Tuesday, November 30, 2010
The Committee was asked to review current data and make a
5 Servings Fruits and Vegetables a Day
10 Minutes of Silence or Relaxation a Day
30 Body Mass Index below 30
150 Minutes of Exercise a week
You knew this already...but are you really doing it?
Monday, November 29, 2010
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.
Sunday, November 28, 2010
Monday, November 22, 2010
Overturning ACA would cause 32 million Americans
Sunday, November 21, 2010
We don't know if more patients age 45-64 are getting
Saturday, November 20, 2010
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?
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.
Friday, November 19, 2010
We know that most hypertension diagnoses have no etiology (cause). We also know that in the U.S. escherichia coli
Thursday, November 18, 2010
#1 - Actinic Keratosis - these dry crusty bumps are on sun damaged skin and can be either flat or raised in appearance. They occur after long periods of sun exposure and damage. They are not life threatening and can be treated with
Tuesday, November 16, 2010
I spent last weekend at the Weston A. Price Foundation Wise Traditions conference in King of Prussia, PA. Here are some highlights:
Spending time with several people in the diet-health community who I’ve been wanting to meet in person, including Chris Masterjohn, Melissa McEwen and John Durant. John and Melissa are the public face of the New York city paleo movement. The four of us spent most of the weekend together tossing around ideas and making merry. I’ve been corresponding with Chris quite a bit lately and we’ve been thinking through some important diet-health questions together. He is brimming with good ideas. I also got to meet Sally Fallon Morell, the founder and president of the WAPF.
Attending talks. The highlight was Chris Masterjohn’s talk “Heart Disease and Molecular Degeneration: the New Paradigm”, in which he described his compelling theory on oxidative damage and cardiovascular disease, among other things. You can read some of his earlier ideas on the subject here. Another talk I really enjoyed was by Anore Jones, who lived with an isolated Inuit group in Alaska for 23 years and ate a mostly traditional hunter-gatherer diet. The food and preparation techniques they used were really interesting, including various techniques for extracting fats and preserving meats, berries and greens by fermentation. Jones has published books on the subject that I suspect would be very interesting, including Nauriat Niginaqtuat, Plants that We Eat, and Iqaluich Niginaqtuat, Fish that We Eat. The latter is freely available on the web here.
I attended a speech by Joel Salatin, the prolific Virginia farmer, writer and agricultural innovator, which was fun. I enjoyed Sally Fallon Morell’s talk on US school lunches and the politics surrounding them. I also attended a talk on food politics by Judith McGeary, a farmer, attorney and and activist, in which she described the reasons to oppose or modify senate bill 510. The gist is that it will be disproportionately hard on small farmers who are already disfavored by current regulations, making high quality food more difficult to obtain, more expensive or even illegal. It’s designed to improve food safety by targeting sources of food-borne pathogens, but how much are we going to have to cripple national food quality and farmer livelihood to achieve this, and will it even be effective? I don’t remember which speaker said this quote, and I’m paraphrasing, but it stuck with me: “I just want to be able to eat the same food my grandmother ate.” In 2010, that’s already difficult to achieve. Will it be impossible in 2030?
Giving my own talk. I thought it went well, although attendance was not as high as I had hoped. The talk was titled “Kakana Dina: Diet and Health in the Pacific Islands”, and in it I examined the relationship between diet and health in Pacific island cultures with different diets and at various stages of modernization. I’ve covered some of this material on my blog, in my posts on Kitava, Tokelau and sweet potato eating cultures in New Guinea, but other material was new and I went into greater detail on food habits and preparation methods. I also dug up a number of historical photos dating back as far as the 1870s.
The food. All the meat was pasture-raised, organic and locally sourced if possible. There was raw pasture-raised cheese, milk and butter. There was wild-caught fish. There were many fermented foods, including sauerkraut, kombucha and sourdough bread. I was really impressed that they were able to put this together for an entire conference.
The vendors. There was an assortment of wholesome and traditional foods, particularly fermented foods, quality dairy and pastured meats. There was an entire farmer’s market on-site on Saturday, with a number of Mennonite vendors selling traditional foods. I bought a bottle of beet kvass, a traditional Russian drink used for flavor and medicine, which was much better than the beet kvass I’ve made myself in the past. Beets are a remarkable food, in part due to their high nitrate content—beet juice has been shown to reduce high blood pressure substantially, possibly by increasing the important signaling molecule nitric oxide. I got to meet Sandeep Agarwal and his family, owners of the company Pure Indian Foods, which domestically produces top-quality pasture-fed ghee (Indian-style clarified butter). They now make tasty spiced ghee in addition to the plain flavor. Sandeep and family donated ghee for the big dinner on Saturday, which was used to cook delicious wild-caught salmon steaks donated by Vital Choice.
There were some elements of the conference that were not to my taste. But overall I’m glad I was able to go, meet some interesting people, give my talk and learn a thing or two.
Each year 30% of people age 65 or older fall and sustain serious injuries so preventing falls and fractures is important. Vitamin D prevents both falls and fractures, but mega doses of
Sunday, November 14, 2010
One way to have a lot of fun on the internet and get a
Thursday, November 11, 2010
Making healthy food choices can be tough during the holidays, especially at gatherings where festive snacks abound But who says holiday snacks
Tuesday, November 9, 2010
I've received several e-mails from readers about a recent experiment by nutrition professor Mark Haub at Kansas State university (thanks to Josh and others). He ate a calorie-restricted diet in which 2/3 of his calories came from junk food: Twinkies, Hostess and Little Debbie cakes, Dorito corn chips and sweetened cereals (1). On this calorie-restricted junk food diet (800 calorie/day deficit), he lost 27 pounds in two months.
Therefore, junk food doesn't cause fat gain and the only thing that determines body fatness is how much you eat and exercise. Right?
Let's start with a few things most people can agree on. If you don't eat any food at all, you will lose fat mass. If you voluntarily force-feed yourself with a large excess of food, you will gain fat mass, whether the excess comes from carbohydrate or fat (2). So calories obviously have something to do with fat mass.
But of course, the situation is much more subtle in real life. Since a pound of body fat contains roughly 3,500 calories, eating an excess of 80 calories per day (1 piece of toast) should lead to a weight gain of 8 lbs of fat per year. Conversely, if you're distracted and forget to eat your toast, you should lose 8 lbs of fat per year, which would eventually be dangerous for a lean person. That's why we all record every crumb of food we eat, determine its exact calorie content, and match that intake precisely with our energy expenditure to maintain a stable weight.
Oh wait, we don't do that? Then how do so many people maintain a stable weight over years and decades? And how do wild animals maintain a stable body fat percentage (except when preparing for hibernation) even in the face of food surpluses? How do lab rats and mice fed a whole food diet maintain a stable body fat percentage in the face of literally unlimited food, when they're in a small cage with practically nothing to do but eat?
The answer is that the body isn't stupid. Over hundreds of millions of years, we've evolved sophisticated systems that maintain "energy homeostasis". In other words, these systems act to regulate fat mass and keep it within the optimal range. The evolutionary pressures operating here are obvious: too little fat mass, and an organism will be susceptible to starvation; too much, and an organism will be less agile and less efficient at locomotion and reproduction. Energy homeostasis is such a basic part of survival that even the simplest organisms regulate it.
Not only is it clear that we have an energy homeostasis system, we even know a thing or two about how it works. Early studies showed that lesioning a part of the brain called the ventromedial hypothalamus causes massive obesity (3; this is also true in humans, when a disruption results from cancer). Investigators also discovered several genetic mutations in rats and mice that result in massive obesity*. Decades-long research eventually demonstrated that these models have something in common: they all interfere with an energy homeostasis circuit that passes information about fat mass to the hypothalamus via the hormone leptin.
The leptin system is a classic negative feedback loop: the more fat mass accumulates, the more leptin is produced. The more leptin is produced, the more the hypothalamus activates programs to reduce hunger and increase energy expenditure, which continues until fat mass is back in the optimal range. Conversely, low fat mass and low leptin lead to increased hunger and energy conservation by this same pathway**.
So if genetic mutants can become massively obese, I guess that argues against the idea that voluntary food intake and energy expenditure are the only determinants of fat mass. But a skeptic might point out that these are extreme cases, and such mutations are so rare in humans that the analogy is irrelevant.
Let's dig deeper. There are many studies in which rodents are made obese using industrial high-fat diets made from refined ingredients. The rats eat more calories (at least in the beginning), and gain fat rapidly. No big surprise there. But what may come as a surprise to the calorie counters is that rodents on these diets gain body fat even if their calorie intake is matched precisely to lean rodents eating a whole food diet (4, 5, 6). In fact, they sometimes gain almost as much fat as rodents who are allowed to eat all the industrial food they want. This has been demonstrated repeatedly.
How is this possible? The answer is that the calorie-matched rats reduce their energy expenditure to a greater degree than those that are allowed free access to food. The most logical explanation for this behavior is that the "set point" of the energy homeostasis system has changed. The industrial diet causes the rodents' bodies to "want" to accumulate more fat, therefore they will accomplish that by any means necessary, whether it means eating more, or if that's not possible, expending less energy. This shows that a poor diet can, in principle, dysregulate the system that controls energy homeostasis.
Well, then why did Dr. Haub's diet allow him to lose weight? The body can only maintain body composition in the face of a calorie deficit up to a certain point. After that, it has no choice but to lower fat mass. It will do so reluctantly, at the same time increasing hunger, and reducing lean mass***, muscular strength and energy dedicated to tissue repair and immune function. However, I hope everyone can agree that a sufficient calorie deficit can lead to fat loss regardless of what kind of food is eaten. Dr. Haub's 800 calorie deficit qualifies. I think only a very small percentage of people are capable of maintaining that kind of calorie deficit for more than a few months, because it is mentally and physically difficult to fight against what the hypothalamus has decided is in your best interest.
My hypothesis is that, in many people, industrial food and an unnatural lifestyle lead to gradual fat gain by dysregulating the energy homeostasis system. This "breaks" the system that's designed to automatically keep our fat mass in the optimal range by regulating energy intake, energy expenditure and the relative partitioning of energy resources between lean and fat tissue. This system is not under our conscious control, and it has nothing to do with willpower.
I suspect that if you put a group of children on this junk food diet for many years, and compared them to a group of children on a healthy diet, the junk food group would end up fatter as adults. This would be true if neither group paid any attention to calories, and perhaps even if calorie intake were identical in the two groups (as in the rodent example). The result of Dr. Haub's experiment does not contradict that hypothesis.
So do calories matter? Yes, but in a healthy person, all the math is done automatically by the hypothalamus and energy balance requires no conscious effort. In 2010, many people have already accumulated excess fat mass. How that may be sustainably lost is another question entirely, and a more challenging one in my opinion. As they say, an ounce of prevention is worth a pound of cure. There are many possible strategies, with varying degrees of efficacy that depend highly on individual differences, but I think overall the question is still open. I discussed some of my thoughts in a recent series on body fat regulation (7, 8, 9, 10, 11).
* ob/ob and db/db mice. Zucker and Koletsky rats. Equivalent mutations in humans also result in obesity.
** Via an increase in muscular efficiency and perhaps a decrease in basal metabolism. Thyroid hormone activity drops.
*** Loss of muscle, bone and connective tissue can be compensated for by strength training during calorie restriction. Presumed loss of other non-adipose tissues (liver, kidney, brain, etc.) is probably not affected by strength training.
Monday, November 8, 2010
The reasons are not that hard to understand. Medicine has become a complex and difficult business. Dealing with dozens of different insurance
Thursday, November 4, 2010
Wednesday, November 3, 2010
1. Atrophic candidiasis
3. lingual thyroid
4. Median rhomboid glossitis
5. Tertiary syphillis
Tuesday, November 2, 2010
The internet is a wonderful place to get medical information when and how you want it. You may not be interested in the topic of "Coumadin" until you or a family member is prescribed the drug. What does it mean when your father tells you his doctor wants to do a "laparoscopy" or that your mother has a "venous thrombosis"? It is important to get your medical information from a reputable source