

References

  1. Sugar: The Bitter Truth https://www.youtube.com/watch?v=dBnniua6-oM
  2. Longo et al., Harrison’s Manual of Medicine. 18th edition. McGraw Hill. 2013.
  3. Artificial sweeteners could cause spikes in blood sugar by By Brady Dennis September 17, 2014
  4. Washington Post: http://www.washingtonpost.com/national/health-science/study-suggests-sweeteners-could-contribute-to-obesity-and-diabetes/2014/09/17/c3c04ea6-3dc2-11e4-b03f-de718edeb92f_story.html
  5. Artificial sweeteners could lead to obesity, diabetes. By Michelle Castillo CBS NEWS July 10, 2013, 4:28 PM
  6. CBS News: http://www.cbsnews.com/news/artificial-sweeteners-could-lead-to-obesity-diabetes/
  7. Artificial sweeteners may promote diabetes, claim scientists
  8. The Guardian: http://www.theguardian.com/science/2014/sep/17/artificial-sweeteners-diabetes-saccharin-blood-sugar
  9. Do Artificial Sweeteners Really Cause Diabetes? By Published: June 7, 2013 By Jessica Chia
  10. Women’s Health Magazine: http://www.womenshealthmag.com/health/artificial-sweeteners-cause-diabetes
  11. Could artificial sweetener CAUSE diabetes? Splenda ‘modifies way the body handles sugar’, increasing insulin production by 20% by Rachel Reilly Published: 12:27 Est, 30 May 2013 | Updated: 12:27 Est, 30 May 2013
  12. The Daily Mail: http://www.dailymail.co.uk/health/article-2333336/Could-artificial-sweetener-CAUSE-diabetes-Splenda-modifies-way-body-handles-sugar-increasing-insulin-production-20.html
  13. How To Starve Cancer To Death By Removing This One Thing From Your Diet
  14. Organic Health: http://organichealth.co/starve-cancer-to-death-by-removing-this/
  15. Is sugar a toxin? Experts debate the role of fructose in our obesity epidemic By Tamar Haspel, September 2, 2013
  16. Washington Post: http://www.washingtonpost.com/national/health-science/is-sugar-a-toxin-experts-debate-the-role-of-fructose-in-our-obesity-epidemic/2013/08/30/58a906d6-f952-11e2-afc1-c850c6ee5af8_story.html
  17. Scientific team sounds the alarm on sugar as a source of disease. By Barbara Sadick Chicago Tribune
  18. The Chicago Tribune: http://www.chicagotribune.com/lifestyles/health/sc-health-1210-sugar-metabolic-syndrome-20141205-story.html#page=1

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Fluoroquinolone Antibiotics Linked to Diabetes Onset

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Lisa Bloomquist flouroquinolone antibiotics

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.

Correlation between fluoroquinolone use rates and prevalence of diabetes.
(A) Incidence of diabetes in the non-institutionalized U. S. population aged 18–79. (B) U.S. national outpatient prescription rates of fluoroquinolone antibiotics from Refs. [3] and [27] (squares) and [28] (diamonds). (C) Correlation between incidence of diabetes in a given year and outpatient fluoroquinolone prescription rate 2years previously. (D) Prevalence of diabetes in the whole U.S. population plotted with prevalence of obesity. Posted with permission of the author.

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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A Global Contamination: Persistent Organic Pollutants

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For personal reasons, I have been investigating environmental toxins and their effects on hormonal, neurological and reproductive health. The bioaccumulation of Persistent Organic Pollutants (POPs) within our bodies and the proliferation of POPs across the entire planet is frightening, but like most, I was not aware of the dangers. Despite the abundance of research linking POPs to many of the health epidemics we face here in the United States, such as Type II Diabetes and obesity, the public’s attention has not been directed to this man-made creation. Here is some of the research I found on persistent organic pollutants and what is being done to control our exposure to them.

What are Persistent Organic Pollutants?

Persistent Organic Pollutants, or POPs, are a number of organic (mostly man-made) compounds resistant to degradation by natural environmental processes. A number of POPs became widely utilized during the increase in industrial production post-World War II, a time when thousands of chemicals were introduced into commercial use. Many of these chemicals were proven effective in pest and disease control, crop production, manufacturing and industrial processes. Also in existence are a number of POPs which are “unintentionally produced chemicals” as the result of combustion (e.g., trash burning or municipal/medical waste incineration).

Why are Persistent Organic Pollutants So Bad?

Since they cannot be broken down via natural degradation in the environment, they are transported by wind and water. POPs are known for bioaccumulation in human and animal tissue and have become a part of the food chain, affecting all life on earth. Isolated communities, such as indigenous populations in the Arctic Circle, have a particularly high exposure risk to POPs.  POPs have been linked to disruption of our endocrine, reproductive and immune systems, neurological problems, diabetes, obesity and cancer. According to The United Nations Industrial Development Organization (UNIDO), the international community has been calling for “urgent global actions to reduce and eliminate releases of these chemicals.” A number of POPs are compounds the reader may be familiar with, such as DDT, PCBs, and HCH.

“The Dirty Dozen” and the Stockholm Convention

Coordinated by the United Nations Environment Programme (UNEP), The Stockholm Convention serves as “a global legally-binding instrument for targeting persistent organic pollutants.” The purpose of the Convention is to direct us toward a future free of POPs and re-shape the global economy in order to eliminate reliance on such dangerous pollutants.

The Convention initially identified twelve POPs (“The Dirty Dozen”) considered to be the most detrimental to the well-being of humans, animals and the environment. This measure created a system that allows for a greater number of chemicals to be identified as “unacceptably hazardous.” In accordance with the Convention, governments are obliged to eliminate or reduce the introduction of POPs into the environment. Such is done by channeling resources into “cleaning up existing stockpiles and dumps of POPs that litter the world’s landscapes.” The Convention was ratified May 17, 2004, with 150 signatory countries. As of February 20, 2013, Afghanistan acceded to the Convention as its 179th party. According to Kyoto Energy, the Convention aims to prohibit the production of POPs, with the exception of equipment currently in use; they have set a deadline for the elimination of the remaining usage for 2025.

Destroying and Transforming POPs in the Environment

The UNIDO website suggests that POPs stockpiles “must be destroyed in a manner which does not further degrade the environment by generating or releasing POPs.” The Convention calls for community participation, safety of the community, full disclosure of information, monitoring and release of data.

Details regarding the destruction process on the UNIDO website are vague; they suggest that traditional methods use “landfilling, ground storage, deepwell injection and combustion by open burning, incineration or in cement kilns or metal furnaces.” UNIDO stresses that there are “serious limitations” to the “normal incineration process,” considering that incineration can lead to the creation of dioxins, PCBs and HCBs. The quantities of POPs are rather difficult to estimate; almost no inventory exists. Kyoto Energy estimates that one million tons of PCBs and 100,000 tons of obsolete pesticides exist within countries that are not member to the Organization for Economic Co-operation and Development (OECD).

Are We Burying POPs for Future Generations?

Many of these methods do not entirely eliminate the problem. Rather, we are, quite literally, burying them for future generations to deal with – if we don’t burn this stuff and release it into the atmosphere first.

The United Nations Environment Programme (UNEP) suggests that high temperature incinerators, incineration in cement kilns and chemical treatment are proven methods of destruction. There is no evidence of this being true, and most research indicates that POPs are created as a result of incineration.  

A number of countries have continued to produce POPs such as DDT, with a staggering 3,314 tons (7,306,119 pounds) produced globally in 2009. On the bright side, this signifies a 43% reduction in DDT production from 2007. Considering the stability of POPs (i.e., resistant to degradation), it’s difficult to imagine any concerted effort can “undo” the damage that has already been dealt to the planet, especially since a number of POPs like DDT continue to be produced and exported in such exorbitant quantities.

It’s time to rethink our reliance on dangerous chemicals and the industries that use them. Though, many of these chemicals were developed before we understood their dangers, now that we know, it is difficult to support their continued use. With all of the advances in science, one would think we could design better, safer tools for industry, than the non-degradable, persistent organic pollutants we have now.

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Thanksgiving Dinner: Ideas for Diabetics, Vegetarians and Everyone in Between

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The holidays symbolize a joyous time of family, friends and food. As a big proponent of a plant-based diet, this time of year has usually served as a conundrum for me. While my family is carving the turkey and noshing on honey-baked ham, I have always found myself turning to the carbohydrate-heavy side dishes. I have decided I am done torturing myself and have taken to the Internet and vegan/vegetarian cookbooks for help in planning a healthy, plant-based holiday. Rather than turkey, I indulge in acorn squash stuffed with spinach and a bit of Gorgonzola (or, for my vegan audience, try a quinoa mushroom pilaf stuffing instead). The traditional turkey, stuffing and mashed potatoes is not necessary for a fulfilling holiday.  If you are curious about plant-based Thanksgiving dishes, I highly recommend sites such as The Post Punk Kitchen, Vegetarian Times or One Green Planet. For me, experimenting with new, healthier foods has been an exciting and challenging adventure.

Regardless of dietary status, it is important to recognize that the average person consumes anywhere between 5,000 to 6,000 calories throughout Thanksgiving Day. Such a deluge of food into the human body overworks our system. According to Joanna Gorman, a registered dietitian quoted in the Las Vegas Review Journal, insulin and the breakdown of fat kick into high gear and cause unnecessary strain and stress. For those among us who must monitor their insulin, there are a number of substitutions one can make on Thanksgiving, such as switching out potatoes for mashed rutabagas, parsnips or cauliflower for more fiber and lower carbs. Try sautéed green beans with garlic instead of casserole, which can be heavy with cheese and cream. Use whole-grain bread crumbs (or even brown rice) and double the veggies for your stuffing. The Mayo Clinic and dLife (a Diabetes resource site) both share a number of recipes and ideas for a healthful holiday.

The best way to avoid overeating for one big meal is to partake in smaller meals throughout the day. Portion control and light exercise is key; rather than sitting on the couch all day, maybe take a little walk around the block with a loved one instead. Listen to your body and don’t keep allowing yourself to eat out of boredom or based on the deliciousness of a particular dish. Not only should we keep ourselves from overeating, we shouldn’t push our loved ones to eat more when they are already sated either.

It is important to enter the holiday season armed with knowledge on how we can better care for each other and ourselves. Many choices we make during this time of year, such as overindulging in sweets or tripling our calorie count can be harmful to our bodies. I know I have made these mistakes many times and felt remorse and physical pain as a result of my overeating. I truly hope these resources will allow my readers to seek out new and interesting recipes and partake in a healthy and happy holiday season.

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My Experience with Women’s Health, Endometriosis and Hormone Research

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My journey into the fascinating world of hormone research officially commenced in 2007, when I joined together with group of psychology and anthropology students who decided to create the Hormones and Disease Group at University of Nevada, Las Vegas. Our goal was to disseminate information about diseases and research via workshops, lectures and presentations to the UNLV community, as well as the greater Las Vegas community. We wanted to not only enlighten ourselves, but to help other students and community members who may suffer from health problems such as Polycystic Ovarian Syndrome (PCOS), endometriosis, diabetes and cancer (to name a few).

Hormone Research, Endometriosis and Misdiagnosis

I became further involved with hormonal research in the winter of 2008 after one of my professors from UNLV’s Anthropology Department introduced me to Dr. Chandler Marrs and the Maternal Health Lab. At the time, I was under the impression (thanks to a misdiagnosis) that I suffered from endometriosis, and with a desire to learn more about myself and other health issues specific to women, I became an undergraduate research assistant for Dr. Marrs. I believed that women’s health research was severely under-funded (a position I maintain), so in my mind, Dr. Marrs and her students were a beacon of light in a confusing, dark world filled with many questions and not nearly enough answers. Personally, I assisted with human menstrual cycle research and the role hormone fluctuation plays in the lives of young women. I believe this type of research is incredibly necessary for understanding the connection between our bodies and minds.

As someone who lived approximately 6 years of her life believing she suffered from a disease she did not have, I understand the desire to self-educate as well as assist others in understanding their own bodies, pain management techniques and alternative treatments. Not only was I coping physically with pain, I had to psychologically deal with my diagnosis and what the possible implications of endometriosis are. I went through a number of gynecologists and it took many years for my diagnosis to be corrected (I had a hernia that was creating scar tissue around my uterus and intestines). The discovery of this was a shock; not only can a hernia be fixed rather easily, I had grown accustomed to the role of an endometriosis patient seeking answers for herself and others in the same situation. However, looking at this from a positive perspective, this misdiagnosis had opened me up to a realm of health I likely would have not been so interested in.

In tandem to my position with the Maternal Health Lab, I have also conducted independent, original research for diabetes and alternative medicine as a student of medical anthropology. For me, food is a large aspect of our lives that can either hurt or harm us; it can be poison or medicine. In my opinion, the link between diet and health is incontrovertible. The more this is part of the public discussion, the further we can raise awareness and help people make better lifestyle choices. Personally, I am curious about the connections that exist between our dietary choices and how they can interact with our hormonal pathways. I believe Lucine Biotechnology is a sorely needed resource for women who are tired of having unanswered concerns and questions and I look forward to contributing to the Lucine community.

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