I was reading an interview with Rudolph L. Leibel and doubly-labeled water was mentioned. This sort of stuff fascinates me. Using doubly-labeled water, a mass spectrometer, loads of measurements and some mathematics, it's possible to work out how many kcals someone is burning. This method costs an arm & a leg. So, how does doubly-labeled water work?
Chemistry 101:
Water has the formula H2O. H stands for Hydrogen and O stands for Oxygen.
Elements have isotopes. Hydrogen has two isotopes, Deuterium and Tritium. Deuterium oxide, or D2O is known as heavy water and one use for heavy water is the manufacture of atomic bombs, if you recall the film "The heroes of Telemark". Deuterium is non-radioactive, as is heavy water. Tritium is radioactive.
Oxygen has three stable non-radioactive isotopes one of which is O-18. This can be used to make labeled water H2O-18. Mix D2O with a bit of H2O-18 and you have doubly-labeled water. Now what? To quote Leibel:-
"The interesting thing is that when you give somebody water like this, the deuterium comes out of the body which is determined by water turnover in the individual. The O-18 is in equilibrium with carbon dioxide, so the O-18 comes out by two mechanisms: first with normal water by transpiration, perspiration and urine, but also in the breath.
The difference between those two decay curves (the O-18 comes out faster), which we obtain by getting urine from these patients every day for 10 days-that gap is proportional to carbon dioxide production in that individual. By doing this, we can figure out how much carbon dioxide this person made over a period of 10 days. Knowing that, and knowing what the so-called diet quotient is - in other words, what the ratio of carbohydrates to fat in their diet is - you can back-calculate the amount of oxygen used to produce that amount of carbon dioxide.
So by some simple algebra using the rate of carbon dioxide excretion, you can actually calculate how much oxygen their body used in the process of oxidative metabolism. That is a very critical number because it tells you how much energy they burned. Oxygen consumption can be immediately converted into calories.
So we measure caloric expenditure both by figuring out how many calories it takes to make their body weight absolutely stable, and checking that number by also using this double-doped water excretion technique using mass spectroscopy. It's quite expensive: the isotopes to do such a study cost about $500, not including the spectroscopy."
See A comparative study of different means of assessing long-term energy expenditure in humans.
Ain't science wonderful?
Saturday, January 30, 2010
Thursday, January 28, 2010
Chocolate Sorbet- Vegan and Dairy-Free
 |
| Rich chocolate sorbet- without dairy. Pass the spoon. |
Two trends are sneaking in to recipe searches this week. The first? Super bowl recipes. You know, guy-style chicken chili and Crock-Pot crowd pleasers. Party food for the Big Game. Guacamole and hummus. Nachos. The second trend is a search closer to my own heart and its tender sensibilities. You may have already guessed it. Because you, Wonderful Reader, are smart, savvy and, well. Let's just gush a minute with appreciation. You are downright fabulous (with impeccable taste and discernment, I might add).
The second big trend is a search for romantic recipes and Valentine's Day inspiration. You're not surprised, are you? (See, I knew you were brilliant).
I'd much rather conjure up chocolate recipes than beans and burgers. Sexy food is more interesting than AstroTurf and lines of scrimmage and backfields in motion. And what the Hail Mary is a down, anyway? First down, fourth down. All these downs and off sides. It makes my head spin.
The key to happiness
AC-CENT-TCHU-ATE THE POSITIVE (Mister In-Between)
(Johnny Mercer/Harold Arlen, sung by Bing Crosby)
You've got to accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
You've got to spread joy up to the maximum
Bring gloom down to the minimum
Have faith or pandemonium
Liable to walk upon the scene
(To illustrate his last remark
Jonah in the whale, Noah in the ark
What did they do
Just when everything looked so dark)
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No, do not mess with Mister In-Between
Do you hear me, hmm?
(Oh, listen to me children and-a you will hear
About the elininatin' of the negative
And the accent on the positive)
And gather 'round me children if you're willin'
And sit tight while I start reviewin'
The attitude of doin' right
(You've gotta accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between)
You've got to spread joy (up to the maximum)
Bring gloom (down) down to the minimum
Otherwise (otherwise) pandemonium
Liable to walk upon the scene
To illustrate (well illustrate) my last remark (you got the floor)
Jonah in the whale, Noah in the ark
What did they say (what did they say)
Say when everything looked so dark
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No! Don't mess with Mister In-Between
(Johnny Mercer/Harold Arlen, sung by Bing Crosby)
You've got to accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
You've got to spread joy up to the maximum
Bring gloom down to the minimum
Have faith or pandemonium
Liable to walk upon the scene
(To illustrate his last remark
Jonah in the whale, Noah in the ark
What did they do
Just when everything looked so dark)
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No, do not mess with Mister In-Between
Do you hear me, hmm?
(Oh, listen to me children and-a you will hear
About the elininatin' of the negative
And the accent on the positive)
And gather 'round me children if you're willin'
And sit tight while I start reviewin'
The attitude of doin' right
(You've gotta accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between)
You've got to spread joy (up to the maximum)
Bring gloom (down) down to the minimum
Otherwise (otherwise) pandemonium
Liable to walk upon the scene
To illustrate (well illustrate) my last remark (you got the floor)
Jonah in the whale, Noah in the ark
What did they say (what did they say)
Say when everything looked so dark
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No! Don't mess with Mister In-Between
Wednesday, January 27, 2010
When good science goes bad
I was rummaging through PubMed (as you do) and it occurred to me that there's a problem.
1) The conclusions in the abstracts don't always tie-up with the data in the full studies.
2) There is no mention of who funded the studies.
3) There is no mention of any conflict of interest for the authors.
Some abstracts link to a free full study and some don't. This makes it difficult to know which studies have been "fixed" to achieve a desired outcome by tweaking the methodology. For example, here are some studies involving Hunter SJ, in chronological order:-
Elderly women in northern New England exhibit seasonal changes in bone mineral density and calciotropic hormones which is about seasonal variations in Vitamin D status affecting bone density and was co-authored by Michael Holick.
Demonstration of Glycated Insulin in Human Diabetic Plasma and Decreased Biological Activity Assessed by Euglycemic-Hyperinsulinemic Clamp Technique in Humans which is about how high blood glucose glycates insulin before it's even secreted, resulting in it working less well in muscle cells.
Reduced prevalence of limited joint mobility in type 1 diabetes in a U.K. clinic population over a 20-year period which pretty much does what it says on the tin.
Then, Hunter starts working for The Sugar Bureau and begins co-authoring studies like this:-
Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, scrutinised in Who pays the piper
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial, scrutinised in Who pays the piper part 2
and
Session 4: CVD, diabetes and cancer Diet, insulin resistance and diabetes: the right (pro)portions, which concludes "based on the results of diabetes prevention trials focusing on lifestyle measures, evidence favours low-fat diets as the preferred approach for weight loss and diabetes prevention."
Evidence favours low-fat diets for weight loss and diabetes prevention, huh? See Low-carb diet pitted against low-fat PLUS medication (low-carb still wins) and Diabetes Update
So, getting paid by an organisation which promotes the consumption of sugar makes good science go bad.
1) The conclusions in the abstracts don't always tie-up with the data in the full studies.
2) There is no mention of who funded the studies.
3) There is no mention of any conflict of interest for the authors.
Some abstracts link to a free full study and some don't. This makes it difficult to know which studies have been "fixed" to achieve a desired outcome by tweaking the methodology. For example, here are some studies involving Hunter SJ, in chronological order:-
Elderly women in northern New England exhibit seasonal changes in bone mineral density and calciotropic hormones which is about seasonal variations in Vitamin D status affecting bone density and was co-authored by Michael Holick.
Demonstration of Glycated Insulin in Human Diabetic Plasma and Decreased Biological Activity Assessed by Euglycemic-Hyperinsulinemic Clamp Technique in Humans which is about how high blood glucose glycates insulin before it's even secreted, resulting in it working less well in muscle cells.
Reduced prevalence of limited joint mobility in type 1 diabetes in a U.K. clinic population over a 20-year period which pretty much does what it says on the tin.
Then, Hunter starts working for The Sugar Bureau and begins co-authoring studies like this:-
Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, scrutinised in Who pays the piper
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial, scrutinised in Who pays the piper part 2
and
Session 4: CVD, diabetes and cancer Diet, insulin resistance and diabetes: the right (pro)portions, which concludes "based on the results of diabetes prevention trials focusing on lifestyle measures, evidence favours low-fat diets as the preferred approach for weight loss and diabetes prevention."
Evidence favours low-fat diets for weight loss and diabetes prevention, huh? See Low-carb diet pitted against low-fat PLUS medication (low-carb still wins) and Diabetes Update
So, getting paid by an organisation which promotes the consumption of sugar makes good science go bad.
Monday, January 25, 2010
Quinoa Mushroom Pilaf
 |
| Quinoa pilaf with mushrooms, scallions and bell peppers. |
New Queen on the Block
In between bouts of rain and nostalgia (I prickle using the word nostalgia, to be honest; it smacks of sentimentality, not a trait I cultivate or suffer gladly, but I'll get to that later) I've been craving quinoa
like there's no tomorrow, as if I'm living in my own post-apocalyptic genre movie
, foraging for nuts and berries on a desert highway in my fashionably shredded mud spattered get-up complete with goggles and chain link bracelets, wishing I had the taut burnished thighs of Tina Turner
instead of my own wobbly, pale set of limbs.Yeah. I'm talking voracious.
Read more + get the recipe >>
Saturday, January 23, 2010
The Body Fat Setpoint, Part III: Dietary Causes of Obesity
[2013 update: I've edited this post to remove elements that I feel were poorly supported. I now think that changes in the setpoint are at least partially secondary to passive overconsumption of calories, particularly low quality calories]
What Caused the Setpoint to Change?
We have two criteria to narrow our search for the cause of modern fat gain:
In the last post, I described two mechanisms that may contribute to elevating the body fat set point by causing leptin resistance: inflammation in the hypothalamus, and impaired leptin transport into the brain due to elevated triglycerides. After more reading and discussing it with my mentor, I've decided that the triglyceride hypothesis is on shaky ground*. Nevertheless, it is consistent with certain observations:
The Role of Digestive Health
What causes inflammation in the hypothalamus? One of the most interesting hypotheses is that increased intestinal permeability allows inflammatory substances to cross into the circulation from the gut, irritating a number of tissues including the hypothalamus.
Dr. Remy Burcelin and his group have spearheaded this research. They've shown that high-fat diets cause obesity in mice, and that they also increase the level of an inflammatory substance called lipopolysaccharide (LPS) in the blood. LPS is produced by gram-negative bacteria in the gut and is one of the main factors that activates the immune system during an infection. Antibiotics that kill gram-negative bacteria in the gut prevent the negative consequences of high-fat feeding in mice.
Burcelin's group showed that infusing LPS into mice on a low-fat chow diet causes them to become obese and insulin resistant just like high-fat fed mice (4). Furthermore, adding 10% of the soluble fiber oligofructose to the high-fat diet prevented the increase in intestinal permeability and also largely prevented the body fat gain and insulin resistance from high-fat feeding (5). Oligofructose is food for friendly gut bacteria and ends up being converted to butyrate and other short-chain fatty acids in the colon. This results in lower intestinal permeability to toxins such as LPS. This is particularly interesting because oligofructose supplements cause fat loss in humans (6).
A recent study showed that blood LPS levels are correlated with body fat, elevated cholesterol and triglycerides, and insulin resistance in humans (7). However, a separate study didn't come to the same conclusion (8). The discrepancy may be due to the fact that LPS isn't the only inflammatory substance to cross the gut lining-- other substances may also be involved. Anything in the blood that shouldn't be there is potentially inflammatory.
Overall, I think gut dysfunction could play a role in obesity and other modern metabolic problems.
Exiting the Niche
I believe that we have strayed too far from our species' ecological niche, and our health is suffering. One manifestation of that is body fat gain. Many factors probably contribute, but I believe that diet is the most important. A diet heavy in nutrient-poor refined carbohydrates and industrial omega-6 oils, high in gut irritating substances such as gluten and sugar, and a lack of direct sunlight, have caused us to lose the robust digestion and good micronutrient status that characterized our distant ancestors. I believe that one consequence has been the dysregulation of the system that maintains the fat mass "setpoint". This has resulted in an increase in body fat in 20th century affluent nations, and other cultures eating our industrial food products.
In the next post, I'll discuss my thoughts on how to reset the body fat setpoint.
* The ratio of leptin in the serum to leptin in the brain is diminished in obesity, but given that serum leptin is very high in the obese, the absolute level of leptin in the brain is typically not lower than a lean person. Leptin is transported into the brain by a transport mechanism that saturates when serum leptin is not that much higher than the normal level for a lean person. Therefore, the fact that the ratio of serum to brain leptin is higher in the obese does not necessarily reflect a defect in transport, but rather the fact that the mechanism that transports leptin is already at full capacity.
What Caused the Setpoint to Change?
We have two criteria to narrow our search for the cause of modern fat gain:
- It has to be new to the human environment
- At some point, it has to cause leptin resistance or otherwise disturb the setpoint
In the last post, I described two mechanisms that may contribute to elevating the body fat set point by causing leptin resistance: inflammation in the hypothalamus, and impaired leptin transport into the brain due to elevated triglycerides. After more reading and discussing it with my mentor, I've decided that the triglyceride hypothesis is on shaky ground*. Nevertheless, it is consistent with certain observations:
- Fibrate drugs that lower triglycerides can lower fat mass in rodents and humans
- Low-carbohydrate diets are somewhat effective for fat loss and lower triglycerides
- Fructose can cause leptin resistance in rodents and it elevates triglycerides (1)
- Fish oil reduces triglycerides. Some but not all studies have shown that fish oil aids fat loss (2)
The Role of Digestive Health
What causes inflammation in the hypothalamus? One of the most interesting hypotheses is that increased intestinal permeability allows inflammatory substances to cross into the circulation from the gut, irritating a number of tissues including the hypothalamus.
Dr. Remy Burcelin and his group have spearheaded this research. They've shown that high-fat diets cause obesity in mice, and that they also increase the level of an inflammatory substance called lipopolysaccharide (LPS) in the blood. LPS is produced by gram-negative bacteria in the gut and is one of the main factors that activates the immune system during an infection. Antibiotics that kill gram-negative bacteria in the gut prevent the negative consequences of high-fat feeding in mice.
Burcelin's group showed that infusing LPS into mice on a low-fat chow diet causes them to become obese and insulin resistant just like high-fat fed mice (4). Furthermore, adding 10% of the soluble fiber oligofructose to the high-fat diet prevented the increase in intestinal permeability and also largely prevented the body fat gain and insulin resistance from high-fat feeding (5). Oligofructose is food for friendly gut bacteria and ends up being converted to butyrate and other short-chain fatty acids in the colon. This results in lower intestinal permeability to toxins such as LPS. This is particularly interesting because oligofructose supplements cause fat loss in humans (6).
A recent study showed that blood LPS levels are correlated with body fat, elevated cholesterol and triglycerides, and insulin resistance in humans (7). However, a separate study didn't come to the same conclusion (8). The discrepancy may be due to the fact that LPS isn't the only inflammatory substance to cross the gut lining-- other substances may also be involved. Anything in the blood that shouldn't be there is potentially inflammatory.
Overall, I think gut dysfunction could play a role in obesity and other modern metabolic problems.
Exiting the Niche
I believe that we have strayed too far from our species' ecological niche, and our health is suffering. One manifestation of that is body fat gain. Many factors probably contribute, but I believe that diet is the most important. A diet heavy in nutrient-poor refined carbohydrates and industrial omega-6 oils, high in gut irritating substances such as gluten and sugar, and a lack of direct sunlight, have caused us to lose the robust digestion and good micronutrient status that characterized our distant ancestors. I believe that one consequence has been the dysregulation of the system that maintains the fat mass "setpoint". This has resulted in an increase in body fat in 20th century affluent nations, and other cultures eating our industrial food products.
In the next post, I'll discuss my thoughts on how to reset the body fat setpoint.
* The ratio of leptin in the serum to leptin in the brain is diminished in obesity, but given that serum leptin is very high in the obese, the absolute level of leptin in the brain is typically not lower than a lean person. Leptin is transported into the brain by a transport mechanism that saturates when serum leptin is not that much higher than the normal level for a lean person. Therefore, the fact that the ratio of serum to brain leptin is higher in the obese does not necessarily reflect a defect in transport, but rather the fact that the mechanism that transports leptin is already at full capacity.
Ghrelin, the other "in"
Having just written about Leptin, it's Ghrelin's turn now. When your stomach is empty, serum ghrelin level is high and when your stomach is full, serum ghrelin level is low. Interestingly, high serum ghrelin has a beneficial effect on the hippocampus (responsible for learning stuff) so do your studying when you're hungry!
As a full stomach reduces serum ghrelin and thus reduces appetite, anything that keeps the stomach full for longer reduces appetite for longer. This is where enterogastrones come in. The most useful one in terms of appetite control is cholecystokinin, the secretion of which is stimulated by proteins & fats. This is one reason why diets high in proteins & fats keep you full for longer. Another useful filler is fibre/fiber, of course. As shown on the BBC programme "The Truth about Food", blending a meal with water or some other low-calorie liquid like soup also slows stomach emptying.
Finally, sleep deprivation raises ghrelin so I must try harder to spend less time on my computer and get some shut-eye.
As a full stomach reduces serum ghrelin and thus reduces appetite, anything that keeps the stomach full for longer reduces appetite for longer. This is where enterogastrones come in. The most useful one in terms of appetite control is cholecystokinin, the secretion of which is stimulated by proteins & fats. This is one reason why diets high in proteins & fats keep you full for longer. Another useful filler is fibre/fiber, of course. As shown on the BBC programme "The Truth about Food", blending a meal with water or some other low-calorie liquid like soup also slows stomach emptying.
Finally, sleep deprivation raises ghrelin so I must try harder to spend less time on my computer and get some shut-eye.
Friday, January 22, 2010
Don't fight it, if you like it.
I was listening to "Scream" by Timbaland in the car today and the first part of the title made me think of dieting. Sometimes our bodies fight our every effort to change our weight. This is a particular problem for people who are trying to lose weight. They feel cold, hungry & listless and they really want to EAT SOMETHING, damn it! It's because they are trying to change their set point weight. For information about set point weight, see Good Science: Dr. Leibel Explains Metabolic Slowdown with Weight Loss.
The problem with getting fat is that adipocytes (fat cells) can only hypertrophy (become larger in size) so much. When they reach a certain size, they secrete something (I don't know how this works so don't ask) that stimulates preadipocytes to become adipocytes. A larger number of something is called hyperplasia. Once adipocyte hyperplasia has occurred, we are stuck with them for life depending on what part of the body they've formed in. Visceral fat (the harmful fat around your internal organs) cannot be removed by liposuction. Only sub-cutaneous fat can. Losing weight & bodyfat results in adipocytes becoming smaller. However, the more of them there are, the smaller they have to become to achieve a given fat mass.
Adipocytes secrete leptin, the amount secreted reducing with reducing size. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP). Reducing serum leptin level acts on the hypothalamus, increasing our appetites and reducing our energy expenditures. When adipocytes become smaller than normal, leptin secretion reduces considerably and even though there are more of them, net serum leptin decreases and the end result is feeling cold, hungry & listless.
There's another problem that can occur with leptin. In the above example, there's a lack of leptin and the body doesn't work properly. This is analogous to type 1 diabetes. In some people, the hypothalamus becomes insensitive to leptin. Leptin resistance is analogous to type 2 diabetes in that the stuff's present at the correct level but it doesn't have the desired effect and the body doesn't work properly. The end result is also feeling cold, hungry & listless.
It's supposedly possible to restore the sensitivity of the hypothalamus to leptin, but that's for another blog post. So a fat person could say "I'm not fat, I'm hypothalamically-challenged!"
The problem with getting fat is that adipocytes (fat cells) can only hypertrophy (become larger in size) so much. When they reach a certain size, they secrete something (I don't know how this works so don't ask) that stimulates preadipocytes to become adipocytes. A larger number of something is called hyperplasia. Once adipocyte hyperplasia has occurred, we are stuck with them for life depending on what part of the body they've formed in. Visceral fat (the harmful fat around your internal organs) cannot be removed by liposuction. Only sub-cutaneous fat can. Losing weight & bodyfat results in adipocytes becoming smaller. However, the more of them there are, the smaller they have to become to achieve a given fat mass.
Adipocytes secrete leptin, the amount secreted reducing with reducing size. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP). Reducing serum leptin level acts on the hypothalamus, increasing our appetites and reducing our energy expenditures. When adipocytes become smaller than normal, leptin secretion reduces considerably and even though there are more of them, net serum leptin decreases and the end result is feeling cold, hungry & listless.
There's another problem that can occur with leptin. In the above example, there's a lack of leptin and the body doesn't work properly. This is analogous to type 1 diabetes. In some people, the hypothalamus becomes insensitive to leptin. Leptin resistance is analogous to type 2 diabetes in that the stuff's present at the correct level but it doesn't have the desired effect and the body doesn't work properly. The end result is also feeling cold, hungry & listless.
It's supposedly possible to restore the sensitivity of the hypothalamus to leptin, but that's for another blog post. So a fat person could say "I'm not fat, I'm hypothalamically-challenged!"
Wednesday, January 20, 2010
Gluten-Free Chili - Our Favorite Recipe
 |
Our favorite gluten-free chili- hearty winter comfort. |
FADE IN:
INT. 5TH FLOOR APARTMENT - DAY
A chilly winter light slices into a SANTA MONICA apartment and illuminates every cobweb. (Obviously, a certain individual has been neglecting house work again). Said individual sighs audibly. Glances sideways into the mirror hanging above the kitchen sink cluttered with coffee spoons, grilled cornbread crumbs and half-filled tea mugs. She could never pass for Martha Stewart. Not in a million years.
DISHEVELED GLUTEN-FREE GODDESS
Good gravy. Look at all the dust balls.
STEVE (HUSBAND)
So what. What's a dust bunny or two?
(glancing up from his laptop)
I’ll vacuum later. Or next Tuesday.
DISHEVELED GLUTEN-FREE GODDESS
My hero.
(dragging out the Crock Pot from under the sink)
My hero.
(dragging out the Crock Pot from under the sink)
This calls for chili.
FADE TO BLACK
Krauss's New Article on Saturated Fat Intervention Trials
Dr. Ronald Krauss's group just published another article in the American Journal of Clinical Nutrition, this time on the intervention trials examining the effectiveness of reducing saturated fat and/or replacing it with other nutrients, particularly carbohydrate or polyunsaturated seed oils. I don't agree with everything in this article. For example, they cite the Finnish Mental Hospital trial. They openly acknowledge some contradictory data, although they left out the Sydney diet-heart study and the Rose et al. corn oil study, both of which suggested increased mortality from replacing animal fats with polyunsaturated seed oils. Nevertheless, here is the conclusion:
Particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.
Tuesday, January 19, 2010
Ban Butter, Part 4,400?
By the time I've finished typing this, there will probably be over 4,400 blogs containing the phrase "Ban Butter". I'm not going to call Shyam Kolvekar rude names. He's a heart surgeon so he's probably very good at cutting people's chests open, removing clogged coronary arteries and grafting in veins removed from legs or whatever it is they do. I don't really wanna know!
He obviously doesn't read our blogs, or he wouldn't have said what he did. If he didn't get any money from Unilever for saying it, that's rather foolish. If I'm going to risk being called every rude name under the sun, I want it to be worth my while.
Anyway, in case you missed it, here's Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.
See also Fats and Fatty Acids in Human Nutrition and specifically Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials.
I personally use Anchor Spreadable (kept in the 'fridge) or Anchor/Kerrygold (kept out of the 'fridge) as they're from grass-fed cows.
Finally, for a little light relief, see Butter vs Margarine.
Update: From Hartke Is Online!
He obviously doesn't read our blogs, or he wouldn't have said what he did. If he didn't get any money from Unilever for saying it, that's rather foolish. If I'm going to risk being called every rude name under the sun, I want it to be worth my while.
Anyway, in case you missed it, here's Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.
See also Fats and Fatty Acids in Human Nutrition and specifically Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials.
I personally use Anchor Spreadable (kept in the 'fridge) or Anchor/Kerrygold (kept out of the 'fridge) as they're from grass-fed cows.
Finally, for a little light relief, see Butter vs Margarine.
Update: From Hartke Is Online!
Monday, January 18, 2010
Mulligatawny Soup with Jasmine Rice
 |
| Warm up with a bowl of this delicious mulligatawny soup. |
Soup weather has arrived in Southern California. The sky is flannel gray and thick with rain. The streets below are slick and shiny wet. Monday morning traffic sounds are hushed and distant. It is even a bit chilly- for L.A. standards. I am wrapped in a sweater. And I am craving mulligatawny- one of my favorite spicy soups. As luck or fate or Plan B foresight would have it, I had enough ingredients on hand to make my favorite soup for lunch today. A simpler, easier version of my well worn favorite recipe for Vegetarian Mulligatawny. I skipped the cabbage and cauliflower and canned tomatoes this time. And upped the carrots for a fresh tasting, healthy soup.
Read more + get the recipe >>
Sunday, January 17, 2010
Good Calories, Bad Calories by Gary Taubes
I haven't yet fully read the book mentioned in the title, but I've read the Cliff Notes. I have the following comments, based on these notes:-
1) I agree with 99% of what Taubes has written. Do I really need to buy Good Calories, Bad Calories?
2) I disagree with the following:-
a) Fattening Diets
▪ it's impossible to fatten people on high-fat, high-protein diets: they just can't eat enough
▪ in one experiment, the volunteers would sit staring at "plates of pork chops a mile high" and refuse to eat enough to get an excess thousand cal/day
b) The Carbohydrate Hypothesis, II: Insulin
▪ so: carbs = glucose = glycerol phosphate = trigs = fattening
a) There's an obvious problem with trying to fatten someone using "plates of pork chops a mile high" and that is BOREDOM. Even I, who loves meat, would baulk at eating pork chops washed down with more pork chops plus a side helping of even more pork chops. However, if I had a plateful of fatty roast beef, pork, lamb & duck with all of the crackling/skin plus lashings of juices, I wouldn't have any difficulty in getting thousands of excess kcals/day. Om, nom, nom!
b) See I have a theory and Enzymes.
P.S. Today's featured article on Wikipedia is....The ketogenic diet!
1) I agree with 99% of what Taubes has written. Do I really need to buy Good Calories, Bad Calories?
2) I disagree with the following:-
a) Fattening Diets
▪ it's impossible to fatten people on high-fat, high-protein diets: they just can't eat enough
▪ in one experiment, the volunteers would sit staring at "plates of pork chops a mile high" and refuse to eat enough to get an excess thousand cal/day
b) The Carbohydrate Hypothesis, II: Insulin
▪ so: carbs = glucose = glycerol phosphate = trigs = fattening
a) There's an obvious problem with trying to fatten someone using "plates of pork chops a mile high" and that is BOREDOM. Even I, who loves meat, would baulk at eating pork chops washed down with more pork chops plus a side helping of even more pork chops. However, if I had a plateful of fatty roast beef, pork, lamb & duck with all of the crackling/skin plus lashings of juices, I wouldn't have any difficulty in getting thousands of excess kcals/day. Om, nom, nom!
b) See I have a theory and Enzymes.
P.S. Today's featured article on Wikipedia is....The ketogenic diet!
Saturday, January 16, 2010
The Body Fat Setpoint, Part II: Mechanisms of Fat Gain
The Timeline of Fat Gain
Modern humans are unusual mammals in that fat mass varies greatly between individuals. Some animals carry a large amount of fat for a specific purpose, such as hibernation or migration. But all individuals of the same sex and social position will carry approximately the same amount of fat at any given time of year. Likewise, in hunter-gatherer societies worldwide, there isn't much variation in body weight-- nearly everyone is lean. Not necessarily lean like Usain Bolt, but not overweight.
Although overweight and obesity occurred forty years ago in the U.S. and U.K., they were much less common than today, particularly in children. Here are data from the U.S. Centers for Disease Control NHANES surveys (from this post):
Together, this shows that a) leanness is the most natural condition for the human body, and b) something about our changing environment, not our genes, has caused our body fat to grow.
Fat Mass is Regulated by a Feedback Circuit Between Fat Tissue and the Brain
In the last post, I described how the body regulates fat mass, attempting to keep it within a narrow window or "setpoint". Body fat produces a hormone called leptin, which signals to the brain and other organs to decrease appetite, increase the metabolic rate and increase physical activity. More fat means more leptin, which then causes the extra fat to be burned. The little glitch is that some people become resistant to leptin, so that their brain doesn't hear the fat tissue screaming that it's already full. Leptin resistance nearly always accompanies obesity, because it's a precondition of significant fat gain. If a person weren't leptin resistant, he wouldn't have the ability to gain more than a few pounds of fat without heroic overeating (which is very very unpleasant when your brain is telling you to stop). Animal models of leptin resistance develop something that resembles human metabolic syndrome (abdominal obesity, blood lipid abnormalities, insulin resistance, high blood pressure).
The Role of the Hypothalamus
The hypothalamus is on the underside of the brain connected to the pituitary gland. It's the main site of leptin action in the brain, and it controls the majority of leptin's effects on appetite, energy expenditure and insulin sensitivity. Most of the known gene variations that are associated with overweight in humans influence the function of the hypothalamus in some way (1). Not surprisingly, leptin resistance in the hypothalamus has been proposed as a cause of obesity. It's been shown in rats and mice that hypothalamic leptin resistance occurs in diet-induced obesity, and it's almost certainly the case in humans as well. What's causing leptin resistance in the hypothalamus?
There are three leading explanations at this point that are not mutually exclusive. One is cellular stress in the endoplasmic reticulum, a structure inside the cell that's used for protein synthesis and folding. I've read the most recent paper on this in detail, and I found it unconvincing (2). I'm open to the idea, but it needs more rigorous support.
A second explanation is inflammation in the hypothalamus. Inflammation inhibits leptin and insulin signaling in a variety of cell types. At least two studies have shown that diet-induced obesity in rodents leads to inflammation in the hypothalamus (3, 4)*. [2013 update: several studies have shown that preventing hypothalamic inflammation attenuates fat gain in obesity models]. If leptin is getting to the hypothalamus, but the hypothalamus is insensitive to it, it will require more leptin to get the same signal, and fat mass will creep up until it reaches a higher setpoint.
The other possibility is that leptin simply isn't reaching the hypothalamus. The brain is a unique organ. It's enclosed by the blood-brain barrier (BBB), which greatly restricts what can enter and leave it. Both insulin and leptin are actively transported across the BBB. It's been known for a decade that obesity in rodents is associated with a lower rate of leptin transport across the BBB (5, 6).
What causes a decrease in leptin transport across the BBB? Triglycerides are a major factor. These are circulating fats going from the liver and the digestive tract to other tissues. They're one of the blood lipid measurements the doctor makes when he draws your blood. Several studies in rodents have shown that high triglycerides cause a reduction in leptin transport across the BBB, and reducing triglycerides allows greater leptin transport and fat loss (7, 8). In support of this theory, the triglyceride-reducing drug gemfibrozil also causes weight loss in humans (9)**. Low-carbohydrate diets, and avoiding sugar and refined carbohydrates in particular, reduce triglycerides and produce weight loss, although that doesn't necessarily mean one causes the other.
In the next post, I'll get more specific about what factors could be causing hypothalamic inflammation and/or reduced leptin transport across the BBB. I'll also discuss some ideas on how to reduce leptin resistance sustainably through diet and exercise.
* This is accomplished by feeding them sad little pellets that look like raw cookie dough. They're made up mostly of lard, soybean oil, casein, maltodextrin or cornstarch, sugar, vitamins and minerals (this is a link to the the most commonly used diet for inducing obesity in rodents). Food doesn't get any more refined than this stuff, and adding just about anything to it, from fiber to fruit extracts, makes it less damaging.
** Fibrates are PPAR agonists, so the weight loss could also be due to something besides the reduction in triglycerides.
Modern humans are unusual mammals in that fat mass varies greatly between individuals. Some animals carry a large amount of fat for a specific purpose, such as hibernation or migration. But all individuals of the same sex and social position will carry approximately the same amount of fat at any given time of year. Likewise, in hunter-gatherer societies worldwide, there isn't much variation in body weight-- nearly everyone is lean. Not necessarily lean like Usain Bolt, but not overweight.
Although overweight and obesity occurred forty years ago in the U.S. and U.K., they were much less common than today, particularly in children. Here are data from the U.S. Centers for Disease Control NHANES surveys (from this post):
Together, this shows that a) leanness is the most natural condition for the human body, and b) something about our changing environment, not our genes, has caused our body fat to grow.Fat Mass is Regulated by a Feedback Circuit Between Fat Tissue and the Brain
In the last post, I described how the body regulates fat mass, attempting to keep it within a narrow window or "setpoint". Body fat produces a hormone called leptin, which signals to the brain and other organs to decrease appetite, increase the metabolic rate and increase physical activity. More fat means more leptin, which then causes the extra fat to be burned. The little glitch is that some people become resistant to leptin, so that their brain doesn't hear the fat tissue screaming that it's already full. Leptin resistance nearly always accompanies obesity, because it's a precondition of significant fat gain. If a person weren't leptin resistant, he wouldn't have the ability to gain more than a few pounds of fat without heroic overeating (which is very very unpleasant when your brain is telling you to stop). Animal models of leptin resistance develop something that resembles human metabolic syndrome (abdominal obesity, blood lipid abnormalities, insulin resistance, high blood pressure).
The Role of the Hypothalamus
The hypothalamus is on the underside of the brain connected to the pituitary gland. It's the main site of leptin action in the brain, and it controls the majority of leptin's effects on appetite, energy expenditure and insulin sensitivity. Most of the known gene variations that are associated with overweight in humans influence the function of the hypothalamus in some way (1). Not surprisingly, leptin resistance in the hypothalamus has been proposed as a cause of obesity. It's been shown in rats and mice that hypothalamic leptin resistance occurs in diet-induced obesity, and it's almost certainly the case in humans as well. What's causing leptin resistance in the hypothalamus?
There are three leading explanations at this point that are not mutually exclusive. One is cellular stress in the endoplasmic reticulum, a structure inside the cell that's used for protein synthesis and folding. I've read the most recent paper on this in detail, and I found it unconvincing (2). I'm open to the idea, but it needs more rigorous support.
A second explanation is inflammation in the hypothalamus. Inflammation inhibits leptin and insulin signaling in a variety of cell types. At least two studies have shown that diet-induced obesity in rodents leads to inflammation in the hypothalamus (3, 4)*. [2013 update: several studies have shown that preventing hypothalamic inflammation attenuates fat gain in obesity models]. If leptin is getting to the hypothalamus, but the hypothalamus is insensitive to it, it will require more leptin to get the same signal, and fat mass will creep up until it reaches a higher setpoint.
The other possibility is that leptin simply isn't reaching the hypothalamus. The brain is a unique organ. It's enclosed by the blood-brain barrier (BBB), which greatly restricts what can enter and leave it. Both insulin and leptin are actively transported across the BBB. It's been known for a decade that obesity in rodents is associated with a lower rate of leptin transport across the BBB (5, 6).
What causes a decrease in leptin transport across the BBB? Triglycerides are a major factor. These are circulating fats going from the liver and the digestive tract to other tissues. They're one of the blood lipid measurements the doctor makes when he draws your blood. Several studies in rodents have shown that high triglycerides cause a reduction in leptin transport across the BBB, and reducing triglycerides allows greater leptin transport and fat loss (7, 8). In support of this theory, the triglyceride-reducing drug gemfibrozil also causes weight loss in humans (9)**. Low-carbohydrate diets, and avoiding sugar and refined carbohydrates in particular, reduce triglycerides and produce weight loss, although that doesn't necessarily mean one causes the other.
In the next post, I'll get more specific about what factors could be causing hypothalamic inflammation and/or reduced leptin transport across the BBB. I'll also discuss some ideas on how to reduce leptin resistance sustainably through diet and exercise.
* This is accomplished by feeding them sad little pellets that look like raw cookie dough. They're made up mostly of lard, soybean oil, casein, maltodextrin or cornstarch, sugar, vitamins and minerals (this is a link to the the most commonly used diet for inducing obesity in rodents). Food doesn't get any more refined than this stuff, and adding just about anything to it, from fiber to fruit extracts, makes it less damaging.
** Fibrates are PPAR agonists, so the weight loss could also be due to something besides the reduction in triglycerides.
Enzymes
I have started to discuss my theory with Gary Taubes and this blog post is intended to go into a bit more detail about how stuff works. Trying to explain the following over the phone with hand-waving is likely to be very difficult, especially when I forget things!
Firstly, see Enzyme. Their name always ends in "ase". The thing about enzymes is that their activity can be increased & decreased by the level of substrate i.e. how much "stuff" there is going in to the reaction and how much "stuff" there is coming out of the reaction. Activation & inhibition can also be produced by other substances not directly involved in the reaction.
To get from Glucose (assuming muscle cells) to Pyruvate involves a multi-step process involving lots of different enzymes and other substances. Here's the first step.
Glucose + 1 molecule of ATP (Adenosine Tri-Phosphate) is converted by Glucokinase (with the aid of 2 Magnesium ions) into Glucose-6-phosphate + 1 molecule of ADP (Adenosine Di-Phosphate) + 1 Hydrogen ion. Here's the last step.
Phosphoenolpyruvate + 1 molecule of ADP is converted by Pyruvate kinase (with the aid of 2 Magnesium ions and 1 Potassium ion) into 1 molecule of Pyruvate + 1 molecule of ATP.
As stated in Everyone is Different , muscle cells at rest derive most of their energy from fat (Tri-Palmitin). Inside the cell mitochondria, molecules of Palmitoyl CoA (from Palmitate from hydrolysed Tri-Palmitin) produce energy starting with a process called beta-oxidation, where Acetyl CoA is repeatedly "snipped-off" yielding a fatty acid that's shorter by 2 carbon groups, 1 molecule of Acetyl CoA, 1 molecule of FADH2 + 1 molecule of NADH+H+ (don't ask!) until all that's left is Acetyl CoA. The molecules of Acetyl CoA enter the Krebs Cycle which produces more energy.
As muscle cells at rest derive most of their energy from Acetyl CoA rather than Pyruvate, Pyruvate accumulates. This inhibits the enzyme Pyruvate kinase causing an accumulation of Phosphoenolpyruvate. This inhibits the enzyme that produces Phosphoenolpyruvate etc etc. This results in an accumulation of Glucose-6-phosphate. This inhibits the enzyme Glucokinase causing an accumulation of Glucose. This inhibits the Glu-T4 transporters making muscle cells temporarily insulin resistant. Blood glucose stops entering muscle cells.
Things change when muscle cells undergoing anaerobic exercise use Pyruvate instead of Acetyl CoA. A lack of Pyruvate activates the enzyme Pyruvate kinase causing a lack of Phosphoenolpyruvate. This activates the enzyme that produces Phosphoenolpyruvate etc etc. This results in a lack of Glucose-6-phosphate. This activates the enzyme Glucokinase causing an lack of Glucose. This activates the Glu-T4 transporters making muscle cells temporarily insulin sensitive. Blood glucose enters muscle cells even if blood insulin level is normal.
The same principle applies to fat cells regarding glycerol-3-phosphate. In conclusion:
Within cells, the biochemical processes that produce "stuff" are not static but vary according to the needs of the cells.
I need a break!
While waiting to get hold of Taube's book Good Calories Bad Calories, I'm reading Toban Wiebe's Complete Notes to Good Calories, Bad Calories by Gary Taubes.
I'm also reading Anthony Colpo's latest articles on http://www.anthonycolpo.com/ . This guy doesn't mince his words!
Firstly, see Enzyme. Their name always ends in "ase". The thing about enzymes is that their activity can be increased & decreased by the level of substrate i.e. how much "stuff" there is going in to the reaction and how much "stuff" there is coming out of the reaction. Activation & inhibition can also be produced by other substances not directly involved in the reaction.
To get from Glucose (assuming muscle cells) to Pyruvate involves a multi-step process involving lots of different enzymes and other substances. Here's the first step.
Glucose + 1 molecule of ATP (Adenosine Tri-Phosphate) is converted by Glucokinase (with the aid of 2 Magnesium ions) into Glucose-6-phosphate + 1 molecule of ADP (Adenosine Di-Phosphate) + 1 Hydrogen ion. Here's the last step.
Phosphoenolpyruvate + 1 molecule of ADP is converted by Pyruvate kinase (with the aid of 2 Magnesium ions and 1 Potassium ion) into 1 molecule of Pyruvate + 1 molecule of ATP.
As stated in Everyone is Different , muscle cells at rest derive most of their energy from fat (Tri-Palmitin). Inside the cell mitochondria, molecules of Palmitoyl CoA (from Palmitate from hydrolysed Tri-Palmitin) produce energy starting with a process called beta-oxidation, where Acetyl CoA is repeatedly "snipped-off" yielding a fatty acid that's shorter by 2 carbon groups, 1 molecule of Acetyl CoA, 1 molecule of FADH2 + 1 molecule of NADH+H+ (don't ask!) until all that's left is Acetyl CoA. The molecules of Acetyl CoA enter the Krebs Cycle which produces more energy.
As muscle cells at rest derive most of their energy from Acetyl CoA rather than Pyruvate, Pyruvate accumulates. This inhibits the enzyme Pyruvate kinase causing an accumulation of Phosphoenolpyruvate. This inhibits the enzyme that produces Phosphoenolpyruvate etc etc. This results in an accumulation of Glucose-6-phosphate. This inhibits the enzyme Glucokinase causing an accumulation of Glucose. This inhibits the Glu-T4 transporters making muscle cells temporarily insulin resistant. Blood glucose stops entering muscle cells.
Things change when muscle cells undergoing anaerobic exercise use Pyruvate instead of Acetyl CoA. A lack of Pyruvate activates the enzyme Pyruvate kinase causing a lack of Phosphoenolpyruvate. This activates the enzyme that produces Phosphoenolpyruvate etc etc. This results in a lack of Glucose-6-phosphate. This activates the enzyme Glucokinase causing an lack of Glucose. This activates the Glu-T4 transporters making muscle cells temporarily insulin sensitive. Blood glucose enters muscle cells even if blood insulin level is normal.
The same principle applies to fat cells regarding glycerol-3-phosphate. In conclusion:
Within cells, the biochemical processes that produce "stuff" are not static but vary according to the needs of the cells.
I need a break!
While waiting to get hold of Taube's book Good Calories Bad Calories, I'm reading Toban Wiebe's Complete Notes to Good Calories, Bad Calories by Gary Taubes.
I'm also reading Anthony Colpo's latest articles on http://www.anthonycolpo.com/ . This guy doesn't mince his words!
Friday, January 15, 2010
An apple a day...
Once upon a time, there were Crab Apples. They were extremely sour (except perhaps for the Chestnut Crabapple) and contained a lot of Pectin, a soluble fibre/fiber. Then, we clever humans selectively bred apple trees over a large number of years and voila! We have the modern-day apple. Note that this contains on average 10.4g of sugar/100g of apple and only 2.4g of fibre/100g of apple. The British Dental Association claims that the Pink Lady, Braeburn and Fuji contain so much sugar that they cause tooth decay.
Different types of fruit vary hugely in their sugar content. Some fruits (blueberries & cranberries) also contain mannose. Bananas also contain starch, which turns into sugars as the banana changes colour from green to yellow to black.
Don't eat/drink too much fructose, as that goes straight to your liver where it tops-up liver glycogen and, once your liver glycogen stores are full, overspills as triglycerides a.k.a. fats into your liver & blood.
For more on fructose, see Sugar: The Bitter Truth by Robert H. Lustig, M.D.
As glucose and fructose have very different effects on the body, this is a situation where "a calorie isn't a calorie".
Different types of fruit vary hugely in their sugar content. Some fruits (blueberries & cranberries) also contain mannose. Bananas also contain starch, which turns into sugars as the banana changes colour from green to yellow to black.
Don't eat/drink too much fructose, as that goes straight to your liver where it tops-up liver glycogen and, once your liver glycogen stores are full, overspills as triglycerides a.k.a. fats into your liver & blood.
For more on fructose, see Sugar: The Bitter Truth by Robert H. Lustig, M.D.
As glucose and fructose have very different effects on the body, this is a situation where "a calorie isn't a calorie".
Thursday, January 14, 2010
New Saturated Fat Review Article by Dr. Ronald Krauss
Dr. Ronald Krauss's group has published a review article titled "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease". As anyone who's familiar with the literature could have predicted (including myself), they found no association whatsoever between saturated fat intake and heart disease or stroke:
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.
Wednesday, January 13, 2010
Awwwww, CRAP!
I've just read Dr A's latest post and it had a link to Jezwyn's Girl Gone Primal. In Australia, they're having a heatwave and as for the food.....................................well!
In the South of England, the weather's like this:-
In the South of England, the weather's like this:-
Sunday, January 10, 2010
Paleo is Going Mainstream
There was an article on the modern "Paleolithic" lifestyle in the New York Times today. I thought it was a pretty fair treatment of the subject, although it did paint it as more macho and carnivorous than it needs to be. It features three attractive NY cave people. It appeared in the styles section here. Paleo is going mainstream. I expect media health authorities to start getting defensive about it any minute now.
[2013 update. Did I call it or what??]
[2013 update. Did I call it or what??]
Mmm. These oxymorons are absolutely delicious!
I like the word oxymoron. I just saw it in Richard's Blog. As you've probably figured out from reading my Blog, the phrase "healthy low-fat" (usually found just before the word "diet") is to me, a presumptuous oxymoron.
If I type the phrase "healthy low-fat" into Google, I get about 148,000 results. Oh, dear! However...
If I type the phrase "healthy low-carb" into Google, I get about 64,400 results. Yee-haw!
So low-fat may be winning the diet war right now, but the tide is definitely turning. Slowly, slowly, catchee monkey.
If I type the phrase "healthy low-fat" into Google, I get about 148,000 results. Oh, dear! However...
If I type the phrase "healthy low-carb" into Google, I get about 64,400 results. Yee-haw!
So low-fat may be winning the diet war right now, but the tide is definitely turning. Slowly, slowly, catchee monkey.
Forget Fad Diets.
"Müller Rice makes the perfect low fat snack. Healthy and tasty, it keeps hunger at bay at any time of the day." says Müller Dairy. Let's take a look at the Nutritional information for Müller Rice Apple Flavour (from http://www.mullerdairy.co.uk/) :-
Milk, Sugar, Rice (7%), Apples (5%), Apple Juice from Concentrate (2%), Egg, Modified Maize Starch, Stabilisers: Carob Bean Gum, Guar Gum; Salt, Acidity Regulators: Ascorbic Acid, Sodium Citrates, Citric Acid; Flavourings.
There's more sugar in it than rice. One 200g serving contains about 6 teaspoonfuls of sugar. Enjoy!
| Nutritional information: | |||||
|---|---|---|---|---|---|
| Per 100g | Per 200g serving | ||||
| Energy | 464 KJ | 928 KJ | |||
| 110 kcal | 220 kcal | ||||
| Protein | 3.2g | 6.4g | |||
| Carbohydrates | 19.3g | 38.6g | |||
| of which sugars | 13.7g | 27.4g | |||
| Fat | 2.2g | 4.4g | |||
| of which saturates | 1.3g | 2.6g | |||
| Fibre | 0.4g | 0.8g | |||
| Sodium | 0.1g | 0.2g | |||
| RDA (per serving) | |||||
| Calcium | 190 mg | 23 % | |||
| Ingredients: | |||||
There's more sugar in it than rice. One 200g serving contains about 6 teaspoonfuls of sugar. Enjoy!
Friday, January 8, 2010
How stuff works.
My last post got a bit technical and delved into the finer points of cell biochemistry. For those who would like to learn more about how cells work, I thoroughly recommend the book Metabolism at a Glance (Paperback) by Jack G Salway, Sen. Lecturer in Medical Biochemistry, University of Surrey. It's crammed with diagrams of metabolic pathways.
I've also got Medical Biochemistry at a Glance (Paperback) by Jack G Salway. EDIT: I thoroughly recommend this book, too.
For more general information on nutrition and metabolism, I recommend the book Introduction to Nutrition and Metabolism (Paperback) by David A Bender, Sen. Lecturer in Biochemistry, UCL.
A good website for medical biochemistry information is MedBio.info by Prof. em. Robert S. Horn.
A good website for enzyme structures is Enzyme Structures Database.
Here's a searchable version of Biochemistry by L Stryer. It's a bit dry, but of interest is Food Intake and Starvation Induce Metabolic Changes and Phosphatidate Is a Common Intermediate in the Synthesis of Phospholipids and Triacylglycerols.
Here's NCBI Bookshelf where you can search many textbooks.
Here's an absolutely humongous diagram in .pdf format of Metabolic Pathways. You need a fast machine to view this.
Update: Here are some cool Animations and Computer-Generated Movies by Harvard University.
Here's a YouTube video of ATP Synthase, which takes a proton gradient and, using a molecular motor-generator, converts ADP + Phosphate into ATP, the energy source that cells use.
Happy reading and viewing!
I've also got Medical Biochemistry at a Glance (Paperback) by Jack G Salway. EDIT: I thoroughly recommend this book, too.
For more general information on nutrition and metabolism, I recommend the book Introduction to Nutrition and Metabolism (Paperback) by David A Bender, Sen. Lecturer in Biochemistry, UCL.
A good website for medical biochemistry information is MedBio.info by Prof. em. Robert S. Horn.
A good website for enzyme structures is Enzyme Structures Database.
Here's a searchable version of Biochemistry by L Stryer. It's a bit dry, but of interest is Food Intake and Starvation Induce Metabolic Changes and Phosphatidate Is a Common Intermediate in the Synthesis of Phospholipids and Triacylglycerols.
Here's NCBI Bookshelf where you can search many textbooks.
Here's an absolutely humongous diagram in .pdf format of Metabolic Pathways. You need a fast machine to view this.
Update: Here are some cool Animations and Computer-Generated Movies by Harvard University.
Here's a YouTube video of ATP Synthase, which takes a proton gradient and, using a molecular motor-generator, converts ADP + Phosphate into ATP, the energy source that cells use.
Happy reading and viewing!
Thursday, January 7, 2010
I have a theory.
I was keeping this theory a bit quiet as it contradicts Gary Taubes , Michael R Eades & Richard D Feinman and Eugene J Fine.
Please note: This post is not criticising low-carb, high-fat diets in any way, shape or form. I'm just trying to point out that if someone on a low-carb, high-fat diet pigs-out on roast lamb/pork/duck etc, they may not lose as much body fat as they expected & they may even gain some.
I don't particularly want to start a sh*t-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied & pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.
"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.
Consider muscle cells undergoing anaerobic activity:-
Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.
This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.
Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."
In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.
Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.
There. I've said it. I expect comments! Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.
As a lot of people report that they appear to be able to eat lots of dietary fat without getting fat (& actually getting slim), there's obviously something magical going on. Now, it's generally accepted that fat is the least thermogenic of all the macronutrients (protein being the most thermogenic). I'm wondering whether this is the case for all types of fat and all types of people.
Stephan Guyenet blogged on Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance and Coconut Oil (high in medium chain fats) is also reported as being less fattening/more slimming than long-chain fats.
As Christopher Gardner said 39m 34s into his lecture Battle of the Weight Loss Diets: Who's Winning (at losing), insulin resistant people do better on high-fat, low-carb (HFLC) diets than high-carb, low-fat diets. Insulin sensitive people are the other way round.
So it's quite possible that in people who do well on a HFLC diet, kcals out on the right hand side of the Energy Balance Equation increase a lot. So, keep on keeping on!
See also:-
More evidence comes to light that fat is not fattening
Is there such as thing as a ‘metabolic advantage’?
They're all MAD!
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?
See also How stuff works and Enzymes.
Please note: This post is not criticising low-carb, high-fat diets in any way, shape or form. I'm just trying to point out that if someone on a low-carb, high-fat diet pigs-out on roast lamb/pork/duck etc, they may not lose as much body fat as they expected & they may even gain some.
I don't particularly want to start a sh*t-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied & pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.
"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.
Consider muscle cells undergoing anaerobic activity:-
Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.
This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.
Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."
In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.
Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.
There. I've said it. I expect comments! Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.
As a lot of people report that they appear to be able to eat lots of dietary fat without getting fat (& actually getting slim), there's obviously something magical going on. Now, it's generally accepted that fat is the least thermogenic of all the macronutrients (protein being the most thermogenic). I'm wondering whether this is the case for all types of fat and all types of people.
Stephan Guyenet blogged on Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance and Coconut Oil (high in medium chain fats) is also reported as being less fattening/more slimming than long-chain fats.
As Christopher Gardner said 39m 34s into his lecture Battle of the Weight Loss Diets: Who's Winning (at losing), insulin resistant people do better on high-fat, low-carb (HFLC) diets than high-carb, low-fat diets. Insulin sensitive people are the other way round.
So it's quite possible that in people who do well on a HFLC diet, kcals out on the right hand side of the Energy Balance Equation increase a lot. So, keep on keeping on!
See also:-
More evidence comes to light that fat is not fattening
Is there such as thing as a ‘metabolic advantage’?
They're all MAD!
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?
See also How stuff works and Enzymes.
Tuesday, January 5, 2010
Changes
Hello everyone. I hope that you're off to a good this year. I can't believe how fast the years are going by, seriously! It seems like it was only a very short while ago that I started calorie restriction. It's certainly not true that; CR doesn't make you live longer, it just seems like it". Well anyway, another year gone, hopefully there are still many to come!
So what have I been up to whilst not posting any new blog updates for a while. Well to be honest, I've just been busy with other stuff and wanted to take a break from blogging while I made some changes. So what are the changes? Well first of all my stats have changed a bit, and so has the level of calorie restriction I'm on. My weight is now 115 - 116 lbs, up from 105 lbs. I was exercising a lot and increased my calorie intake slightly. I concentrated on increasing strength in my arms and my core. My abdominal muscles are pretty well defined now! I think I gained mostly muscle and I've been holding this weight for at least a couple weeks. Also I haven't noticed any significant changes to my body temperature, it still on average around 36.0 degrees! Blood pressure still 90/60. My BMI now is 18.2, which is almost normal for my height.. but still quite a bit lower than the average BMI in the WUSTL study which was closer to 20.
So am I going to increase my weight further? I really don't know, I know the maximum I'll go to is 120 lbs if I were to increase it. Why have I done this? Well because I'm in my 20's and I want to look a little better as you can imagine. Sometimes you I think you need to make choices, and I made mine. Obviously I'm fully in control of what I do with my body. I do not have any sort of eating disorder which prevents me from gaining weight. I gained this weight because I just felt this is what I want to do right now. Simple as that. Pure vanity. I doubt that my health markers have changed all that much, but I will get them tested soon. I assume I'm aging a little quicker, but I think that I'm still quite CR'd relative to what my weight was when I was 18. Some scales even read 10st, I vaguely remember. They could have been wrong... but as I've said in many posts before, my CR journey really started when I was 18, this was the time when family members become concerned because of a big weight loss that I didn't even intend to lose, it just came because I threw out the junk food in favour of fruits and vegetables, whole grains, no sugar... because of reading some stuff from ray kurzweil. And this was losing weight from an already healthy weight, I wasn't anywhere near a BMI of 25 as most adults are.
I've really been improving on my flexibility lately also by being absolutely dedicated, everyday to putting time aside to stretch, do my yoga, sometimes (not as often as i should) meditation for a short while. Haven't been working much on cardiovascular health like running for a while, but that's ok for now.
I've just started to use a really nice skin serum! It's called Skinceuticals CE ferulic acid, and it's making my skin more bright, it also is fading red marks that I have left over from my old acne days.. and there was 1 fine line that I had down my eye which has completely disappeared only after 3 weeks of using the serum. It's very expensive stuff however so I think that I won't be using it in the very long term, only for a period of about 6 months and will switch to a basic vitamin C serum like AOX 10-20 by skin ceuticals. The good thing about this product is that there is some actual peer reviewed studies behind its effects, and it seems to be working far better than anything else I used.
So although my weight has now increased, this isn't forever... I'm still CR'd quite a bit I think, although I can't measure how much! Sometime before I'm 30 I will decrease my calories slightly again.
One thing I'd love to do though is attain a physique like Bruce Lee. You know his stats later on in his life was 125 lbs at 5ft 7" (I have the book the art of expressing the human body). Mine is same height and 116 lbs. I'm a dedicated person, really I am, I could do it... or get somewhere close. When you're young it's very difficult to try find the balance. I think I've found it. I do look a little better, and thats from only gaining 10 lbs. Though I'd like to gain a little fat on my face :-) Just a little! And I'd be pretty happy!
But whatever, I'm still young, I think that I'm doing fairly well, and I think that I also have good genetics on my side too. A lot of my family, including my father and sister all have the same biomarkers as CRers and they're not on CR. My father looks 10 years younger than his age (in his 20's he lived healthy like me), and my sister is 23 but looks 16 years old and she has same kind of biomarkers as me, very low blood pressure, glucose, very low cholesterol, very low inflammation etc etc....
Good genetics, CRON, Raw Food, Strength training all I hope get to escape velocity where aging is being solved quicker than I can age. So although I relaxed my CR, it's only a bit and its most likely a short term thing for the next 5 years at most. And I'm still pretty damn skinny! haha :-)
Foods that I ate today;
First thing cranberry juice, supplements.
Oatmeal
Blueberries
Dark chocolate
Walnuts
Yogurt
almonds
Green smoothie;
Kale
Banana
Mango (w/skin)
Red Apple
Water
Fish Oil
Fruit Smoothie (tesco frozen berries) (best drink I've ever tasted!)
Raspberries
Blackberries
Blackcurrants
Redcurrants
Blueberries
1 Banana
Water
Whey protein
Broccoli
Sweet potato
Red sauce
Tomatoes
Olive Oil
Yogurt
Wholemeal bread
So what have I been up to whilst not posting any new blog updates for a while. Well to be honest, I've just been busy with other stuff and wanted to take a break from blogging while I made some changes. So what are the changes? Well first of all my stats have changed a bit, and so has the level of calorie restriction I'm on. My weight is now 115 - 116 lbs, up from 105 lbs. I was exercising a lot and increased my calorie intake slightly. I concentrated on increasing strength in my arms and my core. My abdominal muscles are pretty well defined now! I think I gained mostly muscle and I've been holding this weight for at least a couple weeks. Also I haven't noticed any significant changes to my body temperature, it still on average around 36.0 degrees! Blood pressure still 90/60. My BMI now is 18.2, which is almost normal for my height.. but still quite a bit lower than the average BMI in the WUSTL study which was closer to 20.
So am I going to increase my weight further? I really don't know, I know the maximum I'll go to is 120 lbs if I were to increase it. Why have I done this? Well because I'm in my 20's and I want to look a little better as you can imagine. Sometimes you I think you need to make choices, and I made mine. Obviously I'm fully in control of what I do with my body. I do not have any sort of eating disorder which prevents me from gaining weight. I gained this weight because I just felt this is what I want to do right now. Simple as that. Pure vanity. I doubt that my health markers have changed all that much, but I will get them tested soon. I assume I'm aging a little quicker, but I think that I'm still quite CR'd relative to what my weight was when I was 18. Some scales even read 10st, I vaguely remember. They could have been wrong... but as I've said in many posts before, my CR journey really started when I was 18, this was the time when family members become concerned because of a big weight loss that I didn't even intend to lose, it just came because I threw out the junk food in favour of fruits and vegetables, whole grains, no sugar... because of reading some stuff from ray kurzweil. And this was losing weight from an already healthy weight, I wasn't anywhere near a BMI of 25 as most adults are.
I've really been improving on my flexibility lately also by being absolutely dedicated, everyday to putting time aside to stretch, do my yoga, sometimes (not as often as i should) meditation for a short while. Haven't been working much on cardiovascular health like running for a while, but that's ok for now.
I've just started to use a really nice skin serum! It's called Skinceuticals CE ferulic acid, and it's making my skin more bright, it also is fading red marks that I have left over from my old acne days.. and there was 1 fine line that I had down my eye which has completely disappeared only after 3 weeks of using the serum. It's very expensive stuff however so I think that I won't be using it in the very long term, only for a period of about 6 months and will switch to a basic vitamin C serum like AOX 10-20 by skin ceuticals. The good thing about this product is that there is some actual peer reviewed studies behind its effects, and it seems to be working far better than anything else I used.
So although my weight has now increased, this isn't forever... I'm still CR'd quite a bit I think, although I can't measure how much! Sometime before I'm 30 I will decrease my calories slightly again.
One thing I'd love to do though is attain a physique like Bruce Lee. You know his stats later on in his life was 125 lbs at 5ft 7" (I have the book the art of expressing the human body). Mine is same height and 116 lbs. I'm a dedicated person, really I am, I could do it... or get somewhere close. When you're young it's very difficult to try find the balance. I think I've found it. I do look a little better, and thats from only gaining 10 lbs. Though I'd like to gain a little fat on my face :-) Just a little! And I'd be pretty happy!
But whatever, I'm still young, I think that I'm doing fairly well, and I think that I also have good genetics on my side too. A lot of my family, including my father and sister all have the same biomarkers as CRers and they're not on CR. My father looks 10 years younger than his age (in his 20's he lived healthy like me), and my sister is 23 but looks 16 years old and she has same kind of biomarkers as me, very low blood pressure, glucose, very low cholesterol, very low inflammation etc etc....
Good genetics, CRON, Raw Food, Strength training all I hope get to escape velocity where aging is being solved quicker than I can age. So although I relaxed my CR, it's only a bit and its most likely a short term thing for the next 5 years at most. And I'm still pretty damn skinny! haha :-)
Foods that I ate today;
First thing cranberry juice, supplements.
Oatmeal
Blueberries
Dark chocolate
Walnuts
Yogurt
almonds
Green smoothie;
Kale
Banana
Mango (w/skin)
Red Apple
Water
Fish Oil
Fruit Smoothie (tesco frozen berries) (best drink I've ever tasted!)
Raspberries
Blackberries
Blackcurrants
Redcurrants
Blueberries
1 Banana
Water
Whey protein
Broccoli
Sweet potato
Red sauce
Tomatoes
Olive Oil
Yogurt
Wholemeal bread
Monday, January 4, 2010
Look after your brain, Part 4.
Ketogenic Diet REALLY WORKS!!!
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.
The above popped-up when I Googled for "ketogenic diet" alzheimer's.
See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.
EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.
It's mum's 80th Birthday today so I'm off to see her now.
Continued on Look after your brain, Part 5.
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.
The above popped-up when I Googled for "ketogenic diet" alzheimer's.
See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.
EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.
It's mum's 80th Birthday today so I'm off to see her now.
Continued on Look after your brain, Part 5.
Sweet Potato Biscuits
 |
| Tender pull-apart biscuits that are gluten-free and vegan. |
It's January, people. It's still winter. Some folks are shoveling snow. Enough already with the bunny food. Dump the word cleanse from your vocabulary.
Have a biscuit.
Have a biscuit.
You can whip up all the low calorie high fiber cleansing smoothies you want if they help you feel virtuous and powerful and fresh as a daisy. I've got nothing against smoothies. I'm a fan of creamy breakfasts, actually. And I love antioxidants as much as the next gluten-free soul (bring on the blueberries, Buster). But I chafe at the word diet. And should. And so I resist the collective push to declare my commitment with a list of New Year's Resolutions for a Better Me.
If I did make a list, though? It might look something like this.
Top Ten Gluten-Free Goals for the New Year
1. Make more biscuits. I'm serious. Warm, fall apart, tender, melt-in-your-mouth biscuits. Life is too short to live without biscuits.
2. Drink more Champagne. It's silly to wait for a special occasion. Every day deserves Champagne.
3. Walk more. And I don't mean power walk. I don't mean buying a pedometer. I mean walk as in stroll. Amble. Look at the sky. People watch. Notice the way the late afternoon sun resembles the color of honey.
4. Play around with some donut recipes. Start with those old fashioned blueberry cake donuts that have a hint of cinnamon and nutmeg.
5. Listen to more music. Discover new artists.
6. Dream up a fabulous gluten-free bialy. Just chant: Yes, I can.
7. Go on more picnics. See goal #2.
8. Take more photos. For fun.
9. Stop feeling guilty for (fill in the blank). Just do it. I said so.
10. Breathe, Baby, breathe. Everyone's doing the best they can to get through the day. And those of us with celiac? We're doing double.
 |
| Sweet potato biscuits are fab with soup. |
Sweet Potato Biscuits Recipe
Make this dough lickity split with a sturdy stand mixer or do it the old fashioned way- with an elbow grease powered wooden spoon.
Ingredients:
In a mixing bowl, combine the dry ingredients and whisk them together:
1/2 cup sorghum flour
1/2 cup potato starch
(not potato flour)1/4 cup millet flour
1 tablespoon baking powder
1/2 teaspoon baking soda
1 teaspoon sea salt
1/2 teaspoon xanthan gum
Pinch nutmeg, to taste (don't put in too much!)
Add in:
3 tablespoons Spectrum Organic Shortening
1 cup canned sweet potato or finely mashed cooked sweet potato
2 tablespoons pure maple syrup
1 1/2 teaspoons Ener-G Egg Replacer
whisked with 2 tablespoons warm water, till frothy
Add in:
3 tablespoons Spectrum Organic Shortening
1 cup canned sweet potato or finely mashed cooked sweet potato
2 tablespoons pure maple syrup
1 1/2 teaspoons Ener-G Egg Replacer
whisked with 2 tablespoons warm water, till frothyBeat to combine. The dough will be smooth and sticky.
Instructions:
Preheat the oven to 375ºF. Prepare a muffin pan (if the pan is non-stick, no need to do anything). You'll be using 9 of the cups.
Spoon the biscuit dough into nine muffin cups. Shape the tops with wet fingers, if you like (I left mine like drop biscuits, a little rough and bumpy).
Bake in the center of a pre-heated oven for 15 to 20 minutes or so- until firm and slightly golden. A wooden pick inserted into the center will emerge clean and the bottoms will be golden and firm. If in doubt, bake for another 3 minutes.
Pop the biscuits out of the muffin pan.
Indulge while they are still warm. Slather with maple butter, apricot jam, whipped honey...
Makes 9 biscuits.
Note:
I tried freezing a few and reheating them in the microwave. They were not nearly as good. This is one of those recipes you make and enjoy. Live in the now.
All images & content are copyright protected, all rights reserved. Please do not use our images or content without prior permission. Thank you.
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.
More gluten-free sweet potato biscuit recipes from food bloggers:
Sweet Potato Biscuits - Gluten-Free at Gluten A Go-Go
Classic Bisquick based biscuits you can tweak to make gluten-free (use a gluten-free baking and pancake mix):
Sunday, January 3, 2010
Look after your computer.
I don't know what I'd do if my lap-top were to die. For starters, I'd stop being an internet smart-arse. I'm on-line virtually all day (& some of the night, too!). I often talk to people on the 'phone with the 'phone in my left hand and my right hand doing 1-finger typing/mousing.
When my 2nd cousin asked me "Can you find out about the osteopath Paul that works in the Foot Pain Clinic, Winchmore Hill?", within a minute I'd found Paul Costin. When my ex-G/F asked me "who's the bloke that was in such & such TV programme?", I immediately went to The Internet Movie Database.
I therefore take PC security very seriously. As I mentioned in a previous blog post, my lap-top has limited memory and, being over 6 years old, limited CPU & graphics processing power. So, anything that can improve what I have is worth a try.
The first utility I shall mention is one that I've been using for ages. It's a watch-dog program called WinPatrol. It prevents programs from altering critical system files and installing start-up programs & services without your permission.
On 1st Jan, I installed Malwarebytes' Anti-Malware (MBAM). It found a load of dodgy stuff in the registry (MyWebSearch & SelectRebates) and deleted it all. The end result was more free memory and a bit more free disk space.
On 2nd Jan, I installed ESET Smart Security 4 (& uninstalled Virgin PCguard) after trying NOD32 Antivirus 4 which detected stuff that Virgin PCguard had missed. I gained ~160MB of free memory and my lap-top ran a bit faster, too.
I test my Firewall from the outside using GRC | ShieldsUP! and from the inside using LeakTest.exe, which I renamed to IEXPLORE.EXE, to try and trick the software. ESET Smart Security 4's firewall, once set to Interactive mode, passed all of the tests.
If I find any other useful programs, I'll let you know.
When my 2nd cousin asked me "Can you find out about the osteopath Paul that works in the Foot Pain Clinic, Winchmore Hill?", within a minute I'd found Paul Costin. When my ex-G/F asked me "who's the bloke that was in such & such TV programme?", I immediately went to The Internet Movie Database.
I therefore take PC security very seriously. As I mentioned in a previous blog post, my lap-top has limited memory and, being over 6 years old, limited CPU & graphics processing power. So, anything that can improve what I have is worth a try.
The first utility I shall mention is one that I've been using for ages. It's a watch-dog program called WinPatrol. It prevents programs from altering critical system files and installing start-up programs & services without your permission.
On 1st Jan, I installed Malwarebytes' Anti-Malware (MBAM). It found a load of dodgy stuff in the registry (MyWebSearch & SelectRebates) and deleted it all. The end result was more free memory and a bit more free disk space.
On 2nd Jan, I installed ESET Smart Security 4 (& uninstalled Virgin PCguard) after trying NOD32 Antivirus 4 which detected stuff that Virgin PCguard had missed. I gained ~160MB of free memory and my lap-top ran a bit faster, too.
I test my Firewall from the outside using GRC | ShieldsUP! and from the inside using LeakTest.exe, which I renamed to IEXPLORE.EXE, to try and trick the software. ESET Smart Security 4's firewall, once set to Interactive mode, passed all of the tests.
If I find any other useful programs, I'll let you know.
Saturday, January 2, 2010
Mum says....
....that Alpro Soya is full of soya bean goodness. Yes, it's another TV advert! I saw it loads of times in the ad-breaks of a programme I was watching on ITV Player. It looks like Alpro aren't allowed to tell us that their soya (soy in just about every other country) milk is full of soya bean goodness, so they have to use argumentum ad verecundiam/ipse dixit.
Alpro. A tasty blend of water, organic soya beans and concentrated organic apple juice. Watch out for all that sugar. You don't want to become addicted, or get tooth decay!
So, do you trust mum? I would rather trust Drew Price BSc, MASc HFI (ACSM).
Alpro. A tasty blend of water, organic soya beans and concentrated organic apple juice. Watch out for all that sugar. You don't want to become addicted, or get tooth decay!
So, do you trust mum? I would rather trust Drew Price BSc, MASc HFI (ACSM).
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