How to prevent diabetes and heart disease for $16

November 26, 2010 in Diabesity | 17 comments


relionIn the last article we discovered that the blood sugar targets established by the American Diabetes Association are far too high, and do not protect people from developing heart disease, diabetes or other complications. And we looked at what the scientific literature indicates are safer targets for fasting blood sugar, hemoglobin A1c and either OGTT or post-meal blood sugar.

In this article I’m going to introduce a simple technique that, when used properly, is one of the most effective ways to maintain healthy blood sugar and prevent cardiovascular and metabolic disease – without unnecessary drugs.

I love this technique because it’s:

  • Cheap. You can buy the equipment you need for $16 online.
  • Convenient. You can perform the tests in the comfort of your home, in your car, or wherever else you might be.
  • Personalized. Instead of following some formula for how much carbohydrate you can safely eat, this method will tell you exactly what your carbohydrate tolerance is, and which carbs are “safe” and “unsafe” for you.
  • Safe. Unlike the oral glucose tolerance test (OGTT), which can produce dangerous and horribly uncomfortable spikes in blood sugar, this strategy simply involves testing your blood sugar after your normal meals.

The strategy I’m referring to is using a glucometer to test your post-meal blood sugars. It’s simple, accessible and completely bypasses the medical establishment and pharmaceutical companies by putting the power of knowledge in your hands.

It’s one of the most powerful diagnostic tools available, and I use it with nearly all of my patients. Here’s how to do it.

Step one: buy a glucometer and test strips

A glucometer is a device that measures blood sugar. You’ve probably seen them before – they’re commonly used by diabetics. You prick your finger with a sterilized lancet, and then you apply the drop of blood to a “test strip” that has been inserted into the glucometer, and it measures your blood sugar.

There are literally hundreds of glucometers out there, and their accuracy, quality and price varies considerably. The one I recommend to my patients is called the Relion Ultima, which can be purchased with 20 test strips for $16.00 online at Walmart.com. (Note: as a rule I don’t like to support Walmart, but I haven’t been able to find this unit anywhere else at a similar price.) Even better, the test strips, which you’ll need on an ongoing basis to monitor your blood sugar, are relatively cheap for the Relion Ultima. You can get a 100 of them for $39 at Walmart online ($0.39/strip).

I’m sure there are many other choices that work well, but this is the unit I have the most experience with, and in general it is very reliable. Another good choice is the TrueTrack meter drugstores sell under their own brand name (i.e. Walgreens, Sav-on, etc.). Other models to consider are the One Touch Ultra or one of the Accu-Chek meters. The problem with these, however, is that the test strips tend to be more expensive than the Relion Ultima.

Step two: test your blood sugar

  1. Test your blood sugar first thing in the morning after fasting for at least 12 hours. Drink a little bit of water just after rising, but don’t eat anything or exercise before the test. This is your fasting blood sugar level.
  2. Test your blood sugar again just before lunch.
  3. Eat your typical lunch. Do not eat anything for the next three hours.Test your blood sugar one hour after lunch.
  4. Test your blood sugar two hours after lunch.
  5. Test your blood sugar three hours after lunch.

Record the results, along with what you ate for lunch. Do this for two days. This will tell you how the foods you normally eat affect your blood sugar levels.

On the third day, you’re going to do it a little differently. On step 3, instead of eating your typical lunch, you’re going to eat 60 – 70 grams of fast acting carbohydrate. A large (8 oz) boiled potato or a cup of cooked white rice will do. For the purposes of this test only, avoid eating any fat with your rice or potato because it will slow down the absorption of glucose.

Then follow steps 4-6 as described above, and record your results.

Step three: interpret your results

If you recall from the last article, healthy targets for blood sugar according to the scientific literature are as follows:

Marker Ideal*
Fasting blood glucose (mg/dL) <86
OGGT / post-meal (mg/dL after 1 hour) <140
OGGT / post-meal (mg/dL after 2 hours) <120
OGGT / post-meal (mg/dL after 3 hours) Back to baseline
Hemoglobin A1c (%) <5.3

*To convert these numbers to mmol/L, use this online calculator.

Hemoglobin A1c doesn’t apply here because you can’t test it using a glucometer. We’re concerned with the fasting blood sugar reading, and more importantly, the 1- and 2-hour post-meal readings.

The goal is to make sure your blood sugar never rises higher than 140 mg/dL an hour after a meal, drops below 120 mg/dL two hours after a meal, and returns to baseline (i.e. what it was before you ate) by three hours after a meal.

There are a few caveats to this kind of testing. First, even reliable glucometers have about a 10% margin of error. You need to take that into account when you interpret your results. A reading of 100 mg/dL could be anything between 90 mg/dL and 110 mg/dL if you had it tested in a lab. This is okay, because what we’re doing here is trying to identify patterns – not nit-pick over specific readings.

Second, if you normally eat low-carb (less than 75g/d), your post-meal readings on the third day following the simple carbohydrate (rice or potato) challenge will be abnormally high. I explained why this occurs in the last article, but in short when you are adapted to burning fat your tolerance for carbohydrates declines. That’s why your doctor would tell you to eat at least 150g/d of carbs for three days before an OGTT if you were having that test done in a lab.

If you’ve been eating low-carb for at least a couple of months before doing the carbohydrate challenge on day three of the test, you can subtract 10 mg/dL from your 1- and 2-hour readings. This will give you a rough estimate of what your results would be like had you eaten more carbohydrates in the days and weeks leading up to the test. It’s not precise, but it is probably accurate enough for this kind of testing.

Step four: take action (if necessary)

So what if your numbers are higher than the guidelines above? Well, that means you have impaired glucose tolerance. The higher your numbers are, the further along you are on that spectrum. If you are going above 180 mg/dL after one hour, I’d recommend getting some help – especially if you’re already on a carb-restricted diet. It’s possible to bring numbers that high down with dietary changes alone, but other possible causes of such high blood sugar (beta cell destruction, autoimmunity, etc.) should be ruled out.

If your numbers are only moderately elevated, it’s time to make some dietary changes. In particular, eating fewer carbs and more fat. Most people get enough protein and don’t need to adjust that.

And the beauty of the glucometer testing is that you don’t need to rely on someone else’s idea of how much (or what type of) carbohydrate you can eat. The glucometer will tell you. If you eat a bowl of strawberries and it spikes your blood sugar to 160 mg/dL an hour later, sorry to say, no strawberries for you. (Though you should try eating them with full-fat cream before you give up!) Likewise, if you’ve been told you can’t eat sweet potatoes because they have too much carbohydrate, but you eat one with butter and your blood sugar stays below 140 mg/dL after an hour, they’re probably safe for you. Of course if you’re trying to lose weight, you may need to avoid them anyways.

You can continue to periodically test your blood sugar this way to see how you’re progressing. You’ll probably notice that many other factors – like stress, lack of sleep and certain medications – affect your blood sugar. In any case, the glucometer is one of your most powerful tools for preventing degenerative disease and promoting optimal function.

Resources

If you haven’t already, check out Jenny Ruhl’s excellent Blood Sugar 101 site. Jenny won’t tell you this herself, but she’s an authority on blood sugar and probably knows more about it than 99.9% of health care practitioners (she’s an author). In particular, check out the “Painless Blood Sugar Testing”, “Frequently Asked Questions” and “How to Lower Your Blood Sugar” sections. I’d link to them directly, but her site uses frames and doesn’t allow it.

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Why your “normal” blood sugar isn’t normal (Part 2)

November 18, 2010 in Diabesity | 48 comments


fat_normalIn 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.

Marker Normal Pre-diabetes Diabetes
Fasting blood glucose (mg/dL) <99 100-125 >126
OGGT / post-meal (mg/dL after 2 hours) <140 140-199 >200
Hemoglobin A1c (%) <6 6-6.4 >6.4

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. A study in Diabetes Care showed that the risk of heart disease increases in a linear fashion as FBG rises above 83 mg/dL. Another study in the same journal showed similar results.

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.

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.

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:

Marker Normal Pre-diabetes Diabetes
Fasting blood glucose (mg/dL) <99 100-125 >126
OGGT / post-meal (mg/dL after 2 hours) <140 140-199 >200
Hemoglobin A1c (%) <6 6-6.4 >6.4

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:

Marker Ideal
Fasting blood glucose (mg/dL) <86*
OGGT / post-meal (mg/dL after 2 hours) <120
Hemoglobin A1c (%) <5.3

*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.

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When your “normal” blood sugar isn’t normal (Part 1)

November 12, 2010 in Diabesity | 35 comments


childhoodobesityIn 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.

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Free public talk on detoxification in San Francisco: Saturday 12/4 11:00am @DIAKADI Body

November 9, 2010 in Toxins | 5 comments


microphoneIn the next few months I’m going to be offering several free talks in the SF Bay Area. The first of these is on the importance of detoxification in promoting health and longevity. It’s on December 4th, from 11:00am – 12:30pm at DIAKADI Body, a fantastic personal training and wellness center in the SoMA area of San Francisco.

You can read more about the talk and register for a space here. Please do register, as we’re expecting a good turnout and we want to make sure we have enough seats for everyone.

You can also download the flyer by clicking on it below.

In other news, last week I posted a link to my new professional website. I’ll be blogging over there as well, and the content and flavor will be a little different than what I do here. Less “research-y”, and more “nuts & bolts” kind of stuff – tips on diet & lifestyle, recipes, supplement recommendations, local SF Bay Area events, book reviews, etc. I’ve published a few blog posts already, so check them out if you haven’t yet. The most recent article is about “stress denial“.

If you’re interested, sign up to receive email updates.

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How toxins are making us fat and diabetic

November 5, 2010 in Diabesity, Toxins | 6 comments


arewetoxicEach year the toxic burden in our air, food and water – and thus our bodies – grows higher than ever before. Companies manufacture 6.5 trillion pounds of 9,000 different chemicals each year. That’s about 3.25 billion tons – enough to fill an ocean supertanker. And the same companies release over 7 billion pounds of 650+ different pollutants into the atmosphere and water.

A recent study by the Environmental Working Group (EWG) found the average person has over 91 toxic chemicals in their body. Some people had as many as 165, including 76 known to cause cancer, 94 known to be toxic to the brain and nervous system, and 79 known to cause birth defects and abnormal fetal development.

Another EWG study found an average of 200 industrial compounds, pollutants, and other chemicals in the umbilical cord blood of 10 newborn babies. Chemicals found in the second study included the organochlorine pesticides DDT and dieldrin, perfluorochemicals, brominated fire retardants, PCBs, polyaromatic hydrocarbons, polychlorinated and polybrominated dioxins and furans, polychlorinated naphthalenes, and mercury.

If that wasn’t enough, the Standard American Diet itself is highly toxic. Processed and refined foods, industrial seed oils, high fructose corn syrup, and even so-called healthy foods like whole grains and soy all have a toxic effect on the body.

How environmental toxins cause diabesity

An increasing amount of evidence has linked exposure to toxins with both obesity and diabetes. Toxins cause inflammation and immune dysregulation. And as you know from reading this series, obesity and diabetes are autoimmune, inflammatory diseases.

I’ve already discussed the role of food toxins in the diabesity epidemic, so in this article we’re going to focus on how industrial chemicals in our air, water and soil contribute.

There are several mechanisms involved. Environmental toxins:

  • interfere with glucose and cholesterol metabolism and induce insulin resistance;
  • disrupt mitochondrial function;
  • cause oxidative stress;
  • promote inflammation;
  • alter thyroid metabolism; and,
  • impair appetite regulation.

There are probably other mechanisms that we don’t yet understand. But the ones I listed above are certainly enough to explain the link between toxins and diabesity.

Evidence supporting the role of toxins in the diabesity epidemic

A while back I wrote about a study showing that a chemical called bisphenol-A (BPA), found in packaged foods and beverages, causes obesity in mice.

A more recent study published in JAMA found that BPA increases the risk of diabetes, heart disease, and abnormal liver function.

A 2010 study in Environmental Health Perspectives found that exposure to organic pollutants leads to insulin resistance and metabolic dysfunction in rats.

A review paper by researchers in Korea reached a similar conclusion:

…the metabolic syndrome is the result of mitochondrial dysfunction, which in turn is caused by exposure to persistent organic pollutants.

A National Health and Nutrition Examination Survey 1999-2002 observed a significant correlation between blood levels of six common persistent organic pollutants and diabetes. Those who had the highest serum levels of pollutants had a dramatically higher risk for diabetes.

Canadian Aboriginals and Great Lakes sport fishermen both have higher rates of diabetes from eating contaminated seafood.

I could go on, but I think you get the point. Toxins are making us fat and diabetic.

Okay, so I’m toxic! What do I do about it?

The most obvious first step is to remove all food toxins from your diet. This means ditching processed and refined foods, industrial seed oils, and high fructose corn syrup, as well as grains, legumes and other foods with toxic effects on the body.

The second step is to take steps to reduce your exposure to chemicals at home. This means choosing non-toxic household cleaning, bath, beauty and hygiene products.

The third step is to support the body’s natural detoxification capacity so you can effectively deal with the toxins you do get exposed to. This is a crucial step, because no matter how careful we are, there’s no way to completely avoid toxins.

Compounds that support health liver detoxification include:

  • Protective compounds like milk thistle and artichoke leaf extract
  • Bile stimulants such as dandelion and curcumin
  • Bile motility enahncers (cholagogues) like dandelion, beet juice and coffee enemas
  • Antioxidants like vitamins C & E, zinc, selenium and lipoic acid

For those of you that would like some support in this area, I’ll be offering a “Paleo Detox” program sometime early next year. It’s a 30-day, supervised detoxification program incorporating a paleo diet, targeted nutrients to support healthy liver function, supportive and educational weekly meetings, and guidelines for integrating the positive changes you’ve made in the program into your day-to-day life. I will offer both local (SF Bay Area) and long-distance (via webinar) programs. Stay tuned for a future announcement on this.

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Do you need a health detective?

October 30, 2010 in Uncategorized | 11 comments


I’m excited to announce that I have officially launched my private practice. I specialize in working with people struggling with complex, chronic illness that haven’t been able to find help anywhere else. I see patients locally in my Berkeley, CA office, and I also offer long-distance consulting to people around the world via telephone and Skype.

If you or someone you know is in need of this kind of support, please watch the video below for an introduction to my approach, and visit my professional website for more information about how I may be able to help.

Special offer for blog subscribers, Facebook fans and Twitter followers!

For the next 30 days I’ll be offering a $50 discount on the Case Review fee for my blog readers, Facebook fans and Twitter followers. Please visit the services page of my website to learn more, and be sure to mention this offer during our initial phone appointment.

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A healthy gut is the hidden key to weight loss

October 29, 2010 in Diabesity | 28 comments


http://thehealthyskeptic.org/images/fatmouse.jpgIn a previous article in this series on diabesity I briefly mentioned the role of gut health in obesity and diabetes. I’d like to go into more detail on that subject here, especially since it’s not a very well known relationship.

Our gut is home to approximately 100,000,000,000,000 (100 trillion) microorganisms. That’s such a big number our human brains can’t really comprehend it. One trillion dollar bills laid end-to-end would stretch from the earth to the sun – and back – with a lot of miles to spare. Do that 100 times and you start to get at least a vague idea of how much 100 trillion is.

The human gut contains 10 times more bacteria than all the human cells in the entire body, with over 400 known diverse bacterial species. In fact, you could say that we’re more bacterial than we are human. Think about that one for a minute.

We’ve only recently begun to understand the extent of the gut flora’s role in human health and disease. Among other things, the gut flora promotes normal gastrointestinal function, provides protection from infection, regulates metabolism and comprises more than 75% of our immune system. Dysregulated gut flora has been linked to diseases ranging from autism and depression to autoimmune conditions like Hashimoto’s, inflammatory bowel disease and type 1 diabetes.

Recent research has shown that the gut flora, and the health of the gut in general, also play a significant role in both obesity and diabetes. I’ve seen this anecdotally in my practice as well. Nearly every patient I treat with a blood sugar issue also has a leaky gut, a gut infection, or some other chronic inflammatory gut condition.

We now know that the composition of the organisms living in your gut determines – to some extent, at least – how your body stores the food you eat, how easy (or hard) it is for you to lose weight, and how well your metabolism functions. Let’s take a closer look at the mechanisms involved.

Intestinal bacteria drive obesity and metabolic disease

A study published this year in Science magazine found that mice without a protein known as toll-like receptor 5 (TLR5) in their gut gain excessive weight and develop full-blown diabetes and fatty liver disease when fed a high-fat diet. If we think of the gut flora as a community, TLR5 is like a neighborhood police force that can keep the houligans in check. Without TLR5, bad bacteria can get out of control.

The study authors found that these bad bacteria caused a low-grade inflammation in the mice, which caused them to eat more and develop insulin resistance. They also found that treating these mice with strong antibiotics (enough to kill most of the bacteria in the gut) reduced their metabolic abnormalities.

But the most interesting part of this study is what happened when the researchers transferred the gut flora from the TLR5-deficient overweight mice into the guts of skinny mice: the skinny mice immediately started eating more and eventually developed the same metabolic abnormalities the overweight mice had. In other words, obesity and diabetes were “transferred” from one group of mice to the other simply by changing their gut flora (as shown in the image below).

tlr5

Other studies have shown that the composition of the gut flora differs in people who are obese and diabetic, and people who are normal weight with no metabolic irregularities.

One possible mechanism for how changes in the gut flora cause diabesity is that different species of bacteria seem to have different effects on appetite and metabolism. In the study on TLR5 deficient mice I mentioned above, the mice with too much bad bacteria in their guts experienced an increase in appetite and ate about 10 percent more food than their regular relatives. But it wasn’t just that these mice were hungrier and eating more; their metabolisms were damaged. When their food was restricted, they lost weight – but still had insulin resistance.

Other studies have shown that changes in the gut flora can increase the rate at which we absorb fatty acids and carbohydrates, and increase the storage of calories as fat. This means that someone with bad gut flora could eat the same amount of food as someone with a healthy gut, but extract more calories from it and gain more weight.

Bad bugs in the gut can even directly contribute to the metabolic syndrome by increasing the production of insulin (leading to insulin resistance), and by causing inflammation of the hypothalamus (leading to leptin resistance).

How modern life screws up our gut and makes us fat and diabetic

What all of this research suggests is that healthy gut bacteria is crucial to maintaining normal weight and metabolism. Unfortunately, several features of the modern lifestyle directly contribute to unhealthy gut flora:

  • Antibiotics and other medications like birth control and NSAIDs
  • Diets high in refined carbohydrates, sugar and processed foods
  • Diets low in fermentable fibers
  • Dietary toxins like wheat and industrial seed oils that cause leaky gut
  • Chronic stress
  • Chronic infections

We also know that infants that aren’t breast-fed and are born to mothers with bad gut flora are more likely to develop unhealthy gut bacteria, and that these early differences in gut flora may predict overweight and obesity in the future.

It’s interesting to note that the diabesity epidemic has neatly coincided with the increasing prevalence of factors that disrupt the gut flora. I’m not suggesting that poor gut health is the single cause of obesity and diabetes, but I am suggesting that it likely plays a much larger role than most people think.

How to maintain and restore healthy gut flora

The most obvious first step in maintaining a healthy gut is to avoid all of the things I listed above. But of course that’s not always possible, especially in the case of chronic stress and infections, and whether we were breast-fed or our mothers had healthy guts.

If you’ve been exposed to some of these factors, there are still steps you can take to restore your gut flora:

  • Remove all food toxins from your diet
  • Eat plenty of fermentable fibers (starches like sweet potato, yam, yucca, etc.)
  • Take a high-quality probiotic, or consider more radical methods of restoring healthy gut flora
  • Treat any intestinal pathogens (such as parasites) that may be present
  • Take steps to manage your stress

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When it comes to fish oil, more is not better

October 25, 2010 in Food & Nutrition, Heart Disease | 73 comments


Article summary

    fishoilmedication
  • The benefits of fish oil supplementation have been grossly overstated
  • Most of the studies showing fish oil benefits are short-term, lasting less than one year
  • The only fish oil study lasting more than four years showed an increase in heart disease and sudden death
  • Fish oil is highly unstable and vulnerable to oxidative damage
  • There’s no evidence that healthy people benefit from fish oil supplementation
  • Taking several grams of fish oil per day may be hazardous to your health

A new study was recently published showing that 3g/d of fish oil in patients with metabolic syndrome increased LDL levels and insulin resistance.

Unfortunately, I don’t read Portuguese so I can’t review the full-text. But this study isn’t alone in highlighting the potential risks of high-dose fish oil supplementation. Chris Masterjohn’s latest article on essential fatty acids, Precious yet Perilous, makes a compelling argument that fish oil supplementation – especially over the long-term – is not only not beneficial, but may be harmful.

This may come as a surprise to you, with all of the current media hoopla about the benefits of fish oil supplementation. Yet the vast majority of the studies done that have shown a benefit have been short-term, lasting less than one year. The only trial lasting more than four years, the DART 2 trial, showed that fish oil capsules actually increase the risk of heart disease and sudden death.

A 2004 Cochrane meta-analysis of trials lasting longer than six months suggests that the cardiovascular benefits of fish oil have been dramatically over-stated. They analyzed 79 trials overall, and pooled data from 48 trials that met their criteria. The only effect that could be distinguished from chance was a reduced risk of heart failure. Fish oil provided no reduction in total or cardiovascular mortality.

Too much fish oil can wreak havoc in your body

Omega-3 fatty acids are highly vulnerable to oxidative damage. When fat particles oxidize, they break down into smaller compounds, like malondialdehyde (MDA), that are dangerous because they damage proteins, DNA, and other important cellular structures.

A study by Mata et al demonstrated that oxidative damage increases as intake of omega-3 fat increases. The results of this study were summarized in the Perfect Health Diet, by Paul and Shou-Ching Jaminet:

oxidativedamage

Notice the clear increase in TBARS (a measure of oxidative damage of the LDL particle) with omega-3 fat. It’s important to note that this was only a 5-week trial. If it had gone on for longer than that, it’s likely the oxidative damage caused by omega-3 fats would have been even worse. This isn’t surprising if you understand the chemical composition of fats. Polyunsaturated fats (PUFA) are highly vulnerable to oxidative damage because they’re the only fatty acids that have two or more double bonds, and it’s the carbon that lies between the double bonds that is vulnerable to oxidation (as shown in the figure below):

diagram of chemical structure of EPA

Another thing worth noting, if you haven’t already, is that intake of saturated and monounsaturated fats does not increase oxidative damage by a significant amount. This is illustrated in both the table and the diagram above: saturated fats have no double bonds, which means they are well protected against oxidation. MUFA is slightly more vulnerable, since it does have one double bond, but not nearly as much as PUFA which has several double-bonds.

A randomized, double blind, placebo-controlled trial likewise showed that 6 grams per day of fish oil increased lipid peroxides and MDA in healthy men, regardless of whether they were supplemented with 900 IU of vitamin E. And consumption of fresh, non-oxidized DHA and EPA has been shown to increase markers of oxidative stress in rats.

Fish oil not as beneficial as commonly believed

To be fair, at least one review suggests that fish oil supplementation is beneficial in the short and even intermediate term. A recent meta-analysis of 11 trials lasting more than one year found that fish oil reduced the relative risk of cardiovascular death by 13 percent and the relative risk of death from any cause by 8 percent.

But the effect seen in this review was mostly due to the GISSI and DART-1 trials. They found that fish oil may prevent arrhythmia in patients with chronic heart failure and patients who have recently survived a heart attack.

However, there is no evidence that people other than those with arrhythmia and chronic heart failure benefit from taking fish oil or that doses higher than one gram of omega-3 fatty acids per day provide any benefit over smaller doses. And then there’s the rather disturbing result of the DART-2 trial, the only fish oil study lasting more than four years, showing an increase in heart disease and sudden death.

It’s logical to assume the effects of oxidative damage would take a while to manifest, and would increase as time goes on. That’s likely the reason we see some benefit in short- and intermediate-term studies (as n-3 displace n-6 in the tissues), but a declining and even opposite effect in the longer-term DART-2 trial (as increased total PUFA intake causes more oxidative damage).

The danger of reductionist thinking in nutritional research

The current fish oil craze highlights the danger of isolated nutrient studies, which unfortunately is the focus of nutritional research today. Kuipers et al. eloquently described the risks of this approach in a recent paper:

The fish oil fatty acids EPA and DHA (and their derivatives), vitamin D (1,25-dihydroxyvitamin D) and vitamin A (retinoic acid) are examples of nutrients that act in concert, while each of these has multiple actions(7,8).

Consequently, the criteria for establishing optimum nutrient intakes via randomised controlled trials (RCT) with single nutrients at a given dose and with a single end point have serious limitations. They are usually based upon poorly researched dose–response relationships, and typically ignore many possible nutrient interactions and metabolic interrelationships.

For instance, the adequate intake of linoleic acid (LA) to prevent LA deficiency depends on the concurrent intakes of α-linolenic acid (ALA), γ-LA and arachidonic acid (AA). Consequently, the nutritional balance on which our genome evolved is virtually impossible to determine using the reigning paradigm of ‘evidence-based medicine’ with RCT.

Interest in fish oil supplementation started with observations that the Inuit had almost no heart disease. It was assumed their high intake of marine oils produced this benefit. While this may be true, at least in part, what was overlooked is that the Inuit don’t consume marine oils in isolation. They eat them as part of a whole-food diet that also includes other nutrients which may help prevent the oxidative damage that otherwise occurs with such a high intake of fragile, n-3 PUFA.

It’s also important to note that there are many other traditional peoples, such as the Masai, the Tokelau, and the Kitavans, that are virtually free of heart disease but do not consume high amounts of marine oils. What these diets all share in common is not a large intake of omega-3 fats, but instead a complete absence of modern, refined foods.

Eat fish, not fish oil – cod liver oil excepted

That is why the best approach is to dramatically reduce intake of omega-6 fat, found in industrial seed oils and processed and refined foods, and then eat a nutrient-dense, whole-foods based diet that includes fatty fish, shellfish and organ meats. This mimics our ancestral diet and is the safest and most sane approach to meeting our omega-3 needs – which as Chris Masterjohn points out, are much lower than commonly assumed.

Some may ask why I continue to recommend fermented cod liver oil (FCLO), in light of everything I’ve shared in this article. There are a few reasons. First, I view FCLO as primarily a source of fat-soluble vitamins (A, D, K2 and E) – not EPA and DHA. Second, in the context of a nutrient-dense diet that excludes industrial seed oils and refined sugar, and is adequate in vitamin B6, biotin, calcium, magnesium and arachidonic acid, the risk of oxidative damage that may occur with 1g/d of cod liver oils is outweighed by the benefits of the fat-soluble vitamins.

So I still recommend eating fatty fish a couple times per week, and taking cod liver oil daily, presuming your diet is as I described above. What I don’t endorse is taking several grams per day of fish oil, especially for an extended period of time. Unfortunately this advice is becoming more and more common in the nutrition world.

More is not always better, despite our tendency to believe it is.

Note: As always, I’m open to discussion and dissenting views. But please don’t link to short-term studies on the efficacy of fish oil, because as I’ve explained in this article, it’s the long-term effects that we’re primarily concerned with. I’d be interested in seeing any studies longer than 2 years showing that 1) fish oil benefits extend beyond reducing arrhythmia in patients with chronic heart failure and patients who have recently survived a heart attack, 2) doses higher than 1g/d produce a larger benefit than doses of 1g/d, and (most importantly) 3) doses of >1g/d or higher do not increase the risk of heart disease or death

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10 ways stress makes you fat and diabetic

October 22, 2010 in Diabesity | 15 comments


stressfatIn the first part of this series on diabesity, we “got under the hood” to look at the underlying mechanisms of both obesity and diabetes. We’ve now moved on to discussing the environmental and lifestyle risk factors that drive these conditions. In the last article we learned about the top 3 dietary causes of diabesity. In this article, we’re going to see how stress can independently cause both obesity and diabetes.

A huge – and I mean huge – amount of research over the past two decades shows that stress causes both obesity and diabetes in a variety of ways. Studies also show that stress makes it hard to lose weight. This is one reason why some people just can’t seem to lose weight no matter how well they eat or how much they exercise. I believe stress is one of the most important – yet most often ignored – factors driving the diabesity epidemic.

Stress is a bigger problem than you think

Hans Selye, the famous physiologist who coined the term “stress”, defined it this way:

…the nonspecific response of the body to any demand made upon it.

The prominent psychologist Richard Lazarus offers a similar definition:

…any event in which environmental demands, internal demands, or both tax or exceed the adaptive resources of an individual…

Most people only think of psychological stress when they hear the term “stress”. When asked what causes stress, they might say things like losing a job, having a fight with your spouse, driving in traffic or getting audited by the IRS.

While it’s true that psychological challenges like this are major stressors, what many people don’t realize is that stress is also caused by physiological challenges, such as:

  • insomnia
  • chronic infections
  • inflammation
  • autoimmune disease
  • environmental toxins
  • dieting
  • too much exercise

Even if your levels of psychological stress are pretty low, any of the conditions listed above can provoke a chronic stress reaction in your body. And as we’ll see in the next section, chronic stress can make you both fat and diabetic.

10 ways stress makes you fat and diabetic

When stress becomes chronic and prolonged, the hypothalamus is activated and triggers the adrenal glands to release a hormone called cortisol. Cortisol is normally released in a specific rhythm throughout the day. It should be high in the mornings when you wake up (this is what helps you get out of bed and start your day), and gradually taper off throughout the day (so you feel tired at bedtime and can fall asleep).

Recent research shows that chronic stress can not only increase absolute cortisol levels, but more importantly it disrupts the natural cortisol rhythm. And it’s this broken cortisol rhythm that wreaks so much havoc on your body. Among other effects, it:

  • raises your blood sugar
  • makes it harder for glucose to get into your cells 1
  • makes you hungry and crave sugar
  • reduces your ability to burn fat
  • suppresses your HPA-axis, which causes hormonal imbalances
  • reduces your DHEA, testosterone, growth hormone and TSH levels 2
  • makes your cells less sensitive to insulin
  • increases your belly fat and makes your liver fatty
  • increases the rate at which you store fat
  • raises the level of fatty acids and triglycerides in your blood

Each one of these consequences alone could make you fat and diabetic, but when added together they’re almost a perfect recipe for diabesity.

Our bodies aren’t made for chronic stress

One of the reasons chronic stress is so destructive is that our bodies didn’t evolve to deal with it. We’re set up to handle short-term, acute stress fairly well. In paleolithic times, this might have been caused by getting chased by a lion or hunting for our next meal. In fact, this type of stress may even be beneficial for our bodies because it improves our ability to react to the challenges of life.

What we’re not adapted for, however, is the chronic, unrelenting stress that has become so common in modern life. This type of stress provokes feelings of hopelessness and helplessness – what psychologists call a “defeat response”. And it’s the defeat response that leads to increased fat storage, abdominal obesity, tissue breakdown, suppression of the immune system, and all of the other effects I listed above that directly cause obesity and diabetes.

A closer look at insomnia, dieting and exercise

I’d like to take a closer look at three often stressors that can make us fat and diabetic: insomnia, dieting and exercise.

More than a third of American suffer from insomnia, with 42 million prescriptions for sleeping medications filled in 2007. Several studies show that sleep deprivation elevates cortisol and makes it more likely that you’ll get fat and develop diabetes.

A very recent paper showed that restricting sleep to 5 hours a night for just one week significantly reduces insulin sensitivity. Another study earlier this year showed that even one night of sleep loss increased appetite in young, healthy adults. Sleep restriction is associated with impairment of carbohydrate tolerance, and research has shown that a loss of 3 hours of sleep each night causes a weight gain of 4-5%.

It’s estimated that between 50-60% of Americans are dieting at any given time. That’s a huge number. And while it may seem counter-intuitive that dieting contributes to obesity and diabetes, it makes perfect sense when you understand that dieting is a stressor that disrupts our cortisol rhythm.

A 2001 study showed that “cognitive dietary restraint” (translation: stressing about food or doing overly restrictive diets) raises your cortisol levels. Studies have also shown that caloric restriction – as is common in low-fat diets – increases cortisol levels. And a recent study reported on by Stephan Guyenet at Whole Health Source found that caloric restriction is especially harmful when combined with sleep deprivation.

Finally, although not common in the general population, too much exercise can also predispose you to weight gain and diabetes by raising cortisol levels, breaking down muscle tissue and increasing fat storage. This is especially true if cortisol levels are already elevated or disrupted by other stressors like gut infections, insomnia, food toxins or psychological factors.

It’s not uncommon (in the paleo/fitness subculture, at least) to encounter someone who eats well and exercises their brains out, but cannot lose weight. In fact, several of my patients fall into this category. They are often surprised when I tell them they need to exercise less if they want to lose weight and recover their health. What they may not realize is that cortisol is a catabolic hormone. It breaks the body down.

While this might sound like a good thing for those trying to lose weight, it’s not. Muscle tissue is metabolically active and actually helps us lose weight. A reduction of lean muscle tissue may drop a few pounds in the short-term, but it will predispose you to weight gain in the future by impairing your metabolism. (This is another reason why caloric restricted diets, which break down muscle tissue, don’t work in the long-term and even make things worse.)

So if you’re struggling with weight or blood sugar control, don’t diet, get plenty of sleep and take it easy with exercise. You’ll be a lot better off.

  1. Talbot, Shawn. The Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health, and What You Can Do About It. Hunter House. 2007. pp. 85-86 ↩
  2. Talbot, Shawn. The Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health, and What You Can Do About It. Hunter House. 2007. pp. 85-86 ↩

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The top 3 dietary causes of obesity & diabetes

October 15, 2010 in Diabesity | 42 comments


donutSo far in this series we’ve focused on a new way of understanding diabesity as an autoimmune, inflammatory disorder, and we’ve looked in a general way at the underlying mechanisms (inflammation, genetics, environmental triggers and leaky gut) that contribute to diabesity.

Now that we’ve laid that foundation, we’re going to take a closer look at some of those mechanisms. In this article, we’ll discuss the three major dietary toxins that trigger diabesity:

  • Cereal grains (especially refined flour)
  • Omega-6 industrial seed oils (corn, cottonseed, safflower, soybean, etc.)
  • Fructose (especially high-fructose corn syrup)
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At the simplest level, a toxin is something capable of causing disease or damaging tissue when it enters the body. When most people hear the word “toxin”, they think of chemicals like pesticides, heavy metals or other industrial pollutants. But even beneficial nutrients like water, which are necessary to sustain life, are toxic at high doses.

In the Perfect Health Diet, Paul & Shou-Ching Jaminet apply the economic principle of declining marginal benefits to toxins:

It implies that the first bit eaten of any toxin has low toxicity. Each additional bit is slightly more toxic than the bit before. At higher doses, the toxicity of each bit continues to increase, so that the toxin is increasingly poisonous.

This is important to understand as we discuss the role of each of the dietary toxins listed above in contributing to diabesity. Most of you won’t develop diabesity by eating a small amount of fructose, cereal grains and even industrial seed oils. But if you eat those nutrients (or rather anti-nutrients) in excessive quantities, your risk of diabesity rises significantly. This is especially true if you have any of the genes that predispose you to diabetes and obesity.

The primary effect toxins have on the body – whether dietary or otherwise – is inflammation. And since we now know that diabesity is an autoimmune, inflammatory disease, it’s clear that anything that causes inflammation is a potential risk factor for both diabetes and obesity.

The impact of each of these dietary toxins could fill a book. And in fact, there are several such books and many other blogs that have covered this material in detail. Rather than re-create the wheel, I’m going to provide a brief summary and then link you to resources if you want more detail.

Cereal grains: the unhealthiest “health food” on the planet?

The major cereal grains – wheat, corn, rice, barley, sorghum, oats, rye and millet – have become the staple crops of the modern human diet. They’ve also become the “poster children” of the low-fat, high-carbohydrate diet promoted by organizations like the American Heart Association (AHA) and American Diabetes Association (ADA). If you say the phrase “whole grains” to most people, the first word that probably comes to their mind is “healthy”.

But the fact is that most animals, including our closest relative (the chimpanzee) aren’t adapted to eating cereal grains and don’t eat them in large quantities. And humans have only been eating them for the past 10,000 years (a tiny blip of time on the scale of evolution). Why?

Because plants like cereal grains are always competing against predators (like us) for survival. Unlike animals, plants can’t run away from us when we decide to eat them. They had to evolve other mechanisms for protecting themselves. These include:

  • producing toxins that damage the lining of the gut;
  • producing toxins that bind essential minerals, making them unavailable to the body; and,
  • producing toxins that inhibit digestion and absorption of other essential nutrients, including protein.

One of these toxic compounds is the protein gluten, which is present in wheat and many of the other most commonly eaten cereal grains. In short, gluten damages the intestine and makes it leaky. As we saw in the last article, a leaky gut is one of the major predisposing factors for diabetes and obesity.

Celiac disease – a condition of severe gluten intolerance – has been well known for decades. These people have a dramatic and, in some cases, potentially fatal immune response to even the smallest amounts of gluten. However, what is less well known is that wheat gluten triggers an immune response and gut inflammation in almost everyone – regardless of whether they are “gluten intolerant” or not. Over 80% of the population develops measurable gut inflammation after eating wheat gluten.

Dr. Kurt Harris, author of one of my favorite blogs (PaleoNu), calls wheat one of the three “neolithic agents of disease” (we agree on the other two as well). For more information on the toxic effect of cereal grains, see Dr. Harris’s two articles “The argument against cereal grains” and “The argument against cereal grains, part II“.

Industrial seed oils: unnatural and unfit for human consumption

Industrial seed oils (corn, cottonseed, soybean, safflower, sunflower, etc.) have not been a part of the human diet up until relatively recently, when misguided groups like the AHA and the ADA started promoting them as “heart-healthy” alternatives to saturated fat.

The graph below shows how dramatically seed oil consumption has risen over the past several decades:

pufaconsumption

Industrial seed oils are extremely harmful when consumed in excess. I’ve written about this at length in my series on essential fatty acids. In the context of this article, researchers have shown that industrial seed oils have played a significant role in the current obesity epidemic.

A recent study showed that a diet with an omega-6:3 ratio of 28 (meaning 28 times more omega-6 than omega-3 fats) caused obesity that progressively increased over four generations of mice. This means that eating too much omega-6 didn’t only cause obesity in the current generation, but it also predisposed future generations eating the same diet to developing obesity.

This is bad news for those eating a Standard American Diet, which contains an omega-6:3 ratio that is very similar to what the mice in the study above were fed.

Omega-6 seed oils have also been shown to cause inflammation, insulin resistance and impaired leptin signaling, all of which directly contribute to diabetes.

Finally, industrial seed oils have been shown to interfere with thyroid function by blocking the binding of thyroid hormone to its receptors. The result is a higher fat mass and a less efficient metabolism.

For more information on how seed oils contribute to diabesity, see The Body Fat Setpoint, Part III: Dietary Causes of Obesity, Have Seed Oils Caused a Multi-Generational Obesity Epidemic?, and my series on Essential Fatty Acids.

Fructose: the sweetest way to get diabesity

White table sugar is composed of two sugars: glucose and fructose. Glucose is an important nutrient in our bodies and is healthy, as long as it’s consumed in moderation. Fructose is a different story.

Fructose is found primarily in fruits and vegetables, and sweeteners like sugar and high-fructose corn syrup (HFCS). A recent USDA report found that the average American eats 152 pounds of sugar each year, including almost 64 pounds of HFCS.

Unlike glucose, which is rapidly absorbed into the bloodstream and taken up by the cells, fructose is shunted directly to the liver where it is converted to fat. Excess fructose consumption causes a condition called non-alcoholic fatty liver disease (NAFLD), which is directly linked to both diabetes and obesity.

A 2009 study showed that shifting 25% of dietary calories from glucose to fructose caused a 4-fold increase in abdominal fat. Abdominal fat is an independent predictor of insulin sensitivity, impaired glucose tolerance, high blood pressure and high cholesterol and triglycerides.

In a widely popular talk on YouTube, Dr. Robert H. Lustig explains that fructose has all of the qualities of a poison. It causes damage, provides no benefit and is sent directly to the liver to be detoxified so that it doesn’t harm the body.

Another danger of fructose is that it reacts with polyunsaturated fats and proteins to form toxic compounds called Advanced Glycation End-Products (AGEs) in a process known as “fructation”. (Who comes up with these words?) AGEs wreak all kinds of havoc on the body; they damage DNA, speed up the aging process and cause high blood pressure and kidney disease. And studies have shown that fructose is up to 10 times more likely to produce AGEs than glucose.

For more on the toxic effects of fructose, see The Perfect Health Diet and Robert Lustig’s YouTube talk: Sugar, The Bitter Truth.

A toxin-free diet prevents and even reverses diabetes

In addition to all of the evidence above, we have two other lines of evidence that strongly indicate that cereal grains, seed oils and fructose contribute to diabesity.

First, diabesity is either non-existent or extremely rare in hunter-gatherer cultures that don’t consume these toxic foods.

Second, two studies have shown that a paleolithic diet (free of cereal grains, seed oils and excessive fructose) produced dramatic improvements in cardiovascular and metabolic markers.

The first study, performed by Dr. Staffan Lindeberg and colleagues, found that a paleolithic diet was superior to the mediterranean diet in several ways. These are summarized in Stephan Guyenet’s article on Lindeberg’s study:

  • Greater fat loss in the the midsection and a trend toward greater weight loss
  • Greater voluntary reduction in caloric intake (total intake paleo= 1,344 kcal; Med= 1,795)
  • A remarkable improvement in glucose tolerance that did not occur significantly in the Mediterranean group
  • A decrease in fasting glucose
  • An increase in insulin sensitivity (HOMA-IR)

The most remarkable outcome of the study is that, although 12 of 14 participants had elevated fasting blood sugar at the beginning of the trial, every single participant had normal fasting blood sugar at the end of the trial.

Dr. Lindeberg published a follow-up study in 2009. In this case they compared a paleolithic diet with a conventional ADA low-fat “diabetes diet”. While the results weren’t quite as impressive as the first one, they were still very encouraging. Participants in the paleolithic group:

  • Reduced HbA1c more than the diabetes diet (a measure of average blood glucose)
  • Reduced weight, BMI and waist circumference more than the diabetes diet
  • Lowered blood pressure more than the diabetes diet
  • Reduced triglycerides more than the diabetes diet
  • Increased HDL more than the diabetes diet

At the end of the trial, 8 out of 13 patents still had diabetic blood glucose levels. However, in this study the patients had well-established diabetes for an average of 9 years. Over time diabetes progresses to beta cell destruction, which reduces insulin output. Once this point has been reached, dietary changes can be helpful but cannot completely reverse diabetes.

What this means, of course, is that the earlier you remove these toxins from your diet, the better chance you have of preventing and even reversing diabesity. And while a paleolithic diet may not reverse diabetes in those that have had it for several years, it still produces significant improvements.

** A donut is the perfect diabesity food. It’s got refined flour (cereal grains), industrial seed oils (plus trans fats for an added bonus), and plenty of high-fructose corn syrup.

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