Hi folks,

...just dropping in with a few bits that may be helpful:

In physiology a calorie is a unit equal to the kilocalorie used to express the heat output of an organism and the fuel or energy value of food. In other words, a calorie is about how much heat you get when you burn it.

If you can't burn it, the body has to store it or eject it in excreta.

A gallon of gasoline (about 4 liters) contains about 31,000 calories. Obviously you cannot drink it, but people can drink vegetable oil, which contains nearly the same number of calories per gallon. 

If you drink a few spoons of it, that's all the calories you theoretically need in a day. If you drank half a bottle of it a day and ate nothing, you'd still die of malnutrition despite taking in thousands more calories than you need every day.

If we're gonna store it, it must have somewhere to go. Adipose tissue for fat storage forms mainly during our first year of life, and STOPPING making it relies on a gene that's transcripted by breast milk. If it isn't turned off after that firt year or so, we carry on making too many fat-storing cells.

When we take in more calories than needed and already have some stored, the body should eject the excess straight down the toilet. If there are too many adipose cells, it will try to keep on storing it instead.

To store excess calories they must be turned into fat.

Excess sugars from some foods (eg low GI) cannot be turned into fat very economically due to their chemical composition; by the time the body gets to extracting enough sugars to make fat, the remains are already going down the toilet.

Some foods (eg high GI) can be turned into fats with ease. If we have the combination of too much fast release sugar and too many adipose cells, we store too much fat and get sick.

Water retention is the body's attempt to keep toxins out of tissues. Toxins accumulate in the stored water, and can be excreted over time. Sadly they often build up faster than we can excrete them.

Food composition signals the genome, and most people's idea of 'good food' is not the same as biology's. If food is poor in nutrients (eg, most of our western diet, particularly processed cereals & sucrose) the genome 'assumes' there is a shortage of good food, and starts making more adipose tissue for storing fat.

In short, when we live on cattle food for long preiods of time, the body thinks there is a famine 'out there'. It's storing fat to try to save our lives, but it doesn't know there is way too much adipose tissue; its programmed instructions code for: 'fill the available space and then excrete the rest'. If the available space is ever-expanding, where does that leave the poor program?

Habitual low GI signals the genome that there is nutritious food available and no famine. Adipose tissue stops being made and starts being dismantled for recycling. Fat has only a limited amount of space to be stored IN, so most of it is excreted. That's how we can get away with eating junk once the genome's switched, as long as we keep signaling it that there's nutritious food as well.

Best,
AR

Alex wrote:

Hi folks,

Sakiro Wrote:
I know that alex has another opinion than me

There is misunderstanding here, and I can't yet figure out where it's coming from.
Firstly, our opinions are not relevant here; we need facts. Hopefully none of us expresses our opinions on this site unless they are specifically asked for. I haven't told anybody mine, so how can anyone know if they disagree with it?
AR

Hi dude, when i wrote that word i tought than something like this could come =)

I don't know what word is more appropiate to use when you have a "insert word here" (i used opinion) based in your interpretation of the research (facts) about the topic?? i only could come with opinion but just tell me what could be a better word to avoid misunderstood in the future.

Alex wrote:

Second, I am unable to understand what your (Sakiro's) argument is so far. I think this is often the main problem for me; I don't understand exactly what it is that is either not understood or being disagreed with, and I end up taking 'shots in the dark' hoping to provide enough bits of information to help clarify things by adding extra data, which of course makes things even more complicated  :  )

This is good productive chat and I'm hoping that at some point I'll think "Aha!" and understand where to go from there. Simplicity and formality help me to grasp concepts, and I'm still getting used to how to pull information out of our casual chat style.

AR

Well, i was looking for research of "the stuff" that happend in your body when you eat permanently only Low GI foods for about 6 months, and after that, the theorically epignetic changes that turn fat store genes OFF so you could eat above your caloric maintanance and still don't gain weight because they will not be absorved and you will pee/poo that calories? (that's something new i learned in this chat because i thought the body has no option but to store any "excess" not used)

So based on that, i was looking for some peer review study, with good methodology (metabolic warden, in humans, etc) where they do something as simple as this:

- Find 20-30 people to eat Low GI foods for the time neccesary to tigger that change (in the tutorials is about 6 months)

- Calculate theirs metabolism accurately (this can't be done for any of us without the tools)

- After the epigenetic change, give them 20-30% above his mainteneance calories every day, if is 2000 calories, give them about 2600-2800 (with still low GI foods) , for like 1 month, and see if they don't gain weight (in fat).

- If they don't, bingo.

So is something as simple like that, but, again, i can't find any study like that?

A few study i read who are similar, are flawed because the calories are "self-reported" and people lie or just don't know how many calories eat in reality (specially obese people, the one who say they "can't lose weight") and that is not science is a waste of time.

Undereating and underrecording of habitual food intake in obese men: selective underreporting of fat intake

http://www.ajcn.org/content/71/1/130.full

And there is a lot of more research like that one.

Alex wrote:

Here's a small example:
Sakiro wrote:
"the reason that for a lot of people is a lot easier to not get hungry so fast with low carbs than high carbs (a lot of this depend of insulin sensitivty i think)"
...Does 'low carbs' mean "low quantities of carbohydrates" OR "low GI carbohydrate" OR "Low GL carbohydrate"?  Simple things like that trip me up.
AR

Well with that i tried to say that a lot of "anti carb" people, misunderstood that one mechanism which a low carb (quantity) diet appear to be better than one that is not, is all the water and glucogen loss in the muscle in the first days, they lose more weight (but not fat) and they think that "carbs make you fat", or the relationship with carbs and insulin when now is know (at least i recently found this) that even protein spike up your insulin.

Measures of postprandial wellness after single intake of two protein-carbohydrate meals.

http://www.ncbi.nlm.nih.gov/pubmed/20060863

And about flawed research, a few weeks ago this study make a lot of noise

Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance

http://jama.jamanetwork.com/article.asp … id=1199154

And at first glance, it seemed like a solid proof to the advantage of "low gi diet".

Objective  To examine the effects of 3 diets differing widely in macronutrient composition and glycemic load on energy expenditure following weight loss.

And i thought, one finally! (i'm glad to change my mind because the only thing i want is the truth not matter what it turned to be, if i found it, i improved myself)

But right now a lot of experts in the field are debunking the study because it have a lot of errors in their implementation (i'm still reading it so probably i update this later for anyone interested)

So, in resume, my argument is:

There is evidence that "something more" is going on .. and is not only a "calorie in Vs calorie out" stuff (even if it works to lose weight anyways, if you are in a caloric deficit you can't avoid the reality that your body must pull off the energy somewhere)

I'm saying that till today, 25 jul 2012, i couldn't find any reliable research who could replicate the epiginetic changes (agouti gene) in humans (here was posted something, but it was in rats) and after that is proved (the change, triggered by the consume of low gi foods) probe the theory just making that people eat above his caloric expending (all controlled by laboratory, not self-reported data) and see if they don't gain weight in fat after a reasonable amount of time.

The End =)

I hope that now is "Spock enough", and sorry if i confused someone with my posture in this topic.

And i was wondering, i don't think (from a survival point of view) very "smart" to the body don't get stored fat? if no food is available the people who had that genes stored off will be the first to die!

PS: I think that maybe we need to create a new thread for this? it started at the 3rd post.  All the people looking for "nootropic info" could get a little lost LOL =)

Cheers

...Okay I catch up with the rest now  :  )

[s] So, in resume, my argument is:
There is evidence that "something more" is going on .. and is not only a "calorie in Vs calorie out" stuff (even if it works to lose weight anyways, if you are in a caloric deficit you can't avoid the reality that your body must pull off the energy somewhere)

Great; that's very clear to me. My interpretation of what research I've read so far is: Calories are completely unimportant in low GI because EITHER: if there are 'too many', the excess can't be stored as 'white' fat. It looks like some of it is excreted out and some of it is turned into brown fat and burned for energy, OR: calories from low GI foods can't be turned into fats. I don't know which yet but it may be both (eg, it may be that calories from low GI are very difficult to turn into fats, and doing that takes energy in itself?)
...so your interpretation is: 'there's more involved than calories', and my interpretation is: 'calories are not necessarily involved at all'.
That's a good position for us to go hunting from  :  )

Hopefully some human trials have now been viewed by both of us (and don't forget we're human trials too)  :  )

[s] I hope that now is "Spock enough", and sorry if i confused someone with my posture in this topic.

That's great thankyou Captain, hopefully everyone knows we Vulcans get confused on a regular basis. I think we only have 2 neurons in the Amygdala -one's labeled 'fascinating' and the other is labeled 'wtf?'  Shit, I just described my life  LOL  :  )

[s] And i was wondering, i don't think (from a survival point of view) very "smart" to the body don't get stored fat? if no food is available the people who had that genes stored off will be the first to die!

Well yeh obviously there has to be SOME stored fat to protect * warm organs etc, I think we are referring here to the fate of excess fat (consumption above what we need to use & store).

PS: I think that maybe we need to create a new thread for this? it started at the 3rd post.  All the people looking for "nootropic info" could get a little lost LOL =)
Yeh go for it, I'll follow you... keep it in the Lab though, else not everybody can see it.
Best,
AR

Hi dudes'
Re: Can we edit thread titles? 

The best thing to do with a change of subject is start a new thread. Otherwise, what WAS being discussed gets lost in the name change. Afaik, the original authors of threads can change the title.

To get back to nootropics:
Re: do you guys know the mechanism by which modafinil reduces our sleep time needs?

Nobody does  :  )  Well, there are theories, but nobody's sure yet. Modafinil (Provigil) is a complicated drug that does a lot of things; it affects glutamate, GABA, serotonin, dopamine, histamine and norepinephrine. 

One theory is that it works by orexin-receptor stimulation:

"Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation"
http://www.cell.com/retrieve/pii/S009286740081973X

"Hypothalamic arousal regions are activated during modafinil-induced wakefulness"
http://www.jneurosci.org/content/20/22/8620.full

Another theory suggests its mechanism functions via manipulation of glutamate & GABA:
"Modafinil Blocks Reinstatement of Extinguished Opiate-Seeking in Rats: Mediation by a Glutamate Mechanism"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2939923/

"Modafinil reverses hypoexcitability of the motor cortex in narcoleptic patients: a TMS study".
https://www.ncbi.nlm.nih.gov/pubmed/20810311


Re: Joseph B Nelson:
http://www.diabetesselfmanagement.com/a … ement/all/

Best,
AR