diabetes

What If We Are Wrong? Medication, Medical Science and Infallibility

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What if we are wrong? Such a simple question, but one that seems all but absent in modern medicine. Patients, particularly women, routinely present with chronic, treatment refractory, undiagnosed or misdiagnosed conditions. More often than not, the persistence of the symptoms is disregarded as being somehow caused by the patient herself. If the tests come back negative and the symptoms persist, then it is not the tests that are insensitive or incorrect but the patient. If the medication prescribed does not work or elicits ill-understood side effects, then somehow the patient is at fault. If the patient stops taking the medication because of said side-effects, then they are labeled non-compliant and difficult. The patient is always at fault. It is never the test, the disease model, or the treatment.

What if we are wrong? What if the tests to diagnose a particular condition are based on incorrect or incomplete disease models? What if a medication universally prescribed for a given condition doesn’t work or creates adverse reactions in certain populations of people? What if the side-effects listed are incomplete? Is it so difficult to admit that gold standards evolve or that medical science is fluid? Certainly, if a patient is presenting with a constellation of symptoms that create suffering and those symptoms do not remit with a given medication or medications and/or do not appear on the available diagnostic tests, why is it so difficult to consider that either the medication doesn’t work, the diagnostic was insufficient, or the diagnosis itself was incorrect? Why is it that we assume it must be a mental health issue or somehow the patient is causing the symptoms herself?

Here, one doctor tells how he learned that he was wrong about diabetes and metabolic disorder. He gleaned this not from a book or from his training and not from listening to his patients, but when he, a previously healthy young man, developed a metabolic syndrome that led to obesity and type 2 diabetes. It was by his own personal crisis that he began to question the model of diabetes and its relationship with obesity. Dr. Peter Attia asks:

What if we are wrong?

What if we are wrong, indeed. There are so many areas of medicine where we may be wrong; where we are likely wrong, but where no one is asking the question.

We congratulate Dr. Attia for his discovery, but why does it take a personal crisis for a physician to question the status quo? Why is there such fealty to particular disease classifications or disease models even when there is evidence to the contrary? Is it the nature of modern medicine to lay down guidelines and be done or is it simply human nature to resist the notion that we can be wrong? Maybe a combination of both; I don’t know the answer, but I do know that if one is certain of everything there can be no room for learning or discovery.

On the other hand, if we begin with the notion that humans, and thus, the structures humans create are fallible – that we do not know or understand everything – and if we add to that humility a dose empathy, perhaps then we can begin healing patients rather than managing them.

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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.

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This post was published originally on Hormones Matter in July 2013.

Metformin: Medical Marvel or Magical Medicine?

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I am not a big fan of metformin (Glucophage). My disdain for metformin stems not from its efficacy. Metformin is quite adept at lowering blood sugar. In that sense, it is a medical marvel. Consider a pill that will ensure that no matter the individual’s intake of sugar, blood glucose measurements will magically fall within a normal range. What a wonderful invention – to have one’s cake, eat it too, and all the while, maintain normal blood sugar – who wouldn’t want that?

Alas, however, like all magic tricks, when the sleight of hand is revealed, the luster is lost. In the case of metformin, the underlying prestidigitation is not so magical after all. Metformin, like other wonder drugs, treats a symptom of a much greater problem; a symptom that in reality is just a visible sign of a necessary and protective innate process designed for cellular survival. The symptom is insulin resistance, the problem is too much dietary sugar and too few nutrients – an insidious form of high-calorie malnutrition that at once overloads cellular and mitochondrial processing capacities and starves the cells of critical nutrients.

Nutrients – They’re Necessary

A little-appreciated fact in modern medicine, vitamins and minerals power all of the machinery involved in cell function and in mitochondrial energy production. No nutrients, no energy, cellular starvation (even in the face of weight gain), inflammation, dysfunction, and ultimately, death. In the face of too much sugar and not enough nutrition, insulin resistance seems perfectly logical. If cellular fuel is waning, why not keep a little extra floating around, but since the apparatus to process said sugars is crippled, we have to turn down the intake valves. I would argue that it’s not obesity causing insulin resistance, after all not all overweight folks have type 2 diabetes, and not all insulin-resistant diabetics are overweight. It’s the damned sugar and lack of other nutrients initiating insulin resistance. Both the insulin resistance and fat storage are survival mechanisms; ones that ultimately have pathological consequences, but survival mechanisms nevertheless. In fact, folks who are diabetic and overweight have a lower all-cause mortality rate than those who are diabetic and thin.

If the problem is high-calorie malnutrition, which manifests as elevated blood sugar and in many cases, increased fat storage, wouldn’t the more prudent solution be to rectify the problem, to cease sugar intake, and address the nutrient deficiency? Wouldn’t that unwind the damage and heal the body? I think so, but alas, that’s not what we do in modern medicine. No, we don’t correct the problem, we treat the symptom(s) and then we revel in all the cool mechanisms we can interrupt, never considering the bigger picture.

Metformin Usurps Cell Signaling

Metformin bypasses our cells’ innate response to too much of anything – downregulation or desensitization – by overriding the communication systems that control these functions. In this case, metformin becomes the signaling molecule that tells the liver if and when to release glucose into the bloodstream. From an engineering standpoint, it’s a fantastic workaround. No need to address the core problem, just rewire the communication and continue on as if nothing is wrong. The added bonus is that for all intents and purposes, it works. Blood sugar declines, as does some of the pathology associated with elevated blood sugar. A medical marvel, right?

Well, not so fast. It just so happens that we need those pesky nutrients to function and to survive. When we give metformin to individuals who are already in a state of malnutrition, we are effectively ignoring and extending the underlying deficiencies that initiated the insulin resistance in the first place. More importantly, and this is something that is missed almost entirely in western medicine, we are adding to the metabolic mess a chemical that directly leaches a whole bunch of nutrients on its own (which further disables cell function, increases insulin resistance, increases fat storage in the long term and all of the associated pathologies we have come to know and love). Furthermore, we’re disrupting energy metabolism – energy that all cells need to function – and while that may quell some pathologies in the short term, in the long term, we’re all but guaranteeing a progressive decline into ill-health, despite the cheerleading that suggests otherwise.

We Get It. Metformin Treats a Symptom Not the Root Cause. So What?

Why am I blustering on about metformin now, when I have done so on several occasions previously (here, here, and here)? Well, an emerging body of research is showing yet another set of mechanisms by which metformin derails health. It turns out, that in addition to depleting vitamins B12 and B9, which are responsible for 100s of enzymatic reactions and particularly important in central nervous system function including myelination (how many cases of diabetic neuropathy or multiple sclerosis are really vitamin b12 deficiency?) and tanking CoEnzyme Q10 which effectively cripples mitochondrial ATP production in muscles (and likely exercise capabilities) with the resultant loss inducing a whole host of pathological processes (muscle weakness, cognitive decline among a few), metformin also blocks vitamin B1 – thiamine – uptake by multiple mechanisms. And for kicks and giggles, it appears to interfere with the body’s innate toxicant metabolism pathways, the P450 enzymes, rendering those who use this drug less capable of effectively metabolizing a whole host of other medications and environmental toxicants.

Thiamine is Critically Important to Health

For those of you who don’t read our blog and/or are not familiar with thiamine and thiamine deficiency, let’s just say, thiamine is the granddaddy of nutrients, an essential cofactor at the top of the fuel processing pyramid. Without thiamine, food fuel from carbs and, to a lesser extent, fats cannot be converted into ATP. With declining fuel sources, mitochondrial functioning degrades as well and all sorts of diseases processes ensue.

Sit with that for a moment. We’re giving folks who already have an issue with converting foods to energy and who are already very likely nutrient deficient, a medication that blocks the very first step in that conversion process. Since metformin also blocks the lactate pathway and acetyl-coenzyme A carboxylase (an enzyme necessary to process fatty acids into fuels), blocking thiamine effectively shunts the mitochondrial input pathways. Mind you, this is in addition to blocking the critical electron transport functions – via CoQ10 – found at the back of ATP processing. Talk about an induction of energetic stress.

So What If a Few Vitamins Are Depleted?

I bet you’re thinking if these nutrients are so important and metformin is so dangerous, why isn’t metformin more toxic? After all, metformin has been on the market for over 50 years, is considered the first line of treatment for type 2 diabetes, and just about every research article published on this drug begins with a blanket statement that metformin has an excellent safety record.

Why, indeed? Let us consider what constitutes a safe drug?

In modern medicine, the notion of drug safety and toxicology are equated with acute reactions. For decades, we have been operating under the false assumption in medical and environmental toxicology that if something doesn’t kill us immediately it must be safe (and the equally false assumption that toxicological responses are necessarily linear). Many drugs (and environmental toxicants) are much more subtle in their damage. They disrupt systems that, in many cases, have the capacity to compensate, at least for a period of time and until a critical threshold is met. Mitochondrial energetics is one of those systems that is remarkably resilient in the face of a myriad of stressors, sometimes taking years for the damage to be recognized. With nutrient deficiencies, in particular, compensation is aided by continuously changing environmental and lifestyle considerations. Sometimes we eat very well and other times we don’t; sometimes life is good, other times, it is not. Stressors vary.

Nutrient Deficiencies Wax and Wane

With nutrients deficiencies, especially essential nutrients that require dietary intake, there can be waxing and waning of the symptoms that these deficits evoke as diet and other variables change. It’s not until one reaches a critical threshold that the deficiency is recognized if it is recognized at all. With thiamine deficiency, in particular, animal research suggests the threshold for severe symptoms may be as high as 80% depletion. Imagine a system that can maintain life in the face of up to an 80% deficiency. That is remarkable.

Symptoms of severe thiamine deficiency include those associated with a condition called Wernicke’s Encephalopathy, a serious and potentially fatal medical emergency with neurological and cognitive impairments, oculomotor and gait disturbances, and cardiac instability. With milder deficiencies, however, we see things like fatigue, muscle pain, mental fuzziness, GI disturbances, autonomic dysregulation, and a host of symptoms that can easily and incorrectly be attributed to other conditions and/or modern life in general.

Interestingly, once thiamine depletion reaches that critical threshold, it doesn’t take much thiamine to begin seeing improvement in the symptoms. In those same animal studies mentioned above, it took an increase of only 6% of the total thiamine concentration to begin the improvement. So with a change from 20 to 26% of recommended thiamine concentration, symptoms begin to dissipate, at least temporarily. Sit with than one for a moment – what a remarkable bit of resilience. It takes a full 80% reduction in thiamine stores before serious symptoms are recognized but improvement begins with only an additional 6% – when the system is still depleted by 74%.

Given the metabolic capacity to maintain survival in the face of all but critical deficiencies, it is easy to see how and why blocking these nutrients would not be considered dangerous or at least obviously so. The decline is so gradual in most cases, and likely waxes and wanes, that it becomes near impossible to attribute symptoms and underlying nutrient deficiencies to the offending medication(s). Unfortunately, just because we don’t recognize those patterns, doesn’t mean that they do not exist.

How Metformin Blocks Thiamine: The Technicals

Backing up just a bit, it is important to understand the mechanisms by which metformin reduces thiamine. When metformin is present, a set of transporters that normally bring thiamine into the cell to perform its task as a cofactor in the machinery that converts carbs to ATP, brings metformin into the cell instead, replacing thiamine altogether. The transporters involved are the SLC22A1, also called the organic cation transporter 1, [OAT1], and the SLC19A3. Conversely, when metformin is not present or at least not overwhelming all of the transporters as it is during the initial phases of absorption post intake, thiamine becomes available for transport. Since these transporters are not completely and continuously blocked (and there are other thiamine transporters), thiamine uptake occurs, just not continuously and just not at full capacity. This may be one reason why metformin is not as acutely damaging as some of the other drugs in its class, but make no mistake, it is still dangerous. Thiamine deficiency is deadly. With the right combination of thiamine blocking variables (other medications/vaccines block thiamine as well), thiamine concentrations can tank and even if the thiamine concentrations hover at a subclinical deficit, the likelihood of chronic illness is high.

Thiamine and Diabetes: Connecting a Few More Dots

A little over a year ago, I stumbled upon some research showing a high rate of thiamine deficiency in individuals with both type 1 and type 2 diabetes (75% and 64%, respectively). I wrote about that research in Diabetes and Thiamine: A Novel Treatment Opportunity. According to several studies, diabetics appear to excrete higher amounts of thiamine than non-diabetics. The research attributes this to either poor kidney reabsorption and/or mutations in the thiamine transporter genes that prevent absorption. None of the research detailed the medication usage of the participants, but one might expect a good percentage of the type 2 diabetics were using metformin. It seems reasonable that if metformin supplants thiamine uptake via the thiamine transporters mentioned above, then the body would excrete the unused thiamine, leading to a higher rate of thiamine excretion than observed in non-diabetics and a higher rate of thiamine deficiency in diabetics versus non-diabetics. Based upon this, additional clinical research has shown that thiamine supplementation normalizes, the aberrant processes activated by sustained hyperglycemia including:

Metformin, in treating a symptom rather than a root cause, is likely exacerbating, and perhaps even initiating, some of the very disease processes that it is intended to prevent. Although metformin is not often acutely toxic, the underlying mechanisms manipulated by this drug suggest that it is likely to induce and not prevent, as is so frequently suggested, chronic illness. From my perspective, that makes metformin a very dangerous drug.

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, and like it, please help support it. Contribute now.

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This article was published originally on Hormones Matter on February 16, 2016. 

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Food Composition and Hyperglycemia

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Over the last few months, I have written a number of white papers on thiamine for contract. They may or may not be published in part or in full at some future date. Among them, I was contracted to write separate papers about thiamine in diabetes, cardiovascular disease, and Alzheimer’s disease. As I began writing the first article, I realized that these were not separate topics. Rather, each disease process was simply a different manifestation of the same core problem: persistent hyperglycemia. This, in turn, was a direct response to our current ultra-processed, chemically-laden, refined sugar, garbage-food environment; a problem we all seem reticent to confront.

The garbage foods that we consume lead to metabolic dysfunction marked by, among other things, hyperglycemia. Hyperglycemia, in turn, leads to specific metabolic adaptations that result in the inability to efficiently convert consumed foods, not just sugars, but amino and fatty acids as well, into energy. (See here for details.) Poor energy metabolism then drives cravings and overeating as a compensatory reaction to increase metabolic energy, which in turn, further entrenches hyperglycemia and its metabolic cascades. It is a deadly spiral, the likes of which are evident in skyrocketing rates of metabolic ill-health. A recent study found that only 12% of the population, 20% if the authors were generous in their description, could be considered metabolically healthy.

From my perspective, it is this shift in metabolic capacity, in the pathways used to metabolize food that drives much, if not all, modern illness. Importantly, many of the disease processes we now consider to be separate entities, like diabetes, the various cardiovascular diseases, the neurodegenerative diseases like Alzheimer’s and dementia, cancer, and even the litany of chronic autoimmune, inflammatory, or pain and fatigue related disease processes, may not be separate at all. They may just represent the way the consumption of ultra-processed foods and the resulting hyperglycemia mix with the individual’s unique genetic and environmental circumstances to form disease. In other words, food provides the spark, hyperglycemia is the kindling, and how and where the flame burns is determined by the individual’s genetics and the totality of his or her life, lifestyle, and environmental exposures. It all begins with food though.

What Are Ultra-processed Foods?

Just about everything in the middle aisles of a super market or purchased from a fast food establishment would be considered ultra-processed. These products are:

…formulations of several ingredients which, besides salt, sugar, oils and fats, include food substances not used in culinary preparations, in particular, flavours, colours, sweeteners, emulsifiers and other additives used to imitate sensorial qualities of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product.

In other words, most of the American diet. These products are highly palatable, densely caloried (because of all of added sugars and fats), and loaded with synthetic chemicals, but have no discernable endogenous nutrient content. Sadly, almost 60% of the American diet for adults and close to 70% for kids aged 2-19 years is comprised of ultra-processed food products.

Processing is not the only problem though. Conventionally grown and raised food and livestock have all but bred out of their products any semblance of nutrition in favor of bigger, faster-growing, and more attractive products. In the place of nutrients, we get excess sugars (yes, conventionally grown produce has a higher sugar content than organic or that was grown in the past), along with lots of herbicides, pesticides, hormones, antibiotics and veritable laundry list additional mitochondrial poisons. From farm to table, the composition of modern food products is lacking nutrients while rich with potential anti-nutrient and toxicant compounds. Is it any wonder only 12-20% of the population can be considered metabolically healthy or that hyperglycemia drives modern illness?

Why Hyperglycemia?

Backing up just a bit, let us talk about how discussions of hyperglycemia are framed conventionally and what that has to do with the composition of the foods we ingest. Most discussions of hyperglycemia involve either the absence of sufficient insulin as in the case of Type 1 diabetes or a developed resistance to insulin as in the case of Type 2 diabetes. In either case, there is insufficient insulin available, either absolutely or relative to need, to transport glucose from the bloodstream into the cells and this results in hyperglycemia. Much of the research involves defects in pancreatic islet cell function, glucose receptors and transporters relative to these diseases. In general, diet exacerbates hyperglycemia. With type 2 diabetes, however, diet accounts for almost all of the disease process itself. In many, but not all cases of type 2 diabetes, diet also induces obesity and may provoke a host of additional disease process affecting the heart and the brain. Indeed, Alzheimer’s disease is now considered an outgrowth of persistent hyperglycemia and has been categorized as type 3 diabetes.

This linkage of diabetes with obesity leads many to conclude that if the individual just reduces his/her calories and/or increases activity and loses weight, the diabetes, the obesity, and the assortment of other disease processes that ensue, would resolve and/or be prevented. For some this may be true, but if the persistent rates of obesity, despite reductions in caloric intake are any indicator, this aspect of diet is only indirectly related to the disease at hand. My research involving the some of the metabolic pathways associated with hyperglycemia, leads me to believe that hyperglycemia represents more than just an excess of calories, carbohydrate or otherwise, and that changes to pancreatic islet function, and glucose receptors and transporters are simply adaptive response to ailing mitochondrial metabolism. What is causing metabolism to fail? The American diet of ultra-processed food-like products that are high refined sugars, trans fats and chemical toxins, but low in usable macronutrients and micronutrients – that is the root of these illnesses.

Micronutrient Deficiency Underlies Hyperglycemia

Adenosine triphosphate (ATP), the fuel source for cellular function, the energy currency that all organisms require to survive, is derived entirely from food. The foods we eat provide the macronutrients – protein, fats, and carbohydrates, and the micronutrients –vitamins and minerals – that, with a little oxygen, are then processed by the mitochondria into ATP. Absent frank starvation, the key variables in this process are the micronutrients. Thiamine and its activating partner magnesium are especially important because they manage the gates to this process. Micronutrients derived from foods allow for the catabolism of consumed macronutrients so that it may be turned into ATP. Vitamins and minerals fuel the enzymatic machinery that allows energy factory to work. Insufficient micronutrients slow down enzyme capacity (the energy machinery), causing a backup of macronutrients (a supply excess), at the gates. That excess has to be dealt with. Some of it is forced through alternate pathways that, through a variety processes, break down and salvage some of the macronutrients as a way to temper the backup, but most of the excess either just floats around in the blood or is stored in the fat cells. The glucose that floats around in the blood and desensitizes the glucose receptors and transporters and re-regulates pancreatic islet function – that is hyperglycemia. The glucose that is stored as fat – that is obesity.

Those macronutrients that cannot be processed because of absent micronutrients, not only lead to the hyperglycemia cascades and the various diseases processes associated therewith, but their consumption produces little to no energy or ATP and, in most cases, consumes it. In other words, despite ingesting an excess of calories, the mitochondria, and thus the human in which they reside, are starving. If macronutrients cannot get into the factory, the factory cannot produce ATP. The result is cravings and overeating, which no amount of willpower will overcome. This is why a simple reduction of caloric intake, absent recognition of food composition, does not work for many with type 2 diabetes. They are already starved for energy. Proteomic studies in rodents fed comparable diets illustrate this pattern of poor energetic capacity with reduced expression of the proteins involved in energy metabolism and increased expression of those marking oxidative stress and aberrant cell proliferation (cancer pathways).

A Technical Aside

In more technical terms, when the excess sugars cannot be processed via oxidative phosphorylation or through the pentose phosphate pathway – processes that ultimately produce ATP and other important substrates – they are diverted through salvage pathways like the polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE pathways. This leads not only to decrements in ATP production but the macro- and microvascular cell damage associated with persistent hyperglycemia leading to heart disease and neurological dysfunction.

Similarly, in the absence of sufficient micronutrients, thiamine in particular, the catabolism of branched chain amino acids suffers, resulting in increased branched chain keto acids, especially short and medium chain acylcarnitines. Surplus acylcarnitines then overwhelm the b-oxidation pathway involved in fatty acid metabolism. This, in turn, leads to incomplete fatty acid metabolism (dyslipidemia) and the formation of the pro-inflammatory diacylglycerol and ceramides associated with metabolic dysfunction. The hyper-activation of ceramide synthesis expedites cell death, blocking complex 3 of the electron transport chain in the mitochondria.

Inadequate micronutrient availability, and again, thiamine and magnesium especially, further imperials the alpha oxidation of fatty acids. This is the step before beta-oxidation. Poor alpha-oxidation results in increased phytanic acid and disrupted sphingolipid homeostasis; two patterns with linked with a variety of neurological sequelae. All of this is linked to persistent hyperglycemia, which evolves from inadequate micronutrient content relative to demands.

Coincidently, COVID death is linked to both increased ceramide synthesis and disturbed sphingolipid homeostasis.

We postulate that SARS[1]CoV-2 causes endothelial damage by binding ACE2 and misbalancing the renin-angiotensin pathway, dysregulating sphingolipids and activating the ceramide pathway, known to mediate endothelial cell apoptosis in the setting of radiation damage. Such injury also generates reactive oxygen species, vasoconstriction and hypoxia, and ultimately the deposition of platelets on an exposed vessel basement membrane initiating the intravascular coagulopathy and multi-organ failure, pathognomonic of severe COVID-19 and death.

Underlying both processes are micronutrient deficient patterns of hyperglycemia, e.g. insufficient thiamine, magnesium and likely other nutrients, but most have not been investigated. Inasmuch hyperglycemia accounts for much of the risk for COVID severity, it is difficult not wonder if these pathways were not already entrenched pre-virus and the virus simply escalated the negative adaptations beyond rescue.

Food Composition Matters More Than Caloric Intake

From this perspective, it is clear that it is not solely an excess of calories that causes hyperglycemia, or even an excess of carbohydrates, although both play a large role. It is the quality or composition of the food that is the problem. Modern foods are calorie dense, sure, primarily because of the use of refined sugars and added fats. They are also loaded with chemical poisons, which we all seem to disregard as important. Carbohydrates derived from natural, organic, and unadulterated fruits, vegetables and grains, carry with them vitamins, minerals, fiber, and proteins that allow the body to convert the macronutrient substrates into useable energy. Indeed, a diet rich in these types of foods is unlikely to induce hyperglycemia or obesity. In contrast, processed foods, while high in carbohydrates, fats, and chemicals that are toxic to the mitochondria, carry few to no micronutrients, little to no fiber, or other compounds that can be used by the body to produce ATP all the while carrying an abundance of chemical toxins. From a metabolic standpoint, ultra-processed foods are nothing more than edible poisons. They demand more energy to process than they add and wreak havoc with far more systems than were illustrated here. The hyperglycemia and associated damage that ensues is evidence of this process. If we are to tackle these health issues, the entirety of modern food landscape relative to metabolic health must be addressed.

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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.

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This article was published originally on October 28, 2021. 

A Rant About Diet and Responsibility

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The American diet is atrocious and largely responsible for the growing epidemics of diabetes, cardiovascular disease, and obesity, not just in America, but worldwide. The highly processed, high calorie, high fructose corn syrup and hydrogenated fat, and high chemical additive products that line grocery stores are products of American ingenuity; products that we have exported internationally, and sadly, products that are responsible for the declining metabolic health worldwide. This is a fact that many of us are reticent to accept. We are poisoning ourselves and everyone else around us by the products we make and consume.

A recent study found that fully 80% of metabolic disease can be attributed to lifestyle, e.g. poor diet and a lack exercise. Eighty percent. That is a staggering finding especially when one considers that 476 million people worldwide have diabetes, most of them Type 2 (T2). This represents a 129% increase since 1990, when the number stood 211.2 million. During the same time frame, the rates of cardiovascular disease have increased from 271 million to 523 million. Underlying a significant percentage of these conditions is the obesity epidemic, with 13% of the world’s population considered obese and 39% considered overweight and heading towards obesity.

In the US, the situation is quite dire, only 12-20% of the population, depending upon the criteria utilized, are considered metabolically healthy. Clearly, our approach to metabolic health is not working and yet, much of the focus in health research remains centered on either identifying that one medication or combination of medications that resolve all of our bad choices or an overly simplistic approach to health represented by balancing the calories in/calories out equation. As evidenced by the exploding numbers of metabolic disease, neither of these perspectives seems particularly useful.

While both personal choice and calories play a role in these epidemics, the problem is much broader. The food ecosystem has been decimated and in its place, we have non-nutritive chemical-toxicant food-like products that were designed to be highly addictive. When consumed, these products fundamentally change the metabolism of the individual who consumes them, and not for the better. Every bite of a chemically processed food is one step closer to metabolic disease. Beyond that however, the choice to allow industry to create, utilize, and ultimately dump these chemicals into food, other products, and into the environment, rests on us as well. Those are choices too; choices that affect the metabolic health of communities, and more broadly, the world.

We tend to think of industry and the pollution they create as amorphous, self-propelling and promoting agents of doom, forgetting of course, that each and every one of these organizations is made of people; people like you and me who make decisions to produce and promote these chemical poisons; people who choose to put poisons in foods under the auspices of the pathetically weak and ineffective GRAS guidelines. People make these choices. We do not get forever chemicals that fundamentally disrupt all aspects of metabolism without people who chose to create them, others who chose to use them in common products (and deny any and all risk), and all of us who relish in the novelty of these products. We do not get 80,000 synthetic chemical entities currently on the market without people putting them there. We do not get 1.8 billion pounds of glyphosate used every year, enough for every person on the planet to consume 4lbs annually without people that made choices to produce, use, and not regulate this chemical. We are the problem. We made these choices. We are the ones who are destroying our health and the health of others by the choices we make.

So when we look at the skyrocketing numbers of diabetes, cardiovascular disease, and obesity, it is not enough to say ‘eat better and eat less’. We need to clean house, top to bottom. We need to stop producing the garbage food that pollutes our bodies and the environment. We need to take responsibility for all of the choices that lead us to the point where only 12-20% of the population can be considered metabolically healthy.

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. 

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Pregnancy Toes – What Sugar Does to Feet

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Pregnancy toes are really swollen feet and swollen toes. The name stuck in my mind because one of my daughter-in-laws is pregnant and I was sent a photo from her winter vacation in her flip flops in the snow and winter coat—she was not able to put her boots on because of her swollen feet (swollen even in the cold!).

I did not think much about it until she came to visit me yesterday and I noticed the flip flops and her chubby toes. She had “pregnancy toes” again she said. It then suddenly all became clear. I asked her: did you by any chance have any sugar today? And she said “as a matter of fact, yes!”

I reached for my salt pills that I use for my migraines as do all members in my migraine group on Facebook and handed her one. I really should have photographed what happened but I did not think the effect was going to be so fast and so big. Less than 15 minutes after she took the salt pill and a glass of water, her toes went back to normal. We ended up laughing it away. Had she known this, she could have worn her boots in the snow after all!

So what did her pregnancy toes have to do with sugar and salt you may ask? Previously, I quoted from the Harrison’s Manual of Medicine an important paragraph that I repeat here:

…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)

The above means glucose (part of sugar) and sodium (part of salt) are in inverse relationship. As you increase sugar, salt drops and water is sucked out of your cells by sugar like a giant Slurpee machine. The water then collects on the outside of your cells rather than the inside, thereby dehydrating your cells and at the same time make your body swell. Edema is often associated with too much salt, but in fact, it is too much sugar. Being always thirsty is associated with Type 2 Diabetes but it is also associated with not having enough salt in the body since without salt the cells cannot get hydrated.

In light of this fragile balance between sodium and glucose in the blood, are we treating pregnancy edema, gestational diabetes, and other maternity complications, the way we should? Consider that with pre-eclampsia (gestational hypertension), women are told not to eat salt. You can see what happens when we reduce sodium: glucose increases and we also induce an ionic imbalance. This ionic level imbalance is visible (like the swollen toes) and may lead to further complications. There are two problems that we are facing here: first if she does not eat salt, her sodium-potassium pumps cannot work–this may cause migraines and headaches as I often see in my migraine group. Secondly, as you saw the fragile balance between the see-saw action of glucose and sodium, if she stops eating sodium her glucose may increase, causing swelling. This is an interesting theory to ponder – one that merits research.

Sodium and Glucose Work Together

Salt breaks up in the body into sodium and chloride. Sodium attracts water and holds onto it inside the cells. It keeps chloride outside of the cells to ensure proper voltage and electrolyte balance with the aid of potassium. When you eat sugar, the glucose part of it removes the water from the cells via osmotic channels that are too narrow for the sodium ions to exit. Thus, one ends up with a ton of water outside the cells with sodium inside hugging a tiny amount of water. Swelling occurs as the water leaves the cells but remains between cells.

Given the inverse nature of glucose and sodium in the blood, if one is swollen as a result of too much sugar, eating salt will take the water back from sugar and move it back into the cells–as it did for my daughter-in-law’s pregnancy toes. What is important in this information is this:

  1. If you feel swollen after eating sweets, you need to eat salt and drink a bit of water to reduce your swelling.
  2. If you have Type 2 Diabetes or are hypoglycemic, eating a salty meal can give you a major sugar crash and land you in the hospital!
  3. Eating sugar of any quantity will dehydrate your cells and you and make you run to the toilet every 30 minutes.

Because glucose takes water out of the cells, the edema that follows increases extra-cellular water and causes swelling in the body. This extra-cellular water needs to be reabsorbed into the circulation for the kidneys to be eliminated. To be reabsorbed, sodium is necessary since without sodium, the cells cannot operate their voltage gated sodium pumps and so the gates cannot open to grab glucose to take it into the cells and to get the water back into the cells. I think you can already see the contradictions in the logic of reduced salt: the mom-to-be is told to not eat salt, this causes extra-cellular water and swelling, which needs salt to be reabsorbed into her cells for clearance by the kidneys but which she is not allowed to eat. This way ionic level balance is not possible and chain reactions may occur with negative consequences. She may have protein leaching into her urine, extra hard kidney work, and a whole other long chain of complex events may kick in to make pregnancy a rather unpleasant experience risking the health of the fetus.

The amount of extra-cellular water is very hard for the body to get back into circulation without salt and may take days, taxing the kidneys with the volume of water leaving and increasing pressure on the blood vessels from the outside, causing high BP. However, as the volume of water is leaving the body finally, this reduces blood pressure. When a pregnant woman’s blood pressure drops as a result of all that water leaving, the dehydrated blood cells carry less oxygen. This indicates reduced oxygen for both her and the baby.

By telling mothers to reduce salt intake, glucose increases, which increases blood pressure (BP) rather than reduces it. The similar phenomenon happens in gestational diabetes. In gestational diabetes (and gestational hypoglycemia as well) the sugar level is unstable and is either too high or too low, respectively. Should the mother-to-be eat a salty pickle (as cravings always dictate pickles), she may end up in a major sugar crash and in the hospital for immediate treatment.

The balance between sodium and glucose is very fragile and extremely quick changing as you could see on my daughter-in-law’s foot. Interestingly we now also know that salt does not increase blood pressure but sugar does and so a reduced salt diet automatically increases blood pressure because of the glucose and sodium inverse connection and sugar’s dehydrating properties. Reduced salt also increases triglycerides (Graudal, 2011), causing a lot of problems for people with preexisting heart conditions. So by reducing the salt intake of the mothers to be, are we creating diabetic mothers and/or babies? Babies have been born with diabetes 2!

Is it possible that we are giving the wrong advise to pregnant women about salt and sugar? It’s an interesting question to pose and further research is badly needed. Knowing that salt and sugar are in inverse proportion in the blood, one may suggest eating them together. In fact, eating them together is a much better idea than eating sugar alone. It is best to not eat sugar at all but if you must eat sugar, consider eating salt too.

Sources:

Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Graudal et al., Cochrane Database Syst Rev. 2011 Nov 9; (11).

This article was published originally on Hormones Matter on February 15, 2015. 

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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.

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Thiamine Deficiency and Sugar in Diabetes

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Thiamine is one of the B vitamins and I need to explain its action. To put it as simply as possible, it regulates sugar metabolism in every cell within the body and has a special importance in the brain. About four years ago a researcher in England reported that there was a mild deficiency of thiamine (vitamin B1) in diabetic patients, a disease that affects sugar metabolism. He said that all diabetics should have a supplement of thiamine because he had anticipated that it will prevent complications in this devastating disease. If that is not enough to make a diabetic sit up and take notice I would be very surprised.  I will try to explain this a little further.

A program on PBS television called “The Quiet Revolution” reported that there were 29 million patients in the United States with type two diabetes and as many as 70 million with pre-diabetes, meaning that they were on their way  to contract the disease. If we had 29 million cases of “flu” it would be called a pandemic. Most people with type 2 diabetes have no idea that their health before the onset of the disease is within their own responsibility. Our culture says “go ahead, do what you like, eat what you like, drink what you like; if you get sick, it is just bad luck and you go to one of those clever characters called Dr. who will produce the magic bullet that “cures” you because of the wonders of modern scientific medicine.

Although both types one and two have different causative factors, I want to emphasize very strongly that both types are not purely genetically determined. The genetic risk in type 1 is much greater than in type 2 and is certainly the major component as the underlying cause. Type 2 is much more clearly initiated by dietary indiscretion in a person who might be, shall we say, at genetic risk. Much of our diet today involves the consumption of man-made foods developed by the food industry. Of course, the main drive of this industry is to sell their products and so it appeals to our palatability, a sensory phenomenon that has nothing to do with good nutrition. We all know what pleasure we get from tasting anything that is sweet. Since sweetness sells, it explains why so many man-made foods are laced with sugar, so long thought to be harmless and even good for you by supplying quick energy.

Sweet and Dangerous: Sugar and Thiamine Deficiency

In 1973, John Yudkin, a professor of nutrition in a large London Hospital wrote a book with the title “Sweet and Dangerous”, the result of his many years of research into the dangers of sugar.  He reported that many diseases, including heart disease, were related to its ingestion. As so often happens, this terribly important book was ignored and cholesterol became the demon for the cause of heart disease. Now, 40 years later, many people know that the cholesterol story has been debunked. Because sugar requires vitamin B 1 to metabolize it, in much the same way as gasoline requires a spark plug to burn it, taking sugar on its own in the form of empty calories easily overwhelms the power of thiamine to carry out its function.

That means that you have an imbalance between the calories and the vitamin or a relative deficiency of thiamine. Your daily intake of thiamine may be sufficient for a good diet but not enough to take care of the overload of sugar represented as the bad diet which is so common.  It may easily be accomplished by the consumption of the stuff that we consume in our social activities.  Yes, there is no doubt that it makes the mouth water and the sweetness underlies the joy of the social event but if it is causing widespread disease, I ask you, is it worth it?

The lower part of the human brain is particularly sensitive to thiamine deficiency and because this part of the brain organizes the entire body in its performance of adapting to the environment in which we find ourselves, we easily become maladapted. For example, we may feel cold when it is hot or hot when it is cold, a mistake in sensory input and brain interpretation. The nervous system involved in this reaction is known as the autonomic nervous system and is entirely automatic.  The message from the brain to the heart causes it to accelerate when it is a necessary adaptive need as, for example, running for a bus.  But when this happens spontaneously for no apparent reason at all, we might take this to a physician and tell him that “I have palpitations of my heart”.  Unfortunately the medical focus would be on the heart not on the nervous system that caused the acceleration. For this reason one of the complications in diabetes is called “autonomic neuropathy”, meaning that the autonomic nervous system is disorganized. Thiamine protects diabetics from complications because it improves the ability of our cells to produce adequate energy for function by “burning sugar as brain fuel”.  Think of it as a change of inefficient spark plugs in a car engine.

Thiamine deficiency is sometimes referred to as pseudo (or false) hypoxia because it results in exactly the same symptoms as those from a mild to moderate deprivation of oxygen. Its effect on the lower part of the brain is to make it more reactive to all input signals. When you read a telegram giving you bad news, your eyes send a signal to the brain that has to interpret the meaning of the signal. I refer to the input signals, whether they are physical or mental, as “stress”. Your response to the stress is organized by the lower brain with “advice and consent” from the higher brain. Freud referred to the lower brain as the “id”. It reacts automatically to anything perceived as danger or self indulgence and the upper brain as the “ego” because it either permits or prevents the ensuing action. It is our moral censor.

I have studied the effects of this kind of “high calorie malnutrition” and it is responsible for a huge amount of mental illness and unpredictable bad behavior. It makes the “id” irritable and weakens the “ego” making a person much more likely to act in response to a whim or a nursed grievance.  There is much evidence that it can even affect criminal behavior.  This kind of malnutrition is widespread in America, but I have never seen it discussed in relation to whether the behavior exhibited at inexplicable school shootings is a potential factor. A recent exhibition of “road rage” projected on TV news might just be comprehensible because it was otherwise well beyond civilized behavior. Although this may sound too far-fetched, we have an epidemic of Attention Deficit Disorder, with or without hyperactivity, learning disability and obesity in our children that defies a genetically determined cause. Nature does not make that kind of mistake in so many individuals. Their young brains are irritable and disorganized because of dietary indulgence.

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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.

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Diabetes: Another Problem With Hormonal Birth Control

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Diabetes is the 7th leading cause of death in the United States according to the American Diabetes Association. Tens of millions of people have diabetes and are at increased risk for a whole host of other problems because of it. The estimated economic cost of diabetes is nearly $245 billion each year. BILLION! So shouldn’t we take a look at how to decrease these risks, lessen this economic burden, save lives?

I’ve done a lot of research on birth control pills, their side effects, and how those risks are communicated to women. My interest in the topic is both personal (I suffered a stroke from hormonal birth control at age 28) and professional. I’ve been reviewing the Nelson Pill hearings and what I’ve found is shocking. Beyond the obvious correlation between blood clots and hormonal birth control, even back in 1970 doctors and scientists knew that these medications affected, contributed to, and caused a myriad of health problems from weight gain to stroke. One of the most surprising to me, because I hadn’t come across it in any of my previous research, was the link between synthetic hormones and diabetes. Dr. Hugh J. Davis, the first doctor to testify at the Nelson Pill Hearings said the following (page 5930):

“A woman, for example, who has a history of diabetes or even a woman with a strong family history of diabetes is not an ideal candidate for using oral contraceptives… [they] produce changes in carbohydrate metabolism which tends to aggravate existing diabetes and can make it difficult to manage.”

Hormonal birth control elevates blood glucose levels, can increase blood pressure, increases triglycerides and cholesterol, and accelerates the hardening of the arteries, among other things. They knew this in 1970. But what about the research now? Well, if you’ve read any of my other articles it probably won’t surprise you that the current research is… wait for it… you guessed it… INCONCLUSIVE! Here’s a look at what I’ve found:

“Cardiovascular disease is a major concern, and for women with diabetes who have macrovascular or microvascular complications, nonhormonal methods are recommended. There is little evidence of best practice for the follow-up of women with diabetes prescribed hormonal contraception. It is generally agreed that blood pressure, weight, and body mass index measurements should be ascertained, and blood glucose levels and baseline lipid profiles assessed as relevant. Research on hormonal contraception has been carried out in healthy populations; more studies are needed in women with diabetes and women who have increased risks of cardiovascular disease.

 

And:

“The four included randomised controlled trials in this systematic review provided insufficient evidence to assess whether progestogen-only and combined contraceptives differ from non-hormonal contraceptives in diabetes control, lipid metabolism and complications. Three of the four studies were of limited methodological quality, sponsored by pharmaceutical companies and described surrogate outcomes. Ideally, an adequately reported, high-quality randomised controlled trial analysing both intermediate outcomes (i.e. glucose and lipid metabolism) and true clinical endpoints (micro- and macrovascular disease) in users of combined, progestogen-only and non-hormonal contraceptives should be conducted.

 

Not enough evidence is available to prove that hormonal contraceptives do not influence glucose and fat metabolism in women with diabetes mellitus.”

For women with polycystic ovarian syndrome (PCOS), this is particularly troubling. They are already at an increased risk for diabetes. “Researchers in Australia collected data from 6,000 women and found that those who had PCOS were three to five times more likely to develop type 2 diabetes than women who didn’t.” Yet the first treatment doctors usually prescribe for PCOS is birth control pills. It’s unclear whether the PCOS alone increases a woman’s risk or just that most women with PCOS are treated with hormones that make her more likely to develop diabetes.

It begs the question, why are we treating a woman for a condition that increases her risk for diabetes with a drug that increases her risk for diabetes?

Even if you don’t have PCOS, you are still at risk. A recent study showed that “women who used hormonal methods of birth control had higher odds for gestational diabetes than did women who used no contraception.” So using hormonal birth control may prevent you from getting pregnant but at the cost of making a future pregnancy more dangerous? It’s not just dangerous for pregnant women, however. Hormonal contraceptives seem to predispose women to diabetes across the lifespan. For example, another study found:

“The prevalence of diabetes was significantly higher in post-menopausal participants who had taken OCs (oral contraceptives) for more than 6 months than in those who had never taken OCs. The duration of OC use was also positively associated with the prevalence of diabetes. Furthermore, taking OCs for more than 6 months led to a significant increase in fasting insulin levels and HOMA-IR in nondiabetic participants. Past use of OCs for more than 6 months led to a significant increase in the prevalence of diabetes in post-menopausal women, and increased IR in nondiabetic participants. These results suggested that the prolonged use of OCs at reproductive age may be an important risk factor for developing diabetes in post-menopausal women.”

This is further proof that taking hormonal birth control affects women for much longer than the duration they take it. A correlation between synthetic hormones and diabetes was evident to doctors and researchers back in 1970 and we’re still trying to understand those effects today. Dr. Hugh Davis testified (pg 5928) about hormonal birth control:

“While you are accomplishing your contraceptive objective you are producing very, very widespread and generalized changes.”

I’m starting to feel like a broken record here, but at what point are these risks not acceptable? And why do we still not fully understand these risks? The goal of the Nelson Pill Hearings was to determine if these medications were safe and they are clearly not. Over and over, experts testified and said the pill should not be taken off the market but that it should be studied more and replaced by something better as soon as possible. As we can see, that hasn’t happened. Women are still having to make the choice between convenient contraception and their health and safety. The risks involved with hormonal contraceptives are still being downplayed, skewed, and hidden. If a serious and potentially life-threatening condition like diabetes is not too high a price to pay to avoid pregnancy, what is? How about loss of libido? Mental health? Weight gain? Blood clots? Stroke? Loss of life? Dr. Davis also said (pg 5925):

“In using these agents (hormonal contraceptives), we are in fact embarked on a massive endocrinologic experiment with millions of healthy women.”

I couldn’t agree more. And the experiment continues.

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. 

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5 Surprising Reasons Not to Use Hormonal Birth Control

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The following is a list of some the health factors that increase your risk of side effects from taking hormonal birth control. It is by no means a complete list of contraindications but you may find some of these surprising. I know I did.

Five Reasons You May Want to Reconsider Hormonal Birth Control

Reason 1: Smoking and Age

You are probably familiar with these warnings. You may have heard them on television commercials or seen them on magazine advertisements. Or maybe you read my article about risk communication and saw them there. The problem with these warnings is that the wording makes it seem like you are only at risk if you are over 35 and a smoker. But the truth is that these two risk factors stand independent of each other. You are at increased risk if you are over 35 years of age. You are at increased risk if you are a smoker of any age. And if you are a smoker who is over 35, you have an exponentially higher risk for blood clots when using hormonal birth control.

Reason 2: Migraines

According to a 2010 article in the Reviews in Obstetrics and Gynecology, 43% of women in the United States suffer from migraines. That’s a huge number of women. Also, according to the same article, 43% of women using birth control are using hormonal contraception (the pill, rings, shots, implants, etc.). I’m not a statistician but I’m guessing there is some overlap between the women that suffer migraines and the ones using hormonal birth control. This is problematic for two reasons:

  1. A great deal of evidence suggests that migraine, particularly migraine with aura, is associated with an increased risk of ischemic stroke, and that this risk may be further elevated with the use of hormonal birth control. But if you don’t believe me, both the American College of Obstetricians and Gynecologists and the World Health Organization advise that women who suffer migraines with aura should not use hormonal contraception.
  2. Reevaluation or discontinuation of combination hormonal contraception is advised for women who develop escalating severity/frequency of headaches, new-onset migraine with aura, or nonmigrainous headaches persisting beyond 3 months of use.

A 2016 meta-analysis of seven research studies demonstrated “a two- to fourfold increased risk of stroke among women with migraine who use combined oral contraceptives (COCs) compared with nonusers.” But once again, like so many other things about hormonal birth control, the authors of the study report that research is lacking in this area and more studies need to be done.

Reason 3: Family Clotting Disorders

Many people have a clotting disorder and simply don’t know it. When I had my stroke while on birth control pills, I had no idea that I had the fairly common clotting disorder Factor V Leiden (FVL affects between 3-8% of people). But what I did know was that my grandmother had had two strokes. And my aunts and uncle had all had blood clots.

Unfortunately, women are not systematically tested for clotting disorders before they begin using hormonal birth control. This is very dangerous and why it’s so important to give your doctor a thorough family history; something I know I wouldn’t have considered that vital when I was 18 years old.

A lot of health professionals don’t take the time to review your family history, making it even more important that you mention your family history of blood clots and your concerns about hormonal contraception. You might even insist on being tested for clotting disorders before increasing your risk of a dangerous and sometimes deadly blood clot.

Reason 4: Depression and Mental Health

I explore this further in this article but the basics are:

  • Hormonal contraceptives can cause mental health issues
  • Women who suffer from mental health issues are much more likely to suffer from increased symptoms when on hormonal contraception
  • Often the longer hormonal contraception is used, the greater the symptoms
  • Discontinuation of hormonal contraception can usually alleviate mental health symptoms

Reason 5: Diabetes

Dr. Hugh J. Davis, the first doctor to testify at the Nelson Pill Hearings said the following (page 5930):

“A woman, for example, who has a history of diabetes or even a woman with a strong family history of diabetes is not an ideal candidate for using oral contraceptives… [they] produce changes in carbohydrate metabolism which tends to aggravate existing diabetes and can make it difficult to manage.”

Hormonal birth control elevates blood glucose levels, can increase blood pressure, increases triglycerides and cholesterol, and accelerates the hardening of the arteries, among other things. They knew this in 1970. But what about the research now? Well, if you’ve read any of my other articles it probably won’t surprise you that the current research is… wait for it… you guessed it… INCONCLUSIVE! Here’s a look at what I’ve found:

“Cardiovascular disease is a major concern, and for women with diabetes who have macrovascular or microvascular complications, nonhormonal methods are recommended.

There is little evidence of best practice for the follow-up of women with diabetes prescribed hormonal contraception. It is generally agreed that blood pressure, weight, and body mass index measurements should be ascertained, and blood glucose levels and baseline lipid profiles assessed as relevant. Research on hormonal contraception has been carried out in healthy populations; more studies are needed in women with diabetes and women who have increased risks of cardiovascular disease.”

And:

The four included randomised controlled trials in this systematic review provided insufficient evidence to assess whether progestogen-only and combined contraceptives differ from non-hormonal contraceptives in diabetes control, lipid metabolism and complications. Three of the four studies were of limited methodological quality, sponsored by pharmaceutical companies and described surrogate outcomes. Ideally, an adequately reported, high-quality randomised controlled trial analysing both intermediate outcomes (i.e. glucose and lipid metabolism) and true clinical endpoints (micro- and macrovascular disease) in users of combined, progestogen-only and non-hormonal contraceptives should be conducted.

Not enough evidence is available to prove that hormonal contraceptives do not influence glucose and fat metabolism in women with diabetes mellitus.”

As a side note, a recent study demonstrated a link between hormonal contraceptives and gestational diabetes.

Contraception is a very personal choice. I believe all women should research the risks associated with using hormonal contraception, but especially if you experience any of the health conditions above. Should you weigh the risks and benefits of using hormonal birth control and decide it’s still the right choice for you, please take a moment to review the symptoms of the blood clot and seek help immediately if you notice any of these.

Real Risk Study: Birth Control and Blood Clots

Lucine Health Sciences and Hormones Matter are conducting research to investigate the relationship between hormonal birth control and blood clots. If you or a loved one have suffered from a blood clot while using hormonal birth control, please consider participating. We are also looking for participants who have been using hormonal birth control for at least one year and have NOT had a blood clot, as well as women who have NEVER used hormonal birth control. For more information or to participate, click here.