Right then, seeing as I have been tardy, let me bring you all up to speed. I had my unfill which was wonderful... too wonderful. I have been able to eat everything and it's dog.
So I booked to have a top up and had it done last Sunday. I had 0.5mls put back in (for free) and to be honest there is not a lot of difference. I have not been eating quite so much, but apart from that I am able to eat pretty much all things except for sliced bread/rolls.
I am finding that pitta is a really good thing for me to eat. I have had 3 pitta bread over the course of the day with hummus. Tonight's tea is roast gammon with cauliflower cheese and for afters we are having apple and blackberry crumble and custard.
I am not hungry right now, and all I have consumed all day has been pitta bread and hummus, orange juice and coffee.
If you asked me have I had a lot to eat today I would say "yes" and in the back of my min think "too much" but actually this is BECAUSE of the band causing the sensation of satisfaction. I only FEEL like I have eaten too much, when in fact I haven't.
I hope to see a difference with my eating with this fill. Not so tight that I cannot eat more than a bite, but enough so that I can keep healthy and just lose maybe even 1/2 pound per week.
I am conscious that I am not really at my 1 year out yet (Band Mk2 that is - counting November 9th as band day.), and I have lost about a 1/3rd of the weight I want to ideally lose. I hope to have knocked half the weight on its head by my Band (mk2) Anniversary.
What damage did I do to my weight whilst at open free for all... 4 lb gain. This was analysed as 1 pound of water, 1 pound of muscle and 2 pounds of fat. Not bad when you consider I ate like a hog for 2 weeks solid. Mind you, eating like a hog for someone with a band, whatever their restriction is like, is significantly reduced from the Hardcore Hog that I was pre banding!!
So, I am not going to update my weight bar and add on the 4pound gain, as I will feel horrible and it will put me in a bad place, and I will adjust it when I have lost 4 and a half pounds instead and then I will be happy.
I have exactly 6mls in my band.
I suffered with a lot of pain in my port over the last few days where I have had to resort to codeine (Thanks Dad! He gave me all 200 packets of 90 tablets given to him from the hospital after his cancer operation - bargain!). Codeine was the only thing that touched my pain before when my band broke. However, it was NOT that kind of pain, but really from the injection site. There has been no swelling, redness or anything else and I still definitely have restriction, so I am not worried, although paranoia did start to set in during the long sleepless night after the fill! Today is fine though and I have been decorating, sawing, painting and all kinds of stuff without a problem.
As for the normal lark... we have our new lodger Josh. He arrived this afternoon at 3:30 with all his stuff. He is really excited about staying and starting his apprenticeship etc. Seems like a nice lad. He has a brother aged 9 too so just like home really!
Right, over and out for today.
Wednesday, August 27, 2008
Tuesday, August 26, 2008
Eating Down the Food Chain
Europe once teemed with large mammals, including species of elephant, lion, tiger, bear, moose and bison. America was also home to a number of huge and unusual animals: mammoths, dire wolves, lions, giant sloths and others.
The same goes for Australia, where giant kangaroos, huge wombats and marsupial 'lions' once roamed.
What do these extinctions have in common? They all occurred around when humans arrived. The idea that humans caused them is hotly debated, because they also sometimes coincided with climactic and vegetation changes. However, I believe the fact that these extinctions occurred on several different continents about when humans arrived points to an anthropogenic explanation.
A recent archaeological study from the island of Tasmania off the coast of Australia supports the idea that humans were behind the Australian extinctions. Many large animals went extinct around the time when humans arrived in Australia, but that time also coincided with a change in climate. What the new study shows is that the same large animals survived for another 5,000 years in Tasmania... until humans arrived there from the mainland. Then they promptly went extinct. That time period didn't correspond to a major climate change, so it's hard to explain it away.
It's a harsh reality that our big brains and remarkable adaptability give us the power to be exceptionally destructive to the environment. We're good at finding the most productive niches available, and exploiting them until they implode. Jared Diamond wrote an excellent book on the subject called Collapse, which details how nearly every major civilization collapse throughout history was caused at least in part by environmental damage. It's been a hallmark of human history since the beginning.
I don't think it will take much to convince you that the trend has accelerated in modern times. Ocean life, our major source of nutrient-rich wild food, has already been severely depleted. The current extinction rate is estimated to be over 1,000 times the baseline, pre-modern level, and rising.
Humans have always been top-level predators. We kill and eat nutrient-dense prey that is often much larger than we are. But today, the extinction of such walking meat lockers has caused us to eat down the food chain. We're turning to jellyfish and sea cucumbers and... gasp... lobsters!
While it's true that we've probably always eaten things like shellfish and insects, I find it disturbing that we've depleted the oceans to the point where we can no longer sustainably eat formerly abundant carnivorous fish like tuna. We need to make a concerted effort to preserve these species because extinction is permanent.
I don't want to live in a future where the only thing on the menu is bacteria patties, the other other other other white meat.
Monday, August 25, 2008
Saharan Hunter-Gatherers Unearthed
The media recently covered an archaeological discovery in Niger that caught my attention. In the middle of the Sahara desert, researchers found a hunter-gatherer burial site containing over 200 graves ranging from about 10,000 to 4,500 years old. During this period, the region was lush and productive.
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
Among the Tenerian graves was a heart-rending burial tableaux [SIC!!]: A young woman was lying on her side. Pollen under her body suggested that she was placed on a bed of flowers. Lying on their sides facing her were two young children, their fingers interlocked with hers, leaving a tangle of bones.Haha, I couldn't let the spelling error slide, it should be 'tableau'. Hey, I'm half French, give me a break.
Friday, August 22, 2008
Fit at 70
In my professional life, I study neurodegenerative disease, the mechanisms of aging, and what the two have in common. I was reading through a textbook on aging a few months ago, and I came across an interesting series of graphs.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
Thursday, August 21, 2008
Kitava: Wrapping it Up
There's a lot to be learned from the Kitava study. Kitavans eat a diet of root vegetables, coconut, fruit, vegetables and fish and have undetectable levels of cardiovascular disease (CVD), stroke and overweight. Despite smoking like chimneys. 69% of their calories come from carbohydrate, 21% from fat and 10% from protein. This is essentially a carbohydrate-heavy version of what our paleolithic ancestors ate. They also get lots of sunshine and have a moderately high activity level.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, but most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This suggests that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and witholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? Grains and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed vegetable oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, but most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This suggests that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and witholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? Grains and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed vegetable oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
The Diabetes Miracle Diet
Michael lost 56 pounds recently over about five months. He says eating less of the same foods does not work.Instead he went on The 30-Day Diabetes Miracle
This is a vegetarian diet focused on lots of beans, oatmeal and vegetables. He also walked between 20 and 30 miles per week. His weight loss averaged between 2.5 and 3.5 pounds a week.
Wednesday, August 20, 2008
Cardiovascular Risk Factors on Kitava, Part IV: Leptin
Leptin is a hormone that is a central player in the process of weight gain and chronic disease. Its existence had been predicted for decades, but it was not identified until 1994. Although less well known than insulin, its effects on nutrient disposal, metabolic rate and feeding behaviors place it on the same level of importance.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
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