The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
- Peter @Hyperlipid

I don’t think there are too many people out there familiar with the mechanisms of diabetes and insulin resistance that would disagree with that statement.

But just because a low-carb diet causes fat loss in this population, that doesn’t mean that carbs caused the fat gain or damaged metabolism in the first place.

I wrote about this in a previous article, There is No Single Cause of (or Treatment or) Obesity, but based on some of the comments and discussion I’ve been seeing online recently, I think it bears repeating: in order to properly frame this debate, it’s essential to separate the causes and treatment of obesity. If we don’t do this, we might as well not even have a debate at all because we won’t be talking about the same thing.

We know without a doubt that statins lower cholesterol. But does that mean high cholesterol is caused by a statin deficiency? If you break your arm, your doctor will probably put a cast on to help it heal. Does that mean we should all wear casts on our arms to make sure they don’t break?

Metabolically damaged vs. healthy: apples & oranges

Another important distinction that should be made – but often isn’t – is the difference between how people that are metabolically healthy and metabolically damaged respond to food. Of course excess carbohydrates are more likely to cause problems in someone with leptin and insulin resistance and impaired glucose tolerance. But it doesn’t follow that the same will be true in someone without metabolic problems.

People without gall bladders don’t digest fat very well. Does that mean fat causes indigestion? I have patients with iron overload due to a genetic condition called hemachromatosis. They need to limit their red meat intake because of this. Does this mean we should all avoid red meat to prevent iron overload?

We’re not robot clones. We have different genes, lifestyles, gut flora, immune fitness and exposures to toxins, stress and infections, as well as different emotional and psychological relationships with food. All of these factors play a role in weight regulation.

This explains why two people can react to the same diet in entirely different ways. And it also explains why it’s so ridiculous to extrapolate something that you experience personally to everyone else. (If I read another comment from someone saying that a low-carb diet worked for them, so the insulin-carb theory must be correct, I’m going to lose it. And it takes a lot to make me lose it!)

My unified theory of obesity

For what it’s worth, here’s my “unified theory” on what causes obesity.

Modern lifestyle + genetic predisposition = obesity.

It really is that simple.

Modern lifestyle includes processed, refined and highly rewarding and palatable foods, excess fructose, unprepared grains (especially flour), industrial seed oils, environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.

But the modern lifestyle doesn’t cause obesity in all people. I’m sure we all know someone who eats a horrible diet, doesn’t exercise, is under tons of stress and lives a shockingly unhealthy lifestyle – but doesn’t gain a single pound.

That’s where genetics come in.

Human evolution didn’t stop in the Paleolithic

A commonly held belief in the Paleo-sphere (I held it myself, until fairly recently) is that our genes haven’t changed much since the Paleolithic era. But recent evidence suggests a much more rapid pace of genetic change in humans than was previously estimated.

The birth of agriculture introduced significant selection pressure, and thus mutation, because humans were not well-adapted to this new way of life. And the evolutionary response to agricultural diet differs because different peoples adopted agriculture at different times and in different places.

Agriculture began in the Middle East 10,000 years ago, but it was never adopted by Aboriginal Australians. Might we expect the descendants of people from these two regions to have different responses when exposed to agricultural diets?

Absolutely. Researchers in Iceland have discovered a gene that regulates blood sugar tolerance. (I discussed the role of genetics in obesity and diabetes in a previous article, Are You At Risk For Diabetes and Obesity?) And we know that Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.

Lactase persistence is another example. During Paleolithic times, humans stopped producing lactase (the enzyme required to digest lactose, the sugar in milk) shortly after weaning. There was no need for it, since Paleo people didn’t raise cattle or drink milk. Skeletal remains from northern Europeans 8,000 – 9,000 years ago confirm that there was no lactose tolerance at that time.

However, skeletal remains from northern Europeans living in the Bronze Age 3,000 years ago show roughly 25% of adults produced lactase. And today, in certain Scandanavian countries, more than 95% of adults are now lactose tolerant. ¹

All of these genetic changes happened within the last 8,000 years, after the advent of agriculture.

The hand you were dealt: life isn’t always fair

What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet.

But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.

Does it even matter what causes obesity? I just want to lose weight!

Some might argue that this discussion is irrelevant, since once someone become obese it’s clear their metabolism is damaged. There are two main problems with that argument.

First, not all obese people have deranged metabolisms. Research over the past several years has defined a subset of “metabolically healthy obese” (MHO) people with normal fasting glucose, triglycerides, insulin sensitivity and other markers. I wrote about this in my article Not All Fat People Get Diabetes, and Not All Diabetics Are Fat.

Second, separating the cause and treatment of obesity is necessary to prevent confusion. Something I see all the time in my practice and in the blogosphere is normal or even underweight people following zero- or very-low-carb diets. Why? Because they’ve absorbed the notion that “carbs are bad” from the “carbs-insulin-fat gain” theory, and they avoid them in a misguided attempt to promote health. While this may work for some people, it doesn’t for many others. I know because they end up coming to me with complaints like low energy, hair loss, bad breath, constipation and more.

Food reward vs. the carbohydrate hypothesis: setting the ground rules

I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation.

Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.

Over the last few years doctors are increasingly relying on a test called hemoglobin A1c to screen for insulin resistance and diabetes. It’s more practical (and significantly cheaper) than post-meal glucose testing, and it’s less likely to be skewed by day-to-day changes than fasting blood glucose.

What is hemoglobin A1c?

Sugar has a tendency to stick to stuff. Anyone that has cooked with sugar can tell you that. In our bodies, sugar also sticks – especially to proteins. The theory behind the A1c test is that our red blood cells live an average of three months, so if we measure the amount of sugar stuck to these cells (which is what the hemoglobin A1c test does), it will give us an idea of how much sugar has been in the blood over the previous three months. The number reported in the A1c test result (i.e. 5.2) indicates the percentage of hemoglobin that has become glycated (stuck to sugar).

Why is hemoglobin A1c unreliable?

While this sounds good in theory, the reality is not so black and white. The main problem is that there is actually a wide variation in how long red blood cells survive in different people. This study, for example, shows that red blood cells live longer than average at normal blood sugars. Researchers found that the lifetime of hemoglobin cells of diabetics turned over in as few as 81 days, while they lived as long as 146 days in non-diabetics.

This proves that the assumption that everyone’s red blood cells live for three months is false, and that hemoglobin A1c can’t be relied upon as a blood sugar marker. In a person with normal blood sugar, hemoglobin will be around for a lot longer, which means it will accumulate more sugar. This will drive up the A1c test result – but it doesn’t mean that person had too much sugar in their blood. It just means their hemoglobin lived longer and thus accumulated more sugar. The result is that people with normal blood sugar often test with unexpectedly high A1c levels.

This confused me early in my practice. I was testing blood sugar in three different ways for all new patients: fasting blood glucose, post-meal blood sugar (with a glucometer) and A1c. And I was surprised to see people with completely normal fasting and post-meal blood sugars, and A1c levels of >5.4%.

In fact this is not abnormal, when we understand that people with normal blood sugar often have longer-lived red blood cells – which gives those cells time to accumulate more sugar.

On the other hand, if someone is diabetic, their red blood cells live shorter lives than non-diabetics. This means diabetics and those with high blood sugar will test with falsely low A1c levels. And we already know that fasting blood glucose is the least sensitive marker for predicting future diabetes and heart disease. This is a serious problem, because fasting blood glucose and hemoglobin A1c are almost always the only tests doctors run to screen for diabetes and blood sugar issues.

Another condition that affects hemoglobin A1c levels is anemia. People who are anemic have short-lived red blood cells, so like diabetics, they will test with falsely low A1c levels. In my practice, about 30-40% of my patients have some degree of anemia, so this is not an uncommon problem.

What blood sugar markers are reliable?

Testing accurately for blood sugar is like putting pieces of a puzzle together. Fasting blood glucose, A1c and post-meal blood sugar are all pieces of the puzzle. But post-meal blood glucose testing is by far the most reliable and accurate way to determine what’s happening with blood sugar, and the most sensitive way of predicting future diabetic complications and heart disease.

For more on why post-meal blood sugar is a superior marker, read my article When Your Normal Blood Sugar Isn’t Normal (Part 2). To learn how to test your post-meal blood sugars at home, and what healthy targets should be, read my article How to Prevent Diabetes and Heart Disease for $16.

Another useful – but underused – blood sugar marker is fructosamine. Fructosamine is a compound that results from a reaction between fructose and ammonia or an amine. Like A1c, it’s a measure of average blood sugar concentrations. But instead of measuring the previous 12 weeks like A1c, fructosamine measures the previous 2-3 weeks. And unlike A1c, fructosamine is not affected by the varying length of red blood cell lifespans in different individuals. Fructosamine is especially useful in people who are anemic, or during pregnancy, when hormonal changes cause greater short-term fluctuations in blood glucose levels.

To put the most accurate picture together, I like to have all four: fasting blood glucose, A1c, post-meal glucose and fructosamine. But if I only had to choose one, it would definitely be post-meal glucose.

In the last article we discussed the complex relationship between body weight and type 2 diabetes (T2DM). We learned that although obesity is strongly associated with T2DM, a subset of “metabolically healthy obese” (MHO) people have normal blood sugar and insulin sensitivity and don’t ever develop diabetes.

In this article we’re going to talk about the mirror reflection of the MHO: the “metabolically unhealthy nonobese” (MUN). These are lean people with either full-fledged type 2 diabetes or some metabolic dysfunction, such as insulin resistance.

You might even be surprised to learn that skinny people can and do get T2DM. They are rarely mentioned in the media, and there isn’t much written about them in the scientific literature. Perhaps these folks have been overlooked because type 2 diabetes has been historically viewed as a disease of gluttony and sloth, a self-inflicted outcome of eating too much and not and not exercising enough. But the very existence of the MUN phenotype proves that there’s more to T2DM than overeating and a sedentary lifestyle.

Remember that one in three type 2 diabetics are undiagnosed. It’s possible that a significant number of these people that are lean. They don’t suspect they might have T2DM because they’re under the impression that it’s not a condition that affects thin people. This is one of the biggest dangers of the myth that “only fat people get diabetes”.

It’s well-known that high blood sugar can precede the development of T2DM for as long as ten years. It is during this time that many of the complications associated with diabetes – nerve damage, retinal changes, and early signs of kidney deterioration – begin to develop. This is why it’s just as important for lean people to maintain healthy blood sugar as it is for the overweight and obese.

It’s also important to understand that diabetes is not a disease. It’s a symptom. Every single person with T2DM, whether they are rail thin or morbidly obese, shares a single symptom: high blood sugar. Therefore, anything that interferes with the body’s regulation of blood sugar levels will cause type 2 diabetes.

What causes high blood sugar and T2DM in lean people?

Not surprisingly, the causes of T2DM in lean people are similar to the causes of T2DM in the obese. They can be loosely grouped into the following categories:

1. Genetics
2. Fatty liver
3. Inflammation
4. Autoimmunity
5. Stress

Let’s discuss each of them in turn.

Genetics

Studies of the lean, otherwise healthy offspring of type 2 diabetics has revealed that they are much more likely to be insulin resistant than the lean offspring of non-diabetics. One explanation for this is an inherited defect that causes mitochondrial dysfunction. People with this defect are not able to burn glucose or fatty acids efficiently, which causes lipotoxicity and an accumulation of fat inside of muscle cells.

I will discuss the contribution of genetics in more detail in the next article. What I want you to understand here is that the genetic mechanisms I described above are capable of causing insulin resistance and high blood sugar independently of overweight or obesity.

Fatty liver

Studies of lean, Asian Indian men have found that they have a 3- to 4-fold higher incidence of insulin resistance than their caucasian counterparts. They also have a much higher prevalence of non-alcoholic fatty liver disease (NAFLD) and hepatic (liver) insulin resistance.

NAFLD is an independent predictor of type 2 diabetes. Cross-sectional studies have shown that fatty liver and metabolic abnormalities occur together. It has also been proposed that fatty liver is not just a result, but also a cause of insulin resistance and type 2 diabetes.

Now, keep in mind that these Asian Indian men with NAFLD were not overweight. They were lean, and in some cases, even underweight. This proves that NAFLD occurs in lean people, and together with the evidence above, suggests that NAFLD may be a primary cause of insulin resistance and T2DM in lean people.

If you’re thinking NAFLD might be a rare problem confined to Asian Indian men, you should know that up to 30% (almost 1 in 3) of people in industrialized nations suffer from it. This is a disturbingly high prevalence of a condition that is known to progress to severe liver inflammation and cancer in a small percentage of people – in addition to contributing to T2DM and metabolic syndrome.

While there may be a genetic component that predisposes people to developing NAFLD, we also know that dietary factors play a significant role. Rodent studies have shown that feeding large amounts of sugar and industrial seed oils (like corn, safflower, sunflower, etc.) promote NAFLD, whereas saturated fats such as butter and coconut oil do not. And in human infants, tube-feeding with industrial seed oils causes severe liver damage, whereas the same amount of fat from fish oil does not.

Fructose, especially the high-fructose corn syrup (HFCS) found in sodas, candy and several packaged and refined foods, is perhaps the most significant dietary cause of NAFLD. The liver processes fructose by converting it to fat. The more fructose consumed, the more fatty the liver becomes. Feeding rodents high amounts of fructose promotes NAFLD, and the consumption of soft drinks (by humans) can increase the prevalence of NAFLD independently of metabolic syndrome.

Let me say that again: high fructose intake can cause fatty liver disease independently of overweight, obesity or type 2 diabetes. Do you think that might be a problem in a country where soft drinks account for nearly 10% of total caloric intake?

Since fructose is handled by the liver in the same way the liver handles alcohol, excess fructose produces a similar range of problems as alcohol abuse: hypertension, high triglycerides and low HDL, obesity, cirrhosis and insulin resistance.

Inflammation

In the study of lean Asian Indian men above with T2DM, it was found that they had a 2-fold increase in plasma levels of the inflammatory protein IL-6 when compared to lean subjects without T2DM. In a previous article I showed that chronic, low-grade inflammation associated is an important mechanism in decreasing insulin signaling and causing insulin resistance in muscle, liver and fat cells.

Also, inflammation has been shown to precede the development of diabetes. Infusion of inflammatory cytokines into healthy, normal weight mice causes insulin resistance, and people with other chronic inflammatory conditions are at higher risk of developing T2DM. For example, about one-third of chronic Hepatitis C patients develop T2DM, and those with rheumatoid arthritis are also at higher risk.

Autoimmunity

Up until recently, type 1 and type 2 diabetes were seen as distinct entities. It was understood that type 1 diabetes (or insulin-dependent diabetes) was caused by autoimmune destruction of the beta cells of the pancreas, leading to decreased insulin production, whereas type 2 diabetes was caused by insulin resistance of the liver, muscle and fat cells.

However, recent research has demonstrated that the line separating these two conditions may be much blurrier than previously thought. It is now known that type 1 diabetes, which normally begins in childhood, may slowly develop later in life. This form is referred to as latent autoimmune diabetes (LADA) or more informally as type 1.5 diabetes.

Studies suggest that type 1 diabetes in adults is frequently misdiagnosed as T2DM, and up to 10% of adults with T2DM may actually have the autoimmune form.

Even more relevant to this article is the finding that fully 1 in 4 lean people with T2DM produce antibodies to GAD, the same enzyme in the pancreas that is attacked in type 1 autoimmune diabetes.

These findings suggest that a significant number of lean people with T2DM may be suffering from autoimmune diabetes. This will obviously require a different treatment strategy than those who have the non-autoimmune form. (The way to find out whether you’re in this group is to have your GAD antibodies tested. It’s a fairly standard blood test and is available through Labcorp and Quest.)

(Interestingly enough, approximately 5% of patients with autoimmune thyroid conditions also produce antibodies to GAD. So if you have Hashimoto’s or Graves’ disease along with blood sugar symptoms that don’t respond to dietary changes, you should have your GAD antibodies checked.)

Stress

Under conditions of stress, the body produces higher levels of the hormone cortisol. Cortisol plays a number of important roles, but one of it’s primary functions is to raise blood sugar. This is an incredibly helpful evolutionary mechanism that is part of the “fight or flight” response that prepares us to deal with a challenge or threat.

However, that mechanism was only designed for short bursts of stress. Chronic stress as we experience it today – like worrying about getting audited by the IRS, driving in traffic, and suffering from degenerative disease – wasn’t part of our early ancestors’ lives. This means that our bodies aren’t prepared to deal with the effects of chronic stress, which include chronically elevated levels of cortisol.

Why? Because cortisol is capable of raising blood sugar to unhealthy levels even when a person is fasting. What that also means is that you can be lean, eat a perfect diet, and still have high blood sugar (and thus T2DM) if you suffer from chronic stress. I’ll be writing more about the connection between stress and diabetes in a future article.

Obesity, insulin resistance, metabolic syndrome and type 2 diabetes have reached epidemic proportions. There’s not a person reading this article who isn’t affected by these conditions, either directly or indirectly. Yet as common as these conditions are, few people understand how closely they’re related to one another.

It is now clear that not only do these conditions share the same underlying causes – and thus require the same treatment – they are 100% preventable and, in many cases, entirely reversible.

Because of these similarities, Dr. Francine Kaufman coined the term diabesity (diabetes + obesity) to describe them. Diabesity can be defined as a metabolic dysfunction that ranges from mild blood sugar imbalances to full-fledged type 2 diabetes. Diabesity is a constellation of signs that includes:

• abdominal obesity (i.e. “spare tire” syndrome);
• dyslipidemia (low HDL, high LDL and high triglycerides);
• high blood pressure;
• high blood sugar (fasting above 100 mg/dL, Hb1Ac above 5.5);
• systemic inflammation; and,
• a tendency to form blood clots.

The subjective symptoms of diabesity include (but aren’t limited to):

• sugar cravings, especially after meals;
• eating sweets does not relieve cravings for sugar;
• fatigue after meals;
• frequent urination;
• increased thirst and appetite;
• difficulty losing weight;
• slowed stomach emptying;
• sexual dysfunction;
• visual problems; and,
• numbness and tingling in the extremities.

The term diabesity is misleading in one respect: it suggests one must be obese to experience the metabolic problems I just described above. That’s not true. Thin people can suffer from the entire spectrum of blood sugar imbalances, all the way up to full-fledged type 2 diabetes. The term sometimes used for someone who is thin, yet has insulin resistance, dysglycemia and dyslipidemia is “metabolically obese”. Their metabolism behaves as if they’re obese, even when they’re not.

It’s almost impossible to overstate how serious and far-reaching a problem diabesity is. It affects more than one billion people worldwide (1), including 100 million Americans and 50% of Americans over 65.

More than half of Americans are overweight, and a full one-third are clinically obese. 24 million Americans have type 2 diabetes, with one in three unaware that they have it. (2)

Diabesity is the leading cause of modern, chronic disease. The “diabese” have increased risk of heart disease, stroke, dementia, cancer, kidney failure and blindness – to name only a few.

In the U.S. today, every ten seconds someone dies from diabetes-related causes. (3) Diabetes and cardiovascular disease have now outpaced infectious disease as the primary cause of morbidity and mortality worldwide. In Dr. Bernstein’s Diabetes Solution, Dr. B claims that diabetes is now the 3rd leading cause of death. But death certificates don’t list diabetes or hyperglycemia as the underlying cause of heart attacks, strokes or fatal infections. Nor do they consider the role of obesity, insulin resistance and inflammation in these conditions. If they did, it’s quite possible that diabesity is not only the leading cause of disease, but also the leading cause of death.

Diabesity is literally bankrupting our health care system. The direct and indirect costs of type 2 diabetes were $174 billion in 2007. The cost of obesity in that same year was $113 billion. So the total cost of diabesity to society can be conservatively estimated at nearly $300 billion per year. (4) To put that in perspective, diabesity has cost the U.S. $3 trillion over the past decade. That’s three times the estimated cost of fixing our entire health care system. And it’s only going to get worse. the projected cost of diabetes alone is expected to rise to more than $330 billion by 2034. (5)

With numbers like this, you’d expect a state of emergency to be declared. You’d think we’d be doing everything in our power to figure out the cause of these conditions and how to treat them successfully.

But the reality is that the conventional treatment of diabesity has been a dismal failure. This is reflected in the shocking growth of the conditions that fall under the diabesity umbrella over the past two decades, and the equally alarming projections for the future.

Recent reports suggest that one-third of people born in 2010 will develop diabetes at some point in their lives. (6) What is particularly horrifying about this statistic is that many of those who develop diabetes will be kids. Type 2 diabetes used to be a disease of the middle-aged and elderly. No longer. A recent Yale study indicated that nearly one in four kids between the ages of 4 and 18 have pre-diabetes (glucose intolerance). Some regional studies show type 2 diabetes in kids has jumped from less than 5% before 1994 to 50% in 2004. (7)

Each year, kids are getting fatter. Among American children 2-5 years of age, more than 10% are now obese. (8) Even more alarming is the rise of obesity in infants under 2 years of age. Research from Harvard shows infant obesity has risen more than 70% since 1980. (8) And this isn’t because babies are eating more donuts and cheese doodles while cutting back on their Stairmaster workouts, either. Clearly there’s more to the diabesity story than eating junk food and not exercising enough. But I digress. We’ll be covering causes in future articles.

From 1993 to 2008, the number of people in the world with diabetes increased seven-fold from 35 million to 240 million, and is expected to rise to 380 million by 2030. This is ten times the number of people affected by HIV/AIDS worldwide. In the U.S., the incidence of diabetes is projected to increase to 44 million in the year 2034. (9)

What accounts for such an explosion of new cases? One reason is that the standard treatment for diabesity is not only ineffective, it’s contributing to the problem. Once they have developed, diabetes and obesity are characterized by insulin resistance, which in turn results in carbohydrate intolerance. Yet prominent organizations such as the American Diabetes Association have been recommending a low-fat, high-carbohydrate diet as a treatment for diabetes for decades. It didn’t work in 1985, and it still doesn’t work. Einstein once said that insanity is doing the same thing over and over, and expecting a different result. Clearly the conventional approach to treating diabesity is insane.

In this series, we’re going to get the bottom of the diabesity epidemic. We’ll leave the conventional model of understanding diabesity – which is now about 40 years old – in the dust and replace it with an updated 2010 model that reflects the current scientific literature. We’re going to uncover the real causes of of diabesity, and we’re going to find out exactly how it can be prevented and even reversed in the majority of cases.

As we go along we’ll be busting a number of conventional and alternative myths about diabesity. We’ll learn that:

• Obesity isn’t as simple as eating too much and not exercising enough.
• Diabetes isn’t always progressive, and can be reversed in many people.
• Diabetes isn’t caused by eating too many carbohydrates.
• A fasting blood sugar of 95 mg/dL and Hb1Ac of 5.5% isn’t “normal”.
• Thin people can get type 2 diabetes.
• And more…

As we begin, I’d love to hear from you. Do you have any specific questions about diabesity? Anything you’ve always wondered about but haven’t found the answer to? Leave a comment, and I’ll do my best to address it at some point in the series.

According to the American Association of Clinical Endocrinologists, 27 million Americans suffer from thyroid dysfunction – half of whom go undiagnosed. Subclinical hypothyroidism, a condition in which TSH is elevated but free T4 is normal, may affect an additional 24 million Americans. Taken together, more than 50 million Americans are affected by some form of thyroid disorder.

Metabolic syndrome (MetS), also affects 50 million Americans, and insulin resistance, one of the components of metabolic syndrome, affects up to 105 million Americans. That’s 35% of the population. Metabolic syndrome has become so common that it’s predicted to eventually bankrupt our healthcare system. Both metabolic syndrome and insulin resistance are risk factors for heart disease and diabetes, two of the leading causes of death in the developed world.

With such a high prevalence of both thyroid dysfunction and metabolic syndrome, you might suspect there’s a connection between the two. And you’d be right.

Studies show an increased frequency of thyroid disorders in diabetics, and a higher prevalence of obesity and metabolic syndrome in people with thyroid disorders.

That’s because healthy thyroid function depends on keeping your blood sugar in a normal range, and keeping your blood sugar in a normal range depends on healthy thyroid function.

How high blood sugar affects the thyroid

Metabolic syndrome is defined as a group of metabolic risk factors appearing together, including:

• abdominal obesity;
• high cholesterol and triglycerides;
• high blood pressure;
• insulin resistance;
• tendency to form blood clots; and,
• inflammation.

Metabolic syndrome is caused by chronic hyperglycemia (high blood sugar). Chronic hyperglycemia is caused by eating too many carbohydrates. Therefore, metabolic syndrome could more simply be called “excess carbohydrate disease”. In fact, some researchers have gone as far as defining metabolic syndrome as “those physiologic markers that respond to reduction in dietary carbohydrate.”

When you eat too many carbs, the pancreas secretes insulin to move excess glucose from the blood into the cells where glucose is used to produce energy. But over time, the cells lose the ability to respond to insulin. It’s as if insulin is knocking on the door, but the cells can’t hear it. The pancreas responds by pumping out even more insulin (knocking louder) in an effort to get glucose into the cells, and this eventually causes insulin resistance.

Studies have shown that the repeated insulin surges common in insulin resistance increase the destruction of the thyroid gland in people with autoimmune thyroid disease. As the thyroid gland is destroyed, thyroid hormone production falls.

How low blood sugar affects the thyroid

But just as high blood sugar can weaken thyroid function, chronically low blood sugar can also cause problems.

Your body is genetically programmed to recognize low blood sugar as a threat to survival. Severe or prolonged hypoglycemia can cause seizures, coma, and death. When your blood sugar levels drop below normal, your adrenal glands respond by secreting a hormone called cortisol. Cortisol then tells the liver to produce more glucose, bringing blood sugar levels back to normal.

The problem is that cortisol (along with epinephrine) is also a sympathetic nervous system hormone involved in the “flight or fight” response. This response includes an increase in heart rate and lung action and an increase in blood flow to skeletal muscles to help us defend against or flee from danger. Cortisol’s role is to increase the amount of glucose available to the brain, enhance tissue repair, and curb functions – like digestion, growth and reproduction – that are nonessential or even detrimental in a fight or flight situation.

Unfortunately for hypoglycemics, repeated cortisol release caused by episodes of low blood sugar suppresses pituitary function. And as I showed in a previous article, without proper pituitary function, your thyroid can’t function properly.

Together, hyperglycemia and hypoglycemia are referred to as dysglycemia. Dysglycemia weakens and inflames the gut, lungs and brain, imbalances hormone levels, exhausts the adrenal glands, disrupts detoxification pathways, and impairs overall metabolism. Each of these effects significantly weakens thyroid function. As long as you have dysglycemia, whatever you do to fix your thyroid isn’t going to work.

How low thyroid function affects blood sugar

We’ve seen now how both high and low blood sugar cause thyroid dysfunction. On the other hand, low thyroid function can cause dysglycemia and metabolic syndrome through a variety of mechanisms:

• it slows the rate of glucose uptake by cells;
• it decreases rate of glucose absorption in the gut;
• it slows response of insulin to elevated blood sugar; and,
• it slows the clearance of insulin from the blood.

These mechanisms present clinically as hypoglycemia. When you’re hypothyroid, your cells aren’t very sensitive to glucose. So although you may have normal levels of glucose in your blood, you’ll have the symptoms of hypoglycemia (fatigue, headache, hunger, irritability, etc.). And since your cells aren’t getting the glucose they need, your adrenals will release cortisol to increase the amount of glucose available to them. This causes a chronic stress response, as I described above, that suppresses thyroid function.

How to keep your blood sugar in a healthy range

It’s important to understand that whether you have high or low blood sugar, you probably have some degree of insulin resistance. I described how high blood sugar causes insulin resistance above. But insulin resistance can also cause low blood sugar. This condition, called reactive hypoglycemia, occurs when the body secretes excess insulin in response to a high carbohydrate meal – causing blood sugar levels to drop below normal.

In either case, the solution is to make sure your blood sugar stays within a healthy range. There are two targets to consider. The first is fasting blood glucose, which is a measure of your blood sugar first thing in the morning before eating or drinking anything. I define the normal range for fasting blood glucose as 75 – 95 mg/dL. Although 100 is often considered the cutoff for normal, studies have shown that fasting blood sugar levels in the mid-90s were predictive of future diabetes a decade later. And although 80 mg/dL is often defined as the cutoff on the low end, plenty of healthy people have fasting blood sugar in the mid-to-high 70s (especially if they follow a low-carb diet).

The second, and much more important, target is post-prandial blood glucose. This is a measure of your blood sugar 1-2 hours after a meal. Several studies have shown that post-prandial blood glucose is the most accurate predictor of future diabetic complications and is the first marker (before fasting blood glucose and Hb1Ac) to indicate dysglycemia.

Normal post-prandial blood sugar one to two hours after a meal is 120 mg/dL. Most normal people are under 100 mg/dL two hours after a meal.

Now that we know the targets, let’s look at how to meet them. If you’re hypoglycemic, your challenge is to keep your blood sugar above 75 throughout the day. The best way to do this is to eat a low-to-moderate carbohydrate diet (to prevent the blood sugar fluctuations I described above), and to eat frequent, small meals every 2-3 hours (to ensure a continuous supply of energy to the body.

If you’re hyperglycemic, your challenge is to keep your blood sugar below 120 two hours after a meal. The only way you’re going to be able to do this is to restrict carbohydrates. But how low-carb do you need to go? The answer is different for everyone. You figure your own carbohydrate tolerance by buying a blood glucose meter and testing your blood sugar after various meals. If you’ve eaten too many carbs, your blood sugar will remain above 120 mg/dL two hours after your meal.

I highly recommend you pick up a blood glucose meter if you have a thyroid and/or blood sugar problem. It’s the simplest and most cost-effective way to figure out how much carbohydrate is safe for you to eat. There are tons of meters out there, but one that gets a lot of good recommendations is the ReliOn Ultima. It’s pretty cheap, and the test strips are also cheap, which is where the major expense lies.

Finally, if you have poor thyroid function it’s important that you take steps to normalize it. As I’ve described in this article, the cycle works in both direction. Dysglycemia can depress thyroid function, but thyroid disorders can cause dysglycemia and predispose you to insulin resistance and metabolic syndrome.