An Interview with Dr. C. Vicky Beer, Paleo-friendly MD

As I was preparing my recent article on the Paleo diet (1), I interviewed a local Paleo-friendly MD named C. Vicky Beer.  I was only able to include a snippet of the interview in the article, but I thought WHS readers would be interested to read the rest of the interview with Dr. Beer:

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What Causes Insulin Resistance? Part VII

In previous posts, I outlined the factors I'm aware of that can contribute to insulin resistance.  In this post, first I'll list the factors, then I'll provide my opinion of effective strategies for preventing and potentially reversing insulin resistance.

The factors

These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance.  I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another. 
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What Causes Insulin Resistance? Part VI

In this post, I'll explore a few miscellaneous factors that can contribute to insulin resistance: smoking, glucocorticoids/stress, cooking temperature, age, genetics and low birth weight.

Smoking

Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:

1. Increased inflammation
2. Increased circulating free fatty acids (4)

Paradoxically, since smoking also protects against fat gain, in the very long term it may not produce as much insulin resistance as one would otherwise expect.  Diabetes risk is greatly elevated in the three years following smoking cessation (5), and this is likely due to the fat gain that occurs.  This is not a good excuse to keep smoking, because smoking tobacco is one of the most unhealthy things you can possibly do.  But it is a good reason to tighten up your diet and lifestyle after quitting.

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What Causes Insulin Resistance? Part V

Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance.  In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.

Carbohydrate and Fat

There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity.  What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people.  This will get at what causes insulin resistance in someone who does not already have it.

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What Causes Insulin Resistance? Part IV

So far, we've explored three interlinked causes of insulin resistance: cellular energy excess, inflammation, and insulin resistance in the brain.  In this post, I'll explore the effects on micronutrient status on insulin sensitivity.

Micronutrient Status

There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post.  My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.

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What Causes Insulin Resistance? Part III

As discussed in previous posts, cellular energy excess and inflammation are two important and interlinked causes of insulin resistance.  Continuing our exploration of insulin resistance, let's turn our attention to the brain.

The brain influences every tissue in the body, in many instances managing tissue processes to react to changing environmental or internal conditions.  It is intimately involved in insulin signaling in various tissues, for example by:

• regulating insulin secretion by the pancreas (1)
• regulating glucose absorption by tissues in response to insulin (2)
• regulating the suppression of glucose production by the liver in response to insulin (3)
• regulating the trafficking of fatty acids in and out of fat cells in response to insulin (4, 5)

Because of its important role in insulin signaling, the brain is a candidate mechanism of insulin resistance.

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What Causes Insulin Resistance? Part II

In the last post, I described how cellular energy excess causes insulin resistance, and how this is triggered by whole-body energy imbalance.  In this post, I'll describe another major cause of insulin resistance: inflammation. 

Inflammation

In 1876, a German physician named W Ebstein reported that high doses of sodium salicylate could totally eliminate the signs and symptoms of diabetes in certain patients (Berliner Klinische Wochenschrift. 13:337. 1876). Following up on this work in 1901, the British physician RT Williamson reported that treating diabetic patients with sodium salicylate caused a striking decrease in the amount of glucose contained in the patients' urine, also indicating an apparent improvement in diabetes (2).  This effect was essentially forgotten until 1957, when it was rediscovered.

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What Causes Insulin Resistance? Part I

Insulin is an ancient hormone that influences many processes in the body.  Its main role is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body's two main fuels), keeping them within a fairly narrow range*.  It does this by encouraging the transport of nutrients into cells from the circulation, and discouraging the export of nutrients out of storage sites, in response to an increase in circulating nutrients (glucose or fatty acids). It therefore operates a negative feedback loop that constrains circulating nutrient concentrations.  It also has many other functions that are tissue-specific.

Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids).  It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders. 

Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range?  The answer to that question is the crux of this post. 

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The Brain Controls Insulin Action

Insulin regulates blood glucose primarily by two mechanisms:

1. Suppressing glucose production by the liver
2. Enhancing glucose uptake by other tissues, particularly muscle and liver

Since the cells contained in liver, muscle and other tissues respond directly to insulin stimulation, most people don't think about the role of the brain in this process.  An interesting paper just published in Diabetes reminds us of the central role of the brain in glucose metabolism as well as body fat regulation (1).  Investigators showed that by inhibiting insulin signaling in the brains of mice, they could diminish insulin's ability to suppress liver glucose production by 20%, and its ability to promote glucose uptake by muscle tissue by 59%.  In other words, the majority of insulin's ability to cause muscle to take up glucose is mediated by its effect on the brain. 

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How Does Gastric Bypass Surgery Cause Fat Loss?

Gastric bypass surgery is an operation that causes food to bypass part of the digestive tract.  In the most common surgery, Roux-en-Y bypass, stomach size is reduced and a portion of the upper small intestine is bypassed.  This means that food skips most of the stomach and the duodenum (upper small intestine), passing from the tiny stomach directly into the jejunum (a lower part of the upper small intestine)*.  It looks something like this:
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Fast Food, Weight Gain and Insulin Resistance

CarbSane just posted an interesting new study that fits in nicely with what we're discussing here.  It's part of the US Coronary Artery Risk Development in Young Adults (CARDIA) study, which is a long-term observational study that is publishing many interesting findings.  The new study is titled "Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis" (1).  The results speak for themselves, loud and clear (I've edited some numbers out of the quote for clarity):
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Food Reward: a Dominant Factor in Obesity, Part III

Low-Fat Diets

In 2000, the International Journal of Obesity published a nice review article of low-fat diet trials.  It included data from 16 controlled trials lasting from 2-12 months and enrolling 1,910 participants (1).  What sets this review apart is it only covered studies that did not include instructions to restrict calorie intake (ad libitum diets).  On average, low-fat dieters reduced their fat intake from 37.7 to 27.5 percent of calories.  Here's what they found:
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Dr. Kevin Patterson on Western Diets and Health

A few readers have pointed me to an interesting NPR interview with the Canadian physician Kevin Patterson (link). He describes his medical work in Afghanistan and the Canadian arctic treating cultures with various degrees of industrialization. He discusses the "epidemiological transition", the idea that cultures experience predictable changes in their health as they go from hunter-gatherer, to agricultural, to industrial. I think he has an uncommonly good perspective on the effects of industrialization on human health, which tends to be true of people who have witnessed the effects of the industrial diet and lifestyle on diverse cultures.

A central concept behind my thinking is that it's possible to benefit simultaneously from both:

• The sanitation, medical technology, safety technology, law enforcement and lower warfare-related mortality that have increased our life expectancy dramatically relative to our distant ancestors.


• The very low incidence of obesity, diabetes, coronary heart disease and other non-infectious chronic diseases afforded by a diet and lifestyle roughly consistent with our non-industrial heritage.

But it requires discipline, because going with the flow means becoming unhealthy.

Safflower Oil Study

A few people have sent me a new study claiming to demonstrate that half a tablespoon of safflower oil a day improves insulin sensitivity, increases HDL and decreases inflammation in diabetics (1). Let me explain why this study does not show what it claims.

It all comes down to a little thing called a control group, which is the basis for comparison that you use to determine if your intervention had an effect. This study didn't have one for the safflower group. What it had was two intervention groups, one given 6.4g conjugated linoleic acid (CLA; 50% c9t11 and 50% t10c12-CLA) per day, and one given 8g safflower oil. I have to guess that this study was originally designed to test the effects of the CLA, with the safflower oil group as the control group, and that the interpretation of the data changed after the results came in. Otherwise, I don't understand why they would conduct a study like this without a control group.

Anyway, they found that the safflower oil group did better than the CLA group over 16 weeks, showing a higher insulin sensitivity, higher HDL, lower HbA1c (a marker of average blood glucose levels) and lower CRP (a marker of inflammation). But they also found that the safflower group improved slightly compared to baseline, therefore they decided to attribute the difference to a beneficial effect of safflower oil. The problem is that without a control (placebo) group for comparison, there's no way to know if the improvement would have occurred regardless of treatment, due to the season changing, more regular check-ups at the doctor's office due to participating in a study, or countless other unforeseen factors. A control group is essential for the accurate interpretation of results, which is why drug studies always have placebo groups.

What we can say is that the safflower oil group fared better than the CLA group, because there was a difference between the two. However, what I think really happened is that the CLA supplement was harmful and the small dose of safflower oil had no effect. Why? Because the t10c12 isomer of CLA, which was half their pill, has already been shown by previous well-controlled studies to reduce insulin sensitivity, decrease HDL and increase inflammatory markers at a similar dose and for a similar duration (2, 3). The safflower oil group only looked good by comparison. We can add this study to the "research bloopers" file.

It's worth noting that naturally occurring CLA mixtures, similar to those found in pastured dairy and ruminant fat, have not been shown to cause metabolic problems such as those caused by isolated t10c12 CLA.

The Diabetes Epidemic

The CDC just released its latest estimate of diabetes prevalence in the US (1):

Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.

Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):

These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.

The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.

Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.


* In other words, it's the best predictor of future diabetes risk.

** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (<` href="http://www.ncbi.nlm.nih.gov/pubmed/19924209">5).

Dairy Fat and Diabetes

Introduction

Having access to embargoed news from the Annals of Internal Medicine is really fun. I get to report on important studies at the same time as the news media. But this week, I got my hands on a study that I'm not sure will be widely reported (Mozaffarian et al. Trans-palmitoleic Acid, Metabolic Risk Factors, and New-Onset Diabetes in US Adults. Ann Internal Med. 2010). Why? Because it suggests that dairy fat may protect against diabetes.

The lead author is Dr. Dariush Mozaffarian, whose meta-analysis of diet-heart controlled trials I recently criticized (1). I think this is a good opportunity for me to acknowledge that Dr. Mozaffarian and his colleagues have published some brave papers in the past that challenged conventional wisdom. For example, in a 2005 study, they found that postmenopausal women who ate the most saturated fat had the slowest rate of narrowing of their coronary arteries over time (2). It wasn't a popular finding but he has defended it. His colleague Dr. Walter Willett thinks dietary fat is fine (although he favors corn oil), whole eggs can be part of a healthy diet, and there are worse things than eating coconut from time to time. Dr. Willett is also a strong advocate of unrefined foods and home cooking, which I believe are two of the main pillars of healthy eating.

Let's hit the data

Investigators collected two measures of dairy fat intake in 3,736 Americans:

1. 24 hour dietary recall questionnaires, six times. This records volunteers' food intake at the beginning of the study.
2. Blood (plasma phospholipid) content of trans-palmitoleate. Dairy fat and red meat fat are virtually the only sources of this fatty acid, so it reflects the intake of these foods. Most of the trans-palmitoleate came from dairy in this study, although red meat was also a significant source.

After adjustment for confounding factors, trans-palmitoleate levels were associated with a smaller waist circumference, higher HDL cholesterol, lower serum triglycerides, lower C-reactive protein, lower fasting insulin and lower calculated insulin resistance. Furthermore, people with the highest trans-palmitoleate levels had 1/3 the risk of developing diabetes over the three years volunteers were followed. Keep in mind, however, that this is an observational study and does not prove that dairy fat prevents diabetes.

Even though certain blood fatty acids partially represent food intake, they can also represent metabolic conditions. For example, people on their way to type II diabetes tend to have more saturated blood lipids, independent of diet (3, 4)*. So it's reassuring to see that dietary trans-palmitoleate intake was closely related to the serum level. The investigators also noted that "greater whole-fat dairy consumption was associated with lower risk for diabetes," which increases my confidence that serum trans-palmitoleate is actually measuring dairy fat intake to some degree. However, in the end, I think the striking association they observed was partially due to dairy fat intake, but mostly due to metabolic factors that had nothing to do with dairy fat**.

Here's a nice quote:

Our findings support potential metabolic benefits of dairy consumption and suggest that trans-palmitoleate may mediate these effects***. They also suggest that efforts to promote exclusive consumption of low-fat and nonfat dairy products, which would lower population exposure to trans-palmitoleate, may be premature until the mediators of the health effects of dairy consumption are better established.

Never thought I'd see the day! Not bad, but I can do better:

Our findings support eating as much butter as possible****. Don't waste your money on low-fat cream, either (half-n-half). We're sorry that public health authorities have spent 30 years telling you to eat low-fat dairy when most studies are actually more consistent with the idea that dairy fat reduces the risk obesity and chronic disease.

What are these studies suggesting that dairy fat may be protective, you ask? That will be the topic of another post, my friends.


*Probably due to uncontrolled de novo lipogenesis because of insulin resistance. Many studies find that serum saturated fatty acids are higher in those with metabolic dysfunction, independent of diet. They sometimes interpret that as showing that people are lying about their diet, rather than that serum saturated fatty acids don't reflect diet very well. For example, in one study I cited, investigators found no relationship between dietary saturated fat and diabetes risk, but they did find a relationship between serum saturated fatty acids and diabetes risk (5). They then proceeded to refer to the serum measurements as "objective measurements" that can tease apart "important associations with diabetes incidence that may be missed when assessed by [food questionnaires]." They go on to say that serum fatty acids are "useful as biomarkers for fatty acid intake," which is true for some fatty acids but not remotely for most of the saturated ones, according to their own study. Basically, they try to insinuate that dietary saturated fat is the culprit, and the only reason they couldn't measure that association directly is that people who went on to develop diabetes inaccurately reported their diets! A more likely explanation is that elevated serum saturated fatty acids are simply a marker of insulin resistance (and thus uncontrolled de novo lipogenesis), and had nothing to do with diet.

**Why do I say that? Because mathematically adjusting for dairy and meat fat intake did not substantially weaken the association between phospholipid trans-palmitoleate and reduced diabetes risk (Table 4). In other words, if you believe their math, dairy/meat fat intake only accounted for a small part of the protective association. That implies that healthy people maintain a higher serum phospholipid trans-palmitoleate level than unhealthy people, even if both groups eat the same amount of trans-palmitoleate. If they hadn't mentioned that full-fat dairy fat intake was directly associated with a lower risk of diabetes, I would not find the study very interesting because I'd have my doubts that it was relevant to diet.

***I find it highly doubtful that trans-palmitoleate entirely mediates the positive health outcomes associated with dairy fat intake. I think it's more likely to simply be a marker of milk fat, which contains a number of potentially protective substances such as CLA, vitamin K2, butyric acid, and the natural trans fats including trans-palmitoleate. In addition, dairy fat is low in omega-6 polyunsaturated fat. I find it unlikely that their fancy math was able to tease those factors apart, because those substances all travel together in dairy fat. trans-palmitoleate pills are not going to replace butter.

****That's a joke. I think butter can be part of healthy diet, but that doesn't mean gorging on it is a good idea. This study does not prove that dairy fat prevents diabetes, it simply suggests that it may.

Interview with Chris Voigt of 20 Potatoes a Day

Introduction

Chris Voigt is the executive director of the Washington State Potato Commission, which supports and promotes the Washington state potato industry (1). On October 1st, Mr. Voigt began a two month, potato-only diet to raise awareness about the health properties of potatoes. It was partially in response to the recent decision by the federal WIC (Women, Infants and Children) low-income assistance program to remove potatoes from the list of vegetables it will pay for. Mr. Voigt's potato diet has been a media sensation, leading to widespread coverage in several countries. He maintains a website and blog called 20 Potatoes a Day.


Diet Facts

For 60 days, Mr Voigt's diet consisted of nothing but potatoes and a small amount of cooking oil (canola and olive), with no added nutritional supplements. Based on what he has told me, I estimate that 10-15% of his calories came from fat, 10% from protein and 75-80% from high-glycemic carbohydrate. His calorie intake ranged from 1,600 kcal (first 3 weeks) to 2,200 kcal (remaining 5.5 weeks) per day. Prior to the diet, he estimated that his calorie requirement was 2,200 kcal, so he attempted to stay as close to that as possible.

Health Markers

Mr. Voigt has posted the results of physical examinations, including bloodwork, from the beginning, middle and end of the diet. The change he experienced during that time is nothing short of remarkable. He shed 21 pounds, his fasting glucose decreased by 10 mg/dL (104 to 94 mg/dL), his serum triglycerides dropped by nearly 50%, his HDL cholesterol increased slightly, and his calculated LDL cholesterol dropped by a stunning 41% (142 to 84 mg/dL). The changes in his HDL, triglycerides and fasting glucose are consistent with improved insulin sensitivity (2, 3), and are not consistent with a shift of LDL particle size to the dangerous "small, dense" variety (4).

Interview

What was your diet like prior to the potato diet?

My best estimate is that it was probably a little better than the average US citizen only because of a high rate of produce consumption. I generally would eat about 10 servings of fruits and vegetables a day. But I ate everything else too. I would eat a wide range of food, a little bit of everything, including foods that aren’t considered “healthy”.

You essentially ate nothing but potatoes, fat and flavorings for two months. Can you give us an idea of how much fat you were eating? What kind of fat was it?

I averaged about 2 tablespoons of cooking oil a day over the span of the 60 days. Canola oil was used for frying and olive oil was used for roasting.

How was your digestion?

Potatoes are pretty easy on the digestive system. I actually got a lot of emails from people who suffer from severe digestive disorders and literally, potatoes are the only thing they can eat. My 60 days of potatoes was nothing compared to some folks with these digestive disorders. I was getting a lot of fiber so things were pretty regular, but not too regular :)

You lost 21 pounds during your two months of eating only potatoes. Do you have a sense of whether it came out of fat, muscle or both? For example, did your pants become looser?

Pants definitely became looser. I also noticed it in my neck size for shirts. I’m assuming most all of it was due to fat loss.

Do you think you were able to meet your calorie goal of 2,200 calories per day? Were you hungry during the diet?

I was not meeting the goal of 2,200 calories a day during the first 3 weeks of the diet. During the first three weeks of the diet I only ate until I was full. I didn’t realize that potatoes would give me such a high sense of fullness after each meal. So for those first 3 weeks, I was only consuming about 1,600 calories a day. After the third week I had lost 12 pounds and realized that I needed to change strategy. I then began to eat more potatoes despite the sense of fullness I was experiencing. So for the remaining 5 ½ weeks I was very diligent about eating the 2,200 calories. I continued to lose weight but at a slower place. I lost an additional 9 pounds over the course of those remaining 5 1/2 weeks. At the start of my diet I estimated, via a couple different on line calorie calculators, that I burn about 2,200 calories a day. Since I continued to lose weight, I’m assuming I actually burn closer to 2,800 calories a day. Something that may have also played a role in continued weight loss was the amount of resistant starch I was getting from potatoes. I ate a lot of cooked potatoes that had been refrigerated. These are generally higher in resistant starch. If I were to do the diet again, I would like to set up an experiment to gauge the effect of resistant starch.

What foods did you crave the most?

I craved mostly foods that had a “juicy crunch”, like an apple, or cucumbers, or carrots, or celery. I never acquired a taste for raw potatoes so virtually all the potatoes I consumed were cooked. No matter how you cook your potatoes, you always get that same soft cooked texture. I craved foods with a crisper texture.

How was your energy level?

My energy level was very good the entire time of the diet. I really didn’t notice a change in energy at the start of the diet so I assumed that the potato diet didn’t have a positive or negative effect on my energy level. It wasn’t until I finished the diet and started to consume other foods that I noticed my energy level has seemed to drop a bit.

How did you feel overall? Were there any unexpected effects of the diet?

I felt really good on the diet. I had lots of energy, slept good at night, and seemed to avoid the cold viruses that circulated at home and work.

The only unusual thing that occurred is what my wife told me. I’m a habitual snorer. The day I started eating only potatoes, my snoring stopped. It restarted the day I started to include other foods in my diet. I’m assuming it was just some weird coincidence but that’s what she tells me.

My doctor and I expected my cholesterol to drop but not at the level we saw. I’ve had borderline high cholesterol for the past decade. I started the diet at 214 and saw it drop to 147 at the end of 60 days. We anticipated a drop of maybe 10-25 points. It was a huge surprise to see a 67 point drop.

Your fasting glucose went from 104 mg/dL, which I consider high, to 94 mg/dL, which is on the high side for someone eating a high-carbohydrate diet, but within the clinically normal range. Do you have a family history of diabetes?

No history of diabetes. My parents are in their early eighties and their parents lived to their 70’s and 80’s with no history of type one or two diabetes.

Reading your blog posts, it seemed like you were having a hard time with the diet at first, but after a while you complained less and even seemed to enjoy it at times. Did you get used to it?

I would say that week 2 and 3 were probably the hardest. The first week was easy probably because of the novelty of the diet. Then reality set in for week 2 and 3. After that, I found my groove and it got easier. During the work week was easy but weekends, particularly Sunday’s, were the hardest. During the work week I did most of my eating at my desk so I wasn’t around a lot of other people eating or surrounded by other foods. Weekends were more difficult because I was around other people every meal and always had other foods in front of me at home.

What kinds of potatoes did you eat?

I literally ate every kind of potato I could get my hands on. I ate yellow skin/yellow flesh potatoes, red skin/white flesh, red skin/red flesh, purple skin/white flesh, purple skin/purple flesh, russet potatoes with white flesh, russet potatoes with yellow flesh, white potatoes, yellow potatoes with white flesh, purple fingerlings, yellow fingerlings, red fingerlings and numerous experimental varieties.

Did you peel them or eat the skin?

I ate the skin at least 90% of the time if not more. There is a myth that all the nutrition in a potato is in the skin or right under the skin. That’s not true, there are nutrients spread throughout the potato but most of the fiber is located in the skin.

What variety of potato is your favorite?

It really depended on the cooking method. For frying, I preferred russet potatoes. For baking, I preferred red potatoes. For mashed, I preferred yellow potatoes. For roasting, a toss-up between russets and reds.

How long did it take you after the diet ended to eat another potato?

As strange as it sounds, potatoes were my first two meals after my diet ended. I was saving my first non-potato meal for a special event that was planned at the local Head Start facility. The beef, dairy, apple, and potato producers put together a nice dinner event and nutrition workshop for all the kids and their parents at the Head Start center in Moses Lake. I still eat potatoes pretty regularly, but most of the time now I’m eating them with more than just seasonings.

Are there any other facts about potatoes you think Whole Health Source readers might find interesting?

Just a reminder that I’m not encouraging anyone to follow in my footsteps and eat just potatoes. This diet is not intended to be the next “fad” diet but was simply a bold statement to remind people that there is a tremendous amount of nutrition in a potato. There is no one food product that can meet all of your nutritional needs. I fully support a well balanced healthy diet, which potatoes can be a part of.

In 2008, the United Nations declared it to be the “Year of the Potato”. This was done to bring attention to the fact that the potato is one of the most efficient crops for developing nations to grow, as a way of delivery a high level of nutrition to growing populations, with fewer needed resources than other traditional crops. In the summer of 2010, China approved new government policies that positioned the potato as the key crop to feed its growing population. The Chinese government formed a partnership with the International Potato Center in Peru to help them facilitate this new emphasis on the potato.

Thanks Chris, for doing your experiment and taking the time to share these details with us!

In the next post, I'll give my interpretation of all this.

Glucose Tolerance in Non-industrial Cultures

Background

Glucose is the predominant blood sugar and one of the body's two main fuel sources (the other is fatty acids). Glucose, in one form or another, is also the main form of digestible dietary carbohydrate in nearly all human diets. Starch is made of long chains of glucose molecules, which are rapidly liberated and absorbed during digestion. Sucrose, or table sugar, is made of one glucose and one fructose molecule, which are separated before absorption.

Blood glucose is essential for life, but it can also be damaging if there is too much of it. Therefore, the body tries to keep it within a relatively tight range. Normal fasting glucose is roughly between 70 and 90 mg/dL*, but in the same individual it's usually within about 5 mg/dL on any given day. Sustained glucose above 160 mg/dL or so causes damage to multiple organ systems. Some people would put that number closer to 140 mg/dL.

The amount of glucose contained in a potato far exceeds the amount contained in the blood, so if all that glucose were to enter the blood at once, it would lead to a highly damaging blood glucose level. Fortunately, the body has a hormone designed to keep this from happening: insulin. Insulin tells cells to internalize glucose from the blood, and suppresses glucose release by the liver. It's released by the pancreas in response to eating carbohydrate, and protein to a lesser extent. The amount of insulin released is proportional to the amount of carbohydrate ingested, so that glucose entering the blood is cleared before it can accumulate.

Insulin doesn't clear all the glucose as it enters the bloodstream, however. Some of it does accumulate, leading to a spike in blood glucose. This usually doesn't exceed 130 mg/dL in a truly healthy person, and even if it approaches that level it's only briefly. However, diabetics have reduced insulin signaling, and eating a typical meal can cause their glucose to exceed 300 mg/dL due to reduced insulin action and/or insulin secretion. In affluent nations, this is typically due to type II diabetes, which begins as insulin resistance, a condition in which insulin is actually higher than normal but cells fail to respond to it.  The next step is the failure of insulin-secreting beta cells, which is what generally precipitates actual diabetes.

The precursor to diabetes is called glucose intolerance, or pre-diabetes. In someone with glucose intolerance, blood glucose after a typical meal will exceed that of a healthy person, but will not reach the diabetic range (a common definition of diabetes is 200 mg/dL or higher, 2 hours after ingesting 75g of glucose). Glucose tolerance refers to a person's ability to control blood glucose when challenged with dietary glucose, and can be used in some contexts as a useful predictor of diabetes risk and general metabolic health. Doctors use the oral glucose tolerance test (OGTT), which involves drinking 60-100g glucose and measuring blood glucose after one or two hours, to determine glucose tolerance.

Why do we care about glucose tolerance in non-industrial cultures?

One of the problems with modern medical research is that so many people in our culture are metabolically sick that it can be difficult to know if what we consider "normal" is really normal or healthy in the broader sense. Non-industrial cultures allow us to examine what the human metabolism is like in the absence of metabolic disease. I admit this rests on certain assumptions, particularly that these people aren't sick themselves. I don't think all non-industrial cultures are necessarily healthy, but I'm going to stick with those that research has shown have an exceptionally low prevalence of diabetes (by Western standards) and other "diseases of civilization" for the purposes of this post.

Here's the question I really want to answer in this post: do healthy non-industrial cultures with a very high carbohydrate intake have an excellent glucose tolerance, such that their blood glucose doesn't rise to a high level, or are they simply resistant to the damaging effects of high blood glucose?

The data

I'm going to start with an extreme example. In the 1960s, when it was fashionable to study non-industrial cultures, researchers investigated the diet and health of a culture in Tukisenta, in the highlands of Papua New Guinea. The eat practically nothing but sweet potatoes, and their typical daily fare is 94.6 percent carbohydrate. Whether or not you believe that exact number, their diet was clearly extraordinarily high in carbohydrate. They administered 100g OGTTs and measured blood glucose at one hour, which is a very stringent OGTT. They compared the results to those obtained in the 1965 Tecumseh study (US) obtained by the same method. Here's what they found (1):
Compared to Americans, in Tukisenta they had an extraordinary glucose tolerance at all ages. At one hour, their blood glucose was scarcely above normal fasting values, and glucose tolerance only decreased modestly with age. In contrast, in Americans over 50 years old, the average one-hour value was around 180 mg/dL!

Now let's take a look at the African Bantu in the Lobaye region of the Central African Republic. The Bantu are a large ethnic group who primarily subsist on a diverse array of starchy foods including grains, beans, plantains and root crops. One hour after a 100g OGTT, their blood glucose was 113 mg/dL, compared to 139 mg/dL in American controls (2). Those numbers are comparable to what investigators found in Tukisenta, and indicate an excellent glucose tolerance in the Bantu.

In South America, different investigators studied a group of native Americans in central Brazil that subsist primarily on cassava (a starchy root crop) and freshwater fish. Average blood glucose one hour after a 100g OGTT was 94 mg/dl, and only 2 out of 106 people tested had a reading over 160 mg/dL (both were older women) (Western Diseases: Their Emergence and Prevention, p. 149). Again, that indicates a phenomenal glucose tolerance by Western standards.

I have to conclude that high-carbohydrate non-industrial cultures probably don't experience damaging high blood glucose levels, because their glucose tolerance is up to the task of shuttling a huge amount of glucose out of the bloodstream before that happens.

Not so fast...

Now let's turn our attention to another study that may throw a wrench in the gears. A while back, I found a paper containing OGTT data for the !Kung San (also called the Bushmen), a hunter-gatherer group living in the Kalahari desert of Africa. I reported in an earlier post that they had a good glucose tolerance. When I revisited the paper recently, I realized I had misread it and in fact, their glucose tolerance was actually pretty poor.

Investigators administered a 50g OGTT, half what the other studies used. At one hour, the San had blood glucose readings of 169 mg/dL, compared to 142 mg/dL in Caucasian controls (3)! I suspect a 100g OGTT would have put them close to the diabetic range.

Wait a minute, these guys are hunter-gatherers living the ancestral lifestyle; aren't they supposed to be super healthy?? While I was mulling this over, I recalled a discussion on Peter's blog hyperlipid where commenters were discussing their diabetic OGTT values while on a low-carbohydrate diet. Apparently, carbohydrate refeeding for a few days generally reverses this and allows a normal OGTT in most people. It turns out this effect has been known for the better part of a century.

So what were the San eating? The study was conducted in October of 1970. The San diet changes seasonally, however their main staple food is the mongongo nut, which is mostly fat and which is available year-round (according to The !Kung San: Men, Women and Work in a Foraging Society). Their carbohydrate intake is generally low by Western standards, and at times of the year it is very low. This varies by the availability of other foods, but they generally don't seem to relish the fibrous starchy root crops that are available in the area, as they mostly eat them when other food is scarce. Jean-Louis Tu has posted a nice analysis of the San diet on BeyondVeg (4). Here's a photo of a San man collecting mongongo nuts from The !Kung San: Men, Women and Work in a Foraging Society:

What did the authors of the OGTT study have to say about their diet? Acknowledging that prior carbohydrate intake may have played a role in the OGTT results of the San, they made the following remark:

a retrospective dietary history (M. J. Konner, personal communication, 1971) indicated that the [San], in fact, consumed fairly large amounts of carbohydrate-rich vegetable food during the week before testing.

However, the dietary history was not provided, nor has it been published, so we have no way to assess the statement's accuracy or what was meant by "fairly large amounts of carbohydrate-rich vegetable food." Given the fact that the San diet generally ranges from moderately low to very low in carbohydrate, I suspect they were not getting much carbohydrate as a percentage of calories. Looking at the nutritional value of the starchy root foods they typically ate in appendix D of The !Kung San: Men, Women and Work in a Foraging Society, they are fibrous and most contain a low concentration of starch compared to a potato for example. The investigators may have been misled by the volume of these foods eaten, not realizing that they are not as rich in carbohydrate as the starchy root crops they are more familiar with.

You can draw your own conclusions, but I think the high OGTT result of the San probably reflect a low habitual carbohydrate intake, and not pre-diabetes. I have a very hard time believing that this culture wasn't able to handle the moderate amount of carbohydrate in their diet effectively, as observers have never described diabetic complications among them.

Putting it all together

This brings me to my hypothesis. I think a healthy human body is extraordinarily flexible in its ability to adapt to a very broad range of carbohydrate intakes, and adjusts glucose tolerance accordingly to maintain carbohydrate handling in a healthy range. In the context of a healthy diet and lifestyle (from birth), I suspect that nearly anyone can adjust to a very high carbohydrate intake without getting dangerous blood glucose spikes. A low carbohydrate intake leads to lower glucose handling and better fat handling, as one would expect. This can show up as impaired glucose tolerance or diabetes on an OGTT, but that does not necessarily reflect a pathological state in my opinion.

Every person is different based on lifestyle, diet, personal history and genetics. Not everyone in affluent nations has a good glucose tolerance, and some people will never be able to handle starch effectively under any circumstances. The best way to know how your body reacts to carbohydrate is to test your own post-meal blood glucose using a glucose meter. They are inexpensive and work well. For the most informative result, eat a relatively consistent amount of carbohydrate for a week to allow your body to adapt, then take a glucose measurement 1 and 2 hours after a meal. If you don't eat much carbohydrate, eating a potato might make you think you're diabetic, whereas after a week of adaptation you may find that a large potato does not spike your blood glucose beyond the healthy range.

Exercise is a powerful tool for combating glucose intolerance, as it increases the muscles' demand for glucose, causing them to transport it out of the blood greedily after a meal. Any exercise that depletes muscle glycogen should be effective.


* Assuming a typical carbohydrate intake. Chris Kresser recently argued, based on several studies, that true normal fasting glucose for a person eating a typical amount of carbohydrate is below 83 mg/dL. Low-carbohydrate eating may raise this number, but that doesn't necessarily indicate a pathological change. High-carbohydrate cultures such as the Kitavans, Aymara and New Guineans tend to have fasting values in the low 60s to low 70s. I suspect that a very high carbohydrate intake generally lowers fasting glucose in healthy people. That seems to be the case so far for Chris Voigt, on his diet of 20 potatoes a day. Stay tuned for an interview with Mr. Voigt in early December.

The Big Sleep

This blog usually focuses on diet, because that's my specialty. But if you want Whole Health, you need the whole package: a diet and lifestyle that is broadly consistent with our evolutionary heritage. I think we all know that on some level, but a recent paper has reminded me of it.

I somehow managed to get on the press list of the Annals of Internal Medicine. That means they send me embargoed papers before they're released to the general public. That journal publishes a lot of high-impact diet studies, so it's a great privilege for me. I get to write about the studies, and publish my analysis at the time of general release, which is the same time the news outlets publish their stories.

One of the papers they sent me recently is a fat loss trial with an interesting twist (1; see below). All participants were told to eat 10% fewer calories that usual for two weeks, however half of them were instructed to sleep for 8 and a half hours per night, and the other half were instructed to sleep for 5 and a half hours*. The actual recorded sleep times were 7:25 and 5:14, respectively.

Weight loss by calorie restriction causes a reduction of both fat and lean mass, which is what the investigators observed. Both groups lost the same amount of weight. However, 80% of the weight was lost as fat in the high-sleep group (2.4/3.0 kg lost as fat), while only 48% of it was lost as fat in the low-sleep group (1.4/2.9 kg lost as fat). Basically, the sleep-deprived group lost as much lean mass as they did fat mass, which is not good!

There are many observational studies showing associations between insufficient sleep, obesity and diabetes. However, I think studies like that are particularly vulnerable to confounding variables, so I've never known quite what to make of them. Furthermore, they often show that long sleep duration associates with poor health as well, which I find highly unlikely to reflect cause and effect. I discussed one of those studies in a post a couple of years ago (2). That's why I appreciate this controlled trial so much.

Another sleep restriction trial published in the Lancet in 1999 showed that restricting healthy young men to four hours of sleep per night caused them to temporarily develop glucose intolerance, or pre-diabetes (3).

Furthermore, their daily rhythm of the hormone cortisol became abnormal. Rather than the normal pattern of a peak in the morning and a dip in the evening, sleep deprivation blunted their morning cortisol level and enhanced it in the evening. Cortisol is a stress hormone, among other things, and its fluctuations may contribute to our ability to feel awake in the morning and ready for bed at night.

The term "adrenal fatigue", which refers to the aforementioned disturbance in cortisol rhythm, is characterized by general fatigue, difficulty waking up in the morning, and difficulty going to sleep at night. It's a term that's commonly used by alternative medical practitioners but not generally accepted by mainstream medicine, possibly because it's difficult to demonstrate and the symptoms are fairly general. Robb Wolf talks about it in his book The Paleo Solution.

The investigators concluded:

Sleep debt has a harmful impact on carbohydrate metabolism and endocrine functhon. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.

So there you have it. Besides making us miserable, lack of sleep appears to predispose to obesity and diabetes, and probably sets us up for the Big Sleep down the line. I can't say I'm surprised, given how awful I feel after even one night of six hour sleep. I feel best after 9 hours, and I probably average about 8.5. Does it cut into my free time? Sure. But it's worth it to me, because it allows me to enjoy my day much more.

Keep your room as dark as possible during sleep. It also helps to avoid bright light, particularly in the blue spectrum, before bed (4). "Soft white" bulbs are preferable to full spectrum in the evening. If you need to use your computer, dim the monitor and adjust it to favor warm over cool colors. For people who sleep poorly due to anxiety, meditation before bed can be highly effective. I posted a tutorial here.

1. Nedeltcheva, AV et al. "Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity." Annals of Internal Medicine. 2010. Advanced publication.


* The study was a randomized crossover design with a 3 month washout period, which I consider a rigorous design. I think the study overall was very clever. The investigators used calorie restriction to cause rapid changes in body composition so that they could see differences on a reasonable timescale, rather than trying to deprive people of sleep for months and look for more gradual body fat changes without dietary changes. The latter experiment would have been more interesting, but potentially impractical and unethical.