The department of Health and Human Services has put together an easy-to-read timeline re: what happens when under the federal health care reform law.
Small business health insurance tax credits, for example, started taking effect Jan. 1. The first $250 checks to 4 million senior citizens hitting the gap in Medicare prescription drug coverage were mailed in June.
The big stuff still lies ahead. A major round of provisions start taking effect Sept. 23rd: young adults can stay on their parents' health plan until age 26, there will be no pre-existing condition waiting period for children, insurers can't cancel a policy except in the case of fraud, no lifetime caps on benefits, and there will be no copays, etc. for preventive care. (In general. There are a variety of exceptions and exemptions for grandfathered plans and other factors.)
Tuesday, August 31, 2010
On new digs, Kafka, and getting to it
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| Soroka at dusk. |
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| Here I am, tapping a vein. |
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| Jonathan does his thing. |
We all filled out housing preference forms before we left so the folks here could arrange apartments and houses for us to view. However, as often happens, what you thought would be a good idea changes once you are “boots on the ground.” People changed their minds (me), couldn’t make up their minds, or just went ahead and arranged for something before they got here, bypassing the whole thing. So, there was another series of housing requests put out and a string of apartment viewings set up by our liaisons in the evenings.
So, after a day full of Hebrew and Emergency Medicine, we would meet for extended tours of apartments. I say extended, not because we were seeing so many apartments, but because – even though it had been arranged beforehand – the landlords, as a rule it seemed, would never be at the appointed place, at the appointed time. There was a lot of waiting. Time is a relative thing here. This is one of the things I have learned in my short time in Israel. For example, the Hebrew word for “noon,” our Hebrew teacher explained, does not mean 12 in the afternoon. It means 12 to 3 in the afternoon. So, asking someone to meet you at noon could turn in to a long wait.
This is all part of getting used to living in a totally different culture, but after a long day of class and an evening of uncomfortable walking and waiting, you just want someone to show up on time. But, it is what it is and we dealt with it. As the days dragged on I was more and more afraid we (I threw in with two other first-years) would not find a suitable apartment. But just when hope was at its lowest, we found a place. And none too soon – one of my future roommates was already without a sublet, the other was about to lose his, as was I. (Many of us were unaware until after we’d already been here for a couple of weeks that our sublets did not last through the entire month.) It is a nice place not far from the hospital with cool air and new furnishings. Really, all I wanted was a place to be comfortable and I think we found it.
I must say here too that our liaisons did a great job of making sure we were squared away before we signed our contract. Daniella, one of our liaisons, went to the rental office with us and struck things or added/demanded things as she saw fit. First, we never would have been able to read the contract (because it was in Hebrew) but it was also useful to have someone advocating for us.
With every problem that gets solved, another pops up. With the apartment found, I needed to get an Israeli bank account to write checks for the rent. I wanted to avoid getting an Israeli account but there was no way around it. It was recommended that we go over to the bank on the BGU campus to open our accounts. I’ve opened and closed a fair amount of bank accounts in my time. I’ve done a lot of banking in general. But I’ve never seen anything like this bank.
By appearances, the bank looks like any other bank you would find in the US. But that’s just a set dressing. The reality is something totally unknown. There is a dimension where the mind of Franz Kafka creates and controls everything. This bank was conceived and given life in this place. By some accident of science and sin of physics, this dimension temporarily fused with our own and this bank slipped through and plopped down in the middle of BGU’s campus.
One afternoon I went over to open an account. I found a modest line when I arrived and took my ticket. Other MSIH students were already waiting and some arrived after me. After waiting for an hour or more, a bank official came over and asked if we were “a group.” Some of us tried to explain that while we were all in the same school, we were all independent operators looking to open checking accounts. The official said that would be impossible as she did not have the manpower to handle so many of us. The fact that they had several hours to closing time was not reason enough for her to let us stay and open accounts.
We were invited to crush in to her cubicle and make appointments to open accounts. There were easily 15 of us there. She said she could handle 4 people the next morning, maybe 2 the next day in the afternoon. Any more would just be more than she could schedule. Already it seemed odd to me. We were asking to hand over money to them but that didn’t seem to be very important. A proper scheduling that would allow us to wait for interminable periods of time seemed to be her objective.
I was able to get one of the 2 spots in the afternoon. When I arrived for my appointment, the woman I’d made the appointment with was not there. However, there was another group of about 7 MSIH students. One of our liaisons showed up and there was much discussion apparently pertaining to why the bank would not let us open accounts. These discussions seemed to be acts of futility. I waited for about half an hour or 45 minutes until the lady I had an appointment appeared suddenly and informed us that it would simply be impossible to open accounts today. I protested that I had an appointment. No, she reminded me, I was already there yesterday morning and opened an account. No, that was not me, I answered. Yes, she said.
Our liaison took over the discussion. There was more excited talking and she eventually turned to me and said I had an appointment and I was to wait where I was for a booth to open up. However, the other students were not so “lucky.” They could not open accounts.
There was another 30 minutes of waiting. The lady appeared again and directed me and another student to a cubicle. I wasn’t sure if this cubicle was where an account would be opened, or if it was just another place to wait until we could be sent to another cubicle. A man sat down at the desk across from us and barely responded to our “Shalom!” offerings. I knew this man. I’d been to this bank to exchange money and this had been the bank employee who’d arranged the exchange. It had taken 42 minutes exactly. (Which is really nothing – one student told me a mad story about exchanging money at this bank and in the middle of the process, the employee dropped everything to repair a DVD player.) Inwardly I groaned. I knew I was about to be staring at him for quite some time.
After clarifying with him that the other student and I did not want to open a joint account, he began the process of opening her account. He hardly spoke throughout the process. He never asked her a question other than to see her passport. There was a lot of typing. There was a lot of printing things out, throwing them in the trash, printing out more things, coloring stick men on them and hanging them on my refrigerator. There was grumbling at the computer screen. There were phone calls, extended conversations with passersby, much laughing, some screaming, more crying, and gnashing of teeth. We were required to make plans to take him to dinner, then let him break the plans while he told us he’d found someone cooler to hang out with. Then there were forms to sign. Two metric tons of paper were delivered to the bank exclusively reserved for our signatures. Once that was done, a three legged race took place. At the finish line we were given our new accounts and promises that we would receive our bank cards and checks in due time.
In all, I was at the bank for three hours. It’s never been that hard to give my money to someone so they can take it and do what they want with it until I need it.
One more thing about the bank: I was given online access to my account and told that the English site was self-evident when you visited the website. A few days after opening the account I went to the website and could not find the English site. I was able to log in to my account pasting the prompts in to Google Translate. But once I got in to the account I could not navigate my way around. Google Translate started to get more and more what I’ll call “unstable” in its translations. I gave up after it translated one of the menu options as “successful teaching herpes!” (Based on my previous experience with the bank, that might have actually been what the option said, but it was too much to handle… and the exclamation point is not my addition. That was really in the translator.)
The Emergency Medicine final exam was held on August 27. It consisted of a 2 hour written exam and a 2 hour OSCE exam which is a clinical exam made up of “action stations” where we were required to show off our BLS, PHTLS, and history taking skills. For two days previous the TAs for the course kept the classroom building open for us to come by and practice any of the drills we wanted. From what I can tell, the test went well for all of us. It seems I should have more to say about our first big medical school exam but I don’t. Know why? Because I’m too excited about something we did that amounted to a little over an hour of drill time three weeks into the class… We got to put in IVs!
I knew we would get to do it and I was anticipating it for some time. In part, I was nervous about sticking someone over and over as I fruitlessly searched for their vein. The other part of me was really excited to do something so medical. It seems a simple enough thing to do, but when you’re about to be the sticker instead of the stickie, it’s a pretty exciting thing.
The TAs talked us through the process step by step. We were given fake limbs to practice on and told what to look for when we hit the vein. Quickly we were out in the hall actually doing it on our partners. Like a vampiric picnic, blankets were spread on the group and small groups of us huddled excitedly watching one classmate poke another classmate. In my group, the first person to go got it on her first time. Then I laid down and Jonathan, one of my roommates, did his thing on my vein. I want to make this completely clear: he was a total pro at giving IVs. I’ve had a few IVs and blood draws in my time and Jonathan was the fastest, most efficient, and most painless administer of the needle I’ve experienced. I was well impressed.
The rest of my group went. Everyone tapped it on the first try… except for me. I had to stick my partner, Claire, twice. When Claire had done it, she actually went all the way through her partner’s vein but was able to draw the IV back up and in to the vein… very neat to watch her do it. When I first stuck her and didn’t hit pay dirt, I thought I might be able to do the same thing, but I’d missed completely. I was nervous the first time (I mean I was stabbing someone after all) but the second time I was more so. I’d failed once and I didn’t want to have to keep hurting Claire. I also just wanted to do it correctly.
We switched arms. I knelt down, went through the procedure, and chose my vein. It was a good one. Huge. Obviously juicy. Beautiful. I palpated a few times for good measure, stretched the skin, chose my angle and told her to prepare for a pinch. I put the needle in. Blood appeared in the needle and I was in. Tapped the vein. It was satisfying to do it but after the drill, the afterglow was even better. I wasn’t alone in in feeling that somehow we’d crossed a threshold in our time here. It felt like a significant first step toward bigger and better things.
Putting in an IV is certainly insignificant as far as the range of medical procedures (if you can even call it that) we will learn are concerned. But learning how to do it, and actually doing it, wrestled my mind into another place and reminded me that I am not just back in school. I am in medical school. We are in medical school. Those things we’ve had done to us and for us by doctors over all these years? All of those healing activities? We’re going to do those things someday soon.
It’s good to be reminded where you are now and then. But once you know where you are, you need to know you belong. I have to confess, I still have trouble believing this about myself. I’ve spent more than a month with the class of 2014 and I am impressed. I am impressed with the sort of lives they’ve led. I am impressed with the sort of students they are. And from my roommates to the rest of my class to the second and third years I’ve met, I am impressed with them as people. I am humbled and thankful to be in their company.
August 29 was the first proper day of classes. That is, we had Histology and Biochemistry. It’s really started now. A few things I want to remember as I begin are: I need to remember to keep calm when it gets hard, because it will. I need to remember to laugh at the way places like my bank do things, because it’s not going to change. I need to remember to breathe deep. I need to remember to focus on what’s important and let the incidental fall away. I need to remember to drink water. I need to remember to treat myself to falafel. I need to remember to give myself the good medicine of fellowship with friends on a regular basis. I need to remember that as hot as Be’er Sheva is, the places that need our help are probably much hotter so I better get used to it. I need to remember to help and to ask for help. I need to remember that I don’t know all the things I need to remember and so I need to keep an open mind.
On my way to our first day of classes I thought of something Robert Louis Stevenson said. He paid tribute to the physicians he’d encountered throughout his life by writing the following as a dedication for his book “Underwoods.” I think of it as a description I hope can be applied to me – to all of us – someday when we are the doctors in the sickroom:
“There are men and classes of men that stand above the common herd: the soldier, the sailor and the shepherd not unfrequently; the artist rarely; rarely still, the clergyman; the physician almost as a rule. He is the flower (such as it is) of our civilization; and when that stage of man is done with, and only remembered to be marveled at in history, he will be thought to have shared as little as any in the defects of the period, and most notably exhibited the virtues of the race. Generosity he has, such as is possible to those who practice an art, never to those who drive a trade; discretion, tested by a hundred secrets; tact, tried in a thousand embarrassments; and what are more important, Heraclean cheerfulness and courage. So it is that he brings air and cheer into the sickroom, and often enough, though not so often as he wishes, brings healing.” John Powers, MSIH first-year medical student
Doctors are seeking new ways to prevent muscle loss - buyer beware..
I say buyer beware because drug companies would love to bottle this and sell this as the next life threatening malady that afflicts us which can be bottled, and then sold, side effects and all with the blessing of insurance companies who become convienced this is a true malady that is life threatening.
The reality is that people need to remain active and stimulated. People who work into their late 70's and 80's tend to be sharper mentally and physically, they move better although we have the problems of gravity, our body mechanics, degenerative changes in the spine leading to spinal stenosis which will cause muscular wasting (you cannot solve that in a pill) and there are of course, degenerative processes due to hormonal changes and also changes at the cellular level which are likely not to be helped by a pill.
My solutions are for people to have more active lives (many people are overweight and less active - a problem the army is experiencing with new recruits), to eat better (lets get away from our unhealthy food production methods and corn doping of many things we eventually eat) and to take care of biomechanical problems when we are young (true preventative care). Trying to give someone a pill for a problem that in most cases is because biomechanical issues have been ignored for years because doctors did not understand them is absurd, and will also likely if history repeats itself will be expemsive and give us problems we dont have and are not likely to develop without the pharmaceutical companies help.
We need to embrace aging as a normal process, not a disease and people will have healthier muscles with a properly functioning body, and myofascial system, rather than the next pill to fix a problem that is a natural part of aging, given that most health care practitioners really do not understand human body mechanics very well.
How to become diabetic in 6 hours!? Thanks Dr. Delgado for bringing science to the masses!
(Note: My apologies for the sarcastic tone of this post. I am not really congratulating anybody here!)
Dr. Nick Delgado shows us in this YouTube video how to "become diabetic" in 6 hours!
I must admit that I liked the real-time microscope imaging, and wish he had shown us more of that.
But really!
After consulting with my mentor, the MIMIW, I was reminded that there is at least one post on this blog that shows how one can "become diabetic" in just over 60 minutes – that is, about 6 times faster than using the technique described by Dr. Delgado.
The technique used in the post mentioned above is called "intense exercise", which is even believed to be health-promoting! (Unlike drinking olive oil as if it was water, or eating white bread.)
The advantage of this technique is that one can "become diabetic" by doing something healthy!
Thanks Dr. Delgado, your video ranks high up there, together with this Ali G. video, as a fine example of how to bring real science to the masses.
Dr. Nick Delgado shows us in this YouTube video how to "become diabetic" in 6 hours!
I must admit that I liked the real-time microscope imaging, and wish he had shown us more of that.
But really!
After consulting with my mentor, the MIMIW, I was reminded that there is at least one post on this blog that shows how one can "become diabetic" in just over 60 minutes – that is, about 6 times faster than using the technique described by Dr. Delgado.
The technique used in the post mentioned above is called "intense exercise", which is even believed to be health-promoting! (Unlike drinking olive oil as if it was water, or eating white bread.)
The advantage of this technique is that one can "become diabetic" by doing something healthy!
Thanks Dr. Delgado, your video ranks high up there, together with this Ali G. video, as a fine example of how to bring real science to the masses.
Monday, August 30, 2010
Emergency Medicine… also, the problem (and strange freedom) of illiteracy
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| John in a collar |
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| Soroka from MSIH section |
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| Jakob backboarded |
The lectures are interesting and the drills are enjoyable. I’d never thought of it in these terms but when learning this sort of thing, you’re not learning how to save someone’s life. You are learning how to keep them from dying faster. If Humpty Dumpty falls off his wall and I’m watching it happen, all I can do is keep his shell and yolk intact enough so that a doctor in an OR has enough to work with to put Humpty Dumpty back together again. It is an interesting place to think about existing, philosophically that is. In reality, I’m quite sure I would not be thinking about it if I was actually stabilizing someone’s cervical spine and trying to tell someone how to stop the bleeding from a partial amputation.
It hits me now and again that this course will likely be the last practical, and immediately useful (immediate being an important word there) medical knowledge that we’ll learn for a long time. Between the end of the EM course and the end of the first year, we’ll be in our basic science courses which, in all likelihood, not teach us how to assess if someone is in shock.
Speaking of shock, I have assessed myself and I’d say I’m not quite there. I’m talking about culture shock. I think there is one thing in particular that is staving off my culture shock at the moment, and that is that I am largely illiterate. Yes, Hebrew continues to confound me. I can understand a word here and there but most of what is said to me, and almost all of what I see written around me is mysterious. Perhaps if I could understand what people were saying, or read their billboards, I would be much more shocked by everything.
I learned to read in first grade. That is the last time I could not read or write something besides my name. Obviously, I can’t remember how that felt but, really, it probably felt great since I had people (read here “parents”) to take care of that pesky reading and writing stuff for me. Right now? It feels terrible. At times, it is embarrassing to be unable to speak to or understand what someone is saying. At other times it’s just humiliating. Because it isn’t just illiteracy, I can’t speak many times. I think of it as being mute. And that is an even more unique feeling. I don’t like it. But there is one thing that several people have told us since we got here that is pertinent here: Don’t despair. OK, I won’t. I will continue to stare dumbly and trust that a smile and a shrug mean the same here as it does in the United States until such time as I can effectively say, “I’m sorry I can’t speak your language, but is that falafel really 600 shekels?”
Yes, despairing is no good. And I’m not despairing. In fact, I was having such a terrible time one day that my Hebrew teacher, Nava, let me sit with her after class and go over some problems I was having. After our meeting, I was very encouraged if mostly because she reminded me several times that I am only a child when it comes to Hebrew. Also, and this is just an aside, she often tells our class that she can’t explain all the strange sounds contained in Hebrew because, “It’s a language invented by shepherds and people who run after animals.”
As the title mentioned, I have experienced an unexpected benefit from feeling like a mute, totally cut off from the locals. For some reason, I feel completely comfortable singing out loud with my iPod. I have never done this before. When I lived in New York, I might have been able to get away with it, but my Midwestern sense of propriety keeps me from foisting my singing on innocent bystanders. Here, I feel almost as if, since I can’t understand them and they probably can’t understand me, I can sort of do whatever I want and pass it off as completely normal – like, “oh, that’s what Americans do… walk about singing like madmen.” One evening I was walking through the hospital campus and realized I was doing my best Jeff Buckley impression as I listened to “What Will You Say” on my iPod. It was full on without a shred of self-respect. The Muslim women I was passing at the time barely glanced, not even breaking their conversation. Again, I’m chalking this up to feeling like I can get away with it, but I might be going crazy. I’ll monitor my condition every few minutes and notify you of any further deterioration.
Diversity. It was promised before we came and I can tell you it is here. At the hospital we walk the halls with Russians, Ethiopians, Bedouins, Israelis, and a lot of other folks I can’t identify yet. One might expect that diversity at any hospital but Be’er Sheva reflects it as well. I have been attending the local Catholic church here and it is also a picture of the uniqueness of this area. I attend on Friday nights, which is a popular night for a large group of immigrant workers from southwestern India (the state of Kerala). They are a particular sort of Catholic referred to as Saint Thomas Christians. They are part of the Latin Church but use an Eastern Rite Mass. What does all that mean? Doesn’t matter right now. What I want you to know is that this plays out in an interesting way. The priests here have allowed the Indians, mostly women, to incorporate pieces of the mass they would celebrate at home with the one that is celebrated commonly at the church here. So, the words of the mass are in Hebrew, the Scripture readings are in English, and several responses are sung by the women in (what I think but am not sure) is Malayalam. On Sundays, there is an entirely different group of people who show up. They are Israelis, Americans, Italians, Indians, and the priest is French. Somehow everyone finds a way to communicate and they are all intensely warm and welcoming. It is a hopeful picture.
I bring up religion because one of the lessons I’ve learned about Israel and the people here is that politics and religion are the first thing people talk about instead of the thing they avoid. OK, maybe not the first thing, but I have been surprised at how easily these things have come up in conversation with the local people I have been able to talk with (in English of course). Because I am such a son of America, I will leave it at that and spare you the specifics of what I’ve heard. The last thing I want to do is start talking about religion and politics.
I think I should end by summing up my impressions of Israel and our journey toward the end of orientation and the first day of medical school proper. “Interesting” is the only word I can think of. One can fancy themselves a wordsmith yet they will always be at a loss when they have something important to say. One of the things I found in my (former) career as a writer is that someone has always said what you want to say, and usually they’ve done it better. So, something my Hebrew teacher Nava said comes to mind. It isn’t a summation. It’s just good advice to end on:
“Open your ears and open your eyes… it will be a very interesting trip. This is a crazy and harsh country… but that’s the charm of it.”
How to find flood insurance in WA's Green River Valley
About this time last year, some businesses in Washington state's Green River Valley started discovering that it was extremely difficult to get -- or afford -- flood coverage. The reason was no mystery: The Army Corps of Engineers, citing a weakened abutment to the nearby Howard Hanson Dam, pegged the risk of serious flooding at 1 in 3.
A year later, the Corps and contractors have done extensive work, and the risk is now believed to be about 1 in 60. (The normal risk is about 1 in 140.) As the Corps noted in a recent PowerPoint, the La Nina weather pattern can also bring back-to-back rainstorms, could require the Corps to rapidly draw down the pool of water behind the dam.
We're still urging homeowners in the area to strongly consider flood coverage from the National Flood Insurance Program. And although August may seem like an odd time to be thinking about flooding, the federal coverage doesn't take effect until 30 days after a policy's issued.
For businesses in particular, the federal coverage -- which is limited to $500k for the building and $500k for contents -- may not be enough. So our office launched a "Washington Flood Market Assistance Plan," which is a sort of matchmaking service connecting businesses needing coverage with insurers selling it.
More than two dozen insurance companies are participating, and the program's run by the Surplus Line Association of Washington, an industry association.
To learn more, please see our web page and FAQs on the program.
A year later, the Corps and contractors have done extensive work, and the risk is now believed to be about 1 in 60. (The normal risk is about 1 in 140.) As the Corps noted in a recent PowerPoint, the La Nina weather pattern can also bring back-to-back rainstorms, could require the Corps to rapidly draw down the pool of water behind the dam.
We're still urging homeowners in the area to strongly consider flood coverage from the National Flood Insurance Program. And although August may seem like an odd time to be thinking about flooding, the federal coverage doesn't take effect until 30 days after a policy's issued.
For businesses in particular, the federal coverage -- which is limited to $500k for the building and $500k for contents -- may not be enough. So our office launched a "Washington Flood Market Assistance Plan," which is a sort of matchmaking service connecting businesses needing coverage with insurers selling it.
More than two dozen insurance companies are participating, and the program's run by the Surplus Line Association of Washington, an industry association.
To learn more, please see our web page and FAQs on the program.
Sunday, August 29, 2010
Heavy physical activity may significantly reduce heart disease deaths, especially after age 45
The idea that heavy physical activity is a main trigger of heart attacks is widespread. Often endurance running and cardio-type activities are singled out. Some people refer to this as “death by running”. Others think that strength training has a higher lethal potential. We know based on the Oregon Sudden Unexpected Death Study that this is a myth.
Here is some evidence that heavy physical activity in fact has a significant protective effect. The graph below, from Brooks et al. (2005) shows the number of deaths from coronary heart disease, organized by age group, in longshoremen (dock workers). The shaded bars represent those whose level of activity at work was considered heavy. The unshaded bars represent those whose level of activity at work was considered moderate or light (essentially below the “heavy” level).
The data is based on an old and classic study of 6351 men, aged 35 to 74 years, who were followed either for 22 years, or to death, or to the age of 75. It shows a significant protective effect of heavy activity, especially after age 45. The numbers atop the unshaded bars reflect the relative risk of death from coronary heart disease in each age group. For example, in the age group 65-74, the risk among those not in the heavy activity group is 110 percent higher (2.1 times higher) than in the heavy activity group.
It should be noted that this is a cumulative effect, of years of heavy activity. Based on the description of the types of activities performed, and the calories spent, I estimate that the heavy activity group performed the equivalent of a few hours of strength training per week, plus a lot of walking and other light physical activities. The authors of the study concluded that “… repeated bursts of high energy output established a plateau of protection against coronary mortality.”
Heavy physical activity may not make you lose much weight, but has the potential to make you live longer.
Reference:
Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.
Here is some evidence that heavy physical activity in fact has a significant protective effect. The graph below, from Brooks et al. (2005) shows the number of deaths from coronary heart disease, organized by age group, in longshoremen (dock workers). The shaded bars represent those whose level of activity at work was considered heavy. The unshaded bars represent those whose level of activity at work was considered moderate or light (essentially below the “heavy” level).
The data is based on an old and classic study of 6351 men, aged 35 to 74 years, who were followed either for 22 years, or to death, or to the age of 75. It shows a significant protective effect of heavy activity, especially after age 45. The numbers atop the unshaded bars reflect the relative risk of death from coronary heart disease in each age group. For example, in the age group 65-74, the risk among those not in the heavy activity group is 110 percent higher (2.1 times higher) than in the heavy activity group.
It should be noted that this is a cumulative effect, of years of heavy activity. Based on the description of the types of activities performed, and the calories spent, I estimate that the heavy activity group performed the equivalent of a few hours of strength training per week, plus a lot of walking and other light physical activities. The authors of the study concluded that “… repeated bursts of high energy output established a plateau of protection against coronary mortality.”
Heavy physical activity may not make you lose much weight, but has the potential to make you live longer.
Reference:
Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.
Saturday, August 28, 2010
Saturated Fat, Glycemic Index and Insulin Sensitivity: Another Nail in the Coffin
Insulin is a hormone that drives glucose and other nutrients from the bloodstream into cells, among other things. A loss of sensitivity to the insulin signal, called insulin resistance, is a core feature of modern metabolic dysfunction and can lead to type II diabetes and other health problems. Insulin resistance affects a large percentage of people in affluent nations, in fact the majority of people in some places. What causes insulin resistance? Researchers have been trying to figure this out for decades.*
Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).
The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another darling of the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fat gain (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.
All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).
A large new study just published in the American Journal of Clinical nutrition has placed the final nail in the coffin: neither saturated fat nor high glycemic carbohydrate influence insulin sensitivity in humans, at least on the timescale of most controlled trials (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:
In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.
Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations often run into problems due to reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!
* Excess body fat is almost certainly a major cause. When fat mass increases beyond a certain point, particularly abdominal fat, the fat tissue typically becomes inflamed. Inflamed fat tissue secretes factors which reduce whole-body insulin sensitivity (12, 13). The big question is: what caused the fat gain?
Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).
The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another darling of the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fat gain (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.
All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).
A large new study just published in the American Journal of Clinical nutrition has placed the final nail in the coffin: neither saturated fat nor high glycemic carbohydrate influence insulin sensitivity in humans, at least on the timescale of most controlled trials (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:
- High saturated fat, high glycemic index
- High monounsaturated fat, high glycemic index
- High monounsaturated fat, low glycemic index
- Low fat, high glycemic index
- Low fat, low glycemic index
In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.
Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations often run into problems due to reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!
* Excess body fat is almost certainly a major cause. When fat mass increases beyond a certain point, particularly abdominal fat, the fat tissue typically becomes inflamed. Inflamed fat tissue secretes factors which reduce whole-body insulin sensitivity (12, 13). The big question is: what caused the fat gain?
Friday, August 27, 2010
Getting health coverage for adult children
The number one health insurance problem we get calls about? People trying to find affordable coverage for their adult children. (We're the state insurance regulator in Washington.)
Starting soon -- and some major health insurers have already started to do this -- parents will generally be able to keep their kids covered up to age 26. In many cases, "soon" means next January 1, 2011. But depending on when your policy renews, it could be months later than that.
The New York Times recently did a story aiming to help parents struggling with this figure out what their options are, such as getting coverage through student health plans or buying an individual health insurance policy.
If you live in Washington state and need free help navigating this, give our consumer advocacy staff a call: 1-800-562-6900.
Starting soon -- and some major health insurers have already started to do this -- parents will generally be able to keep their kids covered up to age 26. In many cases, "soon" means next January 1, 2011. But depending on when your policy renews, it could be months later than that.
The New York Times recently did a story aiming to help parents struggling with this figure out what their options are, such as getting coverage through student health plans or buying an individual health insurance policy.
If you live in Washington state and need free help navigating this, give our consumer advocacy staff a call: 1-800-562-6900.
Thursday, August 26, 2010
Coming Soon!!
Exciting things coming up this fall with 3 Healthy Chicks!! Stay tuned to our blog and Facebook fan page as we take our chick bits out on the road. We will be holding the following monthly healthy meet ups:- Explore Your Store: Take a tour of your local supermarket with 3HC to learn how to look for healthy items in conventional stores such as Stop&Shop and Wegmans, or shop health food stores such as Whole Foods and Deans Natural Market.
- Healthy Happy Hour: Meet with us to learn how to choose healthy happy hour beverages and healthier bar fare.
- Lunch and Learn: Pack your lunch and meet up with us to learn about our healthy topic of the month!
We are working hard (as you can see from our photo above) to get these things up and running for you! We'll keep you posted!!!
Dogs and homeowners insurance: Dog bites accounted for $412 million in claims last year
Dog bites accounted for more than one third of all homeowners insurance liability claims paid out last year, according to a new report from the Insurance Information Institute.
Dog bite claims totalled $412 million in 2009, the group says, with an average claim of $24,840. The cost of dog-bite-related claims has risen nearly 30 percent from 2003-2009. The frequency of claims increased slightly, from 15,823 in 2008 to 16,586 a year later.
See the link above for more data, including national stats on dog bites, victim demographics, and the several kinds of liability that dog owners face.
A typical homeowners policy provides $100,000 to $300,000 in liability coverage. And one a dog has bitten someone, the company may boost your premiums, exclude the dog from coverage, or require behavior-modification classes before they'll cover the animal.
Dog bite claims totalled $412 million in 2009, the group says, with an average claim of $24,840. The cost of dog-bite-related claims has risen nearly 30 percent from 2003-2009. The frequency of claims increased slightly, from 15,823 in 2008 to 16,586 a year later.
See the link above for more data, including national stats on dog bites, victim demographics, and the several kinds of liability that dog owners face.
A typical homeowners policy provides $100,000 to $300,000 in liability coverage. And one a dog has bitten someone, the company may boost your premiums, exclude the dog from coverage, or require behavior-modification classes before they'll cover the animal.
Tuesday, August 24, 2010
Chocolicious!
If you missed our August Newsletter, than you missed a wellness tip regarding one of my favorite subjects: chocolate! Need I really say more? I think it’s safe to say that almost everyone loves to indulge in a little decadent chocolate from time to time. And for good reason... it is delicious! But sadly, the indulgence often is paired with guilt for those of us trying to maintain our girlish figures. So, in true healthy chick fashion, I included in our newsletter a super healthy chocolate recipe that coincidentally utilizes none other than coconut oil. (See below!)Terra has already filled you all in on the benefits of coconut oil, but this recipe is all natural and full of healthy, beneficial ingredients! Most chocolate bars and candies are loaded with dairy and refined sugars that are no good for us. But the raw cacao bean, the stuff chocolate is made from, is naturally high in antioxidants and essential minerals. So, eating raw cacao or a high quality dark chocolate can actually be really good for us. Thank goodness! Combine it with some fresh seasonal berries and you have an antioxidant-rich healthful, and delicious treat!
Raw Chocolate Covered Strawberries
1/4 Cup of softened coconut oil (soften oil by placing the jar in a bowl of hot water)
1/2 Cup of raw cacao powder
3 Tbsp raw agave nectar
Pinch of sea salt
Whole strawberries
Mix all ingredients together in a bowl until soft and rich. If your sauce is too runny, continue adding cacao powder until thick, but still a sauce consistency. Dip your strawberries until well coated and refrigerate on a tray lined with parchment paper. It helps to sit your bowl inside another bowl filled slightly with hot water to keep the sauce from hardening as you work.
I looooove chocolate covered strawberries, but there are so many options with this recipe. You can also use sliced bananas, raspberries, mango, dried fruits or raw nuts! You can also sprinkle your chocolate covered fruit with shredded coconut, raw cacao nibs, ground flax or ground nuts before setting the chocolate too! The possibilities are endless! YUM!
Don't forget to sign up for our newsletter so you don't miss out on more delicious recipes and information!
Keep it Fresh!
- Jill
I'm Coocoo for Coconuts!!
I'm not sure how General Mills would feel about me doctoring up one of their best advertising campaigns, but I'm not really worried what those sugar peddlers think! Can you imagine if there were advertising campaigns with delightful cartoon characters pushing wonderful things like kale and coconut water? Creating veggie addicts at the ripe ages of 2-5 rather than sugar addicts? Oh what a wonderful world!! Anyway, I digress. I am coocoo for coconuts!! In all it's beautiful shapes and forms, but specifically two forms; water and oil. Coconut water is quite literally, Mother Nature's energy drink. I always use it in my smoothies for a little added energy. Coconut water contains more potassium than most sports and energy drinks. It has less sodium, and it contains natural sugars where sports and energy drinks contain high amounts of altered sugars. Why bother with sugary drinks like Gatorade, Vitamin Water or Sobe when you can enjoy natural electrolytes from the beautiful coconut?
Who knew a hard shelled hairy fruit could be power packed with so much amazingness!!
For those of you that only recognize the coconut that comes in a bag in shredded form, here's a quick little coconut primer. Coconuts grow in the tropics and are a member of the palm family. The scientific name for coconut is cocos nucifera (nucifera meaning "nut bearing"). Early Spanish explorers called it coco, which means "Monkey Face" because they three eyes on the hair nut resembles the face of a monkey.
Coconut is a nutritious source of meat, juice, milk and oil that has fed and nourished island and tropical populations around the world for generations. The coconut is super nutritious. It's rich in fiber, vitamins and minerals. It is often classified as a "functional" food because it provides many health benefits beyond its nutritional content.
Coconut oil is exactly what makes coconut a functional food. Coconut oil has been used in traditional medicine in Asian and Pacific populations for years. Pacific Islanders consider it to be the cure for all illness. Recently, modern medical science has begun to "validate" coconuts amazing healing powers. I used the quotations around validate because I find it amusing (frustrating and annoying) that modern science needs to play catch up with traditional medicine - "validating" traditional herbs and whole foods cures that have been in use for thousands of years- but that's a separate soap box in its entirety!
Anyway, back to the wonderful coconut!
Coconut oil is a saturated fat, liquid when warm and semi-solid/congealed when cooled. Now, before you start judging our little coconut with a big fat "bad" for its saturated fat content, remember that not all saturated fats are created equal! The structural make up of coconut oil is unique. While it has the highest source of saturated fat at 92%, it also contains 62% of medium chain triglycerides. Half of these triglycerides are made up of lauric acid, the most important essential acid in building and maintaining our immune system. Other than coconut oil, the only other source of lauric acid in such high concentration is breast milk! Check out all ways coconut oil can benefit your health!
I have had a few friends recommend oil pulling with coconut oil. Oil pulling is a traditional Ayurvedic remedy where you swish with oil to remove toxins from the body. Oil pulling is said to benefit many chronic diseases and illnesses such as inflammation, arthritis, allergies, digestive issues including IBS and constipation, and even PMS! After all of this coconut oil research I think I am going to give it a try. I'll let you know how it goes!
Keep it Fresh!
~Terra
Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes
The term “diabetes” is used to describe a wide range of diseases of glucose metabolism; diseases with a wide range of causes. The diseases include type 1 and type 2 diabetes, type 2 ketosis-prone diabetes (which I know exists thanks to Michael Barker’s blog), gestational diabetes, various MODY types, and various pancreatic disorders. The possible causes include genetic defects (or adaptations to very different past environments), autoimmune responses, exposure to environmental toxins, as well as viral and bacterial infections; in addition to obesity, and various other apparently unrelated factors, such as excessive growth hormone production.
Type 2 diabetes and the “tired pancreas” theory
Type 2 diabetes is the one most commonly associated with the metabolic syndrome, which is characterized by middle-age central obesity, and the “diseases of civilization” brought up by Neolithic inventions. Evidence is mounting that a Neolithic diet and lifestyle play a key role in the development of the metabolic syndrome. In terms of diet, major suspects are engineered foods rich in refined carbohydrates and refined sugars. In this context, one widely touted idea is that the constant insulin spikes caused by consumption of those foods lead the pancreas (figure below from Wikipedia) to get “tired” over time, losing its ability to produce insulin. The onset of insulin resistance mediates this effect.
Empirical evidence against the “tired pancreas” theory
This “tired pancreas” theory, which refers primarily to the insulin-secreting beta-cells in the pancreas, conflicts with a lot of empirical evidence. It is inconsistent with the existence of isolated semi/full hunter-gatherer groups (e.g., the Kitavans) that consume large amounts of natural (i.e., unrefined) foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. These groups are nevertheless generally free from type 2 diabetes. The “tired pancreas” theory conflicts with the existence of isolated groups in China and Japan (e.g., the Okinawans) whose diets also include a large proportion of natural foods rich in easily digestible carbohydrates, which cause insulin spikes. Yet these groups are generally free from type 2 diabetes.
Humboldt (1995), in his personal narrative of his journey to the “equinoctial regions of the new continent”, states on page 121 about the natives as a group that: "… between twenty and fifty years old, age is not indicate by wrinkling skin, white hair or body decrepitude [among natives]. When you enter a hut is hard to differentiate a father from son …" A large proportion of these natives’ diets included plenty of natural foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. Still, there was no sign of any condition that would suggest a prevalence of type 2 diabetes among them.
At this point it is important to note that the insulin spikes caused by natural carbohydrate-rich foods are much less pronounced than the ones caused by refined carbohydrate-rich foods. The reason is that there is a huge gap between the glycemic loads of natural and refined carbohydrate-rich foods, even though the glycemic indices may be quite similar in some cases. Natural carbohydrate-rich foods are not made mostly of carbohydrates. Even an Irish (or white) potato is 75 percent water.
More insulin may lead to abnormal fat metabolism in sedentary people
The more pronounced spikes may lead to abnormal fat metabolism because more body fat is force-stored than it would have been with the less pronounced spikes, and stored body fat is not released just as promptly as it should be to fuel muscle contractions and other metabolic processes. Typically this effect is a minor one on a daily basis, but adds up over time, leading to fairly unnatural patterns of fat metabolism in the long run. This is particularly true for those who lead sedentary lifestyles. As for obesity, nobody gets obese in one day. So the key problem with the more pronounced spikes may not be that the pancreas is getting “tired”, but that body fat metabolism is not normal, which in turn leads to abnormally high or low levels of important body fat-derived hormones (e.g., high levels of leptin and low levels of adiponectin).
One common characteristic of the groups mentioned above is absence of obesity, even though food is abundant and often physical activity is moderate to low. Repeat for emphasis: “… even though food is abundant and often physical activity is moderate to low”. Note that having low levels of activity is not the same as spending the whole day sitting down in a comfortable chair working on a computer. Obviously caloric intake and level of activity among these groups were/are not at the levels that would lead to obesity. How could that be possible? See this post for a possible explanation.
Excessive body fat gain, lipotoxicity, and type 2 diabetes
There are a few theories that implicate the interaction of abnormal fat metabolism with other factors (e.g., genetic factors) in the development of type 2 diabetes. Empirical evidence suggests that this is a reasonable direction of causality. One of these theories is the theory of lipotoxicity.
Several articles have discussed the theory of lipotoxicity. The article by Unger & Zhou (2001) is a widely cited one. The theory seems to be widely based on the comparative study of various genotypes found in rats. Nevertheless, there is mounting evidence suggesting that the underlying mechanisms may be similar in humans. In a nutshell, this theory proposes the following steps in the development of type 2 diabetes:
(1) Abnormal fat mass gain leads to an abnormal increase in fat-derived hormones, of which leptin is singled out by the theory. Some people seem to be more susceptible than others in this respect, with lower triggering thresholds of fat mass gain. (What leads to exaggerated fat mass gains? The theory does not go into much detail here, but empirical evidence from other studies suggests that major culprits are refined grains and seeds, as well as refined sugars; other major culprits seem to be trans fats, and vegetable oils rich in linoleic acid.)
(2) Resistance to fat-derived hormones sets in. Again, leptin resistance is singled out as the key here. (This is a bit simplistic. Other fat-derived hormones, like adiponectin, seem to clearly interact with leptin.) Since leptin regulates fatty acid metabolism, the theory argues, leptin resistance is hypothesized to impair fatty acid metabolism.
(3) Impaired fat metabolism causes fatty acids to “spill over” to tissues other than fat cells, and also causes an abnormal increase in a substance called ceramide in those tissues. These include tissues in the pancreas that house beta-cells, which secrete insulin. In short, body fat should be stored in fat cells (adipocytes), not outside them.
(4) Initially fatty acid “spill over” to beta-cells enlarges them and makes them become overactive, leading to excessive insulin production in response to carbohydrate-rich foods, and also to insulin resistance. This is the pre-diabetic phase where hypoglycemic episodes happen a few hours following the consumption of carbohydrate-rich foods. Once this stage is reached, several natural carbohydrate-rich foods also become a problem (e.g., potatoes and bananas), in addition to refined carbohydrate-rich foods.
(5) Abnormal levels of ceramide induce beta-cell apoptosis in the pancreas. This is essentially “death by suicide” of beta cells in the pancreas. What follows is full-blown type 2 diabetes. Insulin production is impaired, leading to very elevated blood glucose levels following the consumption of carbohydrate-rich foods, even if they are unprocessed.
It is widely known that type 2 diabetics have impaired glucose metabolism. What is not so widely known is that usually they also have impaired fatty acid metabolism. For example, consumption of the same fatty meal is likely to lead to significantly more elevated triglyceride levels in type 2 diabetics than non-diabetics, after several hours. This is consistent with the notion that leptin resistance precedes type 2 diabetes, and inconsistent with the “tired pancreas” theory.
Weak and strong points of the theory of lipotoxicity
A weakness of the theory of lipotoxicity is its strong lipophobic tone; at least in the articles that I have read. See, for example, this article by Roger H. Unger in the Journal of the American Medical Association. There is ample evidence that eating a lot of the ultra-demonized saturated fat, per se, is not what makes people obese or type 2 diabetic. Yet overconsumption of trans fats and vegetable oils rich in linoleic acid does seem to be linked with obesity and type 2 diabetes. (So does the consumption of refined grains and seeds, and refined sugars.) The theory of lipotoxicity does not seem to make these distinctions.
In defense of the theory of lipotoxicity, it does not argue that there cannot be thin diabetics. Many type 1 diabetics are thin. Type 2 diabetics can also be thin, even though that is much less common. In certain individuals, the threshold of body fat gain that will precipitate lipotoxicity may be quite low. In others, the same amount of body fat gain (or more) may in fact increase their insulin sensitivity under certain circumstances – e.g., when growth hormone levels are abnormally low.
Autoimmune disorders, perhaps induced by environmental toxins, or toxins found in certain refined foods, may cause the immune system to attack the beta-cells in the pancreas. This may lead to type 1 diabetes if all beta cells are destroyed, or something that can easily be diagnosed as type 2 (or type 1.5) diabetes if only a portion of the cells are destroyed, in a way that does not involve lipotoxicity.
Nor does the theory of lipotoxicity predict that all those who become obese will develop type 2 diabetes. It only suggests that the probability will go up, particularly if other factors are present (e.g., genetic propensity). There are many people who are obese during most of their adult lives and never develop type 2 diabetes. On the other hand, some groups, like Hispanics, tend to develop type 2 diabetes more easily (often even before they reach the obese level). One only has to visit the South Texas region near the Rio Grande border to see this first hand.
What the theory proposes is a new way of understanding the development of type 2 diabetes; a way that seems to make more sense than the “tired pancreas” theory. The theory of lipitoxicity may not be entirely correct. For example, there may be other mechanisms associated with abnormal fat metabolism and consumption of Neolithic foods that cause beta-cell “suicide”, and that have nothing to do with lipotoxicity as proposed by the theory. (At least one fat-derived hormone, tumor necrosis factor-alpha, is associated with abnormal cell apoptosis when abnormally elevated. Levels of this hormone go up immediately after a meal rich in refined carbohydrates.) But the link that it proposes between obesity and type 2 diabetes seems to be right on target.
Implications and thoughts
Some implications and thoughts based on the discussion above are the following. Some are extrapolations based on the discussion in this post combined with those in other posts. At the time of this writing, there were 90 posts on this blog, in addition to many comments. See under "Labels" at the bottom-right area of this blog for a summary of topics addressed. It is hard to ignore things that were brought to light in previous posts.
- Let us start with a big one: Avoiding natural carbohydrate-rich foods in the absence of compromised glucose metabolism is unnecessary. Those foods do not “tire” the pancreas significantly more than protein-rich foods do. While carbohydrates are not essential macronutrients, protein is. In the absence of carbohydrates, protein will be used by the body to produce glucose to supply the needs of the brain and red blood cells. Protein elicits an insulin response that is comparable to that of natural carbohydrate-rich foods on a gram-adjusted basis (but significantly lower than that of refined carbohydrate-rich foods, like doughnuts and bagels). Usually protein does not lead to a measurable glucose response because glucagon is secreted together with insulin in response to ingestion of protein, preventing hypoglycemia.
- Abnormal fat gain should be used as a general measure of one’s likelihood of being “headed south” in terms of health. The “fitness” level for men and women shown on the table in this post seem like good targets for body fat percentage. The problem here, of course, is that this is not as easy as it sounds. Attempts at getting lean can lead to poor nutrition and/or starvation. These may make matters worse in some cases, leading to hormonal imbalances and uncontrollable hunger, which will eventually lead to obesity. Poor nutrition may also depress the immune system, making one susceptible to a viral or bacterial infection that may end up leading to beta-cell destruction and diabetes. A better approach is to place emphasis on eating a variety of natural foods, which are nutritious and satiating, and avoiding refined ones, which are often addictive “empty calories”. Generally fat loss should be slow to be healthy and sustainable.
- Finally, if glucose metabolism is compromised, one should avoid any foods in quantities that cause an abnormally elevated glucose or insulin response. All one needs is an inexpensive glucose meter to find out what those foods are. The following are indications of abnormally elevated glucose and insulin responses, respectively: an abnormally high glucose level 1 hour after a meal (postprandial hyperglycemia); and an abnormally low glucose level 2 to 4 hours after a meal (reactive hypoglycemia). What is abnormally high or low? Take a look at the peaks and troughs shown on the graph in this post; they should give you an idea. Some insulin resistant people using glucose meters will probably realize that they can still eat several natural carbohydrate-rich foods, but in small quantities, because those foods usually have a low glycemic load (even if their glycemic index is high).
Lucy was a vegetarian and Sapiens an omnivore. We apparently have not evolved to be pure carnivores, even though we can be if the circumstances require. But we absolutely have not evolved to eat many of the refined and industrialized foods available today, not even the ones marketed as “healthy”. Those foods do not make our pancreas “tired”. Among other things, they “mess up” fat metabolism, which may lead to type 2 diabetes through a complex process involving hormones secreted by body fat.
References
Humboldt, A.V. (1995). Personal narrative of a journey to the equinoctial regions of the new continent. New York, NY: Penguin Books.
Unger, R.H., & Zhou, Y.-T. (2001). Lipotoxicity of beta-cells in obesity and in other causes of fatty acid spillover. Diabetes, 50(1), S118-S121.
Type 2 diabetes and the “tired pancreas” theory
Type 2 diabetes is the one most commonly associated with the metabolic syndrome, which is characterized by middle-age central obesity, and the “diseases of civilization” brought up by Neolithic inventions. Evidence is mounting that a Neolithic diet and lifestyle play a key role in the development of the metabolic syndrome. In terms of diet, major suspects are engineered foods rich in refined carbohydrates and refined sugars. In this context, one widely touted idea is that the constant insulin spikes caused by consumption of those foods lead the pancreas (figure below from Wikipedia) to get “tired” over time, losing its ability to produce insulin. The onset of insulin resistance mediates this effect.
Empirical evidence against the “tired pancreas” theory
This “tired pancreas” theory, which refers primarily to the insulin-secreting beta-cells in the pancreas, conflicts with a lot of empirical evidence. It is inconsistent with the existence of isolated semi/full hunter-gatherer groups (e.g., the Kitavans) that consume large amounts of natural (i.e., unrefined) foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. These groups are nevertheless generally free from type 2 diabetes. The “tired pancreas” theory conflicts with the existence of isolated groups in China and Japan (e.g., the Okinawans) whose diets also include a large proportion of natural foods rich in easily digestible carbohydrates, which cause insulin spikes. Yet these groups are generally free from type 2 diabetes.
Humboldt (1995), in his personal narrative of his journey to the “equinoctial regions of the new continent”, states on page 121 about the natives as a group that: "… between twenty and fifty years old, age is not indicate by wrinkling skin, white hair or body decrepitude [among natives]. When you enter a hut is hard to differentiate a father from son …" A large proportion of these natives’ diets included plenty of natural foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. Still, there was no sign of any condition that would suggest a prevalence of type 2 diabetes among them.
At this point it is important to note that the insulin spikes caused by natural carbohydrate-rich foods are much less pronounced than the ones caused by refined carbohydrate-rich foods. The reason is that there is a huge gap between the glycemic loads of natural and refined carbohydrate-rich foods, even though the glycemic indices may be quite similar in some cases. Natural carbohydrate-rich foods are not made mostly of carbohydrates. Even an Irish (or white) potato is 75 percent water.
More insulin may lead to abnormal fat metabolism in sedentary people
The more pronounced spikes may lead to abnormal fat metabolism because more body fat is force-stored than it would have been with the less pronounced spikes, and stored body fat is not released just as promptly as it should be to fuel muscle contractions and other metabolic processes. Typically this effect is a minor one on a daily basis, but adds up over time, leading to fairly unnatural patterns of fat metabolism in the long run. This is particularly true for those who lead sedentary lifestyles. As for obesity, nobody gets obese in one day. So the key problem with the more pronounced spikes may not be that the pancreas is getting “tired”, but that body fat metabolism is not normal, which in turn leads to abnormally high or low levels of important body fat-derived hormones (e.g., high levels of leptin and low levels of adiponectin).
One common characteristic of the groups mentioned above is absence of obesity, even though food is abundant and often physical activity is moderate to low. Repeat for emphasis: “… even though food is abundant and often physical activity is moderate to low”. Note that having low levels of activity is not the same as spending the whole day sitting down in a comfortable chair working on a computer. Obviously caloric intake and level of activity among these groups were/are not at the levels that would lead to obesity. How could that be possible? See this post for a possible explanation.
Excessive body fat gain, lipotoxicity, and type 2 diabetes
There are a few theories that implicate the interaction of abnormal fat metabolism with other factors (e.g., genetic factors) in the development of type 2 diabetes. Empirical evidence suggests that this is a reasonable direction of causality. One of these theories is the theory of lipotoxicity.
Several articles have discussed the theory of lipotoxicity. The article by Unger & Zhou (2001) is a widely cited one. The theory seems to be widely based on the comparative study of various genotypes found in rats. Nevertheless, there is mounting evidence suggesting that the underlying mechanisms may be similar in humans. In a nutshell, this theory proposes the following steps in the development of type 2 diabetes:
(1) Abnormal fat mass gain leads to an abnormal increase in fat-derived hormones, of which leptin is singled out by the theory. Some people seem to be more susceptible than others in this respect, with lower triggering thresholds of fat mass gain. (What leads to exaggerated fat mass gains? The theory does not go into much detail here, but empirical evidence from other studies suggests that major culprits are refined grains and seeds, as well as refined sugars; other major culprits seem to be trans fats, and vegetable oils rich in linoleic acid.)
(2) Resistance to fat-derived hormones sets in. Again, leptin resistance is singled out as the key here. (This is a bit simplistic. Other fat-derived hormones, like adiponectin, seem to clearly interact with leptin.) Since leptin regulates fatty acid metabolism, the theory argues, leptin resistance is hypothesized to impair fatty acid metabolism.
(3) Impaired fat metabolism causes fatty acids to “spill over” to tissues other than fat cells, and also causes an abnormal increase in a substance called ceramide in those tissues. These include tissues in the pancreas that house beta-cells, which secrete insulin. In short, body fat should be stored in fat cells (adipocytes), not outside them.
(4) Initially fatty acid “spill over” to beta-cells enlarges them and makes them become overactive, leading to excessive insulin production in response to carbohydrate-rich foods, and also to insulin resistance. This is the pre-diabetic phase where hypoglycemic episodes happen a few hours following the consumption of carbohydrate-rich foods. Once this stage is reached, several natural carbohydrate-rich foods also become a problem (e.g., potatoes and bananas), in addition to refined carbohydrate-rich foods.
(5) Abnormal levels of ceramide induce beta-cell apoptosis in the pancreas. This is essentially “death by suicide” of beta cells in the pancreas. What follows is full-blown type 2 diabetes. Insulin production is impaired, leading to very elevated blood glucose levels following the consumption of carbohydrate-rich foods, even if they are unprocessed.
It is widely known that type 2 diabetics have impaired glucose metabolism. What is not so widely known is that usually they also have impaired fatty acid metabolism. For example, consumption of the same fatty meal is likely to lead to significantly more elevated triglyceride levels in type 2 diabetics than non-diabetics, after several hours. This is consistent with the notion that leptin resistance precedes type 2 diabetes, and inconsistent with the “tired pancreas” theory.
Weak and strong points of the theory of lipotoxicity
A weakness of the theory of lipotoxicity is its strong lipophobic tone; at least in the articles that I have read. See, for example, this article by Roger H. Unger in the Journal of the American Medical Association. There is ample evidence that eating a lot of the ultra-demonized saturated fat, per se, is not what makes people obese or type 2 diabetic. Yet overconsumption of trans fats and vegetable oils rich in linoleic acid does seem to be linked with obesity and type 2 diabetes. (So does the consumption of refined grains and seeds, and refined sugars.) The theory of lipotoxicity does not seem to make these distinctions.
In defense of the theory of lipotoxicity, it does not argue that there cannot be thin diabetics. Many type 1 diabetics are thin. Type 2 diabetics can also be thin, even though that is much less common. In certain individuals, the threshold of body fat gain that will precipitate lipotoxicity may be quite low. In others, the same amount of body fat gain (or more) may in fact increase their insulin sensitivity under certain circumstances – e.g., when growth hormone levels are abnormally low.
Autoimmune disorders, perhaps induced by environmental toxins, or toxins found in certain refined foods, may cause the immune system to attack the beta-cells in the pancreas. This may lead to type 1 diabetes if all beta cells are destroyed, or something that can easily be diagnosed as type 2 (or type 1.5) diabetes if only a portion of the cells are destroyed, in a way that does not involve lipotoxicity.
Nor does the theory of lipotoxicity predict that all those who become obese will develop type 2 diabetes. It only suggests that the probability will go up, particularly if other factors are present (e.g., genetic propensity). There are many people who are obese during most of their adult lives and never develop type 2 diabetes. On the other hand, some groups, like Hispanics, tend to develop type 2 diabetes more easily (often even before they reach the obese level). One only has to visit the South Texas region near the Rio Grande border to see this first hand.
What the theory proposes is a new way of understanding the development of type 2 diabetes; a way that seems to make more sense than the “tired pancreas” theory. The theory of lipitoxicity may not be entirely correct. For example, there may be other mechanisms associated with abnormal fat metabolism and consumption of Neolithic foods that cause beta-cell “suicide”, and that have nothing to do with lipotoxicity as proposed by the theory. (At least one fat-derived hormone, tumor necrosis factor-alpha, is associated with abnormal cell apoptosis when abnormally elevated. Levels of this hormone go up immediately after a meal rich in refined carbohydrates.) But the link that it proposes between obesity and type 2 diabetes seems to be right on target.
Implications and thoughts
Some implications and thoughts based on the discussion above are the following. Some are extrapolations based on the discussion in this post combined with those in other posts. At the time of this writing, there were 90 posts on this blog, in addition to many comments. See under "Labels" at the bottom-right area of this blog for a summary of topics addressed. It is hard to ignore things that were brought to light in previous posts.
- Let us start with a big one: Avoiding natural carbohydrate-rich foods in the absence of compromised glucose metabolism is unnecessary. Those foods do not “tire” the pancreas significantly more than protein-rich foods do. While carbohydrates are not essential macronutrients, protein is. In the absence of carbohydrates, protein will be used by the body to produce glucose to supply the needs of the brain and red blood cells. Protein elicits an insulin response that is comparable to that of natural carbohydrate-rich foods on a gram-adjusted basis (but significantly lower than that of refined carbohydrate-rich foods, like doughnuts and bagels). Usually protein does not lead to a measurable glucose response because glucagon is secreted together with insulin in response to ingestion of protein, preventing hypoglycemia.
- Abnormal fat gain should be used as a general measure of one’s likelihood of being “headed south” in terms of health. The “fitness” level for men and women shown on the table in this post seem like good targets for body fat percentage. The problem here, of course, is that this is not as easy as it sounds. Attempts at getting lean can lead to poor nutrition and/or starvation. These may make matters worse in some cases, leading to hormonal imbalances and uncontrollable hunger, which will eventually lead to obesity. Poor nutrition may also depress the immune system, making one susceptible to a viral or bacterial infection that may end up leading to beta-cell destruction and diabetes. A better approach is to place emphasis on eating a variety of natural foods, which are nutritious and satiating, and avoiding refined ones, which are often addictive “empty calories”. Generally fat loss should be slow to be healthy and sustainable.
- Finally, if glucose metabolism is compromised, one should avoid any foods in quantities that cause an abnormally elevated glucose or insulin response. All one needs is an inexpensive glucose meter to find out what those foods are. The following are indications of abnormally elevated glucose and insulin responses, respectively: an abnormally high glucose level 1 hour after a meal (postprandial hyperglycemia); and an abnormally low glucose level 2 to 4 hours after a meal (reactive hypoglycemia). What is abnormally high or low? Take a look at the peaks and troughs shown on the graph in this post; they should give you an idea. Some insulin resistant people using glucose meters will probably realize that they can still eat several natural carbohydrate-rich foods, but in small quantities, because those foods usually have a low glycemic load (even if their glycemic index is high).
Lucy was a vegetarian and Sapiens an omnivore. We apparently have not evolved to be pure carnivores, even though we can be if the circumstances require. But we absolutely have not evolved to eat many of the refined and industrialized foods available today, not even the ones marketed as “healthy”. Those foods do not make our pancreas “tired”. Among other things, they “mess up” fat metabolism, which may lead to type 2 diabetes through a complex process involving hormones secreted by body fat.
References
Humboldt, A.V. (1995). Personal narrative of a journey to the equinoctial regions of the new continent. New York, NY: Penguin Books.
Unger, R.H., & Zhou, Y.-T. (2001). Lipotoxicity of beta-cells in obesity and in other causes of fatty acid spillover. Diabetes, 50(1), S118-S121.
Monday, August 23, 2010
Produce Labels Explained
Have you ever wondered why all of the produce that you bring home from the grocery store has to have those annoying little stickers on them? While they can be a little irritating they do serve a purpose for grocery stores, and can serve pretty useful to us as well.The information contained on those labels is called a PLU number, or a Price Look-Up number. The International Federation for Produce Coding standardizes these codes for grocery stores, making it easier for the stores to charge appropriately when you check out. But the stickers can be advantageous to the consumer as well. They make it easier to know what we are putting into our shopping carts, by differentiating fruits and veggies. Here’s how:
- Conventional fruits and vegetables are labeled with four digit numbers that begin with a 3 or a 4. Example: a conventional Granny Smith Apple has a PLU of 4017. Conventional means that it is grown on a farm that uses harmful pesticides and chemicals.
- Organic produce has five digit PLU numbers that begin with a 9. Example: an organic Granny Smith Apple has a PLU of 94017. Organic produce is grown on farms using natural fertilizers and without the use of harmful pesticides and chemicals that can be harmful to our bodies.
- Genetically Modified (GM) produce also have five digit PLU numbers, but these begin with an 8. Example: a GM Granny Smith Apple will have a PLU of 84017. GM means that the produce's DNA has been modified through engineering, causing possible safety concerns. Many pre-packaged and processed foods contain GM foods, such as soy or corn oils, but fortunately today GM fruits and vegetables in their whole form are rare.
Ideally, we should purchase most of our fruits and vegetables from local, organic farms and farmer’s markets so we know exactly where our produce was grown and how. But, for most of us, this is not realistic and we have to shop in conventional supermarkets. Supermarkets usually designate organic produce with signage, but do not usually do so for genetically modified foods. So, when perusing the produce section of your favorite supermarket, if you are unsure if something is organic, conventional or GM, all you have to do is look at the PLU! Often, the PLU sticker will also include the country or state of origin, helping us identify how far our produce has traveled as well.
Keep it Fresh!
- Jill
Sunday, August 22, 2010
Parents in NJ are finding reasons to forgo vaccinations. Food for thought
Recently, there have been reports that whooping cough may be returning to our population, even though that population has largely been vaccinated. Could it be that vaccinations are over hyped, religiously pursued by the NJ legislature because of the medical lobby as well as pursued by drug companies trying to cash in on the next flu scare (remember swine flu, H1N1) (http://www.chetday.com/fluscaregame.htm). Our memories are as short as the media but someone made a ton of money scaring the public into getting vaccinated against the maybe disease. In the case of H1N1, our government spent a ton of money, the public did not receive this scare with open arms and they were left with tons of expiring vaccines that were not worth the bottles they were printed on. What is a scare weary public to do?
The thing that really scares me is that one day, when we have a real scare, few people will listen and the chicken little effect will occur (few people will believe it when the sky really is falling). I think that day is nearing and NJ vaccination rates are a symptom of that malaise.
We really need to rethink many of our health policies, since they often amount to scare tactics with little or no health benefit and in many cases, side effects (cholesterol lowering drugs anyone). Somehow, people in other countries have a healthier outlook without having all the stuff done to them. With regard to vaccines, this blog post is not designed to help someone decide weather or not to vaccinate their children. People should read and make their own opinions, rather than have it written into law that they must do this. It is true that some people have vaccine reactions (although a small sampling of the populace) and have neurological impairment or other problems as a result. Somehow, our society has made these risks acceptable even though much of our immunity to many diseases is natural (natural immunity still occurs believe it or not without vaccines) and natural immunity occurs by reacting to the infection.
What would happen if we decided tomorrow that vaccines are no longer mandatory? Would the masses avoid them in droves? My opinion is that it depends on what you believe. The only true way of finding out if vaccination is unnecessary is for the populace to avoid it. It would take many years to see if we need it or if the diseases we have tried to prevent come back or if our improvements in sanitation and living standards are really the reason we no longer see many of the diseases we vaccinate for.
What do you think? As always, I value your opinion.
Saturday, August 21, 2010
The Prettiest Song this Summer
My favorite song this summer. ;) It will always remind me of sunny days on the shore, breezy nights out in town and everything else that the summer has to offer. Enjoy-
Keep it fresh!
- Lauren
Thursday, August 19, 2010
Tropical Plant Fats: Coconut Oil, Part II
Heart Disease: Animal Studies
Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.
The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:
Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.
In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.
What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.
Heart Disease: Human Studies
It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.
Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.
Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).
Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.
Coconut Oil and Body Fat
In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.
Coconut Oil and Cancer
Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.
The Bottom Line
There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.
* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.
Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.
The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:
- Sunflower oil plus added cholesterol
- Copra oil, a coconut oil pressed from dried coconuts, plus added cholesterol
- Freshly pressed virgin coconut oil, plus added cholesterol
Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.
In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.
What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.
Heart Disease: Human Studies
It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.
Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.
Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).
Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.
Coconut Oil and Body Fat
In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.
Coconut Oil and Cancer
Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.
The Bottom Line
There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.
* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.
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