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

Published on March 11, 2024

6715 views

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

Food Composition and Hyperglycemia

by Chandler Marrs, PhD

Published on February 14, 2023

5172 views

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.

Unexplained New Onset Fatigue and Other Symptoms

by William V

Published on May 4, 2022

9038 views

For almost a year, I have suffered from fatigue, morning sinus and congestion problems, and other health issues including type 2 diabetes, insomnia, and depression. For the last four months, I have been dealing with a skin rash on my legs, arms, stomach, and small outbreaks on my face. I have been misdiagnosed by my primary doctor and two different naturopaths. They told me that it was fungal and I was given anti-fungals. I don’t remember the name. After a second visit to a dermatologist, the doctor did a scraping and a biopsy and told me that it definitely wasn’t fungal. They are going to do some patch tests this week. I have had to keep my mental outlook positive because, for the last year, the doctors have had no answers.

My primary has told me that I am an anomaly. Great! But still no answers. She has done a plethora of blood tests, two or three CAT scans, and other imagery. The only blood test that was a little high was my white blood cell count. My iron is high because of my testosterone injections. I was initially told that I had Lyme’s disease but my blood tests found that to be negative. Then I was told that I have Epstein Barr, but my blood tests were negative for that also. I am used to an active lifestyle, lifting weights, hiking, backpacking, fishing, martial arts, etc., but, for the last year, I have been extremely low energy with significant fatigue. I will sleep 8 hours, get up for a while, and just feel like going back to bed. I would like my life back!

Early Thyroid Problems

I take levothyroxine because my thyroid was low about 20 years ago. They did a scan of my thyroid and told me that my thyroid was quite small, probably due to my Graves’ disease treatment when I was 16 years old. I was told that I was close to death at that time. I remember some of the unpleasant things I went through at that time. They gave me a drink called a “nuclear cocktail” and then, for the next 4+ years, they treated me with propylthiouracil. I fought my way through this disease and started lifting weights and working out when I felt better. I was about 16 years old at the time. I continued to work out and have been athletic all of my life.

Back Pain and Spine Curvature

After years of athletics that included snow skiing and martial arts, I began to develop significant back pain. After an MRI in 2004, the doctors asked if I had polio. The test showed curvature of the spine, a bulging disc, and some areas of bone on bone. At that point, I was prescribed oxycodone and have been on it ever since. Despite the back issues, I have functioned fine until this last year when a variety of new symptoms manifested, including unremitting fatigue. I have had a big change in my energy levels, sex drive, and the pain issues have increased and so it is a struggle to lift weights. My hands, shoulders, spine, and feet have increased pain. I have always been very self-motivated, but this last year has been very tough. The doctors say that I have osteoarthritis and fibromyalgia. I don’t know anymore.

Maybe Thiamine for the Fatigue?

Recently, I listened to Elliot Overton’s interview with Dr. Marrs about thiamine and found many of my symptoms were possibly linked to thiamine deficiency. I have taken a myriad of nutritional supplements over the years. They are listed below. All to no avail. I have also started taking thiamine, but the jury is not out on that yet. It has been pretty expensive with all the doctor appointments and nutritional/medical expenses.

There is a lot more that I have probably missed, but I wanted to keep this to a short story, not a novel. What am I missing with my health issues? The fatigue is unending. The doctors have no advice and consider me an anomaly. Am I? Or are we simply missing something?

Current Medications

Levothyroxine-125mcg – for approximately 29 years.
Sertraline-50 mg – last two years
Lisinopril-10mg – last year and a half
Metformin-750mg – last two years
Hydroxyzine-50 mg – at bedtime for sleep issues for the last year and a half
Oxycodone-10 mg up to 4 times a day since 2004. I see my spine doc every 2 months. I have some spine damage and joint issues from the martial arts and various other sports.
Dicloflenac- 50 mg (Rarely use)
Lunesta-3 mg (1 at night) – this was given to wean me off of clonazepam.
Testosterone-.5 ml – injection every 2 weeks – for low testosterone
Aspirin-81 mg-one a day for thick blood due to the testosterone replacement therapy
Kenalog injection for rash. I have had only one injection and the dermatologist told me that it would be good for a month.
Triamcinolone cream to use on the various rash sites.

Current Supplements

Vitamin D3-10,000 IU a day (Kirkland brand)
B12-5000 mcg sublingual 1 a day
Saw Palmetto-450 mg, 1 a day (ZHOU brand)
Ceylon Cinnamon-1200 mg, 1 a day (Spring Valley brand)
Garlic-2 capsules, 1 a day (Kyolic brand)
Niacinamide-500 mg, 2 times a day (Nutricost)
Liposomal Vitamin C-1400 mg, twice a day
Benfotiamine-300 mg, twice a day

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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 February 19, 2020.

Pregnancy Toes – What Sugar Does to Feet

by Angela A Stanton, PhD

Published on December 28, 2020

13541 views

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:

If you feel swollen after eating sweets, you need to eat salt and drink a bit of water to reduce your swelling.
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!
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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The Insulin Resistance Time Bomb

by Angela A Stanton, PhD

Published on September 12, 2017

8684 views

I seldom watch television but for some reason nearly every time I do, the same commercial pops up. It goes something like this: a couple of women are sitting on a bench, chatting, when a guy walks up to them and asks if they have T2D (the answer is “yes”) and then he asks if they know that T2D can cause heart disease. The women act very surprised since they didn’t know. Why did they not know? And how come the pharmaceutical companies know that people don’t know? This commercial always makes me pause because it is so clear that we do not know what is happening to us.

We all know the scary statistics: the CDC admits that 9.3% of US adults are diagnosed with type 2 diabetes (T2D) as of 2010. The key word here is diagnosed. That is because more people are not diagnosed but have T2D than those who are diagnosed. It is estimated that over 30% of the population has T2D only they don’t know they have it. So one must ask a few questions:

Why do so many Americans have T2D?
Why don’t so many Americans know that they have T2D?
What causes T2D?
How does T2D start, why, and when?
Can T2D be prevented?
Can T2D be reversed or at least put to remission?

So let me be the one who tries to explain. The topic is not easy to explain so I am breaking it up into several parts, each at a different level of depth. In part 1 of this series, I will begin by discussing what nutrients are and how they connect to T2D. This will help explain why so many Americans do not know they have T2D and why they remain undiagnosed.

What Are You Eating?

If you look at what is sold in grocery stores today, you will find that over 80% of the stores are filled with commercially prepared foods: cereals, breads, canned foods, frozen pre-cooked foods, juices, soft drinks, candy, dried fruits, health bars, potato or veggie chips, crackers, popcorn, cooking oils, sugar, flour, prepared lunch meals, etc. Fresh dairy, meat, seafood, poultry, and fresh produce represent 10%, and toiletries, kitchen supplies, healthcare products, supplements, and sometimes cosmetics and greeting cards are the remaining 10%. The prices seem to be inversely related to the percentage these occupy in the store. Food-like products that are commercially processed are the cheapest, while fresh produce, dairy, and fresh meat are often prohibitively expensive. Thus, as budget allows, we end up buying a bunch of prepared foods; not only are they cheaper, they are also more convenient. In today’s busy world, who doesn’t want precooked foods that only require re-heating? What a time saver! Indeed, not a health-saver though. The money we save on food will end up in the pockets of medical institutions and pharmaceuticals for healthcare later, because most commercially prepared foods will make us sick.

Unfortunately, the cheapest and most readily available foods contribute most to type 2 diabetes. This takes a little explanation, so I am breaking foods down into the basic nutrient groups; macronutrients. There are three macronutrients: carbohydrates, protein, and fats. Because so many people don’t know what food falls into what macronutrient category, let me help you; some of the foods really aren’t obvious where they belong.

Protein

In our minds, protein refers to meat or fish though a small amount of protein is found in most every food item; even lettuce, only too small to matter. More protein is found in whole foods like unprocessed meats and fish than in processed foods like sausages or hot dogs. Protein is essential, meaning we must eat protein to survive. Proteins are made up of amino acids that form some of the most important macronutrient elements in our body. Protein is not just important for body building but it is essential for our brain and body to function and to survive.

There are a number of amino acids that are nonessential—meaning the body can create them–and others are essential–meaning we must eat them because our body cannot create them. All nonessential amino acids convert only to glucose, some essential amino acids convert to ketones only and some essential amino acids convert to either glucose or ketones based on dietary need. Over 50% of the amino acids convert to glucose. Glucose is in the family of carbohydrates, another macronutrient.

Carbohydrates

The largest nutrient group in most Americans’ life is carbohydrates. Carbohydrates are nonessential nutrients, meaning we can live perfectly healthy lives without a bite of carbohydrates. There is nothing in carbohydrates our body cannot make or we cannot eat in protein. Carbohydrates include the following foods (short list here): candy, sugar of all types (including honey), fruits, vegetables, legumes, nuts, seeds, grains, all foods sweetened with sugar like cookies, pastries, juices, and all natural vegetables, fruits, nuts, legumes, seeds, and alcohol. Carbohydrates are made from starches, glucose, fructose, lactose, and galactose. For example, most fruits contain glucose and fructose, most vegetables have glucose or some have starches (potatoes and carrots contains a lot of starch), milk has lactose, nuts are mostly glucose, and grains are glucose and starches. Although fiber is categorized as a carbohydrate, fiber is not used by the human body; it simply gets eliminated, so I exclude it from this category.

The key factor to know is that all carbohydrates convert to glucose (or to fructose and that partly converts to glucose). The speed with which they convert to glucose makes some difference but ultimately they all become glucose. Starches convert to glucose in our mouths before we swallow them even if they are not sweet (this includes whole wheat bread as well). Since protein is essential and over 50% of protein converts to glucose, carbohydrates become nonessential since we can make glucose without them. Carbohydrates play the biggest role in T2D because they provide excess glucose we don’t need. Although there is genetic predisposition to T2D as well, even those who are genetically so predisposed can prevent T2D by avoiding carbohydrates.

Fats

The third macronutrient group is fats. Fats represent the only nutrient that do not, under normal circumstances, convert to glucose. Fat remains fat. Fat is an essential nutrient in our body made of fatty acids, all of which are essential: omega 3 and omega 6.

From the three macronutrients, carbohydrates is the only one that poses a problem for insulin management and lack of proper insulin management leads to T2D.

How Do We Get T2D?

While most people think that T2D is the start of the problem, in reality it is the outcome, and thus, the end of the problem. There are many ways one can look at the progression to T2D. Most medical professionals (and the general population at large) think that people with T2D are obese. This is far from the truth and this causes the biggest problem in diagnosis. I think the confusion comes from the lack of understanding the progression toward T2D.

T2D starts when a person is thin and knows/cares very little about what she eats. The cause for T2D is too much insulin in response to excess glucose, that cannot be delivered to the liver. Though this sounds simple, it is complex enough to get many confused even in the field of medicine. We must ask a few questions:

Where does excess glucose come from?
Where does excess insulin come from?
Why is insulin not able to pick glucose up from the blood and deliver it to the liver?

Understanding the Liver and Insulin

Insulin is a signaling hormone for many functions, including packaging glucose into the liver for storage. Thus insulin is a storage hormone. Without insulin, people cannot gain weight—a typical problem for type 1 diabetics (T1D) who lack insulin production. T1Ds need to use insulin injections in order to survive, and gain and maintain healthy weight.
Since insulin is a storage hormone, it automatically implies that it stores whatever food we were not able to immediately burn. This is healthy. Think of hibernating bears; they fatten up all summer and then in the winter hibernation they live off of the accumulated energy stored as fat. The key to their health is that they don’t eat during hibernation–meaning all year long. In contrast, humans continue to eat and store excess energy all year long.
Once the storage cabinet of our body has reached its comfortable limit (the liver is our storage cabinet), insulin cannot pack more glucose into it. The liver refuses insulin’s attempts. This is called insulin resistance.
Prediabetes and insulin resistance are the same phenomenon at different stages. Prediabetes usually occurs in people who already have insulin resistance.
During insulin resistance, the excess glucose and the excess insulin circulate in the blood causing damage. They damage arteries by causing inflammation¹ increasing blood pressure as a result, and can cause nerve damage (in the brain as well as in the body). Diabetic neuropathy starts at the stage of insulin resistance for many people and not at a later stage when T2D developed, which is how it is always portrayed.
Insulin resistance is compartmentalized—meaning one may have insulin resistance in one organ (such as the liver) but not in another. This makes insulin resistance very hard to diagnose with conventional tests. The most typical test is the hemoglobin A1c (HbA1c), which measures the average amount of glucose the person had in his blood for a period of two to three months.
Alzheimer’s disease is the insulin resistance (or type 3 diabetes) of the brain but not the body. Hence, the first sign of Alzheimer’s disease is the disease itself and not insulin resistance. This further shows the difficulty of diagnosing insulin resistance.
During the start of insulin resistance, as more and more insulin is released to carry the glucose into the liver that cannot handle any more, the liver becomes ill with non-alcoholic fatty live disease. It makes the liver bigger, inflamed, and less able to do its job, which is the detoxification of the blood.

Since we feel none of this as pain or illness, nearly 100% of the people with insulin resistance have no idea that they have insulin resistance! As insulin resistance continues over decades being undetected, the body slowly degrades in its ability to fight back. Finally, when it is time, T2D arrives. By the time T2D is diagnosed, most people (not all) are overweight, because of the preceding years of insulin resistance that went unnoticed.

Manifestations of Insulin Resistance

Insulin resistance is not felt by anyone (the pain in the legs may be diagnosed as something else) and so its diagnosis is usually accidental and often inaccurate^2,3. The tools used to check for insulin resistance, in the US and elsewhere, require one to be obese or pregnant with gestational diabetes risk. This presents a major problem since obesity tends to develop only after years of insulin resistance. An individual may have insulin resistance at age 11 and not know about it until at age 35, when she suddenly develops neuropathy with hurting feet, or gets shaky and dizzy if the food is five minutes late on her table. The achy feet are often misdiagnosed as a pinched nerve, Plantar fasciitis, or fibromyalgia. If you are ravenously hungry before breakfast and must eat every 3 hours, chances are pretty high you are have insulin resistance, even if you are paper thin, exercise a lot, even at the level of an athlete, and have no aches and pains.

There are two ways insulin resistance can be manifested and there is a bit of confusion in categorizing them so here I cap them under one roof: insulin resistance. The most common is simply being hungry very often with correspondingly high blood sugar—one can use a blood sugar measuring kit (finger poke) to test. This type of insulin resistance is hyperinsulinemia, which only lets itself be known by frequent hunger when the blood sugar levels are still high. The body’s ideal blood sugar level is <100 mg/gL and a healthy individual will not feel hungry while the blood sugar level is at or above 100 mg/dL. A typical hyperinsulinemic person feels hunger pangs at blood sugar of over 110 mg/dL. Normal blood sugar is defined as 70 – 140 mg/dL.

The hardest to treat insulin resistance is reactive hypoglycemia. Its manifestation is feeling shaky, dizzy, cold sweaty, feeling nauseous, whose blood sugar drops below the pre-meal starting blood sugar very shortly after eating. A typical hypoglycemic may start eating with pre-meal blood sugar of 90 mg/dL, an hour after finishing the meal may end up with 70 mg/dl, and an hour and a half later she may drop to 60 mg/dL. The level of glucose in the blood is closely regulated for its healthy minimum. Below 70 mg/dL, the body is in trouble so consider it a major warning. Below 60 mg/dL call the paramedics immediately. Below 50 mg/dL you may be dead—so don’t wait!

Can Insulin Resistance Be Prevented?

Yes it can. Since insulin resistance is too much insulin in response to high dietary glucose (glucose spikes insulin), if you stop eating those foods that give instant glucose access (see the glycemic index of foods), or more glucose than your body needs in general, you can reverse insulin resistance. Examples of foods to avoid include: all sweets with any shape or color, sugar, raw or otherwise, honey, etc., all foods sweetened with sweeteners of any kind (including sugar substitutes and naturals since they may also cause health problems, including obesity and T2D⁴), all juices whether they are sweetened or not, all smoothies and shakes whether they are sweetened or not, all tropical fruits and 90% of other fruits, all vegetables grown below the ground (like potatoes and carrots), peanuts, cereals, pseudo cereals (like quinoa), rice, corn, starches used in place of flour, all breads and pastas of all grain types, including whole grain or whole seed, oats, in general all grains, fermented alcohols, and legumes.

For some people dairy is also insulinogenic but not for all so I am not including dairy on the list. Stop eating all of the high glucose spiking foods listed above and increase animal fats, meats, eggs, and dark green leafy veggies in your diet, and you will be able to prevent insulin resistance.

So what can you eat when you cut out all these great tasting “foods” from your diet? Once you understand that these are really not foods but conveniences, you can see the replacements: increase green leafy vegetables in your diet; eat only those fruits we associate with vegetables: zucchini, bell peppers, squashes, tomatoes, cucumbers, and alike or low carbohydrate veggies like broccoli and cauliflower. Consume only raspberries, blackberries, and strawberries as your fruits with an occasional small orange or if must a very small serving of cantaloupe. Avoid all other fruit. Increase healthy dairy with full fat in your diet, use animal fats for cooking since vegetable oils are unhealthy and can be harmful. More details on the types on fats in part 2 of this series. Animal fats are butter, ghee, pork lard (buy pure pork lard and the not hydrogenated types available in grocery stores), beef tallow, bacon drippings (save it in a ceramic container–no refrigeration needed), poultry fat is super too.

Can Insulin Resistance be Reversed?

One of my migraine group members in the keto mild for migraine group had reactive hypoglycemia–that is the insulin resistance that is harder to treat. I asked her to switch to the zero carbs diet for a short time, after which she wrote the following:

“So looking back Aug 31st was my last low blood sugar [reactive hypoglycemia] day, yay! I followed Angela Stanton’s advice and did the zero carbs program for 6 days; I have reintroduced carbs back now, up to almost my norm for the ketogenic diet and still no low blood sugar!! I’m ecstatic! I have the bruised fingertips as proof of all the poking (I was actually eye spying my toes as an alternative ☺️) for me the increase in protein was the key. I realized I was not eating enough before. So for those of you struggling with reactive hypoglycemia this is the answer.” –LM 9/6/2017

As you can see, she reversed her reactive hypoglycemia by cutting all carbohydrates out of her diet for 6 days, and ate only protein and fat. Why does the zero carbs diet work? This and the rest of the information about nutrition and T2D are going to be discussed in the second part of the series on diabetes. So stay tuned and look for part 2!

Sources:

Dandona P, Chaudhuri A, Ghanim H, Mohanty P. Proinflammatory Effects of Glucose and Anti-Inflammatory Effect of Insulin: Relevance to Cardiovascular Disease. American Journal of Cardiology.99(4):15-26.
Kraft J, R;. Diabetes Epidemic &You. revision 1 ed. North America & International: Trafford; 2011.
Crofts C, Schofield G, Zinn C, Wheldon M, Kraft J. Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Research and Clinical Practice.118:50-57.
Shearer J, Swithers SE. Artificial sweeteners and metabolic dysregulation: Lessons learned from agriculture and the laboratory. Reviews in Endocrine and Metabolic Disorders 2016; 17(2): 179-86.

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Diet Choices: Moving Beyond the Want Culture

by Angela A Stanton, PhD

Published on November 29, 2016

3420 views

I Want versus I Need

I received a message the other day in my Facebook migraine group from one of the members. I am sharing this message (with the migraineur’s permission) because it brought home a few points that most of us don’t ever think about. (There is minor editing and emphasis for clarity).

“Last night I had an awesome breakthrough in my nutritional paradigm. I was hungry and wanted something good to eat. My first thought was “what would taste good right now?” Then I thought, “what does my body NEED right now?” Huge, right? So, I looked at my food journal and noted that I was a little low on protein and fat, so I made myself a nice 150 gr salmon steak with a cream and butter sauce. So, delicious, more importantly, it was just what my body needed. Why was this such a breakthrough?
Because Angela’s [Stanton Migraine Protocol^®] is (or should be) so easy to implement. I find the hardest part, for me, is overcoming the mental conditioning of the last 30+ years: ‘fat is bad, fat makes you fatter, sicker, slower. Animal fat and protein will damage your heart, your kidneys, your liver, and your brain. If you want to live become a vegetarian’. And, of course, calories are king. ‘Every calorie counts. Limit calories to lose weight. If calories eaten exceed calories burned you will get fatter’. It goes on and on.
All my life I have heard (and still hear) this on TV, in newspapers, in magazines, not to mention form my friends, family, medical professionals, and even from complete strangers.
Because of all of that, when I [am] preparing a good [migraine] friendly meal, my brain looks at my daily food log and begins to panic. ‘Good God’ it cries ‘look at all that fat, look at all those calories, are you trying to kill yourself?’
Before the initial panic can set in to a full-blown anxiety I must stop, take a deep breath, and remind myself that all that propaganda is messing with my mind. Calories only matter as a guide to how much fat, protein, and carbs you should be eating. Other than that, they are completely meaningless. Fat is not going to make me fat, quite the opposite, in fact. Fat is good for the brain, the heart, and the rest of the [body].
It will take more time to overcome the 30+ years of brainwashing; [it] will not happen overnight, but I will eventually overcome. And so, will anyone who is willing to ignore [the] ‘conventional wisdom’ and eat healthy animal fats and proteins.
Thanks Angela Stanton for helping me (and hundreds if not thousands of others) to overcome the blatant brainwashing of the 20th and 21st centuries’ nutritional paradigm.”

I found this post an eye opener and a long-awaited awakening of my migraine group members (and people everywhere) since they are not familiar with the details that makes us eat what we want rather than what we need. The food recommendations of the US government, even today, are mostly grains, fruits, and vegetables, minimal skim milk if any, minimal meat and fish if any, and fat is not even on what has been named “My Plate,” which is our current nutritional guideline. My Plate is an improvement over what was the Food Pyramid in the 20^th Century.

With the birth of the misguided Seven Countries Study of Ancel Keys in the 20^th Century, the entire world changed: people suddenly began to get metabolic diseases such as obesity and type 2 diabetes. Even heart disease—the prevention of which was the original goal of Keys–remains the leading cause of death in the US. The food pyramid failed to perform and, instead, created a massive metabolic syndrome epidemic that brought with it a host of other diseases that were unknown or rare before: Alzheimer’s disease, dementia, cancer, Parkinson’s disease, early onset type 2 diabetes which used to be reserved for the elderly and now affects 3-year olds.

Why Do We Eat Grains, Carbohydrates, and Sweets?

Foods, such as grains and carbohydrates recommended by nutritionists are addictive—Wheat is an Opiate! Processed carbohydrates are addictive (bread, pasta, rice, cereal, canned fruits, juices, smoothies, vegetables of all kinds are all carbohydrates, not just candies and sugar). Scanning studies show just how addictive they are and how cravings are generated in people as a result of eating them. Research also shows that the easy availability and constant craving for these foods can modify our brain by changing our perception of satiety and make us continue to eat even when we are already full.

And this brings us to the migraineur’s point, which is an indirect explanation of the biggest problem we face today: we eat what we want to eat and not what we need to eat.

We live to eat rather than eat to live.

Our body needs very different foods from what we have available to us cheaply e.g. pastry, canned and prepared foods, fast foods, soft drinks, sweets. Our fruits and vegetables are bred to be the sweetest and the biggest. Our drinks are flavored and sweetened. Everything is large, sweet, and addictive. Even today, type 2 diabetics are told to follow a high carbohydrate diet, which we know is the cause of type 2 diabetes. Carbohydrates spike insulin and that leads to insulin resistance, e.g. type 2 diabetes.

It is difficult for me to accept that something as simple in cause-and-effect as the metabolic process of carbohydrates is and how that leads to insulin resistance (type 2 diabetes) could defy the understanding of the entire scientific, medical, and nutritional community, and yet it does.

The migraineurs in my Facebook group understand that to become migraine free, they need to change their diet. The human brain is made from fat (over 60% of it) and cholesterol (25% of all cholesterol in our body is in the brain). Therefore, eating low fat anything is akin to shooting ourselves in the foot. Just consider the diseases that have appeared and increased in incidence in parallel to our adoption of a carbohydrate based diet. Diseases like, Alzheimer’s, dementia, Parkinson’s, cancer, and many others, can be linked to diet. Most, except cancer, show signs of myelin damage (myelin is made from cholesterol and is damaged by glucose). Myelin health is the most important factor in brain and body health. To find cancer, researchers inject glucose into our blood—glucose is cancer food.

While most people prefer or want to eat sweets and grains, what they really need to eat is butter and other animal fats, whole fat dairy, whole foods they cook themselves with good sources of meat and fish, low carbohydrate fruits and vegetables, and no grains at all. I am glad that more migraineurs are able to differentiate between what they “want” versus what they “need” for their healthy pain-free and disease-free body.

Can you differentiate between what you want versus what you need?

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The Misguided Battle Against Dietary Fat and Cholesterol

by Angela A Stanton, PhD

Published on August 8, 2016

2955 views

I was at my medical provider the other day waiting for my turn for an MRI test. I shared the lobby with over 100 people. As I looked around, for the first time I noticed something odd. About 80% of the people in the lobby were overweight. I found a seat, the only seat. It was a single small seat. Most of the seats now are double sized to allow the obese to sit. I am claustrophobic and was concerned about this on my way to the MRI machine. The nurse gave me a wink and smile and we walked into the room. I was nailed to the floor. I have never seen anything like this though I have been in MRIs many times before.

I recall having been pushed into a narrow tube many times before where I could not lift a hand, usually dimly lit with some wind blowing in my face and a terribly loud echoing hammering as the image slices were taken. Yet here I was, glided silently into an MRI machine that was almost big enough for me to sit up in. “Ah the benefits of having obese people” I thought as I entered this brightly lit giant tube that was so wide that even the noise was reduced, lacking the echo we all are familiar with and hate. The radiologist told me that all MRI scanners are being replaced. As I was scanned for 45 minutes, I had no claustrophobia at all and not too much noise to block my thinking. The time gave me a chance to pause about the obesity epidemic: how did we get here? Why are entire new industries created to cater to our new weight rather than help us become healthy? Why are so many of us overweight to begin with? What has gone wrong?

Coincidentally, for unrelated reasons, I was already researching the nutritional recommendations of the USDA for the past several months; reading all of the books and academic research papers available to me. The USDA recommendations sparked my interest because I run a migraine group full of glucose intolerant migraineurs. I merely wanted an answer to why migraineurs (like me) are glucose intolerant, when I came across the huge nutritional boxing ring with major academic fights in this arena. The real science was hid, even by the NIH, unpublished.

The obesity epidemic starts with the theory of Ancel Keys who in the mid 20^th Century US decided that coronary heart disease (CHD) was the most important thing to focus on (Eisenhower just had a heart attack). He found support for his hypothesis that high cholesterol is caused by high dietary fat—in particular saturated animal fats—and those with high cholesterol will most certainly have CHD, will flip and die very soon. His findings were dubious at best, but still garnered support (Ancel Keys – Seven Countries Study)

Researchers all over the world presented conflicting evidence but they were not only not able to publish these data in reputable academic journals, they were ostracized for even trying. Eventually so many scientists lost their reputation as a result of trying to fight Keys’ hypothesis that many left academia or changed fields of research and gave up (1-3).

Nina Teicholz spent eight years digging up files never published and hidden in the archives of the NIH (3). The reason for not publishing? The findings did not support Keys’ theories. It was assumed that the results had to have been wrong and therefore could not be published. In scientific research the role of science is to try to refute the theory by proving it wrong. In the case of Keys’ theory, the law of science changed: a theory was accepted as truth and no one could publish anything unless they found supporting evidence to THAT theory. Thus, science moved backwards and has effectively stalled for decades where cholesterol and fat are concerned.

When nutrition research began in the early 20^th Century, we did not have the all of the tools available that we have today. Today we know that cholesterol is not made from fat at all but from Acetyl CoA and Acetoacetyl CoA (source). So if cholesterol is not made from fat, what is the connection of eating saturated fat to CHD? Nothing actually—today we know but shhhhh… this still cannot be said loud!

Cholesterol Is Made from Acetyl CoA and Acetoacetyl CoA, Not Fat

Cholesterol is made from two molecules in a total of about 39 hard steps by our liver (or we can eat it like egg yolks). Would our body go through such hard work of creating something if it ended up causing our death? It is not even plausible that human evolution would have supported such counter mechanism.

A Primer on Metabolism

Acetyl CoA is

“an important biochemical molecule in cellular respiration. It is produced in the second step of aerobic respiration after glycolysis [the breakdown of glucose (think carbohydrates) by enzymes, releasing energy and pyruvic acid] and carries the carbon atoms of the acetyl group to the TCA cycle [Krebs cycle which is a chemical reaction used by all aerobic organisms] to be oxidized for energy production” (source)

and Acetoacetyl CoA is

“intermediate in the oxidation of fatty acids [fats] and in the formation of ketone bodies [fat burning energy bodies]” (source).

Note that neither is a fat but they together form fat (cholesterol) by oxidation. Cholesterol is a lipid (a naturally occurring molecule like fats, waxes, steroids, fat-soluble vitamins like vitamins A, D, E, and K, and also triglycerides). Triglycerides are ester derived from glycerol and three fatty acids – body fat, phospholipids (a major component of all cell membranes), and many other types of lipids. The main biological functions of lipids (such as cholesterol) are storing energy, signaling, and acting as structural components of cell membranes.

It is not the matter of eating fat and oops we now have cholesterol; rather it is a matter of “we must have cholesterol to survive.”

Where do these elements come from in the body to create cholesterol?

As noted above: carbohydrates (glucose is a carbohydrate) and an element that is an intermediate step in oxidizing fatty acid combined create cholesterol, which “then enters the citric acid cycle in the mitochondria…” (source) Note the key word here: carbohydrates. This is important because the “health-heart” movement of Ancel Keys’ “fat causes high cholesterol” is clearly not true if cholesterol is made from carbohydrates and not a fat. How did we end up thinking that cholesterol is made from fat? It certainly is fat but clearly is not made from fat.

Why do we need cholesterol?

Cholesterol is used by our mitochondria (not what we eat but what our mitochondria needs to create energy ATP). (source)

How much cholesterol is needed and what happens when we reduce cholesterol?

You would think that these questions were asked over the 80+ years but no reputable scientist dared asking. The moment such question was asked, the sticker “black sheep” went up the forehead so researchers just let it go. Thus we have no idea how much cholesterol we actually need. Everyone needs a different level: the thought that a 30-year old 7-foot-tall male Marathon runner needs the same cholesterol level as a little old lady, aged 95, in a wheelchair is just preposterous. Clearly each person needs a different level based on mitochondrial respiration intensity and frequency, which is age, gender, and activity related. A cookie-cutter approach just cannot work. What happens when we reduce cholesterol? As noted above, cholesterol stores energy, it is a signaling agent, and acts as structural components of cell membranes among other things. If we reduce cholesterol, we effectively reduce our body functions.

The Combustible Vegetable Oils

Since it was decided that fat creates cholesterol and thus saturated fats had to be removed from everyone’s diet, the research was about how to make vegetable oils, unsaturated or polyunsaturated, edible and digestible (the kind flies won’t eat in your garage). Hydrogenation could only produce dangerous fats, such as hydrogenated vegetable oils (trans fats) or partially hydrogenated vegetable oils, both of which were said to have randomly combusted in delivery trucks while being taken for cleaning and also while taken back to the restaurants after cleaning. Apparently the fumes vegetable oils create settle in the clothing (and the lungs of the chefs) and even after professional cleaning are still capable to burst into flame without any provocation (3). These vegetable oils have polyunsaturated fats that have the unfortunate “poly” (multiple) bonds. These bonds break easily, transforming fats into ugly sticky goo and free radicals. This goo replaces animal fats in human mitochondria, blocking the mitochondria from creating energy.

This makes a lot of sense: fats in vegetable oils are not the same chemical components as fats in animal bodies. There is a huge difference in how they work and to what they bond. Animal fats become energized by thermal heat referred to as internal combustion whereas vegetables use external energy (the sun) and in heat they disintegrate, oxidize, and become goo. They chemically change from being fats to something that cannot be used by the human body as fats (4). Olive oil does not combust but at higher temperatures oxidize, creating free radicals.

Fat provides a lot of energy, 9 Calories per gram as opposed to carbohydrates and proteins, each producing only 4 Calories per gram. This implies that by removing fat calories from our diet, a very large part of the daily calories needed to be made up by something other than fat. Since protein also contained fat (saturated fat in particular), the Food Pyramid and later “My Plate” both reduced the protein amount as well. Thus, what we were left with was increased carbohydrates in our diets. However, as noted above, carbohydrates are part of cholesterol creation. This has become a catch 22 that no one in the “heart-health” supporter group accepted or did not see or decided to ignore because it was too complex or decided to ignore because then they too would become black sheep.

The Catch 22

Perhaps most the most striking aspect of this misunderstanding, is that if we follow the steps, we inadvertently increase the very diseases that we would like to avoid. By increasing carbohydrate intake, we’re increasing cholesterol and inducing metabolic disorders.

reduce cholesterol ==> reduce fats ==> increase carbohydrates ==> increase cholesterol

So here we are today, 80+ years later. Today the Western Diet world has a nightmare of metabolic disorders to fight. Where do metabolic disorder lead to? CHD of course, the very thing Ancel Keys wanted to rid the society from. However, there is more to it than that.

Carbohydrates have some nasty properties—both simple and complex carbohydrates do:

They are addictive; eight times more than cocaine or heroin (5, 6)
Grains (complex carbohydrates we eat the most of) release morphine (7), another drug
Carbohydrates spike insulin and create insulin resistance (8-10)
Insulin in the blood makes us hungry
The more carbohydrates we eat, the more insulin we release and the hungrier we get
Insulin resistance turns into type 2 diabetes
People with type 2 diabetes are at an increased risk of CHD
Carbohydrates create triglycerides, the type of cholesterol that is know to cause CHD (11)

And so now not only are we back at trying to prevent CHD, where we started 80+ years ago, but we also have massive metabolic disorder epidemic and new diseases, such as cancer, that also appear to be connected to high carbohydrate consumption.

Yet, to this day, the nutrition guideline of the USDA for the American population, now called My Plate, does not even include dietary fat! I challenge you to find a baby food with more than 1% fat in it; babies are only eating carbohydrates.

Luckily there is a new movement toward a healthy diet that goes under a couple of different names: Low Carbohydrate High Fat (LCHF) or ketogenic diet. These types of diets are used now therapeutically for many health conditions; health conditions we could probably prevent if we simply added saturated animal fats back into our diet and dumped all that sugar and grain.

Sources

Taubes G (2008) Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Anchor).
Taubes G (2011) Why We Get Fat: And What to Do About It (Anchor) Reprint edition December 27, 2011 Ed p 288.
Teicholz N (2015) The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet (Simon & Schuster; Reprint edition, New York) p 496.
Browner WS, Westenhouse J, & Tice JA (1991) What if americans ate less fat?: A quantitative estimate of the effect on mortality. JAMA 265(24):3285-3291.
Ahmed SH, Guillem K, & Vandaele Y (2013) Sugar addiction: pushing the drug-sugar analogy to the limit. Current Opinion in Clinical Nutrition & Metabolic Care 16(4):434-439.
Lenoir M, Serre F, Cantin L, & Ahmed SH (2007) Intense Sweetness Surpasses Cocaine Reward. PLoS ONE 2(8):e698.
Perlmutter D & Loberg K (2014) Grain Brain: The Surprising Truth About Wheat, Carbs, and Sugar – Your Brain’s Silent Killers (Hodder & Stoughton).
DiNicolantonio JJ & Lucan SC (2014) The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart 1(1):e000167.
Schaefer EJ, Gleason JA, & Dansinger ML (2009) Dietary Fructose and Glucose Differentially Affect Lipid and Glucose Homeostasis. The Journal of Nutrition 139(6):1257S-1262S.
Stanhope KL (2015) Sugar consumption, metabolic disease and obesity: The state of the controversy. Critical Reviews in Clinical Laboratory Sciences:1-16.
Gandotra P & Miller M (2008) The role of triglycerides in cardiovascular risk. Current Cardiology Reports 10(6):505-511.

Tea and Healthy Blood Sugar Levels

by Lauren Chmiel

Published on July 16, 2015

3034 views

It seems to be an almost daily occurrence I am hearing or reading about correlations between specific consumables and better health, whether it is the acai berry, resveratrol or the previously disparaged coconut oil. While some “superfoods” wax and wane in popularity, the benefits of consuming tea continues to intrigue academics, medical professionals and the general public alike. Countless studies have been conducted in order to prove there is a solid relationship between tea consumption and lowering blood sugar levels, or that tea can serve as an inexpensive, alternative method for prevention of diabetes and its pre-diabetic metabolic precursors.

Specifically, I think it is important to sort out the relationship between managing diabetes and how tea can serve as a useful tool in doing such. Diabetes is a complex, chronic disease which, essentially, develops when the pancreas produces too little insulin (Type I) or one’s body can no longer respond to insulin (Type II). Diabetics suffer from blood sugar levels above the healthy range, and when left untreated, can result in a number of debilitating complications. Type II Diabetes, the type which develops usually in adulthood, heavily depends on our lifestyle choices (e.g., diet and exercise). According to the American Diabetes Association, 25.8 million Americans (adults and children), or 8.3% of the population, suffer from diabetes as of 2011. The World Health Organization (WHO) estimates that over 347 million individuals worldwide are diabetic, and approximately 90% of this number has Type II Diabetes.

As an undergraduate, I had the pleasure to conduct research regarding the relationship between Diabetina, an herbal tea blend from Mexico, and blood sugar levels in normal glycemic-level individuals. Although my results were statistically inconclusive, I did notice that Diabetina and black tea consumption (which my participants consumed for a total of 16 weeks) resulted in lower, healthy blood sugar levels. A number of studies concerning black or green tea consumption and blood sugar have proven to be rather promising. A 2012 academic article published in BMJ Open and reviewed in The Huffington Post and WebMD suggests that countries with high black tea consumption patterns have significantly lower rates of diabetes. Nations known for high tea consumption such as Ireland, UK and Turkey enjoyed the lowest levels of diabetes out of the 50 countries surveyed in this study. Green tea and black have both been touted as useful for lowering glucose levels, and in rat studies, have proven to inhibit diabetic cataracts.

It is perfectly acceptable to wonder, what is it about tea that works with lowering our blood sugar? Black, green and oolong teas all are derived from the Camellia sinensis plant and are known to contain polysaccharides which prevent absorption of glucose (sugar) in the body. The relationship between the human race and tea consumption stretches back for at least 5,000 years and has enjoyed a long, colorful life, stemming from its supposed invention by the Chinese Emperor Shennong and has been a prominent member of European history since the late 16th and early 17th century. Not only has the ancient ritual of tea drinking been cultivated for millennia, tea consumption may serve as a healthful participant within a well-balanced diet.

In consideration of everything I have previously mentioned, some current research suggests that one must consume a good amount of tea in order to prevent or reduce one’s risk of diabetes. A European meta-analysis published in May 2012 suggests that consumption of four or more cups of tea a day is associated with a 20% lower risk of diabetes. Those who drink one to three cups of tea daily did not lower their risk of diabetes, comparable to non-tea drinkers. Green tea especially is credited as beneficial for a number of functions, such as deactivating free radicals and boosting metabolism.

We live in a world of modern medicine and often, natural methods of healing are overlooked or dismissed. Perhaps we shouldn’t be so quick to overlook these remedies. As the Pacific College of Oriental Medicine states, “green tea is not a cure for diabetes, but a natural gift for restoring balance in the human system and removing unwanted toxins accumulated from the internalizing of the environment.” In other words, tea may not cure diabetes, but it could be a part of healthy lifestyle, and as my research demonstrated, it might just lower your blood sugar.

This post was published previously in January 2013.

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