As the characters Janice and Ray used to regularly say on the Catherine Tate Show. Having whinged about Channel Five in the past, I shall now whinge about the BBC.
I watched episode 1 of "The Day of the Triffids" on BBC iPlayer and very good it was, too. So far, so good.
I then tried to watch episode 2. It was available in High Definition format only. I bought my lap-top in May 2003 and it isn't up to displaying High Definition programmes on Flash Player 10. I could listen to the programme for a while, but Firefox has a memory leak, which accelerates when trying to play High Definition programmes on Flash Player.
Once all of the memory has been used up, Firefox displays a dialog box, locks-up or just terminates. I disabled Virtual Memory on my lap-top as Hard Disk is ~500,000 times slower than RAM. I have 1GB of memory and that's it. My lap-top won't take more than 1GB of RAM.
So, Aunty Beeb. Why can't I watch programmes in either Low Definition or High Definition formats?
P.S. The BBC messageboards recently changed to the BBC iD system. I tried to migrate Nigeepoo (I've been using that username there since March 2003) to the BBC iD system to be informed "Your username appears to contain a profanity". You couldn't make this stuff up! They will be sorting it out at some point...
I'm temporarily posting there with the username Nigeep00 <- that's two zeros, by the way.
P.P.S. I was so busy whingeing that I completely forgot to wish all my readers a Happy New Year. So......
HAPPY NEW YEAR!
Thursday, December 31, 2009
Look after your tyres.
Many years ago, I used to drive a Signal Yellow Ford Fiesta 1.1S (all 3 of my cars have been bright yellow - it's a very safe colour). In 1982, around Christmas time, I had a minor prang which dented the front offside just beside the headlamp. When I got home, I tried to get my hand up the front wheel arch to inspect the damage but the wheel was in the way so I applied full left lock. What I then saw sent a chill down my spine.
Both front tyres had perfect tread on the outside edges but were worn right down to the steel belts on the inside edges. This was due to tracking error (excessive toe-out) forcing the treads outward as the car moved forward. When I had the tyres replaced and the tracking corrected, the steering felt much lighter (I didn't have power steering).
Fast-forward to 30th December 2009....
I had a slow puncture in my rear nearside tyre (due to a nail) so I went to the garage to get it repaired. The garage informed me that both rear tyres were unserviceable due to a complete lack of tread between the inside & outside edges of the tyres. My car has wide tyres and apparently, this happens even when tyres are inflated to the correct pressure.
Last week, I was driving around on snow & ice on two semi-bald tyres that provide traction, as Mazda MX-5s have Rear Wheel Drive. I got lucky...twice!
Moral of the story:- Check your treads across the full width of the tyres.
Both front tyres had perfect tread on the outside edges but were worn right down to the steel belts on the inside edges. This was due to tracking error (excessive toe-out) forcing the treads outward as the car moved forward. When I had the tyres replaced and the tracking corrected, the steering felt much lighter (I didn't have power steering).
Fast-forward to 30th December 2009....
I had a slow puncture in my rear nearside tyre (due to a nail) so I went to the garage to get it repaired. The garage informed me that both rear tyres were unserviceable due to a complete lack of tread between the inside & outside edges of the tyres. My car has wide tyres and apparently, this happens even when tyres are inflated to the correct pressure.
Last week, I was driving around on snow & ice on two semi-bald tyres that provide traction, as Mazda MX-5s have Rear Wheel Drive. I got lucky...twice!
Moral of the story:- Check your treads across the full width of the tyres.
Wednesday, December 30, 2009
The Body Fat Setpoint
One pound of human fat contains about 3,500 calories. That represents roughly 40 slices of toast. So if you were to eat one extra slice of toast every day, you would gain just under a pound of fat per month. Conversely, if you were to eat one fewer slice per day, you'd lose a pound a month. Right? Not quite.
How is it that most peoples' body fat mass stays relatively stable over long periods of time, when an imbalance of as little as 5% of calories should lead to rapid changes in weight? Is it because we do complicated calculations in our heads every day, factoring in basal metabolic rate and exercise, to make sure our energy intake precisely matches expenditure? Of course not. We're gifted with a sophisticated system of hormones and brain regions that do the "calculations" for us unconsciously*.
When it's working properly, this system precisely matches energy intake to expenditure, ensuring a stable and healthy fat mass. It does this by controlling food seeking behaviors, feelings of fullness and even energy expenditure by heat production and physical movements. If you eat a little bit more than usual at a meal, a properly functioning system will say "let's eat a little bit less next time, and perhaps also burn some of it off." This is one reason why animals in their natural habitat are nearly always at an appropriate weight, barring starvation. The only time wild animals are overweight enough to significantly compromise physical performance is when it serves an important purpose, such as preparing for hibernation.
I recently came across a classic study that illustrates these principles nicely in humans, titled "Metabolic Response to Experimental Overfeeding in Lean and Overweight Healthy Volunteers", by Dr. Erik O. Diaz and colleagues (1). They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume, under controlled conditions where the investigators could be confident of food intake. Macronutrient composition was 12-42-46 % protein-fat-carbohydrate.
After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass. Consistent with what one would expect if the body were trying to burn off excess calories and return to baseline fat mass, the metabolic rate and body heat production of the subjects increased.
Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%). Here is a graph showing changes in fat mass for each individual that completed the study:
.png)
We don't know if they would have lost the remaining fat mass in the following weeks because they were only followed for 6 weeks after overfeeding, although it did appear that they were reaching a plateau slightly above their original body weight. Thus, nearly all subjects "defended" their original body fat mass irrespective of their starting point. Underfeeding studies have shown the same phenomenon: whether lean or overweight, people tend to return to their original fat mass after underfeeding is over. Again, this supports the idea that the body has a body fat mass "set point" that it attempts to defend against changes in either direction. It's one of many systems in the body that attempt to maintain homeostasis.
OK, so why do we care?
We care because this has some very important implications for human obesity. With such a system in place to keep body fat mass in a narrow range, a major departure from that range implies that the system isn't functioning correctly. In other words, obesity has to involve a defect in the system that regulates body fat, because a properly functioning system would not have allowed that degree of fat gain in the first place.
So yes, we are overweight because we eat too many calories relative to energy expended. But why are we eating too many calories? There are a number of reasons, but one reason is that the system that should be defending a low fat mass is now defending a high fat mass. Therefore, the ideal solution is not simply to restrict calories, or burn more calories through exercise, but to try to work with the system that decides what fat mass to 'defend'. Restricting calories isn't necessarily a good solution because the body will attempt to defend its setpoint, whether high or low, by increasing hunger and decreasing its metabolic rate. That's why low-calorie diets, and most diets in general, typically fail in the long term. Restricting calories works for fat loss, but most people find it miserable to fight hunger every day.
This raises two questions:
* The hormone leptin and the hypothalamus are the ringleaders, although there are many other elements involved, such as several gut-derived peptides, insulin, and a number of other brain regions.
How is it that most peoples' body fat mass stays relatively stable over long periods of time, when an imbalance of as little as 5% of calories should lead to rapid changes in weight? Is it because we do complicated calculations in our heads every day, factoring in basal metabolic rate and exercise, to make sure our energy intake precisely matches expenditure? Of course not. We're gifted with a sophisticated system of hormones and brain regions that do the "calculations" for us unconsciously*.
When it's working properly, this system precisely matches energy intake to expenditure, ensuring a stable and healthy fat mass. It does this by controlling food seeking behaviors, feelings of fullness and even energy expenditure by heat production and physical movements. If you eat a little bit more than usual at a meal, a properly functioning system will say "let's eat a little bit less next time, and perhaps also burn some of it off." This is one reason why animals in their natural habitat are nearly always at an appropriate weight, barring starvation. The only time wild animals are overweight enough to significantly compromise physical performance is when it serves an important purpose, such as preparing for hibernation.
I recently came across a classic study that illustrates these principles nicely in humans, titled "Metabolic Response to Experimental Overfeeding in Lean and Overweight Healthy Volunteers", by Dr. Erik O. Diaz and colleagues (1). They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume, under controlled conditions where the investigators could be confident of food intake. Macronutrient composition was 12-42-46 % protein-fat-carbohydrate.
After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass. Consistent with what one would expect if the body were trying to burn off excess calories and return to baseline fat mass, the metabolic rate and body heat production of the subjects increased.
Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%). Here is a graph showing changes in fat mass for each individual that completed the study:
.png)
We don't know if they would have lost the remaining fat mass in the following weeks because they were only followed for 6 weeks after overfeeding, although it did appear that they were reaching a plateau slightly above their original body weight. Thus, nearly all subjects "defended" their original body fat mass irrespective of their starting point. Underfeeding studies have shown the same phenomenon: whether lean or overweight, people tend to return to their original fat mass after underfeeding is over. Again, this supports the idea that the body has a body fat mass "set point" that it attempts to defend against changes in either direction. It's one of many systems in the body that attempt to maintain homeostasis.OK, so why do we care?
We care because this has some very important implications for human obesity. With such a system in place to keep body fat mass in a narrow range, a major departure from that range implies that the system isn't functioning correctly. In other words, obesity has to involve a defect in the system that regulates body fat, because a properly functioning system would not have allowed that degree of fat gain in the first place.
So yes, we are overweight because we eat too many calories relative to energy expended. But why are we eating too many calories? There are a number of reasons, but one reason is that the system that should be defending a low fat mass is now defending a high fat mass. Therefore, the ideal solution is not simply to restrict calories, or burn more calories through exercise, but to try to work with the system that decides what fat mass to 'defend'. Restricting calories isn't necessarily a good solution because the body will attempt to defend its setpoint, whether high or low, by increasing hunger and decreasing its metabolic rate. That's why low-calorie diets, and most diets in general, typically fail in the long term. Restricting calories works for fat loss, but most people find it miserable to fight hunger every day.
This raises two questions:
- What caused the system to defend a high fat mass?
- Is it possible to modify the fat mass setpoint, and how would one go about it?
* The hormone leptin and the hypothalamus are the ringleaders, although there are many other elements involved, such as several gut-derived peptides, insulin, and a number of other brain regions.
Tuesday, December 29, 2009
I'm a secret lemonade drinker...
R. White's, R. White's! I'm a trying to give it up-a but it's one of those nights, R. White's, R. White's! R. White's lemona-a-ade. I'm a secret lemonade drinker...*fade to outtro*
Who remembers the above advert about a man in striped pyjamas creeping downstairs to raid the fridge for R. White's Lemonade and getting caught in the act? It reminds me of another advert currently running for Crunchy Nut Cornflakes where a man is caught eating someone else's Crunchy Nut Cornflakes in the middle of the night having been overheard on a baby monitor. Having had his bowl confiscated, the sound of sobbing is heard on the monitor, which is thrown into a drawer to muffle it. "The trouble is they taste too good!"
Do the above examples sound a bit like drug addicts trying/failing to get their fixes? As Dr John Briffa commented on Losing the taste for sweetness trumps using ‘healthy’ sweeteners, in my book, "Most animals, it turns out, chose saccharin over cocaine. Blimey."
Blimey, indeed! See Intense Sweetness Surpasses Cocaine Reward. Why is this? A possible explanation lies in Hypoglycemia & Neurosis.
"Who is drawn to such "peculiar" diets? The answer, it seems, is those who crave relief from repressed pain and stress in their lives. Sugar somehow elicits the secretion of the body's "feel-good" endorphins, so much so that the pain threshold of baby rats almost doubles. The blood of newborn human babies is routinely sampled by heel prick, a painful procedure that usually causes crying. However, after sugar is given, the tears are brief. Beta-endorphin levels increase in binge-eaters (Blass 1987-1995, Fullerton 1985), which may be why they over-eat.
However, endorphins eventually fall in chronically sugar-fed rats, and their pain thresholds fall with them (Roane 1990). In other words, you need more and more sugar to get the same relief, until you're in Betty Crocker country and your diet has become "peculiar." This kind of "habituation" is found in all opiate-mediated addictions, including chronic alcoholism (Genazzani 1982), in which opiate-like isoquinolones are formed from a breakdown product of alcohol and the neurotransmitter dopamine.
Endorphins, our self-made opiates, have receptors in brain structures mediating emotional feelings as well as those dealing with physical sensations of pain and stress. The sense of urgency we experience with a full bladder is caused by low endorphins. Babies who are breast-fed often appear ecstatic, and this state coincides with high levels of endorphins. In adults, there are high levels of endorphins during and after orgasm. Thus, endorphins motivate as well as providing comfort and gating pain. And they are among the most addictive substances on the face of the planet. So perhaps it's not so surprising that "20 percent [of hypoglycemics] give a history of intense, insatiable and irresistible craving for sweets and carbohydrates" (Buehler 1955), while the rest are strongly attached to their "peculiar" diets. Hypoglycemics are unwittingly trying to self-medicate their profound subconscious malaise with food.
A Canadian who was diagnosed hypoglycemic years ago told me that he was left to cry for the first eight months of his life, until his mother found that sweetened condensed milk comforted him. From then on, he had vast quantities of sugar. In therapy, he realized sugar comforted the buried desolation imprinted in him by his early deprivation, and that eating too little food was a symbolic recreation of this trauma."
As for me, when I was little, I remember eating Rusks, which were very sweet. I also recall getting a regular supply of French fancies and Corona lemonade, which were also very sweet. As we were quite poor, mum used to spend hours on a typewriter doing secretarial stuff to raise extra money. I found comfort in sweet foods. I now have a "sweet tooth" and get great pleasure from eating. Coincidence?
Modern baby formulas are crammed with sugar.
Another Quality Street, anyone? Or how about a wafer-thin mint?
Who remembers the above advert about a man in striped pyjamas creeping downstairs to raid the fridge for R. White's Lemonade and getting caught in the act? It reminds me of another advert currently running for Crunchy Nut Cornflakes where a man is caught eating someone else's Crunchy Nut Cornflakes in the middle of the night having been overheard on a baby monitor. Having had his bowl confiscated, the sound of sobbing is heard on the monitor, which is thrown into a drawer to muffle it. "The trouble is they taste too good!"
Do the above examples sound a bit like drug addicts trying/failing to get their fixes? As Dr John Briffa commented on Losing the taste for sweetness trumps using ‘healthy’ sweeteners, in my book, "Most animals, it turns out, chose saccharin over cocaine. Blimey."
Blimey, indeed! See Intense Sweetness Surpasses Cocaine Reward. Why is this? A possible explanation lies in Hypoglycemia & Neurosis.
"Who is drawn to such "peculiar" diets? The answer, it seems, is those who crave relief from repressed pain and stress in their lives. Sugar somehow elicits the secretion of the body's "feel-good" endorphins, so much so that the pain threshold of baby rats almost doubles. The blood of newborn human babies is routinely sampled by heel prick, a painful procedure that usually causes crying. However, after sugar is given, the tears are brief. Beta-endorphin levels increase in binge-eaters (Blass 1987-1995, Fullerton 1985), which may be why they over-eat.
However, endorphins eventually fall in chronically sugar-fed rats, and their pain thresholds fall with them (Roane 1990). In other words, you need more and more sugar to get the same relief, until you're in Betty Crocker country and your diet has become "peculiar." This kind of "habituation" is found in all opiate-mediated addictions, including chronic alcoholism (Genazzani 1982), in which opiate-like isoquinolones are formed from a breakdown product of alcohol and the neurotransmitter dopamine.
Endorphins, our self-made opiates, have receptors in brain structures mediating emotional feelings as well as those dealing with physical sensations of pain and stress. The sense of urgency we experience with a full bladder is caused by low endorphins. Babies who are breast-fed often appear ecstatic, and this state coincides with high levels of endorphins. In adults, there are high levels of endorphins during and after orgasm. Thus, endorphins motivate as well as providing comfort and gating pain. And they are among the most addictive substances on the face of the planet. So perhaps it's not so surprising that "20 percent [of hypoglycemics] give a history of intense, insatiable and irresistible craving for sweets and carbohydrates" (Buehler 1955), while the rest are strongly attached to their "peculiar" diets. Hypoglycemics are unwittingly trying to self-medicate their profound subconscious malaise with food.
A Canadian who was diagnosed hypoglycemic years ago told me that he was left to cry for the first eight months of his life, until his mother found that sweetened condensed milk comforted him. From then on, he had vast quantities of sugar. In therapy, he realized sugar comforted the buried desolation imprinted in him by his early deprivation, and that eating too little food was a symbolic recreation of this trauma."
As for me, when I was little, I remember eating Rusks, which were very sweet. I also recall getting a regular supply of French fancies and Corona lemonade, which were also very sweet. As we were quite poor, mum used to spend hours on a typewriter doing secretarial stuff to raise extra money. I found comfort in sweet foods. I now have a "sweet tooth" and get great pleasure from eating. Coincidence?
Modern baby formulas are crammed with sugar.
Another Quality Street, anyone? Or how about a wafer-thin mint?
Monday, December 28, 2009
Top Ten Gluten-Free Recipes on Gluten-Free Goddess®
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| Reader's faves: the top gluten-free recipes on Gluten-Free Goddess blog. |
As the first decade of the new millennium chugs to a long slow finish like the spunky little engine that could, top ten lists are sprouting up everywhere. Top ten movies, top ten playlists. Which begs the burning question for celiac survivors. Hello! Where is our own gluten-free top ten list? Where is our shining and sparkly Top Ten Gluten-Free Goodness? It's a new year. A spanking new decade. Let's party.
So without further ado, here is my own humble contribution to the Best of the Best in the expanding gluten-free recipe universe.
Sunday, December 27, 2009
A Bevy of Gluten-Free: Fruit and Vegetables
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| Jewels at the farmers' market -- naturally gluten-free. |
Walking the Santa Monica Farmers' Market beneath dove gray December skies I fell in love with the quiet beauty of seasonal fruits and vegetables protected under netting. There is something so poetic, so archetypal about it. So shy and evocative. Seductive and beckoning. So downright bridal. So understated gorgeous. So rather than waxing all Emily Dickinson on ya and conjuring words for the experience I thought I might use my camera instead.
And let my pictures do the talking.
Friday, December 25, 2009
back after new year!
Hey all! Hope people still are checking back. I think that after the new year i'm gonna be doing some videos on youtube, which i'll post here. Anyway, hope everyone having a lovely holiday, christmas and have a good new year!
These new pictures are from my new camera. 25 years 2 months old in these. Other photos with my webcam
These new pictures are from my new camera. 25 years 2 months old in these. Other photos with my webcam
Rabbits on a High-Saturated Fat Diet Without Added Cholesterol
I just saw another study that supports my previous post Animal Models of Atherosclerosis: LDL. The hypothesis is that in the absence of excessive added dietary cholesterol, saturated fat does not influence LDL or atherosclerosis in animal models, relative to other fats (although omega-6 polyunsaturated oils do lower LDL in some animal models). This appears to be consistent with what we see in humans.
In this study, they fed four groups of rabbits different diets:
Total cholesterol was also the same between all groups except the cholesterol-fed group. TBARS, a measure of lipid oxidation in the blood, was elevated in the cholesterol and sunflower oil groups but not in the chow or coconut groups. Oxidation of blood lipids is one of the major factors in atherosclerosis, the vascular disease that narrows arteries and increases the risk of having a heart attack. Serum vitamin C was lower in the cholesterol-fed groups but not the others.
This supports the idea that saturated fat in the absence of excess dietary cholesterol does not necessarily increase LDL, and in fact in most animals it does not.
Merry Christmas!
In this study, they fed four groups of rabbits different diets:
- Regular low-fat rabbit chow
- Regular low-fat rabbit chow plus 0.5 g cholesterol per day
- High-fat diet with 30% calories as coconut oil (saturated) and no added cholesterol
- High-fat diet with 30% calories as sunflower oil (polyunsaturated) and no added cholesterol
Total cholesterol was also the same between all groups except the cholesterol-fed group. TBARS, a measure of lipid oxidation in the blood, was elevated in the cholesterol and sunflower oil groups but not in the chow or coconut groups. Oxidation of blood lipids is one of the major factors in atherosclerosis, the vascular disease that narrows arteries and increases the risk of having a heart attack. Serum vitamin C was lower in the cholesterol-fed groups but not the others. This supports the idea that saturated fat in the absence of excess dietary cholesterol does not necessarily increase LDL, and in fact in most animals it does not.
Merry Christmas!
Thursday, December 24, 2009
Look after your brain, Part 3.
Funnily enough, on the Mean Forum that I mentioned in my previous post and in the very same discussion, someone suggested two supplements of which I was unaware that can improve mental function.
1) SAMe (S-adenosyl-methionine). See S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's Disease and Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer's Disease: a review.
2) Methylcobalamin, sublingual. See From mild cognitive impairment to Alzheimer's Disease - influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up and Cumulative incidence of vitamin B12 deficiency in patients with Alzheimer's Disease.
Vitamin B12 should be taken sub-lingually (or nasally), as old people's stomachs secrete less Intrinsic Factor (required for B12 absorption in the gut) than young people's. Old people who take a Proton Pump Inhibitor (***prazole) for acid reflux secrete even less Intrinsic Factor still.
I will give these a try.
Continued on Look after your brain, Part 4.
1) SAMe (S-adenosyl-methionine). See S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's Disease and Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer's Disease: a review.
2) Methylcobalamin, sublingual. See From mild cognitive impairment to Alzheimer's Disease - influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up and Cumulative incidence of vitamin B12 deficiency in patients with Alzheimer's Disease.
Vitamin B12 should be taken sub-lingually (or nasally), as old people's stomachs secrete less Intrinsic Factor (required for B12 absorption in the gut) than young people's. Old people who take a Proton Pump Inhibitor (***prazole) for acid reflux secrete even less Intrinsic Factor still.
I will give these a try.
Continued on Look after your brain, Part 4.
Tuesday, December 22, 2009
What's the Ideal Fasting Insulin Level?
[2013 update. I'm leaving this post up for informational purposes, but I think it's difficult to determine the "ideal" insulin level because it depends on a variety of factors including diet composition. Also, insulin assays are not always comparable to one another, particularly the older assays, so it's difficult to compare between studies]
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin is a marker of metabolic problems and may contribute to some of them as well.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. This is despite a substantial intake of carbohydrate, including fruit and vegetable sugars. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, and a relatively healthy diet growing up. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template.
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin is a marker of metabolic problems and may contribute to some of them as well.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. This is despite a substantial intake of carbohydrate, including fruit and vegetable sugars. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, and a relatively healthy diet growing up. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template.
Chocolate Quinoa Brownies- Gluten-Free and Vegan
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| Vegan gluten-free brownies made with quinoa flakes. |
Your stubborn and chocolate obsessed gluten-free goddess has been working overtime. In between shooting photographs of the holiday lights and skaters in Santa Monica and battling the return of the flu I fought off some weeks ago (I believe in recycling, Darling, but this is a wee bit ridiculous) I have been utterly possessed. Haunted by the ghost of chocolate brownies. Vegan chocolate brownies, to be exact (because I've already served up the best egg-based gluten-free brownie I can think of, so if you haven't tried my Dark Chocolate Brownie recipe or the Chocolate Brownie made with pecan meal, Darling- Go!).
Baking failures do not sit pretty with yours truly. Especially when I am achy and voiceless and my head feels like a giant damp wad of gluten-free dough with too much xanthan gum added (you gluten-free bakers know exactly what I'm talking about). I feel like the goddess of sticky, thick and dull. And there ain't no cure. Except maybe a hot toddy. Or three.
Lucky for me I have a husband who likes to bake. A husband who says (as his brittle, grumpy hot-flashing wife is muttering expletives and scraping another gooey not-in-a-good-way gluten-free vegan brownie failure into the perky polka dotted trash can), So.
How can we make this work?
For a split second I panic and think, He's over it. He's finally tired of living gluten-free. Living without baguettes and bagels and croissants out of love, a sense of duty, or comradeship and support.
He's done. Finished. He's out the door, no looking back.
Monday, December 21, 2009
Happy Winter Solstice!
Wishing you and your family
the warmest of winter greetings
for a safe, healthy and beautiful holiday season.
xox
Karina
Sunday, December 20, 2009
How many working brain cells do drug company lackeys have?
In Elvis lives!, I referred to the study Intensive lipid lowering with atorvastatin in patients with coronary heart disease and chronic kidney disease: the TNT (Treating to New Targets) study*, which came to the conclusion:
"Aggressive lipid lowering with atorvastatin 80 mg was both safe and effective in reducing the excess of cardiovascular events in a high-risk population with CKD and CHD."
I then pointed out the following teensy-weensy flaw in the conclusion:
"What the abstract failed to mention was the fact that there were 26 more deaths in the 80mg Atorvastatin group than in the 10mg group. What's worse? Having a major cardiovascular event or being dead?"
On a Mean Forum far away, I pointed out this teensy-weensy flaw in the conclusion and was told "are you really that retarded?" Funnily enough, I never got an answer from that person as to how the conclusion in red was justified by the data in green. I helpfully suggested that it might have something to do with the fact that Atorvastatin 80mg is a 700% increase in sales compared to Atorvastatin 10mg.
I then received an e-mail from Pfizer ® Customer Service with a spoofed sending address (it was fairly obvious that it was spoofed as it was my e-mail address!). There was the usual helpful Outlook Express "Some pictures have been blocked to help prevent the sender from identifying your computer. Click here to download pictures" message. I didn't click. Well, would you? I deleted the e-mail. I've now enabled comment moderation just in case this 'tard feels like spamming my Blog.
Pfizer manufactures Atorvastatin. Ho-hum!
*Funding for the study was provided by Pfizer Inc., New York, New York. Dr. Shepherd has received consulting fees from AstraZeneca, GlaxoSmithKline, Merck, Oxford Biosensors, Pfizer Inc., and Schering-Plough, and lecture fees from AstraZeneca, Merck, and Schering-Plough. Dr. Kastelein has received consulting fees and lecture fees from Pfizer Inc., AstraZeneca, Merck, and Schering-Plough, and grant support from Pfizer Inc. and AstraZeneca. Dr. Bittner has received consulting fees from CV Therapeutics, Novartis, Pfizer Inc., Abbott, and Reliant, and grant support from Pfizer Inc., Atherogenics, Merck, Kos Pharmaceuticals, Abbott, CV Therapeutics, and the National Institutes of Health. Dr. Deedwania has received consulting fees and lecture fees from Pfizer Inc. and AstraZeneca. Dr. Breazna, Dr. Wilson, and Dr. Zuckerman are all employees of Pfizer Inc. Mr. Dobson is an employee of Envision Pharma Ltd., which was a paid consultant to Pfizer Inc. in connection with the development of the manuscript. Dr. Wenger has received consulting fees from CV Therapeutics, Sanofi-Aventis, Schering-Plough, AstraZeneca, Abbott, Merck, and Pfizer Inc., and grant support from Pfizer Inc., Merck, and the National Heart, Lung, and Blood Institute.
"Aggressive lipid lowering with atorvastatin 80 mg was both safe and effective in reducing the excess of cardiovascular events in a high-risk population with CKD and CHD."
I then pointed out the following teensy-weensy flaw in the conclusion:
"What the abstract failed to mention was the fact that there were 26 more deaths in the 80mg Atorvastatin group than in the 10mg group. What's worse? Having a major cardiovascular event or being dead?"
On a Mean Forum far away, I pointed out this teensy-weensy flaw in the conclusion and was told "are you really that retarded?" Funnily enough, I never got an answer from that person as to how the conclusion in red was justified by the data in green. I helpfully suggested that it might have something to do with the fact that Atorvastatin 80mg is a 700% increase in sales compared to Atorvastatin 10mg.
I then received an e-mail from Pfizer ® Customer Service with a spoofed sending address (it was fairly obvious that it was spoofed as it was my e-mail address!). There was the usual helpful Outlook Express "Some pictures have been blocked to help prevent the sender from identifying your computer. Click here to download pictures" message. I didn't click. Well, would you? I deleted the e-mail. I've now enabled comment moderation just in case this 'tard feels like spamming my Blog.
Pfizer manufactures Atorvastatin. Ho-hum!
*Funding for the study was provided by Pfizer Inc., New York, New York. Dr. Shepherd has received consulting fees from AstraZeneca, GlaxoSmithKline, Merck, Oxford Biosensors, Pfizer Inc., and Schering-Plough, and lecture fees from AstraZeneca, Merck, and Schering-Plough. Dr. Kastelein has received consulting fees and lecture fees from Pfizer Inc., AstraZeneca, Merck, and Schering-Plough, and grant support from Pfizer Inc. and AstraZeneca. Dr. Bittner has received consulting fees from CV Therapeutics, Novartis, Pfizer Inc., Abbott, and Reliant, and grant support from Pfizer Inc., Atherogenics, Merck, Kos Pharmaceuticals, Abbott, CV Therapeutics, and the National Institutes of Health. Dr. Deedwania has received consulting fees and lecture fees from Pfizer Inc. and AstraZeneca. Dr. Breazna, Dr. Wilson, and Dr. Zuckerman are all employees of Pfizer Inc. Mr. Dobson is an employee of Envision Pharma Ltd., which was a paid consultant to Pfizer Inc. in connection with the development of the manuscript. Dr. Wenger has received consulting fees from CV Therapeutics, Sanofi-Aventis, Schering-Plough, AstraZeneca, Abbott, Merck, and Pfizer Inc., and grant support from Pfizer Inc., Merck, and the National Heart, Lung, and Blood Institute.
Thursday, December 17, 2009
Jewels at the Santa Monica Farmers Market
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| Gorgeous fresh picked carrots in a rainbow of colors. |
This week at the Santa Monica Farmers' Market the jewels of the season glow. Among my favorites? The rainbow carrots in orange, ruby, purple and gold. Some roots were so young they were the tiniest of crooked fingers, delicate and naturally sweet. These carrots make wonderful crudities for hummus.
Serve raw with:
Roasted Red Pepper Hummus
Jalapeño Lime Hummus
Classic Hummus Tahini with Spiced Olive Oil
Read more + get the recipe >>
Roasted Red Pepper Hummus Recipe
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| Red pepper hummus - a fab gluten-free vegan snack. |
Get your hummus on. It's party time! The holiday season is upon us and that means it's time to whip up your favorite hummus and dip recipes. After all, the days are still getting shorter (my personal excuse for partying). And Winter Solstice- also known as the shortest, darkest day of the year- is only days away.
Then it's here comes the sun, Baby. So. Huzzah! Let's celebrate. To help in such a worthy cause, here's one of our favorite hummus recipes.
Let the sun shine in.
Roasted Red Pepper Hummus Recipe
Forget store bought hummus that's been sitting in the deli case for weeks. It's laden with soybean oil. Or worse. And hummus is such an easy treat to make at home- especially if you have a food processor. Five minutes prep- and you're ready to rock.Ingredients:
1 16-oz. (or 14-15-ounce) can chilled chickpeas
or garbanzo beans, drainedJuice of one fresh lemon
2 tablespoons sesame tahini
, sunflower seed or nut butter
4 cloves fresh garlic, peeled
1/3 cup roasted red peppers (if using jarred, drain the peppers)
3 tablespoons tasty extra virgin olive oil
2 tablespoons fresh parsley or basil, roughly chopped
Pinch of sea salt, to taste
Instructions:
Combine all of the ingredients in a food processor until creamy smooth.
Combine all of the ingredients in a food processor until creamy smooth.
Taste test and adjust the olive oil and seasoning to your liking. Cover and chill until serving.
Fab with fresh organic veggies, rice crackers, or organic blue corn chips. Or serve with my gluten-free easy Brown Rice Tortilla Chips, Buttermilk Flat Bread, or Savory Grain-free Crackers.
Recipe Source: glutenfreegoddess.blogspot.com
All images & content are copyright protected, all rights reserved. Please do not use our images or content without prior permission. Thank you.
Karina's Note:
This naturally gluten-free hummus is also fab as a side dish with a plate of roasted vegetables and brown rice. It's a perfect way to add a complementary protein to a vegan meal.
More (Gluten-Free and Fabulous) Hummus Recipes To Dip Your Chip In
and last but by no means least...
It looks molto yummy and me, I'm thinking, why not puree it into a party dip?
Recipe Source: glutenfreegoddess.blogspot.com
All images & content are copyright protected, all rights reserved. Please do not use our images or content without prior permission. Thank you.
Tuesday, December 15, 2009
The Dirty Little Secret of the Diet-Heart Hypothesis
The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. What have these studies found?
The large majority of observational studies have found no connection between habitualsaturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. The abstract claims that saturated fat was associated with heart attack risk. However, the association disappeared when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is a dominant cause of cardiovascular disease, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be complete, some studies have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was very small.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. In case you're concerned that I'm cherry-picking studies, here are links to review papers on the same data that have reached the same conclusion:
Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition. 2010. "A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association between saturated fat consumption and heart attack risk.
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov challenges the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. Could this hypothesis be less well supported than it appears? The data that are used to support it come almost exclusively from short-term feeding studies (<3 and="" association="" between="" blood="" consumption="" effect="" fat="" found="" habitual="" have="" here="" how="" information="" is="" lipids.="" little="" long="" months="" most="" nbsp="" observational="" on="" p="" persists="" saturated="" studies="" surprisingly="" this="">
The large majority of observational studies have found no connection between habitualsaturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. The abstract claims that saturated fat was associated with heart attack risk. However, the association disappeared when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is a dominant cause of cardiovascular disease, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be complete, some studies have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was very small.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. In case you're concerned that I'm cherry-picking studies, here are links to review papers on the same data that have reached the same conclusion:
Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition. 2010. "A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association between saturated fat consumption and heart attack risk.
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov challenges the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. Could this hypothesis be less well supported than it appears? The data that are used to support it come almost exclusively from short-term feeding studies (<3 and="" association="" between="" blood="" consumption="" effect="" fat="" found="" habitual="" have="" here="" how="" information="" is="" lipids.="" little="" long="" months="" most="" nbsp="" observational="" on="" p="" persists="" saturated="" studies="" surprisingly="" this="">
Monday, December 14, 2009
Thumbprint Cookies with Buckwheat Flour + Brown Sugar
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| Gluten-free thumbprint cookies made with buckwheat flour + brown sugar. |
'Tis the season for baking cookies. So I feel no guilt at all tempting you with my latest gluten-free baking success. What kind of gluten-free goddess would I be if I didn't keep conjuring up cookie recipes? I ask you. Not a goddess worth her salt- er- sugar. So I am not going to apologize for the calories, or the fat or the organic golden brown sugar in this recipe. Goddesses do not apologize for their cookies. Not during cookie season, anyway. And besides, Sweetcakes, a treat should be a treat. Life is short. Daylight is dwindling.
Live a little.
Read more + get the recipe >>
Saturday, December 12, 2009
How many working brain cells do researchers have?
Apparently (according to a Japanese study referred to in Am I Missing Something??? ), eating/drinking lots of sugary & starchy carbohydrate causes postprandial hyperglycemia (high blood glucose after meals) in people with type 2 Diabetes. No sh*t, Sherlock! Postprandial hyperglycemia "causes damage to blood vessels, inflammation and oxidation and these cause clogged vessels and heart attacks." I think we're all in agreement that postprandial hyperglycemia is BAD. So, how to tackle this thorny problem? By pharmacological approaches i.e. drug therapies. Like, Duh!
And what is Diabetes-UK's (& the ADA's) dietary advice to people with type 2 Diabetes?
"The actual amount of carbohydrate that the body needs varies depending on your age, weight and activity levels, but it should make up about half of what you eat and drink." & under Ten steps to eating well:
"At each meal include starchy carbohydrate foods
Examples include bread, pasta, chapatis, potatoes, yam, noodles, rice and cereals. The amount of carbohydrate you eat is important to control your blood glucose levels." Like, Duh!
I've been doing a bit of research on methylglyoxal (MG) as a result of reading Methylglyoxal on Atkins... Uh oh! Apparently it's very toxic, therefore ketogenic diets are BAD, mmm-kay? MG causes Insulin Resistance and Advanced Glycation End-products which are both deemed to be undesirable.
Consider this: MG is a glycolysis (conversion of glucose to pyruvate) inhibitor. As MG inhibits glycolysis in cells, uptake of Blood Glucose by cells decreases. Oh, look. Cells have become Insulin Resistant! As uptake of Blood Glucose by cells decreases, Blood Glucose rises. Oh, look. Increased Advanced Glycation End-products! It's bleedin' obvious (to anyone with a sufficient number of working brain cells) that, on a high-carb diet, MG is toxic. It's a no-brainer that MG's toxicity disappears on a low-carb/keto diet, when you actually want cells to burn fatty acids/ketones rather than glucose. Like, Duh!
In fact, strangulating the glucose pathway in cells may have benefits. See Cancer.
Here's another one. According to Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet (KD), "The KD resulted in progressive loss of BMC." And yet, just above, "Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D." Like, Duh!
And what is Diabetes-UK's (& the ADA's) dietary advice to people with type 2 Diabetes?
"The actual amount of carbohydrate that the body needs varies depending on your age, weight and activity levels, but it should make up about half of what you eat and drink." & under Ten steps to eating well:
"At each meal include starchy carbohydrate foods
Examples include bread, pasta, chapatis, potatoes, yam, noodles, rice and cereals. The amount of carbohydrate you eat is important to control your blood glucose levels." Like, Duh!
I've been doing a bit of research on methylglyoxal (MG) as a result of reading Methylglyoxal on Atkins... Uh oh! Apparently it's very toxic, therefore ketogenic diets are BAD, mmm-kay? MG causes Insulin Resistance and Advanced Glycation End-products which are both deemed to be undesirable.
Consider this: MG is a glycolysis (conversion of glucose to pyruvate) inhibitor. As MG inhibits glycolysis in cells, uptake of Blood Glucose by cells decreases. Oh, look. Cells have become Insulin Resistant! As uptake of Blood Glucose by cells decreases, Blood Glucose rises. Oh, look. Increased Advanced Glycation End-products! It's bleedin' obvious (to anyone with a sufficient number of working brain cells) that, on a high-carb diet, MG is toxic. It's a no-brainer that MG's toxicity disappears on a low-carb/keto diet, when you actually want cells to burn fatty acids/ketones rather than glucose. Like, Duh!
In fact, strangulating the glucose pathway in cells may have benefits. See Cancer.
Here's another one. According to Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet (KD), "The KD resulted in progressive loss of BMC." And yet, just above, "Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D." Like, Duh!
Thursday, December 10, 2009
Why Most Published Research Findings Are False.
Following on from The future: I just saw it, I thought you might find this 2005 study by John P. A. Ioannidis of interest.
"Summary
"Summary
There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research."
For more on this, see Who pays the piper and Who pays the piper part 2.
Tuesday, December 8, 2009
Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance?
An Interesting Finding
Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:
The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.
Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:
I found this study thought-provoking, so I looked into butyrate further.
Butyrate Suppresses Inflammation in the Gut and Other Tissues
In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.
It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Some investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.
Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal permeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).
Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.
Butyrate Increases Resistance to Metabolic and Physical Stress
Certain types of fiber reduce atherosclerosis in animal models, and this effect may be due to butyrate production produced when the fiber is fermented. Fiber intake was associated with lower blood markers of inflammation in the Women's Health Initiative study, and has been repeatedly associated with lower heart attack risk and reduced progression of atherosclerosis in humans. Butyrate also sharply reduces the harmful effects of type 1 diabetes in rats, as does dietary fiber to a lesser extent.
Butyrate increases the function and survival of mice with certain neurodegenerative diseases. Polyglutamine diseases, which are the most common class of genetic neurodegenerative diseases, are delayed in mice treated with butyrate (1, 2, 3). Many of you have probably heard of Huntington's disease, which is the most common of the class. I did my thesis on a polyglutamine disease called SCA7, and this is the first suggestion I've seen that diet may be able to modify its course.
Yet another interesting finding in the first paper I discussed: mice treated with butyrate were more cold-resistant than the comparison group. When they were both placed in a cold room, body temperature dropped quite a bit in the comparison group, while it remained relatively stable in the butyrate group, despite the fact that the butyrate group was leaner****. This was due to increased heat production in the butyrate group.
Due to the potent effect butyrate has on a number of bodily processes, it may be a fundamental controller of metabolism, stress resistance and the immune system in mammals.
An Ancient Line of Communication Between Symbiotic Organisms
Why does butyrate have so much control over inflammation? Let's think about where it comes from. Bacteria in the gut produce it. It's a source of energy, so our bodies take it up readily. It's one of the main molecules that passes from the symbiotic (helpful) bacteria in the gut to the rest of the body. Could it be that the body receives butyrate as a signal that there's a thriving colony of symbiotic bacteria in the gut, inducing immune tolerance to them? The body may alter its immune response (inflammation) in order to permit a mutually beneficial relationship between itself and its symbionts.
Sources of Butyrate
There are two main ways to get butyrate and other short-chain fatty acids. The first is to eat fiber and let your intestinal bacteria do the rest. Whole plant foods such as sweet potatoes, properly prepared whole grains, beans, vegetables, fruit and nuts are good sources of fiber. Refined foods such as white flour, white rice and sugar are very low in fiber. Clinical trials have shown that increasing dietary fiber increases butyrate production, and decreasing fiber decreases it (free full text).
Butyrate also occurs in significant amounts in food. What foods contain butyrate? Hmm, I wonder where the name BUTYR-ate came from? Butter perhaps? Butter is 3-4 percent butyrate, the richest known source. But everyone knows butter is bad for you, right?
After thinking about it, I've decided that butyrate may have been a principal component of Dr. Weston Price's legendary butter oil. Price used this oil in conjunction with high-vitamin cod liver oil to heal tooth decay and a number of other ailments in his patients. The method he used to produce it would have concentrated fats with a low melting temperature, including butyrate, in addition to vitamin K2*****. Thus, the combination of high-vitamin cod liver oil and butter oil would have provided a potent cocktail of fat-soluble vitamins (A, D3, K2), omega-3 fatty acids and butyrate. It's no wonder it was so effective in his patients.
* According to insulin tolerance test.
** Acetate (acetic acid, the main acid in vinegar), propionate and butyrate are the primary three fatty acids produced by intestinal fermentation.
*** The lowest concentration used in this study, 30 micromolar, is probably higher than the concentration in peripheral serum under normal circumstances. Human serum butyrate is in the range of 4 micromolar in British adults, and 29 micromolar in the hepatic portal vein which brings fats from the digestive tract to the liver (ref). This would likely be at least two-fold higher in populations eating high-fiber diets.
**** Due to higher mitochondrial density in brown fat and more mitochondrial uncoupling.
***** Slow crystallization, which selectively concentrates triglycerides with a low melting point.
Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:
The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:
Butyrate and its derivatives may have potential application in the prevention and treatment of metabolic syndrome in humans.There's one caveat, however: the butyrate group at less food. Something about the butyrate treatment caused their food intake to decline after 3 weeks, dropping roughly 20% by 10 weeks. The investigators cleverly tried to hide this by normalizing food intake to body weight, making it look like the food intake of the comparison group was dropping as well (when actually it was staying the same as this group was gaining weight). This does cast some doubt on the health-promoting effects of high-dose butyrate.
I found this study thought-provoking, so I looked into butyrate further.
Butyrate Suppresses Inflammation in the Gut and Other Tissues
In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.
It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Some investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.
Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal permeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).
Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.
Butyrate Increases Resistance to Metabolic and Physical Stress
Certain types of fiber reduce atherosclerosis in animal models, and this effect may be due to butyrate production produced when the fiber is fermented. Fiber intake was associated with lower blood markers of inflammation in the Women's Health Initiative study, and has been repeatedly associated with lower heart attack risk and reduced progression of atherosclerosis in humans. Butyrate also sharply reduces the harmful effects of type 1 diabetes in rats, as does dietary fiber to a lesser extent.
Butyrate increases the function and survival of mice with certain neurodegenerative diseases. Polyglutamine diseases, which are the most common class of genetic neurodegenerative diseases, are delayed in mice treated with butyrate (1, 2, 3). Many of you have probably heard of Huntington's disease, which is the most common of the class. I did my thesis on a polyglutamine disease called SCA7, and this is the first suggestion I've seen that diet may be able to modify its course.
Yet another interesting finding in the first paper I discussed: mice treated with butyrate were more cold-resistant than the comparison group. When they were both placed in a cold room, body temperature dropped quite a bit in the comparison group, while it remained relatively stable in the butyrate group, despite the fact that the butyrate group was leaner****. This was due to increased heat production in the butyrate group.
Due to the potent effect butyrate has on a number of bodily processes, it may be a fundamental controller of metabolism, stress resistance and the immune system in mammals.
An Ancient Line of Communication Between Symbiotic Organisms
Why does butyrate have so much control over inflammation? Let's think about where it comes from. Bacteria in the gut produce it. It's a source of energy, so our bodies take it up readily. It's one of the main molecules that passes from the symbiotic (helpful) bacteria in the gut to the rest of the body. Could it be that the body receives butyrate as a signal that there's a thriving colony of symbiotic bacteria in the gut, inducing immune tolerance to them? The body may alter its immune response (inflammation) in order to permit a mutually beneficial relationship between itself and its symbionts.
Sources of Butyrate
There are two main ways to get butyrate and other short-chain fatty acids. The first is to eat fiber and let your intestinal bacteria do the rest. Whole plant foods such as sweet potatoes, properly prepared whole grains, beans, vegetables, fruit and nuts are good sources of fiber. Refined foods such as white flour, white rice and sugar are very low in fiber. Clinical trials have shown that increasing dietary fiber increases butyrate production, and decreasing fiber decreases it (free full text).
Butyrate also occurs in significant amounts in food. What foods contain butyrate? Hmm, I wonder where the name BUTYR-ate came from? Butter perhaps? Butter is 3-4 percent butyrate, the richest known source. But everyone knows butter is bad for you, right?
After thinking about it, I've decided that butyrate may have been a principal component of Dr. Weston Price's legendary butter oil. Price used this oil in conjunction with high-vitamin cod liver oil to heal tooth decay and a number of other ailments in his patients. The method he used to produce it would have concentrated fats with a low melting temperature, including butyrate, in addition to vitamin K2*****. Thus, the combination of high-vitamin cod liver oil and butter oil would have provided a potent cocktail of fat-soluble vitamins (A, D3, K2), omega-3 fatty acids and butyrate. It's no wonder it was so effective in his patients.
* According to insulin tolerance test.
** Acetate (acetic acid, the main acid in vinegar), propionate and butyrate are the primary three fatty acids produced by intestinal fermentation.
*** The lowest concentration used in this study, 30 micromolar, is probably higher than the concentration in peripheral serum under normal circumstances. Human serum butyrate is in the range of 4 micromolar in British adults, and 29 micromolar in the hepatic portal vein which brings fats from the digestive tract to the liver (ref). This would likely be at least two-fold higher in populations eating high-fiber diets.
**** Due to higher mitochondrial density in brown fat and more mitochondrial uncoupling.
***** Slow crystallization, which selectively concentrates triglycerides with a low melting point.
Thursday, December 3, 2009
Some more nails for the coffin of the "healthy low-fat" diet.
Every time someone writes "I'm eating a healthy low-fat diet", I cringe. It's presumptuous to assume that, because the fat content is low, the diet is automatically healthy. The media tell us it's healthy. The government tells us it's healthy. "Experts" tell us it's healthy. It must be healthy, right? Um...
See After-eating effects: Carbohydrates vs. fats and Reduced oxidation of dietary fat after a short term high-carbohydrate diet.
The low-fat diet was white bread, potatoes, tuna, chicken, carrots, canned fruit, fruit juices, cola, jam, marmalade, sweets, and sugar cubes.
The higher-fat diet was less of the above, plus a fat spread, which consisted of a mixture of lard, palm oil, olive oil, and corn oil (the ratio of polyunsaturated to saturated fat was 0.5:1).
Please excuse the following "shouting", but some facts need to be shouted from the rooftops:-
1) LDL CHOLESTEROL (LDL-C) DOES NOT CLOG YOUR ARTERIES. LDL-C IS NOT BAD CHOLESTEROL.
2) OXIDISED LDL-C (OX-LDL-C) DOES CLOG YOUR ARTERIES. OX-LDL-C IS BAD CHOLESTEROL.
3) LARGE, FLUFFY (PHENOTYPE A) LDL-C OXIDISES SLOWLY.
4) SMALL, DENSE (PHENOTYPE B) LDL-C OXIDISES RAPIDLY.
5) AS THE PERCENTAGE OF CALORIES FROM FAT DECREASES, YOU GET LESS PHENOTYPE A AND MORE PHENOTYPE B.
If you don't believe me (and why should you?), see A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins, with particular reference to the following figure:-
At 50% fat intake, ~15% of the subjects have phenotype B. At 20% fat intake, ~50% of the subjects have phenotype B. At 10% fat intake, over 60% of the subjects have phenotype B. The subjects were all men, but women are no different in this respect.
And now we have Dietary fat intake and subsequent weight change in adults: results from the European Prospective Investigation into Cancer and Nutrition cohorts.
"Results:...The difference in mean annual weight change was 0.90 g/y (95% CI: –0.54, 2.34 g/y) for men and –1.30g/y (95% CI: –3.70, 1.11 g/y) for women per 1 g/d energy-adjusted fat intake (residual method).
Conclusions: We found no significant association between the amount or type of dietary fat and subsequent weight change in this large prospective study. These findings do not support the use of low-fat diets to prevent weight gain."
Note: -1.30g/y means that as dietary fat intake increased, weight decreased.
See After-eating effects: Carbohydrates vs. fats and Reduced oxidation of dietary fat after a short term high-carbohydrate diet.
The low-fat diet was white bread, potatoes, tuna, chicken, carrots, canned fruit, fruit juices, cola, jam, marmalade, sweets, and sugar cubes.
The higher-fat diet was less of the above, plus a fat spread, which consisted of a mixture of lard, palm oil, olive oil, and corn oil (the ratio of polyunsaturated to saturated fat was 0.5:1).
Please excuse the following "shouting", but some facts need to be shouted from the rooftops:-
1) LDL CHOLESTEROL (LDL-C) DOES NOT CLOG YOUR ARTERIES. LDL-C IS NOT BAD CHOLESTEROL.
2) OXIDISED LDL-C (OX-LDL-C) DOES CLOG YOUR ARTERIES. OX-LDL-C IS BAD CHOLESTEROL.
3) LARGE, FLUFFY (PHENOTYPE A) LDL-C OXIDISES SLOWLY.
4) SMALL, DENSE (PHENOTYPE B) LDL-C OXIDISES RAPIDLY.
5) AS THE PERCENTAGE OF CALORIES FROM FAT DECREASES, YOU GET LESS PHENOTYPE A AND MORE PHENOTYPE B.
If you don't believe me (and why should you?), see A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins, with particular reference to the following figure:-
At 50% fat intake, ~15% of the subjects have phenotype B. At 20% fat intake, ~50% of the subjects have phenotype B. At 10% fat intake, over 60% of the subjects have phenotype B. The subjects were all men, but women are no different in this respect.
And now we have Dietary fat intake and subsequent weight change in adults: results from the European Prospective Investigation into Cancer and Nutrition cohorts.
"Results:...The difference in mean annual weight change was 0.90 g/y (95% CI: –0.54, 2.34 g/y) for men and –1.30g/y (95% CI: –3.70, 1.11 g/y) for women per 1 g/d energy-adjusted fat intake (residual method).
Conclusions: We found no significant association between the amount or type of dietary fat and subsequent weight change in this large prospective study. These findings do not support the use of low-fat diets to prevent weight gain."
Note: -1.30g/y means that as dietary fat intake increased, weight decreased.
Malocclusion: Disease of Civilization, Part IX
A Summary
For those who didn't want to wade through the entire nerd safari, I offer a simple summary.
Our ancestors had straight teeth, and their wisdom teeth came in without any problem. The same continues to be true of a few non-industrial cultures today, but it's becoming rare. Wild animals also rarely suffer from orthodontic problems.
Today, the majority of people in the US and other affluent nations have some type of malocclusion, whether it's crooked teeth, overbite, open bite or a number of other possibilities.
There are three main factors that I believe contribute to malocclusion in modern societies:
In one, he made more space in her jaws by extracting teeth. In the other, he put in an apparatus that broadened her dental arch, which roughly mimics the natural process of arch growth during childhood and adolescence. This had profound effects on the girls' subsequent occlusion and facial structure:
The girl on the left had teeth extracted, while the girl on the right had her arch broadened. Under ideal circumstances, this is what should happen naturally during development. Notice any differences?
Thanks to the Weston A Price foundation's recent newsletter for the study reference.
For those who didn't want to wade through the entire nerd safari, I offer a simple summary.
Our ancestors had straight teeth, and their wisdom teeth came in without any problem. The same continues to be true of a few non-industrial cultures today, but it's becoming rare. Wild animals also rarely suffer from orthodontic problems.
Today, the majority of people in the US and other affluent nations have some type of malocclusion, whether it's crooked teeth, overbite, open bite or a number of other possibilities.
There are three main factors that I believe contribute to malocclusion in modern societies:
- Maternal nutrition during the first trimester of pregnancy. Vitamin K2, found in organs, pastured dairy and eggs, is particularly important. We may also make small amounts from the K1 found in green vegetables.
- Sucking habits from birth to age four. Breast feeding protects against malocclusion. Bottle feeding, pacifiers and finger sucking probably increase the risk of malocclusion. Cup feeding and orthodontic pacifiers are probably acceptable alternatives.
- Food toughness. The jaws probably require stress from tough food to develop correctly. This can contribute to the widening of the dental arch until roughly age 17. Beef jerky, raw vegetables, raw fruit, tough cuts of meat and nuts are all good ways to exercise the jaws.
In one, he made more space in her jaws by extracting teeth. In the other, he put in an apparatus that broadened her dental arch, which roughly mimics the natural process of arch growth during childhood and adolescence. This had profound effects on the girls' subsequent occlusion and facial structure:
The girl on the left had teeth extracted, while the girl on the right had her arch broadened. Under ideal circumstances, this is what should happen naturally during development. Notice any differences?Thanks to the Weston A Price foundation's recent newsletter for the study reference.
Tuesday, December 1, 2009
Gluten-Free Chicken Soup for Body and Soul
Gluten-Free Chicken Soup for Body and Soul
We've been living on soup since Sunday. No, not turkey leftovers soup. Jewish penicillin soup. You see, Steve- that ordinarily upbeat and tenacious husband of mine- has been feeling a tad under the weather these past few days. In truth, more than a tad. He's caught a nasty cold. The kind of cold where you ache all over and do nothing but lay in bed watching a marathon of Lost
on your laptop because to even zombie-walk to the sofa loveseat too-small-to-lay-on requires functional navigation skills and balance beyond your sinus-throbbing capacity.Poor guy.
Lucky for me, I've not succumbed to the zombie-walk inducing bug. Yet. And just in case, I've been cranking out soups. An ounce of prevention and all that. And medicine. Because when I'm not in top gluten-free goddess form conserving energy means dragging out the Crock Pot
for some easy slow-cooked comfort.
for some easy slow-cooked comfort.This is a simple healing soup with the goodness of cabbage (so beneficial to a celiac's tummy) and lots of garlic (an all-purpose fighter of evil and undead mayhem not to mention, a natural immune booster and cold-fighter). Green chiles.
I made this recipe like a peasant-style stew, starting with a layer of split chicken breasts on the bottom of the crock pot- drizzled with extra virgin olive oil, of course. Then I added eight cloves of fresh chopped garlic, lots of cut-up veggies, herbs, a can of fire roasted diced tomatoes, green chiles, and just enough organic chicken broth to cover the veggies. Good stuff.
But is my chicken soup powerful enough to stave off zombies
?
?Ah, that is the question. And here is another. I ask you (in honor of my zombie literate son who knows from zombies).
Please. Do zombies run? Go.
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