http://www.ncbi.nlm.nih.gov/pubmed/20595541
It took 2 days of fasting to increase myostatin levels significantly, 1 day of fasting did not affect myostatin.
Friday, 23 July 2010
Glutamine prevents Myostatin hyperexpression
http://www.ncbi.nlm.nih.gov/pubmed/20623149
More support for glutamine supplementation.
More support for glutamine supplementation.
Friday, 16 July 2010
Eating Animal Adipose Tissue
http://vimeo.com/10533993
Bacteria ferment plant material into short chain fatty acids.
Barry mentions how prized fatty meat was in our past. So lets all eat more animal adipose tissue, something that so rarely happens these times.
Bacteria ferment plant material into short chain fatty acids.
Barry mentions how prized fatty meat was in our past. So lets all eat more animal adipose tissue, something that so rarely happens these times.
Adaption : Reminder to myself
Your bodies metabolism will ultimately adjust to whatever diet your consuming. Regardless of macronutrient content.
To break a weight loss plateau, change from high protein to high fat or vice versa if you was doing the other. Always try to keep it ketogenic however!
To break a weight loss plateau, change from high protein to high fat or vice versa if you was doing the other. Always try to keep it ketogenic however!
Body Fat Set Point
Muscle is controlled by the protein myostatin. Your expression of myostatin is genetic. Therefore your set point of musculature is also primarily genetic.
You can change how much muscle you have by doing exercise, your body compensates by building more muscle. Or you can lower muscle mass by being extremely sedentary. This change in activity must be maintained, for once it is abandoned, you slowly but surely go back to your muscle "setpoint".
Bone density is essentially the same. Bone will change its mass and density dynamically, depending on what happens to it.
So is adipose tissue size the same as the analogy above? Is there really a fundamental genetically determined setpoint controlled by some mysterious gene or protein.
You can change how much muscle you have by doing exercise, your body compensates by building more muscle. Or you can lower muscle mass by being extremely sedentary. This change in activity must be maintained, for once it is abandoned, you slowly but surely go back to your muscle "setpoint".
Bone density is essentially the same. Bone will change its mass and density dynamically, depending on what happens to it.
So is adipose tissue size the same as the analogy above? Is there really a fundamental genetically determined setpoint controlled by some mysterious gene or protein.
Thursday, 15 July 2010
Going to bed in a insulin sensitive state
Im still intrigued by the study posted recently were lean subjects got a spike in ghrelin during sleeping hours and obese subjects didnt.
In the study, the subjects were eating high carb meals all day, in the last 2 meals they had a blunted response to ghrelin, suggesting that they may be insulin resistent at this point. Going to bed in an insulin resistent state is perhaps not sufficient to make a ghrelin response becuase ghrelin itself will cause a kind of physiological insulin resistence so that we can switch to FFA for fuel.
This is just trial and error and speculation at the moment, tomorrow I will look for more studies to piece together the puzzle of ghrelin.
In the study, the subjects were eating high carb meals all day, in the last 2 meals they had a blunted response to ghrelin, suggesting that they may be insulin resistent at this point. Going to bed in an insulin resistent state is perhaps not sufficient to make a ghrelin response becuase ghrelin itself will cause a kind of physiological insulin resistence so that we can switch to FFA for fuel.
This is just trial and error and speculation at the moment, tomorrow I will look for more studies to piece together the puzzle of ghrelin.
High Intensity Exercise boosts Adiponectin
http://jcem.endojournals.org/cgi/content/full/90/11/5970
Their definition of high intensity exercise is 80-85% of 1RM. 3 Sets of each exercise were performed with 6 mins rest between!
Thats alot of rest, but then again the subjects were elderly.
Adiponectin was raised for 24hrs following this.
Their definition of high intensity exercise is 80-85% of 1RM. 3 Sets of each exercise were performed with 6 mins rest between!
Thats alot of rest, but then again the subjects were elderly.
Adiponectin was raised for 24hrs following this.
My Dandruff has vanished
Its been a problem for most of my life.
Currently the supplements im taking are...
l-glutamine + fizzy vit c in morning
Vitamin D 7500iu in morning
Butter Oil
Cod Liver Oil
Krill Oil 2g per day
ZMA at night before bed 4-5 times per week.
Niacin 500mg , few times a week, randomly
I started taking Inositol today aswell, will see how it goes.
I suspect it is the Vitamin D, since I only started taking large doses of it again recently and spending more time in the summer sun. Theres also a small chance it could be the krill oil, as I added it back to my supplement list at the same time as the D3.
Currently the supplements im taking are...
l-glutamine + fizzy vit c in morning
Vitamin D 7500iu in morning
Butter Oil
Cod Liver Oil
Krill Oil 2g per day
ZMA at night before bed 4-5 times per week.
Niacin 500mg , few times a week, randomly
I started taking Inositol today aswell, will see how it goes.
I suspect it is the Vitamin D, since I only started taking large doses of it again recently and spending more time in the summer sun. Theres also a small chance it could be the krill oil, as I added it back to my supplement list at the same time as the D3.
Tuesday, 13 July 2010
Ghrelin and Adiponectin
http://www.ncbi.nlm.nih.gov/pubmed/15231997
First, in this study we see from the graphs that ghrelin increases dramatically in response to sleep for lean people, however it remains unchanged for obese people.
We also see a marked drop in adiponectin during sleeping for lean people, while for obese people, nothing happens to thier adiponectin levels.
For breakfast and lunch, the pattern of ghrelin remained the same for obese and lean people, then we get to dinner, ghrelin goes down markedly for lean people, but stays the same for obese people, then the evening snack comes, ghrelin goes up for obese people, while for lean people it stays low, right up until sleepy time.
Then we have the leptin graph, notice it stays the same for lean people constantly, while for obese people its shooting all over the place.
There is clearly something wrong with an obese persons adipocyte functions.
Unfortauntely the study doesnt say what the dinner consisted of, as this is when the trouble starts for the obese people with ghrelin.
http://www.ncbi.nlm.nih.gov/pubmed/20464707
This study offers a discussion on ghrelin and adiponectin,
Circulating ghrelin concentrations are also regulated by longer term changes in energy homeostasis. Ghrelin levels are lower in humans with higher body weight and rise after diet-induced weight loss (31). The usual postprandial fall in plasma ghrelin is absent or attenuated in the obese, suggesting that ghrelin may be involved in the pathophysiology of obesity (32, 33). We have shown that iv ghrelin administration stimulates appetite in obese humans, suggesting that they are not ghrelin resistant
2002 Food fails to suppress ghrelin levels in obese humans. J Clin Endocrinol Metab
2005 Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects
The above study showed that meals high in carbs didnt really do alot for ghrelin levels in the obese, but in lean people ghrelin was surpressed more as calories went up.
Now, we have already seen that fat digestion is needed for ghrelin supression after a meal, and we have also seen that carb rich meals make ghrelin bounce back, while protein rich meals supressed ghrelin for along time.
Today we also saw that obese people secret markedly lower bile acids after food.
Could it be that obese people are not properly digesting thier food?
First, in this study we see from the graphs that ghrelin increases dramatically in response to sleep for lean people, however it remains unchanged for obese people.
We also see a marked drop in adiponectin during sleeping for lean people, while for obese people, nothing happens to thier adiponectin levels.
For breakfast and lunch, the pattern of ghrelin remained the same for obese and lean people, then we get to dinner, ghrelin goes down markedly for lean people, but stays the same for obese people, then the evening snack comes, ghrelin goes up for obese people, while for lean people it stays low, right up until sleepy time.
Then we have the leptin graph, notice it stays the same for lean people constantly, while for obese people its shooting all over the place.
There is clearly something wrong with an obese persons adipocyte functions.
Unfortauntely the study doesnt say what the dinner consisted of, as this is when the trouble starts for the obese people with ghrelin.
http://www.ncbi.nlm.nih.gov/pubmed/20464707
This study offers a discussion on ghrelin and adiponectin,
Circulating ghrelin concentrations are also regulated by longer term changes in energy homeostasis. Ghrelin levels are lower in humans with higher body weight and rise after diet-induced weight loss (31). The usual postprandial fall in plasma ghrelin is absent or attenuated in the obese, suggesting that ghrelin may be involved in the pathophysiology of obesity (32, 33). We have shown that iv ghrelin administration stimulates appetite in obese humans, suggesting that they are not ghrelin resistant
2002 Food fails to suppress ghrelin levels in obese humans. J Clin Endocrinol Metab
2005 Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects
The above study showed that meals high in carbs didnt really do alot for ghrelin levels in the obese, but in lean people ghrelin was surpressed more as calories went up.
Now, we have already seen that fat digestion is needed for ghrelin supression after a meal, and we have also seen that carb rich meals make ghrelin bounce back, while protein rich meals supressed ghrelin for along time.
Today we also saw that obese people secret markedly lower bile acids after food.
Could it be that obese people are not properly digesting thier food?
Obese slower digestion of fat?
http://www.ncbi.nlm.nih.gov/pubmed/20595403
A while ago I posted how fat digestion was needed for ghrelin supression post meal.
This study shows how obese people secret markedly less bile salts for fat digestion.
Also note that lean people typically have higher levels of ghrelin in a fasted state.
A while ago I posted how fat digestion was needed for ghrelin supression post meal.
This study shows how obese people secret markedly less bile salts for fat digestion.
Also note that lean people typically have higher levels of ghrelin in a fasted state.
Monday, 12 July 2010
The coming together of Leptin
http://forum.lowcarber.org/showthread.php?t=409492
This interesting thread links Leptin with Glutamate, its quite common for people to stall weight loss on ketogenic diets. And those very obese who loose weight tend to have very very low leptin levels after the weight loss.
On a ketogenic diet, gluconeogenesis is most likely massively increased. The liver, at all costs, needs to maintain normoglycemia as hypoglycemia is death very quickly. This would suggest that following a ketogenic diet, the pathway of gluconeogenesis is massively upregulated becuase the liver cannot afford to ever let the 5g of glucose in the blood drop too low.
Obviously, ketones reduce the need for glucose in the brain, but whatever way we swing it, that 5g of blood glucose rules the day. That must be maintained.
Anyway, there is lots of anecdotal evidence that one of the ways to break a fat loss stall on a ketogenic diet is to kind of carb binge for sometime. Such a carb binge will completely refuel liver glycogen and thus down regulate the pathway of gluconeogenesis, perhaps finally allowing glutamate to cause intense leptin secretion from white adipocytes.
With gluconeogenesis so high during a ketogenic diet, my theory is that glutamine is massively and preferentially turned into liver glycogen, instead of being turned into glutamate or reaching white adipocytes where we can crank up leptin.
I intend to experiment with honey and l-glutamine powder mega-dosing over the coming week.
This interesting thread links Leptin with Glutamate, its quite common for people to stall weight loss on ketogenic diets. And those very obese who loose weight tend to have very very low leptin levels after the weight loss.
On a ketogenic diet, gluconeogenesis is most likely massively increased. The liver, at all costs, needs to maintain normoglycemia as hypoglycemia is death very quickly. This would suggest that following a ketogenic diet, the pathway of gluconeogenesis is massively upregulated becuase the liver cannot afford to ever let the 5g of glucose in the blood drop too low.
Obviously, ketones reduce the need for glucose in the brain, but whatever way we swing it, that 5g of blood glucose rules the day. That must be maintained.
Anyway, there is lots of anecdotal evidence that one of the ways to break a fat loss stall on a ketogenic diet is to kind of carb binge for sometime. Such a carb binge will completely refuel liver glycogen and thus down regulate the pathway of gluconeogenesis, perhaps finally allowing glutamate to cause intense leptin secretion from white adipocytes.
With gluconeogenesis so high during a ketogenic diet, my theory is that glutamine is massively and preferentially turned into liver glycogen, instead of being turned into glutamate or reaching white adipocytes where we can crank up leptin.
I intend to experiment with honey and l-glutamine powder mega-dosing over the coming week.
Thursday, 8 July 2010
The body works on a system of thresholds
http://www.ncbi.nlm.nih.gov/pubmed/20570821
some may well be as good as none. and more may not be any better than some.
One thing that is prevalent in biology is that cell surface receptors for the most part determine what a cell will do.
There is no point in having high serum growth hormone for example if all your cells dont have the receptor for it to bind. Same for Testosterone. Same for ANY hormone.
With Testosterone there is a strong negative feedback loop, such that high serum T will cause your balls to churn out less. This has implications as increasing serum T through whatever means is largely a mission in futility, your testis will adjust accordingly.
Meanwhile, having the T cell surface receptor is upregulated does not have a negative feedback loop, infact, having your cells sucking in more T will ofcourse make your testis produce more as serum levels drop.
some may well be as good as none. and more may not be any better than some.
One thing that is prevalent in biology is that cell surface receptors for the most part determine what a cell will do.
There is no point in having high serum growth hormone for example if all your cells dont have the receptor for it to bind. Same for Testosterone. Same for ANY hormone.
With Testosterone there is a strong negative feedback loop, such that high serum T will cause your balls to churn out less. This has implications as increasing serum T through whatever means is largely a mission in futility, your testis will adjust accordingly.
Meanwhile, having the T cell surface receptor is upregulated does not have a negative feedback loop, infact, having your cells sucking in more T will ofcourse make your testis produce more as serum levels drop.
Sunday, 4 July 2010
Ghrelin Antagonism = Hypertension
http://www.ncbi.nlm.nih.gov/pubmed/20596792
Given that protein supresses ghrelin for the longest period of time, again intermittent fasting looks to be a magic bullet for reducing metabolic syndrome.
I have high blood pressure but I dont worry about it too much becuase its I tend to get dizzy quickly with even slight drops in blood pressure.
Given that protein supresses ghrelin for the longest period of time, again intermittent fasting looks to be a magic bullet for reducing metabolic syndrome.
I have high blood pressure but I dont worry about it too much becuase its I tend to get dizzy quickly with even slight drops in blood pressure.
l-glutamine stimulates Growth Hormone
http://www.ncbi.nlm.nih.gov/pubmed/7733028
Basically it looks like glutamine taken in isolation supresses FFA in the blood, which once again stimulates a nice GH response.
They used 2g but I suspect its dose dependent, I would imagine 5-10g would be optimal depending on body weight.
The study author speculates that the the smaller GH spikes are more beneficial becuase of the negative feedback loops associated with the large spikes.
Area under curve is likely important, but his theory does need testing.
Basically it looks like glutamine taken in isolation supresses FFA in the blood, which once again stimulates a nice GH response.
They used 2g but I suspect its dose dependent, I would imagine 5-10g would be optimal depending on body weight.
The study author speculates that the the smaller GH spikes are more beneficial becuase of the negative feedback loops associated with the large spikes.
Area under curve is likely important, but his theory does need testing.
Friday, 2 July 2010
L-Glutamine induces insulin resistence in adipocytes
http://www.ncbi.nlm.nih.gov/pubmed/17604977
I remember when I first started my ketogenic diet again, the weight loss at the beginning was very dramatic and at the time I was still finishing off my bottle of l-glutamine. taking about 5g per day.
Its unclear how much glutamine the rodents in this study were getting per kg of body weight since I don't have access to the full article. But I think that in general obesity is characterised by an upregulation of fat storage compared to fat oxidation gene's.
Taubes comment on obesity being a disorder of excess fat accumulation rather than a result of over-eating mirror's this theory.
I remember when I first started my ketogenic diet again, the weight loss at the beginning was very dramatic and at the time I was still finishing off my bottle of l-glutamine. taking about 5g per day.
Its unclear how much glutamine the rodents in this study were getting per kg of body weight since I don't have access to the full article. But I think that in general obesity is characterised by an upregulation of fat storage compared to fat oxidation gene's.
Taubes comment on obesity being a disorder of excess fat accumulation rather than a result of over-eating mirror's this theory.
Thursday, 1 July 2010
Current Hormone Understanding
Leptin - So far this looks to be more of an anti-starvation hormone. The fact that it is highly elevated in obese people is irrelevant, probably due to the fact that receptor levels are saturated.
However, problems occur when Leptin is low, although it does not seem to affect percieved hunger it does have an effect of sex hormones and depression.
Ghrelin - It seems to this hormone is also not completely involved in hunger and apetite.
http://www.ncbi.nlm.nih.gov/pubmed/16014402 - The satiating effect of dietary protein is unrelated to postprandial ghrelin secretion.
Leptin production is mainly regulated by insulin-induced changes of adipocyte metabolism - http://www.ncbi.nlm.nih.gov/pubmed/11790963
I also found another eye opening study here - http://www.ncbi.nlm.nih.gov/pubmed/12679444
Despite cutting out 95% of bypass patients stomach's, levels of circulating ghrelin remained in measurable quantities.
However, problems occur when Leptin is low, although it does not seem to affect percieved hunger it does have an effect of sex hormones and depression.
Ghrelin - It seems to this hormone is also not completely involved in hunger and apetite.
http://www.ncbi.nlm.nih.gov/pubmed/16014402 - The satiating effect of dietary protein is unrelated to postprandial ghrelin secretion.
Leptin production is mainly regulated by insulin-induced changes of adipocyte metabolism - http://www.ncbi.nlm.nih.gov/pubmed/11790963
I also found another eye opening study here - http://www.ncbi.nlm.nih.gov/pubmed/12679444
Despite cutting out 95% of bypass patients stomach's, levels of circulating ghrelin remained in measurable quantities.
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