A Gluten-free January

Are You Gluten Sensitive?

Many people are totally unaware of the fact that they react poorly to gluten. Because they've been eating wheat, barley and/or rye products every day for virtually their entire lives, they don't know what their bodies feel like without gluten. In susceptible people, eating gluten is linked to a dizzying array of health problems that stem from an immune reaction to gliadins and other proteins in gluten (1). Are you a susceptible person? How do you know?

The gold standard way to detect a gluten sensitivity is to do a gluten "challenge" after a period of avoidance and see how you feel. People who react poorly to gluten may feel better after a period of avoidance. After a gluten challenge, symptoms can range from digestive upset, to skin symptoms, to fatigue or irritability within minutes to days of the gluten challenge.

With 2011 approaching, why not make your new year's resolution to go gluten-free for a month? A man named Matt Lentzner e-mailed me this week to ask if I would help with his (non-commercial) project, "A Gluten-free January". I said I'd be delighted. Although I don't typically eat much gluten, this January I'm going 100% gluten-free. Are you on board? Read on.

A Message from Matt Lentzner

Hi There.

My name is Matt Lentzner. I'm just some guy who lifts weights on his patio and tries to eat healthy. That's not important, but I have an idea that just might be.

I am trying to get as many people as possible to go gluten-free for one month - this January 2011.

I've considered this whole ancestral diet thing and I've come to a conclusion. If you could only do just one thing to improve your health then not eating gluten would be it. This is not to say that avoiding other nasty things like fructose or industrial vegetable oil is not important. They are, but you'd get the most bang for your buck from not eating gluten.

"Eat No Gluten" is simple and easy to remember. I think that sometimes the rules get so complicated and overwhelming and people just give up on it. We're keeping it simple here. Even at this simplified level I see that it's difficult for a lot of folks. I think people, Americans especially, tend not to pay much attention to what they're eating - what it is, where it came from, etc.

Getting people to get out of their eating ruts and think a little about what goes into their mouths is a valuable exercise. It sets the stage for better choices in the future. I hope that some success with the simple step will encourage people to further improve their diets.

I have a website at www.glutenfreejan.com. If you want to sign up just send an email with your first name, last initial, and town of residence to glutenfreejan@gmail.com. If you are on Facebook there's a community you can 'Like' called: Gluten Free January. So far I have over 120 people all over the world signed up. If you are already gluten-free then I still want you to sign up - the more the merrier. You can also use this opportunity to spread the word and sign up your family and friends.

Merry Christmas - Looking forward to a gluten-free New Year.

Matt

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.

Potato Diet Interpretation

If you read my post on December 16th, you know that Chris Voigt saw remarkable fat loss and improvements in health markers as a result of two months of eating almost nothing but potatoes. This has left many people scratching their heads, because potatoes are not generally viewed as a healthy food. This is partially due to the fact that potatoes are very rich in carbohydrate, which also happens to be a quickly digested type, resulting in a high glycemic index. The glycemic index refers to the degree to which a particular food increases blood glucose when it's eaten, and I've questioned the relevance of this concept to health outcomes in the past (1, 2, 3). I think Mr. Voigt's results once again argue against the importance of the glycemic index as a diet-health concept.

It's often pointed out that potatoes are low in vitamins and minerals compared to vegetables on a per-calorie basis, but I think it's a misleading comparison because potatoes are much more calorie-dense than most vegetables. Potatoes compare favorably to other starchy staples such as bread, rice and taro.

Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).

On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But as Gary Taubes would say, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.

Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?

I believe Mr. Voigt's diet lowered his fat mass 'setpoint'. In other words, for whatever reason, the diet made his body 'want' to be leaner that it already was. His body began releasing stored fat that it considered excess, and therefore he had to eat less food to complete his energy needs. You see this same phenomenon very clearly in rodent feeding studies. Changes in diet composition/quality can cause dramatic shifts in the fat mass setpoint (5, 6). Mr. Voigt's appetite would eventually have returned to normal once he had stabilized at a lower body fat mass, just as rodents do.

Rodent studies have made it clear that diet composition has a massive effect on the level of fat mass that the body will 'defend' against changes in calorie intake (5, 6). Human studies have shown similar effects from changes in diet composition/quality. For example, in controlled diet trials, low-carbohydrate dieters spontaneously reduce their calorie intake quite significantly and lose body fat, without being asked to restrict calories (7). In Dr. Staffan Lindeberg's Paleolithic diet trials, participants lost a remarkable amount of fat, yet a recent publication from his group shows that the satiety (fullness) level of the Paleolithic group was not different from a non-Paleolithic comparison group despite a considerably lower calorie intake over 12 weeks (8, 9). I'll discuss this important new paper soon. Together, this suggests that diet composition/quality can have a dominant impact on the fat mass setpoint.

One possibility is that cutting the wheat, sugar, most vegetable oil and other processed food out of Mr. Voigt's diet was responsible for the fat loss. I think that's likely to have contributed. Many people find, for example, that they lose fat simply by eliminating wheat from their diet.

Another possibility that I've been exploring recently is that changes in palatability (pleasantness of flavor) influence the fat mass setpoint. There is evidence in rodents that it does, although it's not entirely consistent. For example, rats will become massively obese if you provide them with chocolate flavored Ensure (a meal replacement drink), but not with vanilla or strawberry Ensure (10). They will defend their elevated fat mass against calorie restriction (i.e. they show a physiological starvation response when you try to bring them down to a lower weight by feeding them less chocolate Ensure) while they're eating chocolate Ensure, but as soon as you put them back on unpurified rodent pellets, they will lose fat and defend the lower fat mass. Giving them food in liquid or paste form often causes obesity, while the same food in solid pellet form will not. Eating nothing but potatoes is obviously a diet with a low overall palatability.

So I think that both a change in diet composition/quality and a decrease in palatability probably contributed to a decrease in Mr. Voigt's fat mass setpoint, which allowed him to lose fat mass without triggering a starvation response (hunger, fatigue).

The rest of his improvements in health markers were partially due to the fat loss, including his decreased fasting glucose, decreased triglycerides, and presumably increased insulin sensitivity. They may also have been partially due to a lack of industrial food and increased intake of certain micronutrients such as magnesium.

One of the most striking changes was in his calculated LDL cholesterol ("bad" cholesterol), which decreased by 41%, putting him in a range that's more typical of healthy non-industrial cultures including hunter-gatherers. Yet hunter-gatherers didn't eat nothing but potatoes, often didn't eat much starch, and in some cases had a high intake of fat and saturated fat, so what gives? It's possible that a reduced saturated fat intake had an impact on his LDL, given the relatively short timescale of the diet. But I think there's something mysterious about this setpoint mechanism that has a much broader impact on metabolism than is generally appreciated. For example, calorie restriction in humans has a massive impact on LDL, much larger than the impact of saturated fat (11). And in any case, the latter appears to be a short-term phenomenon (12). It's just beginning to be appreciated that energy balance control systems in the brain influence cholesterol metabolism.

Mr. Voigt's digestion appeared to be just fine on his potato diet, even though he generally ate the skins. This makes me even more skeptical of the idea that potato glycoalkaloids in common potato varieties are a health concern, especially if you were to eliminate most of the glycoalkaloids by peeling.

I asked Mr. Voigt about what foods he was craving during the diet to get an idea of whether he was experiencing any major deficiencies. The fact that Mr. Voigt did not mention craving meat or other high-protein foods reinforces the fact that potatoes are a reasonable source of complete protein. The only thing he craved was crunchy/juicy food, which I'm not sure how to interpret.

He also stopped snoring during the diet, and began again immediately upon resuming his normal diet, perhaps indicating that his potato diet reduced airway inflammation. This could be due to avoiding food allergies and irritants (wheat anyone?) and also fat loss.

Overall, a very informative experiment! Enjoy your potatoes.


*Until the last 5.5 weeks, when he deliberately stuffed himself beyond his appetite because his rapid weight loss worried him. Yet, even with deliberate overfeeding up to his estimated calorie requirement of 2,200 calories per day, he continued to lose weight. He probably was not quite reaching his calorie goal, or his requirement is higher than he thought.

Trouble With RSS Feed?

I've received several comments that my blog posts are no longer showing up in peoples' RSS feeds. I've gone into my settings, and the blog is still set to full feed mode, so I don't know why that would be. I'm trying to understand if the problem is widespread or only affects a few people. Please let me know in the comments section if new posts (since the potatoes and human health series) are not showing up in your reader. Also, please let me know if new posts are showing up. Thanks!

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.

Dr. Mellanby's Tooth Decay Reversal Diet

I have a lot of admiration for Drs. Edward and May Mellanby. A husband-and-wife team, they discovered vitamin D, and determined that rickets is caused by poor calcium (or phosphorus) status, typically due to vitamin D deficiency. They believed that an ideal diet is omnivorous, based on whole foods, and offers an adequate supply of fat-soluble vitamins and easily absorbed minerals. They also felt that grain intake should be modest, as their research showed that unsoaked whole grains antagonize the effect of vitamins D and A.

Not only did the Mellanbys discover vitamin D and end the rickets epidemic that was devastating Western cities at the time, they also discovered a cure for early-stage tooth decay that has been gathering dust in medical libraries throughout the world since 1924.

It was in that year that Dr. May Mellanby published a summary of the results of the Mellanby tooth decay reversal studies in the British Medical Journal, titled "Remarks on the Influence of a Cereal-free Diet Rich in Vitamin D and Calcium on Dental Caries in Children". Last year, I had to specially request this article from the basement of the University of Washington medical library (1). Thanks to the magic of the internet, the full version of the paper is now freely available online (2).

You don't need my help to read the study, but in this post I offer a little background, a summary and my interpretation.

In previous studies, the Mellanbys used dogs to define the dietary factors that influence tooth development and repair. They identified three, which together made the difference between excellent and poor dental health (from Nutrition and Disease):

1. The diet's mineral content, particularly calcium and phosphorus
2. The diet's fat-soluble vitamin content, chiefly vitamin D
3. The diet's content of inhibitors of mineral absorption, primarily phytic acid

Once they had defined these factors, they set about testing their hypotheses in humans. They performed eight trials, each one in children in an institutionalized setting where diet could be completely controlled. The number of cavities in each child's mouth was noted at the beginning and end of the period. I'll only discuss the three most informative, and only the most successful in detail. First, the results:

I'll start with diet 1. Children on this diet ate the typical fare, plus extra oatmeal. Oatmeal is typically eaten as an unsoaked whole grain (and soaking it isn't very effective in any case), and so it is high in phytic acid, which effectively inhibits the absorption of a number of minerals including calcium. These children formed 5.8 cavities each and healed virtually none-- not good!

Diet number 2 was similar to diet 1, except there was no extra oatmeal and the children received a large supplemental dose of vitamin D. Over 28 weeks, only 1 cavity per child developed or worsened, while 3.9 healed. Thus, simply adding vitamin D to a reasonable diet allowed most of their cavities to heal.

Diet number 3 was the most effective. This was a grain-free diet plus supplemental vitamin D. Over 26 weeks, children in this group saw an average of only 0.4 cavities form or worsen, while 4.7 healed. The Mellanbys considered that they had essentially found a cure for this disorder in its early stages.

What exactly was this diet? Here's how it was described in the paper (note: cereals = grains):

...instead of cereals- for example, bread, oatmeal, rice, and tapioca- an increased allowance of potatoes and other vegetables, milk, fat, meat, and eggs was given. The total sugar, jam, and syrup intake was the same as before. Vitamin D was present in abundance in either cod-liver oil or irradiated ergosterol, and in egg yolk, butter, milk, etc. The diet of these children was thus rich in those factors, especially vitamin D and calcium, which experimental evidence has shown to assist calcification, and was devoid of those factors- namely, cereals- which interfere with the process.

Carbohydrate intake was reduced by almost half. Bread and oatmeal were replaced by potatoes, milk, meat, fish, eggs, butter and vegetables. The diet is reminiscent of what Dr. Weston Price used to reverse tooth decay in his dental clinic in Cleveland, although Price's diet did include rolls made from freshly ground whole wheat. Price also identified the fat-soluble vitamin K2 MK-4 as another important factor in tooth decay reversal, which would have been abundant in Mellanby's studies due to the dairy. The Mellanbys and Price were contemporaries and had parallel and complementary findings. The Mellanbys did not understand the role of vitamin K2 in mineral metabolism, and Price did not seem to appreciate the role of phytic acid from unsoaked whole grains in preventing mineral absorption.

Here are two sample meals provided in Dr. Mellanby's paper. I believe the word "dinner" refers to the noon meal, and "supper" refers to the evening meal:

Breakfast- Omelette, cocoa, with milk.
Lunch- Milk.
Dinner- Potatoes, steamed minced meat, carrots, stewed fruit, milk.
Tea- Fresh fruit salad, cocoa made with milk.
Supper- Fish and potatoes fried in dripping, milk.

Breakfast- Scrambled egg, milk, fresh salad.
Dinner- Irish stew, potatoes, cabbage, stewed fruit, milk.
Tea- Minced meat warmed with bovril, green salad, milk.
Supper- Thick potato soup made with milk.

In addition, children received vitamin D daily. Here's Dr. Mellanby's summary of their findings:

The tests do not indicate that in order to prevent dental caries children must live on a cereal-free diet, but in association with the results of the other investigations on animals and children they do indicate that the amount of cereal eaten should be reduced, particularly during infancy and in the earlier years of life, and should be replaced by an increased consumption of milk, eggs, butter, potatoes, and other vegetables. They also indicate that a sufficiency of vitamin D and calcium should be given from birth, and before birth, by supplying a suitable diet to the pregnant mother. The teeth of the children would be well formed and more resistant to dental caries instead of being hypoplastic and badly calcified, as were those in this investigation.

If I could add something to this program, I would recommend daily tooth brushing and flossing, avoiding sugar, and rinsing the mouth with water after each meal.

This diet is capable of reversing early stage tooth decay. It will not reverse advanced decay, which requires professional dental treatment as soon as possible. It is not a substitute for dental care in general, and if you try using diet to reverse your own tooth decay, please do it under the supervision of a dentist. And while you're there, tell her about Edward and May Mellanby!

Preventing Tooth Decay
Reversing Tooth Decay
Images of Tooth Decay Healing due to an Improved Diet
Dental Anecdotes

Interview with a Kitavan

Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.

I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.

How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.

Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.

Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.

What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.

Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.

Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.

How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.

Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.

Thanks for your help, Job! I know many people will appreciate reading these responses.

Diet-Heart Controlled Trials: a New Literature Review

Many controlled studies have measured the cardiovascular effects of replacing animal ("saturated") fats with seed oils (predominantly the omega-6 polyunsaturated fat linoleic acid) in humans. A number of these studies recorded heart attacks and total mortality during the following 1-8 years. Several investigators have done meta-analyses (literature reviews) to try to tease out overall conclusions from these studies.

I'm pleased to point out a new meta-analysis of these controlled trials by Dr. Christopher Ramsden and colleagues (1). This paper finally cleans up the mess that previous meta-analyses have made of the diet-heart literature. One recent paper in particular by Dr. Dariush Mozaffarian and colleagues concluded that overall, the controlled trials show that replacing animal fat with linoleic acid (LA)-rich seed oils reduces heart attack risk (2). I disagreed strongly with their conclusion because I felt their methods were faulty (3).

Dr. Ramsden and colleagues pointed out several fundamental flaws in the review paper by Dr. Mozaffarian and colleagues, as well as in the prevailing interpretation of these studies in the scientific literature in general. These overlap with the concerns that I voiced in my post (4):

1. Omission of unfavorable studies, including the Rose corn oil trial and the Sydney diet-heart trial.
2. Inclusion of weak trials with major confounding variables, such as the Finnish mental hospital trial.
3. Failure to distinguish between omega-6 and omega-3 fatty acids.
4. Failure to acknowledge that seed oils often replaced large quantities of industrial trans fats in addition to animal fat in these trials.
   

Dr. Ramsden and colleagues accounted for all of these factors in their analysis, which has never been done before. They chose inclusion criteria* that made sense, and stuck with them. In addition, they did an impressive amount of historical work, digging up old unpublished data from these trials to determine the exact composition of the control and experimental diets. The paper is published in the British Journal of Nutrition, an excellent journal, and overall is written in a scientific and professional manner.

What did they find?

• Interventions that replaced animal and trans fat with seed oils that were rich in LA but low in omega-3 caused a non-significant trend toward increased heart attacks (13% increase) and overall mortality.
  
• Interventions that replaced animal and trans fat with a combination of LA and omega-3 fats significantly reduced heart attacks (by 22%). The numbers for total mortality followed a similar trend.

In other words, LA-rich seed oils do not prevent heart attacks (and may actually promote them), but correcting an omega-3 deficiency and reducing industrial trans fat intake may be protective. This is similar to what I've been saying for a while now, based on my own interpretation of the same studies and others. However, Dr. Ramsden and colleagues have taken the idea to a new level by their thorough and sophisticated detective work and analysis. For example, I didn't realize that in virtually all of these controlled trials, the intervention group reduced its trans fat intake substantially in addition to reducing animal fat. From the paper:

...experimental diets replaced common ‘hard’ margarines, industrial shortenings and other sources of [trans fat] in all seven of the [controlled trials] included in the meta-analysis by Mozaffarian et al. The mean estimated [trans fat] content of the seven control diets was 3·0 [% of calories] (range 1·5–9·6 [%]).
...the displacement of [trans fat], rather than the substitution of mixed n-3/n-6 [polyunsaturated fat] for [saturated fat], may account for some or all of the 22% reduction in non-fatal [heart attacks and heart attack] death in our meta-analysis. By contrast, the increased [heart attack] risks from n-6 specific [polyunsaturated fat] diets in our meta-analysis may be underestimated as n-6 [polyunsaturated fat] also replaced substantial quantities of [trans fat] (Table 3). The consistent trends towards increased [heart attack] risk of n-6 specific [polyunsaturated fat] diets may have become significant if the n-6 [polyunsaturated fat] replaced only [saturated fat], instead of a combination of [saturated fat] and [trans fat].

In other words, it looks like trans fat is probably the issue, not animal fat, but these trials replaced both simultaneously so we can't know for sure. I will note here that trans fat does not generally promote atherosclerosis (thickening and hardening of arteries) in animal models, so if it does truly increase heart attack risk as many studies suggest, it's probably through a mechanism that is independent of atherosclerosis.

The article also contains an excellent discussion of the Finnish mental hospital trial (5, 6) and why it was excluded from the meta-analysis, in which Dr. Ramsden and colleagues point out major design flaws, some of which I was not aware of. For example, trans fat intake was on average 13 times higher in the control groups than in the experimental groups. In addition, one of the control groups received more than twice as much of the antipsychotic drug thioridazine, which is known to be highly toxic to the heart, as any other group. Ouch. I'm glad to see this study finally discussed in an open and honest manner. I discussed my own problems with the Finnish trial in an earlier post (7).

I was also glad to see an open discussion of the Oslo Diet-heart study (8), in which diet changes led to a reduction in heart attack risk over five years. Dr. Mozaffarian and colleagues included it in their analysis as if it were a controlled trial in which animal fat was replaced by seed oils only. In reality, the investigators changed many variables at once, which I had also pointed out in my critique of Dr. Mozaffarian's meta-analysis (9). Here's what Dr. Ramsden and colleagues had to say about it:

First, experimental dieters were instructed to substitute fish, shellfish and ‘whale beef’ for meats and eggs, and were actually supplied with ‘considerable quantities of Norwegian sardines canned in cod liver oil, which proved to be popular as a bread spread’(32)... Second, the experimental group consumed massive amounts of soybean oil, which provided large quantities of both LA (15·6 en %) and ALA (2·7 en %). ALA consumption was about 4·5 times average US intake(42), or about twelve typical flax oil pills (1 g pill ¼ 560 mg ALA) per d. In addition, the fish and cod liver oil consumption provided Oslo (598N latitude) dieters with 610 IU (15·25 mg) of daily vitamin D3, recently linked to lower blood pressure, plaque stabilisation, and reduced [heart attack risk] (64). Furthermore, experimental dieters were encouraged to eat more nuts, fruits, and vegetables; to limit animal fats; and to restrict their intake of refined grains and sugar.

trans fat intake was also reduced substantially by excluding margarine in the experimental group. Other review papers have used this trial as a justification to replace animal fat with seed oils. Hmm... The only reason they get away with this is because the trial was published in 1966 and almost no one today has actually read it.

One criticism I have of Dr. Ramsden's paper is that they used the Oslo trial in their analysis, despite the major limitation described above. However, they were extremely open about it and discussed the problem in detail. Furthermore, the overall result would have been essentially the same even if they had excluded the Oslo trial from the analysis.

Overall, the paper is an excellent addition to the literature, and I hope it will bring a new level of sophistication to the dialogue on dietary prevention of cardiovascular disease. In the meantime, brace yourselves for an avalanche of criticism from the seed oil brigade.


* Guidelines that determine which studies to include in the analysis. For example, you want to exclude any study that wasn't randomized, because it will not be interpretable from a statistical standpoint. You also want to exclude trials where major variables differ between groups besides the specific variable you're trying to test. The Finnish mental hospital trial fails by both criteria.

Choline and Fatty Liver

I've been writing about non-alcoholic fatty liver disorder (NAFLD) since the early days of this blog, because it's an alarmingly common disorder (roughly a quarter of Americans affected) that is typically undiagnosed. It often progresses into its more serious cousin non-alcoholic steatohepatitis (NASH), an inflammatory condition that causes liver damage and can progress to cancer. In a number of previous posts, I pinpointed excess sugar and seed oil consumption as culprits in NAFLD and NASH (1, 2, 3, 4, 5).

Chris Masterjohn recently published two very informative posts on NAFLD/NASH that add a major additional factor to the equation: choline (6, 7). Choline is an essential nutrient that's required for the transport of fat out of the liver (8). NAFLD can be caused, and cured, simply by removing or adding dietary choline, and it appears to be dominant over other dietary factors including fat, sugar and alcohol. Apparently, certain researchers have been aware of this for some time, but it hasn't entered into the mainstream consciousness.

Could that be because the richest dietary sources are liver and eggs*? Choline is also found in smaller amounts in a variety of whole animal and plant foods. Most people don't get the officially recommended amount. From a recent review article (9):

Mean choline intakes for older children, men, women, and pregnant women are far below the adequate intake level established by the [Institute of Medicine]. Given the importance of choline in a wide range of critical functions in the human body, coupled with less-than-optimal intakes among the population, dietary guidance should be developed to encourage the intake of choline-rich foods.

I've dubbed beef liver the Most Nutritious Food in the World, Nature's Multivitamin, and I'll probably invent other titles for it in the future. Add yours to the comments. Learn to love liver! I think it's an excellent food to eat on a weekly basis.

Head over to Chris's blog and read about the classic studies he unearthed. And add The Daily Lipid to your RSS reader, because there's more interesting material to come!

The Sweet Truth about Liver and Egg Yolks
Does Choline Deficiency Contribute to Fatty Liver in Humans?


* For the brave: brain is actually the richest source of choline.

Predicting future demand for medical tourism: Health tourism blog is moving to IMTJ

To keep things simple, this blog is moving to the IMTJ web site. You can find the Health Tourism Blog here, in future.

Here's an extract of the latest blog post on "Predicting future demand for medical tourism".

The latest data on hospital activity within the UK National Health Service provides a useful indicator of where future demand for medical tourism may lie. One of the advantages of the UK public health system is that with one provider....the NHS, and one payor....the NHS it means that an enormous amount of meaningful data can be captured about the state of the nation’s health, about demand for health services and about how the health profile of the population is changing.

Like many developed countries with established health systems, the UK is facing the challenge of meeting the needs of an ageing population at a time when there is massive pressure to reduce or put a hold on public spending, and in effect reduce expenditure on health services. All UK hospitals collect data in the same way (well almost...) and the data is collected centrally by the NHS.

The following data is taken from the recent report “Hospital Episode Statistics: Admitted Patient Care – England 2009/10”, published by the NHS Information Centre.

Take a look at how demand for NHS hospital services has changed over the last ten years. First let’s examine the age profile of patients admitted to UK hospitals:

In 2009/10 there were:

• 16,806,200 hospital stays, a 38 per cent rise on 1999/2000.
• 1,939,190 stays for patients aged 0 to 14; a 15 per cent rise on 1999/2000.
• 7,333,110 stays for patients aged 15 to 59; a 29 per cent rise on 1999/2000.
• 3,642,940 stays for patients aged 60 to 74; a 48 per cent rise on 1999/2000.
• 3,837,990 stays for patients aged 75 and over, a 66 per cent rise on 1999/2000.

Read the full article at IMTJ: Go to "Predicting future demand for medical tourism".

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 160 mg/dL in a 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 clearance. 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 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 approaching the diabetic range!

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 (come on guys, you have to call me on this stuff!).

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.

Comparing the costs of (accidental) medical tourism

Whereas much of the attention in the medical travel sector is focused on medical tourism (i.e. where the primary reason for travel is some form of surgery or treatment), a more established and mature market sector is the provision of healthcare services for the tourist or business traveller who falls ill when abroad.

The structure and maturity of this sector means that it is far easier to gather comparative data such as the cost of healthcare and actual treatment in different countries. Cost management is in the hands of the international insurers, the travel insurance companies and the assistance companies who negotiate prices with hospital providers worldwide.A recent analysis of travel insurance claims, published by the UK based travel insurer, Sainsbury’s Travel Insurance, provides an insight into the variation in hospital costs across the world and the rising trend in hospital costs.

According to their analysis:

• In 2009, a record number of people needed medical treatment whilst abroad.
• The most expensive country for inpatient hospital treatment was the United States, with the average hospital visit costing £6,000.
• The average cost of hospital treatment in a foreign country has climbed to £2,040 over the last 12 months, an increase of 6.25% year-on-year.
• The most significant increase in treatment costs were seen in Turkey (+10%), the USA (+10%) and Spain (+7.5%).
• Over the summer months (May to September), the most common reason for hospitalisation was gastroenteritis with the average bill for inpatient treatment amounting to £1,200.
• The most expensive hospital bills were for those who suffered a heart attack abroad, resulting in medical expenses that averaged £12,500.

It’s interesting that the international assistance companies who deal with these "accidental" medical tourists have shown little or no interest in entering the medical tourism business. They have everything in place to become the world’s number one facilitator and blow everyone else out of the market:

• They have a network of “approved” hospitals around the world.
• They facilitate treatment for thousands of international patients in foreign countries every day.
• They have call centres to deal with patient enquiries.
• They have extensive technology and systems to manage the patient process.
• They have people on the ground in major destinations who can provide local support.
• They have comparative data on treatment outcomes and comparative costs in hospitals around the world.

So, why haven’t companies like Europ Assistance, Mondial Assistance and AXA Assistance entered the medical tourism market and used their expertise to attain a dominant market position?

The answer is probably quite simple. The medical tourism market is just not big enough to be attractive to them, nor worth the hassle. Which is good news for the existing operators...but puts the medical tourism market opportunity in perspective compared to the long established international assistance market.

The slumbering giant of medical travel?

Where do you think the international patients' centre shown above is? Singapore? Thailand? Malaysia? India? Korea?

Read on to find out...

This week’s International Medical Travel Journal covers a recent announcement by the UK Department of Health (See: Liberated UK hospitals to attract medical tourists) that it plans to remove the cap on the proportion of income that NHS hospitals can earn from private surgery. NHS hospitals are allowed to treat private patients (both domestic and international patients) in addition to their primary responsibility for serving the needs of the UK public.

Many NHS hospitals have private patient wards or dedicated units which benefit from their location close to the extensive clinical resources and medical technology which are available with an NHS general or teaching hospital. These are well supported by private patients but these NHS units have been restricted in terms of their revenue potential; across the UK, NHS hospitals were not allowed to generate more than 2% of their income from private paying patients. Some individual hospitals were allowed to generate a much greater proportion but were still limited in their revenue earning potential.

At medical tourism conferences around the world, the UK gets barely a mention. Yet it ranks in the top ten destination countries in terms of medical tourist numbers and probably in the top five in terms of revenue generated (Source: Team Tourism Consulting 2010). London continues to attract high value medical travellers seeking expertise and quality rather than the lowest prices. The average treatment cost for these patients is around £20,000, and for individual patients it can be much more. London also benefits significantly from the related expenditure of these medical travellers e.g. accommodation for friends and family during these extended patient stays.

Private patient facilities at leading London teaching hospitals such as Moorfields Eye Hospital, Great Ormond Street Children's Hospital, Royal Brompton & Harefield Hospitals, Kings College Hospital, Royal Marsden Hospital, and Guy’s & St Thomas’ Hospital have always been attractive to international patients and they compete with other international centres of excellence in countries such as the USA and Germany . Indeed, these NHS private patient facilities earn more from international private patients (medical tourists) than they do from UK private patients.

The Harris International Patient Centre at Great Ormond Street (pictured above) is a good example. The Centre has 130 staff, working with over 170 clinicians in Great Ormond Street Children's Hospital. It’s bigger than most international patient departments serving “medical tourists” that you would find anywhere in the world. And it’s very busy. But, until now Great Ormond Street and similar NHS run international patient facilities have been limited by the private patient income cap.

That is about to change... London “the slumbering giant of medical travel” may wake up to some of the newly emerging opportunities presented by the international patient market:

• The London hospitals mentioned above have a long and impressive track record in attracting international patients.


• They were involved in medical tourism long before the term was invented.


• And they are able to provide quality and prices that will be attractive to many emerging source markets for medical travel. For example, if US derived medical tourism does eventually take off, and American patients can make significant savings by travelling to London for major surgery (not far short of those available in Singapore or Thailand), would London be an attractive option? Same language (...almost), same culture (...almost).

This American who travelled to Wales for surgery may be the start of a growing trend....

Change in UK regulations may reduce infertility tourism

One factor that can affect any aspect of medical travel and medical tourism is that the market sector can be a victim of its own success. Constantine Constantinides has highlighted this previously in his IMTJ article “Medical Tourism and the West's Revenge”, arguing that in effect the success of medical travel is self limiting.

How can this success be self limiting?

Where overseas treatment becomes an attractive option for patients, domestic providers and governments may react to this trend by becoming more competitive (e.g. by reducing prices for local treatment) or by removing the causes and drivers for medical travel (e.g. by changing local regualtion of a treatment). Thus, the more patients travel abroad for treatment, the greater will be the reaction within the domestic market and a “balance of trade” will be reached.

An excellent example of this phenomenon is this week’s announcement by the Human Fertilisation and Embryology Authority (HFEA) that it intends to conduct a consultation over changes to the rules governing egg and sperm donation in the UK. There has been a significant shortage of egg and sperm donors in the UK due to the restrictions on the payments that can be made to donors. The £250 maximum "compensation" payment for both men and women donors has meant that demand for donor eggs and sperm has far exceeded supply. Waiting lists can be as long as two to three years for those patients eligible for NHS treatment.

The removal of donor anonymity has also been a contributing factor to the reluctance of donors to come forward. According to the most recent HFEA statistics (2008), only 1,184 women donated eggs and there were only 396 new sperm donors in 2008. Around 2,000 babies a year are born in the UK using donated eggs, sperm or embryos. As a result, we have seen an increasing number of UK couples seeking infertility treatment abroad; it has been one of the fastest growing areas of medical tourism. (For the background see “New research paper provides insight into infertility tourism”). The response from the HFEA to the increasing number of infertile couples going abroad is therefore to consider how to reduce this ...... by increasing the payments and incentives to egg and sperm donors, AND thus increasing the supply of eggs and sperm. Payments may increase to £1,000 plus.

It’s unlikely that the changes will have any immediate effect on the market sector. No decisions will be made until the end of the HFEA public consultation next year. The three-month public consultation will not start until January 2011 and the HFEA is expected to be subsumed into the UK’s Care Quality Commission as a result of the UK public expenditure cuts. But there’s a clear warning here for those involved in medical tourism businesses and the medical travel sector. Don’t put all of your eggs in one basket..... Or more seriously, be aware that any segment of the medical tourism market may be limited by its own success when domestic providers and governments seek to reverse the trend.