In this episode we discuss the following topics:

• A recent study demonstrating that low cholesterol is associated with higher risk of death in women
• What truly normal blood sugar levels during pregnancy are, and cut-offs for pre-diabetic and diabetic women during pregnancy
• Whether there’s any science behind breaking weight loss plateaus by adding carbs back in the diet
• Best practices for people with Hashimoto’s
• Why there has been such an explosion in food sensitivities, celiac disease and leaky gut
• The connection between diet and body odor
• Recommendations for moderate to severe ulcerative colitis

Please note that in the next few weeks, the name of the show will be changing. It will be called “Revolution Health Radio”, with Chris Kresser. There’s nothing you need to do. You’ll just notice that the graphic and show name are different at some point.

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.

I hope you all had happy holidays and are off to a great start this year. I thought I’d share a few thoughts that have been bouncing around my head lately, stimulated most recently by two articles written by fellow health bloggers.

Don Matesz over at Primal Wisdom wrote a thought-provoking piece on the hormone composition of grass-fed and factory-farmed meat. In it he argues (convincingly, I might add) that meat from CAFO (confined animal feeding operations) does not have dangerously high levels of hormones, in spite of claims to the contrary made by advocates of eating grass-fed meat.

Got testicles?

I recommend reading the entire article, I’ll summarize it briefly here. Before CAFO came into being, humans predominantly ate bulls, since eating female animals (cows) was taboo. The taboo made perfect sense in a hunter-gatherer culture, since killing the female could eliminate potential offspring, while killing a few bulls would have no effect on the fecundity of the herd.

Today, CAFO use steer, which are neutered bulls. One reason for this is that steer are a lot easier to manage than bulls. Why? Because hormone levels in bulls (with intact sex organs) are significantly higher than in steer. In fact, bull meat has between 34 and 105 times more testosterone than steer meat. No wonder bulls are harder to manage!

Even when hormones are added to steer in CAFO, the levels are nowhere close to what they are in intact bulls. In fact, studies have found no significant difference in hormone levels between meat from hormone-treated and untreated animals.

This means that Paleo Pete was eating meat with a lot more hormones in it a million years ago than American Andy is when he gets a cheeseburger at McDonalds today.

Hormones in meat are bad – if you eat 200 pounds of meat a day

Studies have also shown that the hormones ingested from food, including CAFO meat, have a negligible effect on human health. From Don’s article:

For example, a prepubertal boy, most vulnerable to adverse effects of excess dietary estrogens, produces about 100 micrograms of estrogen daily. Beef muscle meat contains less than 0.02 micrograms of estrogens per kilogram. To get from beef an intake of estrogens equal to just one percent of his endogenous estrogen production, i.e. 1 microgram, he would have to consume 50 kilograms–110 pounds– of beef in a day!

Another common claim is that adding hormones to meat has increased the rates of cancer and other modern, degenerative diseases. But if that were true, we would have seen these diseases in hunter-gatherer populations that were eating large amounts of bull meat, which has on average 50 times more hormones than the CAFO steer meat eaten today.

So it would seem that there isn’t much difference between grass-fed and CAFO meat when it comes to hormones. So should we all just save some money and eat conventional meat?

It’s not all about hormones. Don’t forget omega-3s!

Not so fast. Mark Sisson published an article earlier this week reporting on a study comparing the effects of eating grass-fed and CAFO meat on omega-3 and omega-6 concentration in human plasma and platelets.

Turns out those that ate the grass-fed meat had significantly higher levels of omega-3 in their plasma and platelets than those that ate CAFO meat, despite the fact that the amount of omega-3 fatty acids in the two types of meat were not hugely different.

The folks consuming grass-finished meat ate, on average, 65 mg/d of long chain omega-3s, while those eating concentrate-finished meat ate about 44 mg/d of long chain omega-6s, yet the lab results – the big improvements in plasma and platelet fatty acid numbers – were lopsided.

What’s happening here? I suspect the answer lies with the difference in omega-6 content in the diets of both groups. Those who ate the CAFO meat had an average intake of 8.5g/d of omega-6 fats, while those that ate grass-fed meat had an average intake of 5.5g/d. In a previous article about how too much omega-6 is making us sick, I explained that omega-6 and omega-3 fatty acids compete for the same conversion enzymes.

Several studies have shown that the biological availability and activity of n-6 fatty acids are inversely related to the concentration of of n-3 fatty acids in tissue. Studies have also shown that greater composition of EPA & DHA in membranes reduces the availability of AA for eicosanoid production.

This works the other way, too. The more omega-6 is consumed, the less omega-3 is available to the tissues. So if two people eat a diet identical in omega-3 content, but one person’s diet is high in omega-6, and the other person’s is low, guess who will end up with more omega-3 in their tissues? That’s right – the one with a low omega-6 intake. This is why I constantly tell people that the most important step they can take in normalizing their omega-3:omega-6 ratio is not boosting omega-3 intake, but reducing omega-6. And this is likely what explains the higher levels of omega-3 in the grass-fed meat eaters in the study, even though grass-fed meat doesn’t have a lot more omega-3 than CAFO meat.

This is important, because the ratio of omega-3 to omega-6 in our tissue is crucial to health. Too much omega-6 in relation to omega-3 has been shown to be a factor in everything from depression and arthritis to heart disease and diabetes. There isn’t a modern disease out there that isn’t influenced by this ratio.

Black, white & shades of grey

So here we have one study suggesting there isn’t much difference between CAFO and grass-fed meat, and another suggesting the opposite. What do we make of this?

As much as we’d all like things to be simple when it comes to food and health, they often aren’t. We have to use our brains to sift through the available information and make intelligent choices based on several different factors.

In the case of grass-fed vs. CAFO meat, there’s a lot more to consider than hormones and fatty acids. There’s also antibiotic use in CAFO cattle and the increased risk of foodborne illness in CAFO meat, and there are several economic and social issues as well. Grass-fed animals are generally treated in a more humane way than CAFO animals. If you’ve ever visited a CAFO you will know what I mean. It’s shocking and disgusting. I personally prefer to support local farmers that use traditional methods of animal husbandry, that pay attention to how the animals are treated and slaughtered, and who care about every phase of the process. I like the money I spend on food to stay in my local community whenever possible.

Clearly this is not a black and white issue, and there’s a lot to take into account when choosing between grass-fed and CAFO meat. As usual, I’d love to hear your thoughts.

Jenny Ruhl over at Diabetes Update posted a notice about a glucometer test strip recall that may affect those of you measuring your own blood sugar:

Aboott Laboratories has just issued a huge recall for blood testing strips which read low. The strips take too long to absorb the drop of blood.

The list of affected lots is given here:

http://www.precisionoptiuminfo.com/img/Lot-Numbers.pdf

Further information can be found here:

http://www.precisionoptiuminfo.com/EN

Apparently, it takes more than 5 seconds for the blood to be absorbed and measured after being applied to the strip. I have some strips in the lot numbers listed in the recall, but they don’t seem to be affected since the blood is absorbed in only 1-2 seconds. I’ve been trying to reach Abbott to determine whether we can consider strips in affected lots that don’t take more than 5 seconds to absorb blood to be functional, but after waiting on hold for 20 minutes and getting hung up on several times, I gave up.

If anyone else is able to get through and find the answer to that question, please report back. For now, I’m assuming if the blood doesn’t take more than the typical 1-2 seconds to be absorbed, the strips are fine.

In the last article I explained the three primary markers we use to track blood sugar: fasting blood glucose (FBG), oral glucose tolerance test (OGTT) and hemoglobin A1c (A1c). We also looked at what the medical establishment considers as “normal” for these markers. The table below summarizes those values.

In this article, we’re going to look at just how “normal” those normal levels are – according to the scientific literature. We’ll also consider which of these three markers is most important in preventing diabetes and cardiovascular disease.

Fasting blood sugar

According to continuous glucose monitoring studies of healthy people, a normal fasting blood sugar is 83 mg/dL or less. Many normal people have fasting blood sugar in the mid-to-high 70s.

While most doctors will tell you that anything under 100 mg/dL is normal, it’s not. In this study, people with FBG levels above 95 had more than 3x the risk of developing future diabetes than people with FBG levels below 90. This study showed progressively increasing risk of heart disease in men with FBG levels above 85 mg/dL, as compared to those with FBG levels of 81 mg/dL or lower.

What’s even more important to understand about FBG is that it’s the least sensitive marker for predicting future diabetes and heart disease. Several studies show that a “normal” FBG level in the mid-90s predicts diabetes diagnosed a decade later.

Far more important than a single fasting blood glucose reading is the number of hours a day our blood sugar spends elevated over the level known to cause complications, which is roughly 140 mg/dl (7.7 mmol/L). I’ll discuss this in more detail in the OGGT section.

One caveat here is that very low-carb diets will produce elevated fasting blood glucose levels. Why? Because low-carb diets induce insulin resistance. Restricting carbohydrates produces a natural drop in insulin levels, which in turn activates hormone sensitive lipase. Fat tissue is then broken down, and non-esterified fatty acids (a.k.a. “free fatty acids” or NEFA) are released into the bloodstream. These NEFA are taken up by the muscles, which use them as fuel. And since the muscle’s needs for fuel has been met, it decreases sensitivity to insulin. You can read more about this at Hyperlipid.

So, if you eat a low-carb diet and have borderline high FBG (i.e. 90-105), it may not be cause for concern. Your post-meal blood sugars and A1c levels are more important.

Hemoglobin A1c

In spite of what the American Diabetes Association (ADA) tells us, a truly normal A1c is between 4.6% and 5.3%

And while A1c is a good way to measure blood sugar in large population studies, it’s not as accurate for individuals. An A1c of 5.1% maps to an average blood sugar of about 100 mg/dL. But some people’s A1c results are always a little higher than their FBG and OGTT numbers would predict, and other people’s are always a little lower.

This is probably due to the fact that several factors can influence red blood cells. Remember, A1c is a measure of how much hemoglobin in red blood cells is bonded (glycated) to glucose. Anything that affects red blood cells and hemoglobin – such as anemia, dehydration and genetic disorders – will skew A1c results.

A number of studies show that A1c levels below the diabetic range are associated with cardiovascular disease. This study showed that A1c levels lower than 5% had the lowest rates of cardiovascular disease (CVD) and that a 1% increase (to 6%) significantly increased CVD risk. Another study showed an even tighter correlation between A1c and CVD, indicating a linear increase in CVD as A1c rose above 4.6% – a level that corresponds to a fasting blood glucose of just 86 mg/dL. Finally, this study showed that the risk of heart disease in people without diabetes doubles for every percentage point increase above 4.6%.

Studies also consistently show that A1c levels considered “normal” by the ADA fail to predict future diabetes. This study found that using the ADA criteria of an A1c of 6% as normal missed 70% of individuals with diabetes, 71-84% with dysglycemia, and 82-94% with pre-diabetes. How’s that for accuracy?

What we’ve learned so far, then, is that the fasting blood glucose and A1c levels recommended by the ADA are not reliable cut-offs for predicting or preventing future diabetes and heart disease. This is problematic, to say the least, because the A1c and FBG are the only glucose tests the vast majority of people get from their doctors.

OGTT / post-meal blood sugars

If you recall, the oral glucose tolerance test (OGTT) measures how our blood sugar responds to drinking a challenge solution of 75 grams of glucose. I don’t recommend this test, because A) it’s not realistic (no one every drinks 75 grams of pure glucose), and B) it can produce horrible side effects for people with poor glucose control.

However, there’s another more realistic and convenient way to achieve a similar measurement, and that is simply using a glucometer to test your blood sugar one and two hours after you eat a meal. This is called post-prandial (post-meal) blood sugar testing. As we go through this section, the numbers I use apply to both OGTT and post-meal testing.

As the table at the beginning of this article indicates, the ADA considers OGTT of between 140 – 199 two hours after the challenge to be pre-diabetic, and levels above 200 to be diabetic.

But once again, continuous glucose monitoring studies suggest that the ADA levels are far too high. Most people’s blood sugar drops below 120 mg/dL two hours after a meal, and many healthy people drop below 100 mg/dL or return to baseline.

This study showed that even after a high-carb meal, normal people’s blood sugar rises to about 125 mg/dL for a brief period, with the peak blood sugar being measured at 45 minutes after eating, and then drops back under 100 mg/dL by the two hour mark.

Another continuous glucose monitoring study confirmed these results. Sensor glucose concentrations were between 71 – 120 mg/dL for 91% of the day. Sensor values were less than or equal to 60 or 140 mg/dL for only 0.2% and 0.4% of the day, respectively.

Even the American Association of Clinical Endocrinologists is now recommending that post-meal blood sugars never be allowed to rise above 140 mg/dL. Unfortunately, less informed groups like the ADA haven’t caught up with the science.

The consequences of this are severe. Nerve damage occurs as blood sugar rises above 140 mg/dL. Prolonged exposure to blood sugars above 140 mg/dL causes irreversible beta cell loss (the beta cells produce insulin). 1 in 2 “pre-diabetics” get retinopathy, a serious diabetic complication. Cancer rates increase as post-meal blood sugars rise above 160 mg/dL. This study showed stroke risk increased by 25% for every 18 mg/dL rise in post-meal blood sugars. Finally, 1-hour OGTT readings above 155 mg/dL correlate strongly with increased CVD risk.

What does it all mean?

Let’s take a look again at what the ADA thinks is “normal” blood sugar:

But as we’ve seen in this article, these levels are only normal if you think increased risk of diabetes, heart disease, cancer and other serious complications is normal. Just because these conditions are common, doesn’t mean they’re normal.

If you’re interested in health and longevity – instead of just slowing the onset of serious disease by a few years – you’d be well advised to shoot for these targets instead:

*If you’re following a low-carb diet, fasting blood sugars in the 90s and even low 100s may not be a problem, provided your A1c and post-meal blood sugars are within the normal range.

Another key takeaway from this article is that fasting blood glucose and A1 are not very reliable for predicting diabetes or CVD risk. Post-meal blood sugars are by far the most accurate marker for this purpose. And the good news is that this can be done cheaply, safely and conveniently at home, without a doctor’s order and without subjecting yourself to the brutality of an OGTT.

I’ll describe exactly how to do this in the next article.

There’s been a lot of discussion about the benefits of intermittent fasting (IF) in the paleo community lately. Paul Jaminet mentions it’s role in boosting the immune system in his book, The Perfect Health Diet, and IF can also be helpful for those trying to lose weight and tune their metabolism.

From an evolutionary perspective, intermittent fasting was probably the normal state of affairs. There were no grocery stores, restaurants or convenience stores, and food was not nearly as readily available or easy to come by as it is today. Nor were there watches, schedules, lunch breaks or the kind of structure and routine we have in the modern world. This means it’s likely that our paleo ancestors often did go 12-16 hours between meals on a regular basis, and perhaps had full days when they ate lightly or didn’t eat at all.

So, while I agree that IF is part of our heritage, and that it can be helpful in certain situations, I don’t believe it’s an appropriate strategy for everyone.

Why? Because fasting can elevate cortisol levels. One of cortisol’s effects is that it raises blood sugar. So, in someone with blood sugar regulation issues, fasting can actually make them worse.

I’ve seen this time and time again with my patients. Almost all of my patients have blood sugar imbalances. And it’s usually not as simple as “high blood sugar” or “low blood sugar”. They often have a combination of both (reactive hypoglycemia), or strange blood sugar patterns that, on the surface, don’t make much sense. These folks aren’t eating a Standard American Diet. Most of them are already on a paleo-type or low-carb diet. Yet they still have blood sugar issues.

In these cases, cortisol dysregulation is almost always the culprit. When these patients try intermittent fasting, their blood sugar control gets worse. I will see fasting blood sugar readings in the 90s and even low 100s, in spite of the fact that they are eating a low-carb, paleo-type diet.

That’s why I don’t recommend intermittent fasting for people with blood sugar regulation problems. Instead, I suggest that they eat every 2-3 hours. This helps to maintain stable blood sugar throughout the day and prevents cortisol and other stress hormones like epinephrine and norepinephrine from getting involved. When my patients that have been fasting and experiencing high blood sugar readings switch to eating this way, their blood sugar numbers almost always normalize.

I don’t think eating every 2-3 hours is “normal” from an evolutionary perspective. But neither is driving in traffic, worrying about your 401k, or staying up until 2:00am on Facebook. The paleo template is there to guide us, but it’s not a set of rules to be followed blindly. This should also be a reminder that there’s no “one size fits all” approach when it comes to healthcare. Successful treatment depends on identifying the underlying mechanisms for each individual and addressing them accordingly.

In the next two articles we’re going to discuss the concept of “normal” blood sugar. I say concept and put normal in quotation marks because what passes for normal in mainstream medicine turns out to be anything but normal if optimal health and function are what you’re interested in.

Here’s the thing. We’ve confused normal with common. Just because something is common, doesn’t mean it’s normal. It’s now becoming common for kids to be overweight and diabetic because they eat nothing but refined flour, high-fructose corn syrup and industrial seed oils. Yet I don’t think anyone (even the ADA) would argue that being fat and metabolically deranged is even remotely close to normal for kids. Or adults, for that matter.

In the same way, the guidelines the so-called authorities like the ADA have set for normal blood sugar may be common, but they’re certainly not normal. Unless you think it’s normal for people to develop diabetic complications like neuropathy, retinopathy and cardiovascular disease as they age, and spend the last several years of their lives in hospitals or assisted living facilities. Common, but not normal.

In this article I’m going to introduce the three markers we use to measure blood sugar, and tell you what the conventional model thinks is normal for those markers. In the next article, I’m going to show you what the research says is normal for healthy people. And I’m also going to show you that so-called normal blood sugar, as dictated by the ADA, can double your risk of heart disease and lead to all kinds of complications down the road.

The 3 ways blood sugar is measured

Fasting blood glucose

This is still the most common marker used in clinical settings, and is often the only one that gets tested. The fasting blood glucose (FBG) test measures the concentration of glucose in the blood after an 8-12 hour fast. It only tells us how blood sugar behaves in a fasting state. It tells us very little about how your blood sugar responds to the food you eat.

Up until 1998, the ADA defined FBG levels above 140 mg/dL as diabetic. In 1998, in a temporary moment of near-sanity, they lowered it to 126 mg/dL. (Forgive me for being skeptical about their motivations; normally when these targets are lowered, it’s to sell more drugs – not make people healthier.) They also set the upward limit of normal blood sugar at 99 mg/dL. Anything above that – but below 126 mg/dL – is considered “pre-diabetic”, or “impaired glucose tolerance” (IGT).

Oral glucose tolerance test (OGTT)

The OGTT measures first and second stage insulin response to glucose. Here’s how it works. You fast and then you’re given 75 grams of glucose dissolved in water. Then they test your blood sugar one and two hours after. If your blood sugar is >140 mg/dL two hours later, you have pre-diabetes. If it’s >199 mg/dL two hours later, you’ve got full-blown diabetes.

Keep in mind these are completely arbitrary numbers. If your result is 139 mg/dL – just one point below the pre-diabetic cut-off – you’ll be considered “normal”. Of course this is perfectly absurd. Diabetes isn’t like catching a cold. You don’t just wake up one day and say, “I’m not feeling so well. I think I got a bad case of diabetes yesterday.” Diabetes, like all disease, is a process. It goes something like this:

malfunction > disease process > symptoms

Before your blood sugar was 139, it was 135. Before it was 135, it was 130. Etcetera. Would you agree that it’s wise to intervene as early as possible in that progression toward diabetic blood sugar levels, in order to prevent it from happening in the first place? Well, the ADA does not agree. They prefer to wait until you’re almost beyond the point of no return to suggest there’s any problem whatsoever.

[End rant]

The other problem with the OGTT is that it’s completely artificial. I don’t know anyone who drinks a pure solution of 75 grams of glucose. A 32-oz Big Gulp from 7-11 has 96 grams of sugar, but 55% of that is fructose, which produces a different effect on blood sugar. The OGTT can be a brutal test for someone with impaired glucose tolerance, producing intense blood sugar swings far greater than what one would experience from eating carbohydrates.

Hemoglobin A1c

Hemoglobin A1c, or A1c for short, has become more popular amongst practitioners in the past decade. It’s used to measure blood glucose in large population-based studies because it’s significantly cheaper than the OGTT test.

A1c measures how much glucose becomes permanently bonded (glycated) to hemoglobin in red blood cells. In layperson’s terms, this test is a rough measure of average blood sugar over the previous three months. The higher your blood sugar has been over the past three months, the more likely it is that glucose (sugar) is permanently bonded to hemoglobin.

The problem with the A1c test is that any condition that changes hemoglobin levels will skew the results. Anemia is one such condition, and sub-clinical anemia is incredibly common. I’d say 30-40% of my patients have borderline low hemoglobin levels. If hemoglobin is low, then there’s less of it around to become bonded to glucose. This will cause an artificially low A1c level and won’t be an accurate representation of your average blood sugar over the past three months.

Likewise, dehydration can increase hemoglobin levels and create falsely high A1c results.

The “normal” range for A1c for most labs is between 4% and 6%. (A1c is expressed in percentage terms because it’s measuring the percentage of hemoglobin that is bonded to sugar.) Most often I see 5.7% as the cutoff used.

In the next article we’ll put these “normal” levels under the microscope and see how they hold up.

Dr. Kharrazian has written an excellent post over at his blog about the importance of proper diet in the treatment of Hashimoto’s. He covers all the bases: the importance of going gluten-free, why gluten-free isn’t enough for most people, how to identify and address food sensitivities, how to balance blood sugar, and how to deal with the psychological and emotional resistance that may arise when making significant dietary changes.

The main obstacle most Americans face in implementing dietary changes, as Dr. K points out, is their addiction to the idea of a “quick fix”:

Americans are infatuated with pills, thanks to decades of conditioning from the pharmaceutical industry. It doesn’t matter whether they come from the pharmacy or the health food store, we have a cultural fixation with finding that magic bullet. It’s no wonder—making genuine, lasting changes to your health takes hard work and discipline, the two last things you’ll see advertised on commercials during your favorite television show.

As long as this mentality prevails, we’ll continue to suffer from increasing rates of disease and morbidity, and our “disease-care” system will continue to buckle and, eventually, collapse.

Dietary and lifestyle changes aren’t easy, but they’re the key to promoting health and preventing disease. And that’s just as true with Hashimoto’s as it is with type 2 diabetes and heart disease.

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.

Note: This is the second article in an ongoing series. Make sure to read the first article before reading this one, and check out the next articles in the series afterwards.

• Chinese Medicine Demystified (Part I): A Case of Mistaken Identity
• Chinese Medicine Demystified (Part II): Origins of the “Energy Meridian” Myth
• Chinese Medicine Demystified (Part III): The “Energy Meridian” Model Debunked
• Chinese Medicine Demystified (Part IV): A Closer Look At How Acupuncture Relieves Pain
• Chinese Medicine Demystified (Part V): A Closer Look At How Acupuncture Relieves Pain
• Chinese Medicine Demystified (Part VI): 5 Ways Acupuncture Can Help You Where Drugs and Surgery Can’t

As an acupuncture student, I often like to ask people if they know what the word qi (sometimes spelled “chi”) means.

I get all kinds of answers. Some people don’t have any idea. Some guess it’s a kind of tea, like chai tea. Some say it has something to do with martial arts. Others say it means balance or flow. But those who’ve been to an acupuncturist, or at least know someone who has, say that qi means energy.

They say that because that’s what their acupuncturist told them. And their acupuncturist told them that because that’s what the acupuncturist was taught in school. That’s the definition of qi in the textbooks about Chinese medicine that we study in the west.

These textbooks teach that qi is an energy that moves through your body in meridians. A meridian is a metaphysical line “juxtaposed” on the body. It has no actual location inside of the body. In other words, it’s not really there. According to these textbooks this mysterious energy called qi flowing through these nonexistent lines called meridians forms the conceptual basis of Chinese medicine.

This is the definition of Chinese medicine that causes snickers, smirks and shaking heads amongst the scientific crowd – which is to say almost every doctor or medical professional trained in the west. But is this definition even accurate?

Much of what we know about Chinese medicine comes from a book called the Huangdi Neijing (HDNJ), or Yellow Emperor’s Internal Classic. There’s some controversy about when it was written, but most scholars agree that it was about 2,000 years ago, sometime between the second and first century BCE. The HDNJ is a massive encyclopedic text of Chinese medicine. You can think of it as their version of the Merck Manual.

The HDNJ had several sections. One was on anatomy. If you recall from the previous post in this series, the Chinese were performing detailed dissections 500 years before the birth of Christ. They listed the average weight, volume and measurements for all of the internal organs. They named the organs and described their functions. (In fact, they knew that the heart is the organ that pumps blood through the body more than 2,000 years ago. This wasn’t discovered in western medicine until the early 16th century.) They knew which vessels flowed away from the heart, which vessels flowed toward the heart, and which vessels supplied which organs.

The HDNJ also had detailed sections on pathology. They described how diseases develop and how to treat those diseases with acupuncture, herbal medicine, massage and dietary and lifestyle changes. In short, the Chinese were practicing truly preventative medicine 2,500 years before the term was even coined.

The HDNJ is a remarkable book. But early western scholars had a problem. The HDNJ is written in a dialect of Chinese that hasn’t been in common use in China for more than a thousand years. You could show it to a modern Chinese person and they wouldn’t be able to read it.

Several westerners took a crack at translating it. One of the first was a Dutch physician named Willem ten Rhijne. Ten Rhijne worked for the Dutch East India Company in Japan from 1683-1685. He reported clinical success by Chinese and Japanese practitioners in treating a wide range of disorders, including pain, internal organ problems, emotional disorders and infectious diseases prevalent at the time. Interestingly enough, Ten Rhijne accurately translated the Chinese character for qi as “air”, not energy, in his reports to the Dutch government.

But the translation we’re most familiar with, and the one that became the source for all of the textbooks used in western schools of Chinese medicine, was done by a man named Georges Soulie de Morant.

De Morant was a French bank clerk who lived in China from 1901 to 1917. He was enamored with Chinese culture and philosophy, and became interested in Chinese medicine during his stay. He decided to translate the HDNJ, in spite of the fact that he had no medical training nor any training in ancient Chinese language.

It was a huge undertaking for a French bank clerk to translate a 2,000 year old medical text written in an extinct Chinese dialect into a modern romance language (French). Under the circumstances, de Morant did well in many respects. But he made some huge mistakes that had serious consequences for how Chinese medicine has been interpreted in the west.

In the next post, we’ll look at those mistakes in more detail. We’ll also replace de Morant’s fictional “energy meridian” model with a new – or rather old – model of Chinese medicine that is both historically accurate and consistent with modern scientific principles of anatomy and physiology.

Continue to the next article.

References

Kendall, Donald, The Dao of Chinese Medicine, Oxford University Press, 2002