This is a simplified summary of the last two posts.
Polyunsaturated fats in the diet are mostly omega-6 or omega-3. These get converted into a diverse and influential class of signaling molecules in the body called eicosanoids. On their way to becoming eicosanoids, they get elongated. These elongated versions can be measured in tissue, and the higher the proportion of elongated omega-6 in the total pool, the higher the risk of a heart attack.
Eicosanoids are either omega-6 or omega-3-derived. Omega-6 eicosanoids, in general, are very potent and participate in inflammatory processes and blood clotting. Omega-3 eicosanoids are less potent, less inflammatory, less clot-forming, and participate in long-term repair processes. This is a simplification, as there are exceptions, but in a broad sense seems to be true.
In the modern U.S. and most other affluent nations, we eat so much omega-6 (mostly in the form of liquid industrial vegetable oils), and so little omega-3, that we create a very inflammatory and pro-clotting environment, probably contributing to a number of chronic diseases including cardiovascular disease.
There are two ways to stay in balance: reduce omega-6, and increase omega-3. In my opinion, the former is more important than the latter, but only if you can reduce omega-6 to below 4% of calories. If you're above 4%, the only way to reduce your risk is to outcompete the omega-6 with additional omega-3. Keeping omega-6 below 4% and ensuring a modest but regular intake of omega-3, such as from wild-caught fish, will probably substantially reduce the risk of cardiovascular disease and other chronic illnesses.
Bottom line: ditch industrial vegetable oils such as corn, soybean, safflower and sunflower oil, and everything that contains them. This includes most processed foods, especially mayonnaise, grocery store salad dressings, and fried foods. We aren't meant to eat those foods and they derail our metabolism on a fundamental level. I also believe it's a good idea to have a regular source of omega-3, whether it comes from seafood, small doses of cod liver oil, or small doses of flax.
Sunday, May 31, 2009
Friday, May 29, 2009
Awards Banquet
The Global Health Council's 2009 Awards Banquet was held last night. As an insider, it was amazing to see how everything has come together to create such a huge gathering of people from around the world. As I stood by the front doors I was shocked to look around at everything in the Regency ballroom - the decorations, the sheer numbers of chairs and tables, and the enormous stage - it all came crashing down upon me. A staff of 45 people organized an event so gigantic and so important. It was amazing!!
After ushering people in to their seats, helping them if they did not know where they were supposed to be seated, I was able to sit down for dinner and enjoy the awards banquet. I sat and discussed global health with others at my table, and listened in quiet awe of the award winners. The work they have done has made such tangible and enormous impact around the world and in their home countries. Dr. Douglas Gwatidzo spoke emotionally of those who he believed were more deserving of the award he received, (The Jonathan Mann Award for Health and Human Rights) and of those who made his work and that of others possible. He has worked tirelessly to help beleaguered colleagues in Zimbabwe's collapsed health sector; and has provided medical and legal documentation and care for victims of state torture in Zimbabwe. His defiance of Robert Mugabe's policies and actions is inspiring and amazing. I had tears in my eyes.
The Award for Best Practices in Global Health was presented to Dr. Harshad Sanghvi, whose work in Kenya, Indonesia, Nepal and Afghanistan focuses on providing post-partem hemorrhaging medicines to women and midwives in rural areas that have no access to doctors. In his speech, he discussed the role that we all play in helping the world to be a better place, saying, "We create change because the current situation regarding the very high mortality and morbidity in developing nations, combined with the inequity in access to health care between poor and rich people is just not acceptable in civilized nations." I don't think anyone could have said what we do, and what we aim to do, better than he did.
And finally, the Gates Award for Global Health was awarded to the London School of Hygiene and Tropical Medicine for the more than 100 years of education and awareness that they have provided to thousands of graduates in more than 140 countries around the world. Truly a global organization, The London School of Hygiene and Tropical Medicine was recognized for its dedication to combating tropical diseases and improving hygiene in the world, and for its off campus program in which students around the world can become educated without having to study in London. The one million dollar grant awarded by the Bill & Melinda Gates foundation will help to improve their ability to educate and create change around the world.
It was an amazing evening, and as an intern, it was frankly humbling and inspiring to see all these amazing individuals all around and to hear such stories of bravery and selflessness. Music was provided by the amazing band, Nation Beat, an outfit of musicians from the Southern United States and Brazil. It was fun music, great food, and inspiration all around as the evening came to an end!
- Geoff Calver
After ushering people in to their seats, helping them if they did not know where they were supposed to be seated, I was able to sit down for dinner and enjoy the awards banquet. I sat and discussed global health with others at my table, and listened in quiet awe of the award winners. The work they have done has made such tangible and enormous impact around the world and in their home countries. Dr. Douglas Gwatidzo spoke emotionally of those who he believed were more deserving of the award he received, (The Jonathan Mann Award for Health and Human Rights) and of those who made his work and that of others possible. He has worked tirelessly to help beleaguered colleagues in Zimbabwe's collapsed health sector; and has provided medical and legal documentation and care for victims of state torture in Zimbabwe. His defiance of Robert Mugabe's policies and actions is inspiring and amazing. I had tears in my eyes.
The Award for Best Practices in Global Health was presented to Dr. Harshad Sanghvi, whose work in Kenya, Indonesia, Nepal and Afghanistan focuses on providing post-partem hemorrhaging medicines to women and midwives in rural areas that have no access to doctors. In his speech, he discussed the role that we all play in helping the world to be a better place, saying, "We create change because the current situation regarding the very high mortality and morbidity in developing nations, combined with the inequity in access to health care between poor and rich people is just not acceptable in civilized nations." I don't think anyone could have said what we do, and what we aim to do, better than he did.
And finally, the Gates Award for Global Health was awarded to the London School of Hygiene and Tropical Medicine for the more than 100 years of education and awareness that they have provided to thousands of graduates in more than 140 countries around the world. Truly a global organization, The London School of Hygiene and Tropical Medicine was recognized for its dedication to combating tropical diseases and improving hygiene in the world, and for its off campus program in which students around the world can become educated without having to study in London. The one million dollar grant awarded by the Bill & Melinda Gates foundation will help to improve their ability to educate and create change around the world.
It was an amazing evening, and as an intern, it was frankly humbling and inspiring to see all these amazing individuals all around and to hear such stories of bravery and selflessness. Music was provided by the amazing band, Nation Beat, an outfit of musicians from the Southern United States and Brazil. It was fun music, great food, and inspiration all around as the evening came to an end!
- Geoff Calver
Thursday, May 28, 2009
Poster session
Everyone come see the New Investigators poster session today! 2:15 in the Blue Room. Tea will be served.
(I had mine yesterday, so I can freely promote my colleagues without being accused of self-aggrandizement)
(I had mine yesterday, so I can freely promote my colleagues without being accused of self-aggrandizement)
Pay No Mind to the Gap
Hans Rosling gave a great talk this morning. The website he founded (along with his son and daughter-in-law) is called Gapminder, which presumably refers to the gap between developed and developing countries.
Ironically, the thrust of his talk was about how we shouldn't be minding the gap so much. He showed how there's no clear division between "developed" and "developing" --- how mixed the countries of the world are in life expectancy, infant mortality, income, HIV infection. It's clearly more of a continuum.
He's a great speaker, and I see his point. But I do think most people who work in global health already understand it. The terms "developing" and "developed" are not perfect, but we need some kind of language to describe the differences between countries. I prefer Low, Middle, and High income myself.
Whatever language we choose, we're inevitably going to divide the world into categories in order to understand it. What Dr. Rosling didn't do today was propose an alternative set of categories.
Maybe that will be his talk next year.....
Ironically, the thrust of his talk was about how we shouldn't be minding the gap so much. He showed how there's no clear division between "developed" and "developing" --- how mixed the countries of the world are in life expectancy, infant mortality, income, HIV infection. It's clearly more of a continuum.
He's a great speaker, and I see his point. But I do think most people who work in global health already understand it. The terms "developing" and "developed" are not perfect, but we need some kind of language to describe the differences between countries. I prefer Low, Middle, and High income myself.
Whatever language we choose, we're inevitably going to divide the world into categories in order to understand it. What Dr. Rosling didn't do today was propose an alternative set of categories.
Maybe that will be his talk next year.....
Wednesday, May 27, 2009
Eicosanoids and Ischemic Heart Disease, Part II
Here's where it gets more complicated and more interesting. The ratio of omega-6 to omega-3 matters, but so does the total amount of each. This is a graph from a 1992 paper by Dr. Lands:
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.
On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that an effective way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that an effective way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Tweeting At The Conference
Twitter is all the rage. A social networking site that allows users to post short messages of 140 characters or less on the web from the comfort of their computers or phones, it has grown exponentially this year, and is now a tool in use at our 2009 conference.
Conference attendees have been posting tweets (the vocabulary for a post on twitter), marked with the "hashtag" #GHC36 so that we can track comments related to the conference, and it has been a resounding success. Hundreds of tweets already, and hundreds more to come! The tweets comment on everything from landing at the airport and DC to being excited about the conference, to thoughts and commentary on all aspects of the conference.
And I was extremely excited today to set up twitter for use in our opening plenary session. The plenary, Tranformations: Discovering New Strategies Using Proven Technologies, focused on the use of mobile devices to transform the way that global health is implemented worldwide. I met with Cyrus Favriar, the moderator, who is a freelance journalist with frequent articles on NPR, the CBC, and more. We briefly discussed the idea of using twitter to ask questions at the plenary, and set it up so that a unique hashtag, #GHCp1, would be used to direct questions from mobile devices. Not only was it amazing to see it in use, but it was amazing to see the effect of mobile devices upon communication in this manner. While the panelists were discussing the use of mobile devices in global health, they were receiving questions on twitter via the same means.
It was a great opportunity for me to set up a new technology for use at our conference, and it was amazing to see it in action. Twitter is a new phenomenon, an internet creation that is a fine example of how technology can enhance and aid everything from large conferences to global health.
- Geoff Calver
Tuesday, May 26, 2009
Can You Hear It?
IntraHealth International hosted a rockin' Tuesday eve party today, for a cause I completely believe in: Open Source. They had a contest where musical groups from all over the world recut, remixed, rearranged, and re-produced the same song. The winner was a group from West Africa called Studio Mali. Since the decision was made last night, the winners couldn't be on hand to receive their prize. But we all got to listen to some good music. The bolder among us even got out there and danced!
(By "bolder among us" I mean "someone other than me.")
(By "bolder among us" I mean "someone other than me.")
The Gist of GIS
I went to a session on Geographic Information Systems, or GIS, this morning. (It occurs to me now, the name conveys absolutely nothing about what GIS is and does...but that's the subject of a different blog post). A very knowledgable guy named Dan De Vries ran the workshop. We used a program called Arc Explorer, which is one of about ten different free programs for mapping health data.
It was a useful session, and a powerful technology. But it's funny how quickly things change. Ten or fifteen years ago, the combination of GPS (the technique for getting latitude and longitudinal coordinates of a site) and GIS (taking those coordinates and layering them on a map) was seen as a powerful new tool for epidemiologists. And it still is. But today it's also a powerful tool for fourth graders.
How did something once so specialized become so universally available. As with so much else: Google.
Google Earth is basically a very user-friendly GIS. It may not have the statistical power of EpiInfo or Arc Explorer, but it allows lay people (and when it comes to epidemiology, I include myself in that category) participate in creating maps and layering data on them.
Does this mean epidemiologists will cease to exist? Obviously not. Access to technology is not the same as knowing how to use it correctly and effectively. Which is why I was in that session today --- to nudge myself slightly from the category "lay person" toward the category "expert."
It was a useful session, and a powerful technology. But it's funny how quickly things change. Ten or fifteen years ago, the combination of GPS (the technique for getting latitude and longitudinal coordinates of a site) and GIS (taking those coordinates and layering them on a map) was seen as a powerful new tool for epidemiologists. And it still is. But today it's also a powerful tool for fourth graders.
How did something once so specialized become so universally available. As with so much else: Google.
Google Earth is basically a very user-friendly GIS. It may not have the statistical power of EpiInfo or Arc Explorer, but it allows lay people (and when it comes to epidemiology, I include myself in that category) participate in creating maps and layering data on them.
Does this mean epidemiologists will cease to exist? Obviously not. Access to technology is not the same as knowing how to use it correctly and effectively. Which is why I was in that session today --- to nudge myself slightly from the category "lay person" toward the category "expert."
Chronicling The Global Health Council's 2009 Conference on Flickr
Flickr is a powerful and amazing website dedicated to sharing photography with the world. Recently, we used Flickr as an outlet for photographer's to post their contributions to our 2009 Photo Contest. Receiving contributions from around the world, our photo contest pooled together wonderful photography that could be shared with people in every corner of the globe.
We are once again using Flickr to highlight photography from this year's Global Health Council Conference. While we have a professional photographer on site who will be chronicling the events of the conference, we would love to have contributions from attendees as well! So, if you have a camera and are snapping photos while at the conference, feel free to join our group and contribute!
The group can be found here: http://www.flickr.com/groups/conference2009/
Instructions for posting and joining the group can be found on the group site. We are looking forward to seeing your photos and sharing our own as well!
- Geoff Calver
Monday, May 25, 2009
Landing on Shoreham
Hi there folks. Just thought I would drop a quick blog post. I'm really excited to be here, looking forward to sharing experiences here in D.C.
A few words about me: I'm a second-year resident in internal medicine at Montefiore Hospital in the Bronx. I spent a year in Kenya doing research on HIV and --- hope you're not eating --- helminths, which are parasites that usually live in the GI tract and are related to tapeworms. I've also done research in Mali and DRC Congo, and traveled in Asia and South America.
Since the conference hasn't started just yet, there's not much to blog about. Stay tuned....
A few words about me: I'm a second-year resident in internal medicine at Montefiore Hospital in the Bronx. I spent a year in Kenya doing research on HIV and --- hope you're not eating --- helminths, which are parasites that usually live in the GI tract and are related to tapeworms. I've also done research in Mali and DRC Congo, and traveled in Asia and South America.
Since the conference hasn't started just yet, there's not much to blog about. Stay tuned....
All a-Twitter
Dr. Gwatidzo, Jonathan Mann Award recipient, having just arrived from Zimbabwe.
The Omni Shoreham Hotel is abuzz with excitement as the the Global Health Council's 36th Annual Conference gets underway. With tote bags stuffed and registration packets at the ready, the Council's board and staff are looking forward to welcoming some 2,000 participants to this yearly event.
This year's conference, which highlights technology, also introduces a few new techological features to the conference. For example, the presenter abstracts are now available on CD. We are also integrating social media, which, in most cases, can be accessed through mobile devices. Find us on Facebook, post your photos to our Flickr pool, and keep tabs on Twitter. In fact, Twitter is already atwitter (pun intended) with plans for the #GHC36 (also known as conference) @GlobalHealthorg. IntraHealth's team, in particular, has been really active about preparations for their various events - all of which sound very exciting. Tomorrow, we launch the blogosphere on http://www.globalhealthconference.org/, which highlights our official conference bloggers.
Our day began at 5:30 this morning with an early morning cab ride to the airport with Dawn Carey, awards coordinator, to meet Dr. Douglas Gwatidzo, chairperson of the Zimbabwe Association of Doctors for Human Rights (ZADHR) and 2009 recipient of the Jonathan Mann Award for Health and Human Rights. Though he had just emerged from a 24-hour journey from Harare, Dr. Gwatidzo showed no sign of weariness and was eager to discuss Zimbabwe with us - the hospital with no running water, the state of the medical community, the positive signs that are slowly emerging, using soccer as a bridge between people... But wait until the awards banquet, where he is sure to wow us all with his speech. He is quite eloquent.
Dr. Gwatidzo discussing Zimbabwe in the cab.
If you don't have a banquet ticket yet, there are still tickets available at the registration desk. If you have a ticket already, make sure and stop by Will Call (where I'll be stationed for most of the day) to pick a seat. Today is, perhaps, the best day to pick-up your registration materials so you can spend the rest of the evening pouring through the final program and posting the sessions you think are interesting on Twitter.
NOTE: Over breakfast, we got word that Dr. Binayak Sen, the imprisoned 2008 Jonathan Mann Award winner, was granted bail by the Supreme Court of India.
- Tina Flores
Sunday, May 24, 2009
Eicosanoids and Ischemic Heart Disease
Dr. William Lands, one of the pioneers of the eicosanoid field, compiled this graph. It may be the single most important clue we have about the relationship between diet and ischemic heart disease (heart attacks).To explain it fully, we have to take a few steps back. Dietary polyunsaturated fatty acids (PUFA) are primarily omega-6 and omega-3. This is a chemical designation that refers to the position of a double bond along the fatty acid's carbon chain. Omega-6 fats are found abundantly in industrial vegetable oils (corn, soybean, sunflower, cottonseed, etc.) and certain nuts, and in lesser amounts in meats, dairy and grains. Omega-3 fats are found abundantly in seafood and a few seeds such as flax and walnuts, and in smaller amounts in meats, green vegetables and dairy.
The body uses a multi-step process to convert omega-3 and omega-6 fats into eicosanoids, which are a diverse and potent class of signaling molecules. The first step is to convert PUFA into highly unsaturated fatty acids, or HUFA. These include arachidonic acid (AA), an omega-6 HUFA, eicosapentaenoic acid (EPA), an omega-3 HUFA, and several others in the 20- to 22-carbon length range.
HUFA are stored in cell membranes and they are the direct precursors of eicosanoids. When the cell needs eicosanoids, it liberates HUFA from the membrane and converts it. The proportion of omega-6 to omega-3 HUFA in the membrane is proportional to the long-term proportion of omega-6 and omega-3 in the diet. Enzymes do not discriminate between omega-6 and omega-3 HUFA when they create eicosanoids. Therefore, the proportion of omega-6- to omega-3-derived eicosanoids is proportional to dietary intake.
Omega-6 eicosanoids are potently inflammatory and thrombotic (promote blood clotting, such as thromboxane A2), while omega-3 eicosanoids are less inflammatory, less thrombotic and participate in long-term repair processes.
Many of the studies that have looked at the relationship between HUFA and heart attacks used blood plasma (serum lipids). Dr. Lands has pointed out that plasma HUFA do not accurately reflect dietary omega-6/3 balance, and they don't correlate well with heart attack risk. What does correlate strikingly well with both dietary intake and heart attack risk is the proportion of omega-6 HUFA in tissue, which reflects the amount contained in cell membranes. That's what we're looking at in the graph above: the proportion of omega-6 HUFA in the total tissue HUFA pool, vs. coronary heart disease death rate.
You can see that the correlation is striking, both between populations and within them. Greenland Inuit have the lowest proportion of omega-6 HUFA, due to a low intake of omega-6 and an exceptionally high intake of seafood. They also have an extraordinarily low risk of heart attack death. The red dots are from the Multiple Risk Factor Intervention Trial (MRFIT), which I'll be covering in a bit more detail in a later post. They're important because they confirm that the trend holds true within a population, and not just between populations.
In the next post, I'll be delving into this concept in more detail, and explaining why it's not just the ratio that matters, but also the total intake of omega-6. I'll also be providing more evidence to support the theory.
Friday, May 22, 2009
Eicosanoids, Fatty Liver and Insulin Resistance
I have to take a brief intermission from the heart disease series to write about a very important paper I just read in the journal Obesity, "COX-2-mediated Inflammation in Fat is Crucial for Obesity-linked Insulin Resistance and Fatty Liver". It's actually related to cardiovascular disease, although indirectly.
First, some background. Polyunsaturated fatty acids (PUFA) come mostly from omega-6 and omega-3 sources. Omega-6 and omega-3 are precursors to eicosanoids, a large and poorly understood class of signaling molecules that play a role in basically everything. Eicosanoids are either omega-6-derived or omega-3-derived. Omega-6 and omega-3 compete for the enzymes that convert PUFA into eicosanoids. Therefore, the ratio of omega-6 to omega-3 in tissues (related to the ratio in the diet) determines the ratio of omega-6-derived eicosanoids to omega-3-derived eicosanoids.
Omega-6 eicosanoids are very potent and play a central role in inflammation. They aren't "bad", in fact they're essential, but an excess of them is probably not good. Omega-3 eicosanoids are generally less potent, less inflammatory, and tend to participate in long-term repair processes. So in sum, the ratio of omega-6 to omega-3 in the diet will determine the potency and quality of eicosanoid signaling, which will determine an animal's susceptibility to inflammation-mediated disorders.
One of the key enzymes in the pathway from PUFA to eicosanoids (specifically, a subset of them called prostanoids) is cyclooxygenase (COX). COX-1 is expressed all the time and serves a "housekeeping" function, while COX-2 is induced by cellular stressors and contributes to the the formation of inflammatory eicosanoids. Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen inhibit COX enzymes, which is why they are effective against inflammatory problems like pain and fever. They are also used as a preventive measure against cardiovascular disease. Basically, they reduce the excessive inflammatory signaling promoted by a diet with a poor omega-6:3 balance. You wouldn't need to inhibit COX if it were producing the proper balance of eicosanoids to begin with.
Dr. Kuang-Chung Shih's group at the Department of Internal Medicine in Taipei placed rats on five different diets:
Rats in group 2 not only gained weight, they also experienced increased fasting glucose, leptin, insulin, triglycerides, blood pressure and a massive decline in insulin sensitivity (seven-fold relative to group 1). Rats in groups 3 and 4 gained weight, but saw much less of a deterioration in insulin and leptin sensitivity, and blood pressure. Group 2 also developed fatty liver, which was attenuated in groups 3 and 4. If you're interested, group 5 (energy restricted high-fat) was similar to groups 3 and 4 on pretty much everything, including insulin sensitivity.
So there you have it folks: direct evidence that insulin resistance, leptin resistance, high blood pressure and fatty liver are mediated by excessive inflammatory eicosanoid signaling. I wrote about something similar before when I reviewed a paper showing that fish oil reverses many of the consequences of a high-vegetable oil, high-sugar diet in rats. I also reviewed two papers showing that in pigs and rats, a high omega-6:3 ratio promotes inflammation (mediated by COX-2) and lipid peroxidation in the heart. Are you going to quench the fire by taking drugs, or by reducing your intake of omega-6 and ensuring an adequate intake of omega-3?
*Of course, they didn't mention the sucrose in the methods section. I had to go digging around for the diet's composition. This is typical of papers on "high-fat diets". They load them up with sugar, and blame everything on the fat.
**Rats gain fat mass when fed a high-fat diet (even if it's not loaded with sugar). But humans don't necessarily gain weight on a high-fat diet (i.e. low-carb weight loss diet). What's the difference? Low-carbohydrate diet trials indicate that humans spontaneously reduce their caloric intake when eating low carbohydrate, high-fat food.
First, some background. Polyunsaturated fatty acids (PUFA) come mostly from omega-6 and omega-3 sources. Omega-6 and omega-3 are precursors to eicosanoids, a large and poorly understood class of signaling molecules that play a role in basically everything. Eicosanoids are either omega-6-derived or omega-3-derived. Omega-6 and omega-3 compete for the enzymes that convert PUFA into eicosanoids. Therefore, the ratio of omega-6 to omega-3 in tissues (related to the ratio in the diet) determines the ratio of omega-6-derived eicosanoids to omega-3-derived eicosanoids.
Omega-6 eicosanoids are very potent and play a central role in inflammation. They aren't "bad", in fact they're essential, but an excess of them is probably not good. Omega-3 eicosanoids are generally less potent, less inflammatory, and tend to participate in long-term repair processes. So in sum, the ratio of omega-6 to omega-3 in the diet will determine the potency and quality of eicosanoid signaling, which will determine an animal's susceptibility to inflammation-mediated disorders.
One of the key enzymes in the pathway from PUFA to eicosanoids (specifically, a subset of them called prostanoids) is cyclooxygenase (COX). COX-1 is expressed all the time and serves a "housekeeping" function, while COX-2 is induced by cellular stressors and contributes to the the formation of inflammatory eicosanoids. Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen inhibit COX enzymes, which is why they are effective against inflammatory problems like pain and fever. They are also used as a preventive measure against cardiovascular disease. Basically, they reduce the excessive inflammatory signaling promoted by a diet with a poor omega-6:3 balance. You wouldn't need to inhibit COX if it were producing the proper balance of eicosanoids to begin with.
Dr. Kuang-Chung Shih's group at the Department of Internal Medicine in Taipei placed rats on five different diets:
- A control diet, eating normal low-fat rat chow.
- A "high-fat diet", in which 45% of calories came from a combination of industrial lard and soybean oil, and 17% of calories came from sucrose*.
- A "high-fat diet" (same as above), plus the COX-2 inhibitor celecoxib (Celebrex).
- A "high-fat diet" (same as above), plus the COX-2 inhibitor mesulid.
- An energy-restricted "high-fat diet".
Rats in group 2 not only gained weight, they also experienced increased fasting glucose, leptin, insulin, triglycerides, blood pressure and a massive decline in insulin sensitivity (seven-fold relative to group 1). Rats in groups 3 and 4 gained weight, but saw much less of a deterioration in insulin and leptin sensitivity, and blood pressure. Group 2 also developed fatty liver, which was attenuated in groups 3 and 4. If you're interested, group 5 (energy restricted high-fat) was similar to groups 3 and 4 on pretty much everything, including insulin sensitivity.
So there you have it folks: direct evidence that insulin resistance, leptin resistance, high blood pressure and fatty liver are mediated by excessive inflammatory eicosanoid signaling. I wrote about something similar before when I reviewed a paper showing that fish oil reverses many of the consequences of a high-vegetable oil, high-sugar diet in rats. I also reviewed two papers showing that in pigs and rats, a high omega-6:3 ratio promotes inflammation (mediated by COX-2) and lipid peroxidation in the heart. Are you going to quench the fire by taking drugs, or by reducing your intake of omega-6 and ensuring an adequate intake of omega-3?
*Of course, they didn't mention the sucrose in the methods section. I had to go digging around for the diet's composition. This is typical of papers on "high-fat diets". They load them up with sugar, and blame everything on the fat.
**Rats gain fat mass when fed a high-fat diet (even if it's not loaded with sugar). But humans don't necessarily gain weight on a high-fat diet (i.e. low-carb weight loss diet). What's the difference? Low-carbohydrate diet trials indicate that humans spontaneously reduce their caloric intake when eating low carbohydrate, high-fat food.
Tuesday, May 19, 2009
The Coronary Heart Disease Epidemic: Possible Culprits Part II
In the last post, I reviewed some of the factors that I believe could have contributed to the epidemic of heart attacks that began in the 1920s and 1930s in the U.S. and U.K., and continues today. I ended on smoking, which appears to be a major player. But even smoking is clearly trumped by another factor or combination of factors, judging by the unusually low incidence of heart attacks in France, Japan and on Kitava.
One of the major changes in diet that I didn't mention in the last post was the rise of industrial liquid vegetable oils over the course of the 20th century. In the U.S. in 1900, the primary cooking fats were lard, beef tallow and butter. The following data only include cooking fats and spreads, because the USDA does not track the fats that naturally occur in milk and meat (source):
Animal fat is off the hook. This is the type of information that makes mainstream nutrition advice ring hollow. Let's see what happened to industrial vegetable oils in the early 1900s:
I do believe we're getting warmer. Now let's consider the composition of traditional American animal fats and industrial vegetable oils:
It's not hard to see that the two classes of fats (animal and industrial vegetable) are quite different. Animal fats are more saturated (blue). However, the biggest difference is that industrial vegetable oils contain a massive amount of omega-6 (yellow), far more than animal fats. If you accept that humans evolved eating primarily animal fats, which is well supported by the archaeological and anthropological literature, then you can begin to see the nature of the problem.
Omega-6 and omega-3 fats are polyunsaturated fatty acids that are precursors to a very important class of signaling molecules called eicosanoids, which have a hand in virtually every bodily process. Omega-6 and omega-3 fats compete with one another for the enzymes (desaturases and elongases) that convert them into eicosanoid precursors. Omega-6-derived eicosanoids and omega-3-derived eicosanoids have different functions. Therefore, the balance of omega-6 to omega-3 fats in the diet influences the function of the body on virtually every level. Omega-6 eicosanoids tend to be more inflammatory, although the eicosanoid system is extraordinarily complex and poorly understood.
What's better understood is the fact that our current omega-6 consumption is well outside of our ecological niche. In other words, we evolved in an environment that did not provide large amounts of omega-6 all year round. Industrial vegetable oils are a product of food processing techniques that have been widespread for about 100 years, not enough time for even the slightest genetic adaptation. Our current level of omega-6 intake, and our current balance between omega-6 and omega-3, are therefore unnatural.
The ideal ratio is probably very roughly 2:1 omega-6:omega-3. Leaf lard is 6.8, beef tallow is 2.4, good quality butter is 1.4, corn oil is 45, cottonseed oil is 260. It's clear that a large qualitative change in our fat consumption occurred over the course of the 20th century.
I believe this was a major factor in the rise of heart attacks from an obscure condition to the primary cause of death. I'll be reviewing the data that convinced me in the next few posts.
The Coronary Heart Disease Epidemic
The Coronary Heart Disease Epidemic: Possible Culprits Part I
The Omega Ratio
A Practical Approach to Omega Fats
Polyunsaturated Fat Intake: Effects on the Heart and Brain
Polyunsaturated Fat Intake: What About Humans?
Vegetable Oil and Homicide
One of the major changes in diet that I didn't mention in the last post was the rise of industrial liquid vegetable oils over the course of the 20th century. In the U.S. in 1900, the primary cooking fats were lard, beef tallow and butter. The following data only include cooking fats and spreads, because the USDA does not track the fats that naturally occur in milk and meat (source):
Animal fat is off the hook. This is the type of information that makes mainstream nutrition advice ring hollow. Let's see what happened to industrial vegetable oils in the early 1900s:
I do believe we're getting warmer. Now let's consider the composition of traditional American animal fats and industrial vegetable oils:
It's not hard to see that the two classes of fats (animal and industrial vegetable) are quite different. Animal fats are more saturated (blue). However, the biggest difference is that industrial vegetable oils contain a massive amount of omega-6 (yellow), far more than animal fats. If you accept that humans evolved eating primarily animal fats, which is well supported by the archaeological and anthropological literature, then you can begin to see the nature of the problem.Omega-6 and omega-3 fats are polyunsaturated fatty acids that are precursors to a very important class of signaling molecules called eicosanoids, which have a hand in virtually every bodily process. Omega-6 and omega-3 fats compete with one another for the enzymes (desaturases and elongases) that convert them into eicosanoid precursors. Omega-6-derived eicosanoids and omega-3-derived eicosanoids have different functions. Therefore, the balance of omega-6 to omega-3 fats in the diet influences the function of the body on virtually every level. Omega-6 eicosanoids tend to be more inflammatory, although the eicosanoid system is extraordinarily complex and poorly understood.
What's better understood is the fact that our current omega-6 consumption is well outside of our ecological niche. In other words, we evolved in an environment that did not provide large amounts of omega-6 all year round. Industrial vegetable oils are a product of food processing techniques that have been widespread for about 100 years, not enough time for even the slightest genetic adaptation. Our current level of omega-6 intake, and our current balance between omega-6 and omega-3, are therefore unnatural.
The ideal ratio is probably very roughly 2:1 omega-6:omega-3. Leaf lard is 6.8, beef tallow is 2.4, good quality butter is 1.4, corn oil is 45, cottonseed oil is 260. It's clear that a large qualitative change in our fat consumption occurred over the course of the 20th century. I believe this was a major factor in the rise of heart attacks from an obscure condition to the primary cause of death. I'll be reviewing the data that convinced me in the next few posts.
The Coronary Heart Disease Epidemic
The Coronary Heart Disease Epidemic: Possible Culprits Part I
The Omega Ratio
A Practical Approach to Omega Fats
Polyunsaturated Fat Intake: Effects on the Heart and Brain
Polyunsaturated Fat Intake: What About Humans?
Vegetable Oil and Homicide
Saturday, May 16, 2009
Mere Rain Cannot Extinguish the Flame of Candlelight Memorial in Haiti
The opening ceremony of the 2009 International AIDS Candlelight Memorial on May 16 in front of the spectacular ruins of Sans Souci Palace in Milot, Haiti was rained out but was still a great success when it was moved to nearby Cap Haitïen, to a dinner following the event that had already been scheduled.
The festivities started when Haitian Prime Minister Michele Duvivier Pierre-Louis arrived at Cap Haitïen Airport in the afternoon and drove to Milot, about 12 kilometers away. She appeared before an enthusiastic crowd of local people at an event promoting the importance of getting tested for HIV. The rains started just before the opening ceremony and, when the rains had continued for over an hour, the program was moved to the dinner in Cap Haitien.
Abbott Fund, one of the donors of the Candlelight Memorial, announced that it was donating 500,000 rapid HIV test kits as the kick-off of a nationwide HIV testing campaign. The testing initiative is a cooperative partnership between the Haitian government, the U.S. government, the Abbott Fund and Haitian health implementing organizations.
The candle-lighting ceremony took place after the dinner, when Prime Minister Pierre-Louis and representatives of the two sponsors of the event — Vice President Kathryn Guare of the Global Health Council and Dr. Myrna Eustache of Promoteurs Objectif Zero Sida (POZ) www.pozsida.org/ — joined people living with HIV and AIDS to light the candles to remember those lost to AIDS, to advocate for improved programs and policies and to celebrate the courage of Haitians living with the disease.
The festivities started when Haitian Prime Minister Michele Duvivier Pierre-Louis arrived at Cap Haitïen Airport in the afternoon and drove to Milot, about 12 kilometers away. She appeared before an enthusiastic crowd of local people at an event promoting the importance of getting tested for HIV. The rains started just before the opening ceremony and, when the rains had continued for over an hour, the program was moved to the dinner in Cap Haitien.
Abbott Fund, one of the donors of the Candlelight Memorial, announced that it was donating 500,000 rapid HIV test kits as the kick-off of a nationwide HIV testing campaign. The testing initiative is a cooperative partnership between the Haitian government, the U.S. government, the Abbott Fund and Haitian health implementing organizations.
The candle-lighting ceremony took place after the dinner, when Prime Minister Pierre-Louis and representatives of the two sponsors of the event — Vice President Kathryn Guare of the Global Health Council and Dr. Myrna Eustache of Promoteurs Objectif Zero Sida (POZ) www.pozsida.org/ — joined people living with HIV and AIDS to light the candles to remember those lost to AIDS, to advocate for improved programs and policies and to celebrate the courage of Haitians living with the disease.
The Coronary Heart Disease Epidemic: Possible Culprits Part I
In the last post, I reviewed two studies that suggested heart attacks were rare in the U.K. until the 1920s -1930s. In this post, I'll be discussing some of the diet and lifestyle factors that preceded and associated with the coronary heart disease epidemic in the U.K and U.S. I've cherry picked factors that I believe could have played a causal role. Many things changed during that time period, and I don't want to give the impression that I have "the answer". I'm simply presenting ideas for thought and discussion.
First on the list: sugar. Here's a graph of refined sugar consumption in the U.K. from 1815 to 1955, from the book The Saccharine Disease, by Dr. T. L. Cleave. Sugar consumption increased dramatically in the U.K. over this time period, reaching near-modern levels by the turn of the century, and continuing to increase after that except during the wars:
Here's a graph of total sweetener consumption in the U.S. from 1909 to 2005 (source: USDA food supply database). Between 1909 and 1922, sweetener consumption increased by 40%:
If we assume a 10 to 20 year lag period, sugar is well placed to play a role in the CHD epidemic. Sugar is easy to pick on. An excess causes a number of detrimental changes in animal models and human subjects, including fatty liver, the metabolic syndrome, and small, oxidized low-density lipoprotein particles (LDL). Small and oxidized LDL associate strongly with cardiovascular disease risk and may be involved in causing it. These effects seem to be mostly attributable to the fructose portion of sugar, which is 50% of table sugar (sucrose), about 50% of most naturally sweet foods, and 55% of the most common form of high-fructose corn syrup. That explains why starches, which break down into glucose (another type of sugar), don't have the same negative effects as table sugar and HFCS.
Hydrogenated fat is the next suspect. I don't have any graphs to present, because no one has systematically tracked hydrogenated fat consumption in the U.S. or U.K. to my knowledge. However, it was first marketed in the U.S. by Procter & Gamble under the brand name Crisco in 1911. Crisco stands for "crystallized cottonseed oil", and involves taking an industrial waste oil (from cotton seeds) and chemically treating it using high temperature, a nickel catalyst and hydrogen gas (see this post for more information). Hydrogenated fats for human consumption hit markets in the U.K. around 1920. Here's what Dr. Robert Finlayson had to say about margarine in his paper "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982":
The next factor is vitamin D. When the industrial revolution became widespread in the late 19th century, people moved into crowded, polluted cities and vitamin D deficiency became rampant. Rickets was a scourge that affected more than half of children in some places. Dr. Edward Mellanby discovered that it's caused by severe vitamin D deficiency, milk was fortified with vitamin D2, and rickets was all but eliminated. However, it only takes a very small amount of vitamin D to avoid rickets, an amount that will not contribute significantly to optimum vitamin D status. Vitamin D modulates the body's inflammatory response, it's ability to resist calcium deposition in the arteries, and seems to be important for so many things I had to include it.
The rise of cigarettes was a major change that probably contributed massively to the CHD epidemic. They were introduced just after the turn of the century in the U.S. and U.K., and rapidly became fashionable (source):
If you look at the second to last graph from the previous post, you can see that there's a striking correspondence between cigarette consumption and CHD deaths in the U.K. In fact, if you moved the line representing cigarette consumption to the right by about 20 years, it would overlap almost perfectly with CHD deaths. The risk of heart attack is so strongly associated with smoking in observational studies that even I believe it probably represents a causal relationship. There's no doubt in my mind that smoking cigarettes contributes to the risk of heart attack and various other health problems.
Smoking is a powerful factor, but it doesn't explain everything. How is it that the Kitavans of Papua New Guinea, more than 3/4 of whom smoke cigarettes, have an undetectable incidence of heart attack and stroke? Why do the French and the Japanese, who smoke like chimneys (at least until recently), have the two lowest heart attack death rates of all the affluent nations? There's clearly another factor involved that trumps cigarette smoke. I have a guess, which I'll expand on in the next few posts.
First on the list: sugar. Here's a graph of refined sugar consumption in the U.K. from 1815 to 1955, from the book The Saccharine Disease, by Dr. T. L. Cleave. Sugar consumption increased dramatically in the U.K. over this time period, reaching near-modern levels by the turn of the century, and continuing to increase after that except during the wars:
Here's a graph of total sweetener consumption in the U.S. from 1909 to 2005 (source: USDA food supply database). Between 1909 and 1922, sweetener consumption increased by 40%:
If we assume a 10 to 20 year lag period, sugar is well placed to play a role in the CHD epidemic. Sugar is easy to pick on. An excess causes a number of detrimental changes in animal models and human subjects, including fatty liver, the metabolic syndrome, and small, oxidized low-density lipoprotein particles (LDL). Small and oxidized LDL associate strongly with cardiovascular disease risk and may be involved in causing it. These effects seem to be mostly attributable to the fructose portion of sugar, which is 50% of table sugar (sucrose), about 50% of most naturally sweet foods, and 55% of the most common form of high-fructose corn syrup. That explains why starches, which break down into glucose (another type of sugar), don't have the same negative effects as table sugar and HFCS. Hydrogenated fat is the next suspect. I don't have any graphs to present, because no one has systematically tracked hydrogenated fat consumption in the U.S. or U.K. to my knowledge. However, it was first marketed in the U.S. by Procter & Gamble under the brand name Crisco in 1911. Crisco stands for "crystallized cottonseed oil", and involves taking an industrial waste oil (from cotton seeds) and chemically treating it using high temperature, a nickel catalyst and hydrogen gas (see this post for more information). Hydrogenated fats for human consumption hit markets in the U.K. around 1920. Here's what Dr. Robert Finlayson had to say about margarine in his paper "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982":
...between 1909-13 and 1924-28, margarine consumption showed the highest percentage increase, whilst that of eggs only increased slightly and that of butter remained unchanged. Between 1928 and 1934, margarine consumption fell by one-third, while butter consumption increased by 57 percent: and increase that coincided with a fall of 48 percent in its price. Subsequently, margarine sales have burgeoned, and if one is correct in stating that the coronary heart disease epidemic started in the second decade of this century, then the concept of hydrogenated margarines as an important aetiological factor, so strongly advocated by Martin, may merit more consideration than hitherto.Partially hydrogenated oils contain trans fat, which is truly new to the human diet, with the exception of small amounts found in ruminant fats including butter. But for the most part, natural trans fats are not the same as industrial trans fats, and in fact some of them, such as conjugated linoleic acid (CLA), may be beneficial. To my knowledge, no one has discovered health benefits of industrial trans fats. To the contrary, compared to butter, they shrink LDL size. They also inhibit enzymes that the body uses to make a diverse class of signaling compounds known as eicosanoids. Trans fat consumption associates very strongly with the risk of heart attack in observational studies. Which is ironic, because hydrogenated fats were originally marketed as a healthier alternative to animal fats. The Center for Science in the Public Interest shamed McDonald's into switching the beef tallow in their deep friers for hydrogenated vegetable fats in the 1990s. In 2009, even the staunchest opponents of animal fats have to admit that they're healthier than hydrogenated fat.
The next factor is vitamin D. When the industrial revolution became widespread in the late 19th century, people moved into crowded, polluted cities and vitamin D deficiency became rampant. Rickets was a scourge that affected more than half of children in some places. Dr. Edward Mellanby discovered that it's caused by severe vitamin D deficiency, milk was fortified with vitamin D2, and rickets was all but eliminated. However, it only takes a very small amount of vitamin D to avoid rickets, an amount that will not contribute significantly to optimum vitamin D status. Vitamin D modulates the body's inflammatory response, it's ability to resist calcium deposition in the arteries, and seems to be important for so many things I had to include it.
The rise of cigarettes was a major change that probably contributed massively to the CHD epidemic. They were introduced just after the turn of the century in the U.S. and U.K., and rapidly became fashionable (source):
If you look at the second to last graph from the previous post, you can see that there's a striking correspondence between cigarette consumption and CHD deaths in the U.K. In fact, if you moved the line representing cigarette consumption to the right by about 20 years, it would overlap almost perfectly with CHD deaths. The risk of heart attack is so strongly associated with smoking in observational studies that even I believe it probably represents a causal relationship. There's no doubt in my mind that smoking cigarettes contributes to the risk of heart attack and various other health problems. Smoking is a powerful factor, but it doesn't explain everything. How is it that the Kitavans of Papua New Guinea, more than 3/4 of whom smoke cigarettes, have an undetectable incidence of heart attack and stroke? Why do the French and the Japanese, who smoke like chimneys (at least until recently), have the two lowest heart attack death rates of all the affluent nations? There's clearly another factor involved that trumps cigarette smoke. I have a guess, which I'll expand on in the next few posts.
Global Health Council and POZ Prepare for AIDS Candlelight Memorial Event
Five members of the Global Health Council are on the ground in northern Haiti preparing furiously for tonight’s grand opening ceremony of the 2009 International AIDS Candlelight Memorial in Milot in front of the Sans Souci Palace, a World Heritage site and the former home of King Henri Christophe between 1804 and 1820.
The Council’s main partner in organizing the event is POZ, Promoteurs Objectif Zéro Sida, a leading Haitian non-governmental organization that provides prevention and counseling services around the country. But many other governmental and non-governmental organizations are also very involved in bringing needed attention to HIV/AIDS and Haiti’s success in dealing with it.
The Council chose Haiti as the site of the opening ceremony of the world’s oldest and premier AIDS awareness raising event principally because of Haiti’s recent progress against HIV/AIDS, particularly in urban areas, and because of POZ’s outstanding record as a country coordinator of the annual event in Haiti over the last 10 years.
The activities begin this afternoon with a march that will include thousands of Haitians and culminate in a symbolic lighting of the candle this evening with a spectacularly lit Sans Souci Palace as the backdrop. Many other activities are being held today leading up to the opening ceremony including HIV counseling and testing, which also serves as the kick-off for a national testing campaign aiming to increase significantly the number of Haitians who know their HIV status.
Friday, May 15, 2009
The 2009 International AIDS Candlelight Memorial
The 2009 International AIDS Candlelight Memorial drew thousands of people to more than 1,000 memorials in 100 countries. The Global Health Council, along with the Promoteurs Objectif Zero Sida, hosted the 26th annual International AIDS Candlelight Memorial Opening Ceremony in Cap Haitian, Haiti on May 16, 2009. The Candlelight Memorial began in 1983 in San Francisco and has since spread throughout the world.
Bound by the theme of “Together, We Are The Solution,” the Candlelight Memorial reinforces our dedication to the cause of HIV/AIDS prevention and education. The Opening Ceremony highlighted Haiti's progress despite its challenges, and promoted the critical partnership between government and civil society worldwide. The event will began with a march through the town of Milot, just outside of Cap Haitian, and ended with the ceremony and lighting of the official candle.
Kathryn Guare, vice president of member resources, and David Olson, policy communications director at the Global Health Council, share their experiences of the events leading up to the opening ceremony and the event itself.
Saturday, May 16: Preparing for Candlelight
Sunday, May 17: The Candlelight Memorial
Bound by the theme of “Together, We Are The Solution,” the Candlelight Memorial reinforces our dedication to the cause of HIV/AIDS prevention and education. The Opening Ceremony highlighted Haiti's progress despite its challenges, and promoted the critical partnership between government and civil society worldwide. The event will began with a march through the town of Milot, just outside of Cap Haitian, and ended with the ceremony and lighting of the official candle.
Kathryn Guare, vice president of member resources, and David Olson, policy communications director at the Global Health Council, share their experiences of the events leading up to the opening ceremony and the event itself.
Saturday, May 16: Preparing for Candlelight
Sunday, May 17: The Candlelight Memorial
Tuesday, May 12, 2009
The Coronary Heart Disease Epidemic
Few people alive today are old enough to remember the beginning of the coronary heart disease (CHD) epidemic in the 1920s and 1930s, when physicians in the U.S. and U.K. began sounding alarm bells that an uncommon disease was rapidly becoming the leading cause of death. By the 1950s, their predictions had come true. A decade later, a new generation of physicians replaced their predecessors and began to doubt that heart attacks had ever been rare. Gradually, the idea that the disease was once uncommon faded from the public consciousness, and heart attacks were seen as an eternal plague of humankind, avoided only by dying of something else first.
According to U.S. National Vital Statistics records beginning in 1900, CHD was rarely given as the cause of death by physicians until after 1930. The following graph is from The Great Cholesterol Con, by Anthony Colpo, which I highly recommend.
The relevant line for CHD deaths begins in the lower left-hand part of the graph. Other types of heart disease, such as heart failure due to cardiomyopathy, were fairly common and well recognized at the time. These data are highly susceptible to bias because they depend on the physician's perception of the cause of death, and are not adjusted for the mean age of the population. In other words, if a diagnosis of CHD wasn't "popular" in 1920, its prevalence could have been underestimated. The invention of new technologies such as the electrocardiogram facilitated diagnosis. Changes in diagnostic criteria also affected the data; you can see them as discontinuities in 1948, 1968 and 1979. For these reasons, the trend above isn't a serious challenge to the idea that CHD has always been a common cause of death in humans who reach a certain age.
This idea was weakened in 1951 with the publication of a paper in the Lancet medical journal titled "Recent History of Coronary Disease", by Dr. Jerry N. Morris. Dr. Morris sifted through the autopsy records of London Hospital and recorded the frequency of coronary thrombosis (artery blockage in the heart) and myocardial infarction (MI; loss of oxygen to the heart muscle) over the period 1907-1949. MI is the technical term for a heart attack, and it can be caused by coronary thrombosis. Europe has a long history of autopsy study, and London Hospital had a long-standing policy of routine autopsies during which they kept detailed records of the state of the heart and coronary arteries. Here's what he found:
The dashed line is the relevant one. This is a massive increase in the prevalence of CHD death that cannot be explained by changes in average lifespan. Although the average lifespan increased considerably over that time period, most of the increase was due to reduced infant mortality. The graph only includes autopsies performed on people 35-70 years old. Life expectancy at age 35 changed by less than 10 years over the same time period. The other possible source of bias is in the diagnosis. Physicians may have been less likely to search for signs of MI when the diagnosis was not "popular". Morris addresses this in the paper:
The solid line is MI mortality. Striking, isn't it? The other lines are tobacco and cigarette consumption. These data are not age-adjusted, but if you look at the raw data tables provided in the paper, some of which are grouped by age, it's clear that average lifespan doesn't explain much of the change. Heart attacks are largely an occurrence of the last 80 years, and were almost totally unknown before the turn of the 20th century.
What caused the epidemic? Both Drs. Morris and Finlayson also collected data on the prevalence of atherosclerosis (plaques in the arteries) over the same time period. Dr. Morris concluded that the prevalence of severe atherosclerosis had decreased by about 50% (although mild atherosclerosis such as fatty streaks had increased), while Dr. Finlayson found that it had remained approximately the same:
He found the same trend in females. This casts doubt on the idea that coronary atherosclerosis is sufficient in and of itself to cause heart attacks, although modern studies have found a strong association between advanced atherosclerosis and the risk of heart attack on an individual level. Heart attacks are caused by several factors, one of which is atherosclerosis. Atherosclerosis can be caused by infectious disease, so this may explain Dr. Morris's finding that it has decreased since the beginning of the 20th century.
What changes in diet and lifestyle associated with the explosion of MI in the U.K. and U.S. after 1920? Dr. Finlayson has given us a hint in the graph above: cigarette consumption increased dramatically over the same time period, and closely paralleled MI mortality. Smoking cigarettes is very strongly associated with heart attacks in observational studies. Animal studies also support the theory. While I believe cigarettes are an aggravating factor, I do not believe they are the main cause of the MI epidemic. Dr. Finlayson touched on a few other factors in the text of the paper, and of course I have my own two cents to add. I'll discuss that next time.
According to U.S. National Vital Statistics records beginning in 1900, CHD was rarely given as the cause of death by physicians until after 1930. The following graph is from The Great Cholesterol Con, by Anthony Colpo, which I highly recommend.
The relevant line for CHD deaths begins in the lower left-hand part of the graph. Other types of heart disease, such as heart failure due to cardiomyopathy, were fairly common and well recognized at the time. These data are highly susceptible to bias because they depend on the physician's perception of the cause of death, and are not adjusted for the mean age of the population. In other words, if a diagnosis of CHD wasn't "popular" in 1920, its prevalence could have been underestimated. The invention of new technologies such as the electrocardiogram facilitated diagnosis. Changes in diagnostic criteria also affected the data; you can see them as discontinuities in 1948, 1968 and 1979. For these reasons, the trend above isn't a serious challenge to the idea that CHD has always been a common cause of death in humans who reach a certain age.
This idea was weakened in 1951 with the publication of a paper in the Lancet medical journal titled "Recent History of Coronary Disease", by Dr. Jerry N. Morris. Dr. Morris sifted through the autopsy records of London Hospital and recorded the frequency of coronary thrombosis (artery blockage in the heart) and myocardial infarction (MI; loss of oxygen to the heart muscle) over the period 1907-1949. MI is the technical term for a heart attack, and it can be caused by coronary thrombosis. Europe has a long history of autopsy study, and London Hospital had a long-standing policy of routine autopsies during which they kept detailed records of the state of the heart and coronary arteries. Here's what he found:
The dashed line is the relevant one. This is a massive increase in the prevalence of CHD death that cannot be explained by changes in average lifespan. Although the average lifespan increased considerably over that time period, most of the increase was due to reduced infant mortality. The graph only includes autopsies performed on people 35-70 years old. Life expectancy at age 35 changed by less than 10 years over the same time period. The other possible source of bias is in the diagnosis. Physicians may have been less likely to search for signs of MI when the diagnosis was not "popular". Morris addresses this in the paper:
The first possibility, of course, is that the increase is not real but merely reflects better post-mortem diagnosis. This is an unlikely explanation. There is abundant evidence throughout the forty years that the department was fully aware of the relation of infarction to thrombosis, of myocardial fibrosis to gradual occlusion, and of the topical pathology of ostial stenosis and infarction from embolism, as indeed were many pathologists last century... But what makes figures like these important is that, unlike other series of this kind, they are based on the routine examination at necropsy of the myocardium and of the coronary arteries over the whole period. Moreover Prof. H. M. Turnbull, director of the department, was making a special case of atheroma and arterial disease in general during 1907-1914 (Turnbull 1915). The possibility that cases were overlooked is therefore small, and the earlier material is as likely to be reliable as the later.Dr. Morris's study was followed by another similar one published in 1985 in the journal Medical History, titled "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982", conducted by Dr. Robert Finlayson. This study, in my opinion, is the coup de grace. Finlayson systematically scrutinized autopsy reports from St. Bartholemew's hospital, which had conducted routine and detailed cardiac autopsies since 1868, and applied modern diagnostic criteria to the records. He also compared the records from St. Bartholemew's to those from the city mortuary. Here's what he found:
The solid line is MI mortality. Striking, isn't it? The other lines are tobacco and cigarette consumption. These data are not age-adjusted, but if you look at the raw data tables provided in the paper, some of which are grouped by age, it's clear that average lifespan doesn't explain much of the change. Heart attacks are largely an occurrence of the last 80 years, and were almost totally unknown before the turn of the 20th century.
What caused the epidemic? Both Drs. Morris and Finlayson also collected data on the prevalence of atherosclerosis (plaques in the arteries) over the same time period. Dr. Morris concluded that the prevalence of severe atherosclerosis had decreased by about 50% (although mild atherosclerosis such as fatty streaks had increased), while Dr. Finlayson found that it had remained approximately the same:
He found the same trend in females. This casts doubt on the idea that coronary atherosclerosis is sufficient in and of itself to cause heart attacks, although modern studies have found a strong association between advanced atherosclerosis and the risk of heart attack on an individual level. Heart attacks are caused by several factors, one of which is atherosclerosis. Atherosclerosis can be caused by infectious disease, so this may explain Dr. Morris's finding that it has decreased since the beginning of the 20th century.
What changes in diet and lifestyle associated with the explosion of MI in the U.K. and U.S. after 1920? Dr. Finlayson has given us a hint in the graph above: cigarette consumption increased dramatically over the same time period, and closely paralleled MI mortality. Smoking cigarettes is very strongly associated with heart attacks in observational studies. Animal studies also support the theory. While I believe cigarettes are an aggravating factor, I do not believe they are the main cause of the MI epidemic. Dr. Finlayson touched on a few other factors in the text of the paper, and of course I have my own two cents to add. I'll discuss that next time.
Thursday, May 7, 2009
Dihydro-Vitamin K1
Step right up ladies and gents; I have a new miracle vitamin for you. Totally unknown to our ignorant pre-industrial ancestors, it's called dihydro-vitamin K1. It's formed during the oil hydrogenation process, so the richest sources are hydrogenated fats like margarine, shortening and commercial deep fry oil. Some of its benefits may include:
This could be another mechanism by which industrially processed vegetable oils degrade health. It's also another example of why it's not a good idea to chemically alter food. We don't understand food, or our bodies, well enough to know the long-term consequences of foods that have been recently introduced to the human diet. I believe these foods should be avoided on principle.
- Inhibiting vitamin K2 metabolism
- Reducing bone mineral density
- Causing organ damage and inhibiting platelet formation in animal models
- Dramatically increasing the death rate of spontaneously hypertensive rats
This could be another mechanism by which industrially processed vegetable oils degrade health. It's also another example of why it's not a good idea to chemically alter food. We don't understand food, or our bodies, well enough to know the long-term consequences of foods that have been recently introduced to the human diet. I believe these foods should be avoided on principle.
Monday, May 4, 2009
Pastured Eggs
Eggs are an exceptionally nutritious food. It's not surprising, considering they contain everything necessary to build a chick! But all eggs are not created equal. Anyone who has seen the tall, orange yolk, viscous white, and tough shell of a true pastured egg knows they're profoundly different. So has anyone who's tasted one. This has been vigorously denied by the American Egg Board and the Egg Nutrition Council, primarily representing conventional egg farmers, which assert that eggs from giant smelly barns are nutritionally equal to their pastured counterparts.
In 2007, the magazine Mother Earth News decided to test that claim. They sent for pastured eggs from 14 farms around the U.S., tested them for a number of nutrients, and compared them to the figures listed in the USDA Nutrient Database for conventional eggs. Here are the results per 100 grams for conventional eggs, the average of all the pastured eggs, and eggs from Skagit River Ranch, which sells at my farmer's market:
Vitamin A:
Looks like the American Egg Board and the Egg Nutrition Council have some egg on their faces...
Eggs also contain vitamin K2, with the amount varying substantially according to the hen's diet. Guess where the A, D, K2, beta-carotene and omega-3 fatty acids are? In the yolk of course. Throwing the yolk away turns this powerhouse into a bland, nutritionally unimpressive food.
It's important to note that "free range" supermarket eggs are nutritionally similar to conventional eggs. The reason pastured eggs are so nutritious is that the chickens get to supplement their diets with abundant fresh plants and insects. Having little doors on the side of a giant smelly barn just doesn't replicate that.
In 2007, the magazine Mother Earth News decided to test that claim. They sent for pastured eggs from 14 farms around the U.S., tested them for a number of nutrients, and compared them to the figures listed in the USDA Nutrient Database for conventional eggs. Here are the results per 100 grams for conventional eggs, the average of all the pastured eggs, and eggs from Skagit River Ranch, which sells at my farmer's market:
Vitamin A:
- Conventional: 487 IU
- Pastured avg: 792 IU
- Skagit Ranch: 1013 IU
- Conventional: 34 IU
- Pastured avg: 136 - 204 IU
- Skagit Ranch: not determined
- Conventional: 0.97 mg
- Pastured avg: 3.73 mg
- Skagit Ranch: 4.02 mg
- Conventional: 10 mcg
- Pastured avg: 79 mcg
- Skagit Ranch: 100 mcg
- Conventional: 0.22 g
- Pastured avg: 0.66 g
- Skagit Ranch: 0.74 g
Looks like the American Egg Board and the Egg Nutrition Council have some egg on their faces...
Eggs also contain vitamin K2, with the amount varying substantially according to the hen's diet. Guess where the A, D, K2, beta-carotene and omega-3 fatty acids are? In the yolk of course. Throwing the yolk away turns this powerhouse into a bland, nutritionally unimpressive food.
It's important to note that "free range" supermarket eggs are nutritionally similar to conventional eggs. The reason pastured eggs are so nutritious is that the chickens get to supplement their diets with abundant fresh plants and insects. Having little doors on the side of a giant smelly barn just doesn't replicate that.
Vitamin A, Vitamin D and Osteoporosis Reprise
Chris Masterjohn just pointed out a new study that examined the relationship of vitamin A to osteoporosis in the context of vitamin D intake. The study is part of the massive Women's Health Initiative, which involved over 75,000 women. The conclusion:
Vitamin A on Trial: Does Vitamin A Cause Osteoporosis?
Is Vitamin A Toxicity a Concern?
No association between vitamin A or retinol intake and the risk of hip or total fractures was observed in postmenopausal women. Only a modest increase in total fracture risk with high vitamin A and retinol intakes was observed in the low vitamin D-intake group.In other words, only women with a low vitamin D intake (less than 440 IU per day) had an increased likelihood of fracture at high vitamin A intakes (more than 8,000 IU per day). This is consistent with the hypothesis that an above-average intake of vitamin A only increases the risk of osteoporosis in the presence of low vitamin D, and that vitamin D deficiency, not vitamin A excess, is the true problem. Hop over to Chris's post for more details.
Vitamin A on Trial: Does Vitamin A Cause Osteoporosis?
Is Vitamin A Toxicity a Concern?
Saturday, May 2, 2009
Iodine
I recently saw a post on Dr. Davis's Heart Scan Blog that reminded me I intended to write about iodine. Iodine is an essential trace mineral. It's required for the formation of activated thyroid hormones T3 and T4. The amount of thyroid hormones in circulation, and the body's sensitivity to them, strongly influences metabolic rate. Iodine deficiency can lead to weight gain and low energy. In more severe cases, it can produce goiter, an enlargement of the thyroid gland.
Iodine deficiency is also the most common cause of preventable mental retardation worldwide. Iodine is required for the development of the nervous system, and also concentrates in a number of other tissues including the eyes, the salivary glands and the mammary glands.
There's a trend in the alternative health community to use unrefined sea salt rather than refined iodized salt. Personally, I use unrefined sea salt on principle, although I'm not convinced refined iodized salt is a problem. But the switch removes the main source of iodine in most peoples' diets, creating the potential for deficiency in some areas. Most notably, the soil in the midwestern United States is poor in iodine and deficiency was common before the introduction of iodized salt.
The natural solution? Sea vegetables. They're rich in iodine, other trace minerals, and flavor. I like to add a 2-inch strip of kombu to my beans. Kombu is a type of kelp. It adds minerals, and is commonly thought to speed the cooking and improve the digestion of beans and grains.
Dulse is a type of sea vegetable that's traditionally North American. It has a salty, savory flavor and a delicate texture. It's great in soups or by itself as a snack.
And then there's wakame, which is delicious in miso soup. Iodine is volatile so freshness matters. Store sea vegetables in a sealed container. It may be possible to overdo iodine, so it's best to eat sea vegetables regularly but in moderation like the Japanese.
Seafood such as fish and shellfish are rich in iodine, especially if fish heads are used to make soup stock. Dairy is a decent source in areas that have sufficient iodine in the soil.
Cod liver oil is another good source of iodine, or at least it was before the advent of modern refining techniques. I don't know if refined cod liver oil contains iodine. I suspect that fermented cod liver oil is still a good source of iodine because it isn't refined.
Omega-6 Linoleic Acid Suppresses Thyroid Signaling
Iodine deficiency is also the most common cause of preventable mental retardation worldwide. Iodine is required for the development of the nervous system, and also concentrates in a number of other tissues including the eyes, the salivary glands and the mammary glands.
There's a trend in the alternative health community to use unrefined sea salt rather than refined iodized salt. Personally, I use unrefined sea salt on principle, although I'm not convinced refined iodized salt is a problem. But the switch removes the main source of iodine in most peoples' diets, creating the potential for deficiency in some areas. Most notably, the soil in the midwestern United States is poor in iodine and deficiency was common before the introduction of iodized salt.
The natural solution? Sea vegetables. They're rich in iodine, other trace minerals, and flavor. I like to add a 2-inch strip of kombu to my beans. Kombu is a type of kelp. It adds minerals, and is commonly thought to speed the cooking and improve the digestion of beans and grains.
Dulse is a type of sea vegetable that's traditionally North American. It has a salty, savory flavor and a delicate texture. It's great in soups or by itself as a snack.
And then there's wakame, which is delicious in miso soup. Iodine is volatile so freshness matters. Store sea vegetables in a sealed container. It may be possible to overdo iodine, so it's best to eat sea vegetables regularly but in moderation like the Japanese.
Seafood such as fish and shellfish are rich in iodine, especially if fish heads are used to make soup stock. Dairy is a decent source in areas that have sufficient iodine in the soil.
Cod liver oil is another good source of iodine, or at least it was before the advent of modern refining techniques. I don't know if refined cod liver oil contains iodine. I suspect that fermented cod liver oil is still a good source of iodine because it isn't refined.
Omega-6 Linoleic Acid Suppresses Thyroid Signaling
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