Barry Groves -has he missed something?

my understanding is that it doesn't quite work that way. When we eat carbs, sugar levels rise in the blood. Insulin takes some of that sugar into the muscles, some into the liver for storage as glycogen, and when the liver is "full", the excess can be stored as fat. To store anything as fat, it has to pass through membranes which requires insulin to let it through. Fat doesn't stimulate the production of insulin so isn't stored. Most fat is actually excreted I believe. (Hence the runny poos if we eat lots some times). We know saturated fat isn't good for us (?) because we're told it's bad for the heart, and probably is, but it's not what makes us fat.
Well, that's my rational for eating loads of bacon anyway!
Malc

From what I've read on other sites he has definitely missed loads, namely the 5 to 7 years it would take to get a Phd if he hadnt bought his off the internet :lol:

I'm not even sure he got past O level, the old standard essay on what happens when you eat a cheese sandwich would have shown him he was wrong.
It is very much easier for fat to be stored as fat than carbs to be stored as fat.
fat storage simplified.
http://science.howstuffworks.com/enviro ... -cell2.htm
edit
added: protein can elicit a high insulin response, I'm not sure what would happen if you ate nothing but pure fat ...not a way anyone would want to eat however, given that insulin is elicited by the smell of food it would probably still be produced)
In one way he is right absolutely no insulin and fat breaks down as in uncontrolled T1 but that is another story. It is a fault when this happens, insulin is a very necessary part of human metabolism.

Hence the runny poos if we eat lots some times

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I was told down to water content in Poo hard ones no water
Runny ones lots of water
Firmish Poo Water level Just right

I take Morphine that removes water from my bowels gives me Hard Ones :evil:
When i take lactulose Liquid pulls water back into bowels I get softer ones


Now we all talk Kcals in and Kcals used

Has Anyone Burnt a good Poo to see how many Kcals we are Wasting :?:

From experience a good Vindaloo does not hang around very long :mrgreen:
So how many of the Kcals in that meal did my body get a chance to use :roll:



Reminds Drink more water

http://www.smellypoop.com/facts_about_poop.php

What is poop made of?
About 3/4 of your average turd is made of water. Of course, this value is highly variable - the water content of diarrhea is much higher, and the amount of water in poop that has been retained (voluntarily or otherwise) is lower. Water is absorbed out of fecal material as it passes through the intestine, so the longer a turd resides inside before emerging, the drier it will be.

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Here is an interesting piece of research - have to admit I have not read the actual paper but it does make you think!

Published on aol today

Quote
Scientists have found out why eating a high fat diet can trigger type 2 diabetes, by carrying out experiments on human tissue samples and mice.

The US research team, who published their work in the Nature Medicine journal, said eating fatty foods disrupts sensors in the body which detect sugar.

Cases of type 2 diabetes have doubled around the world over the last 20 years and one of the major risk factors for the disease is being overweight.

Pancreatic beta cells are responsible for monitoring blood sugar levels in the body. If the levels of sugar in the blood rise too far, the cells release insulin to decrease sugar levels.

An enzyme called GnT-4a is vital to this process as it lets cells soak up glucose and find out how much sugar blood contains.

When scientists fed mice a high-fat diet it interfered with how cells were able to monitor blood sugar levels and mice began to show sign of diabetes.

Lead researcher Dr Jamey Marth said: "The observation that beta cell malfunction significantly contributes to multiple disease signs, including insulin resistance, was unexpected."
He said that if levels of GnT-4a enzymes were boosted, this might prevent type 2 diabetes occurring: "The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment.
"This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function."

If this is followed up then will be interesting!

In practice it seems to echo what I see!

Ally

ally5555 said:

Scientists have found out why eating a high fat diet can trigger type 2 diabetes, by carrying out experiments on human tissue samples and mice.

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This is great news!

Great news for my pet mouse. Now if I stop feeding him cheese, he won't catch the old diabetes.

If only we spent as much money researching a cure for human diabetes as we do researching mouse diabetes, I might have a chance of getting back on the chocolate hobnobs.

Seriously. I'm not sure if I'm allowed to link to it here, but Jenny Ruhl has some interesting things to say about this study (and the legions of other rodent based revelations on diabetes). Picking up on the title of a paper that you haven't read, because you think you agree with its conclusions (which you haven't read), is the worst kind of confirmation bias.

Well many studies use animals but I think the interesting thing here is that it does link in with prof Taylors research.
Jenny Ruhl has not read it either but I guess she would choose to dismiss it!
I think it may come back to the fact that excess fat intake does matter.

Sid Bonkers said:

From what I've read on other sites he has definitely missed loads, namely the 5 to 7 years it would take to get a Phd if he hadnt bought his off the internet :lol:

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I was reading an article that said Barry Groves obtained a doctorate in nutritional science from distance learning Trinity College and University registered in the US, their website states it awards degrees based on 'experience'.......... :shock:

I'll cancel that book........

Nigel

Hi Nigel

I am glad you found that - I looked and could not find where it was from. Sounds a bit like the one Gillian Mckeith awarded herself!

Mckeith awarded herself

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also based on Poo :lol:

Don't dismiss the humble rat!

Research of this nature do give a great undestanding to how things work, helping to guide researchers where they should be looking for answers to cure thing such a diabetes, cancer etc..

And it's is really about time that people such as the Jenny Rulh etc made their minds up on way or the other, as they do tend to one minute dismiss the rat research because it doesn't say what they want it, then use rat research if it happens to indicate in their favour..

You either except all the research as viable, or no researc is viable not change with whether it agrees/supports your view or disagree's with your view point!

As to whether you could survive on fat alone,

Well I know I couldn't has fat makes me feel rather quesy, so must assume if I hate pure fat only it wouldn't be very long before I started vomiting..

But if you could survive on fat alone, doesn't that prove calories do count!

I'd like to know how much carbohydrate the mice were eating along with the fat in their diet. It's that combination that really does for me.

Maybe a research project on 3 types of diet - fat/protein; protein/carb; carb/fat - would show some interesting results?

Viv 8)

Viv said:

Maybe a research project on 3 types of diet - fat/protein; protein/carb; carb/fat - would show some interesting results?

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Interesting, yes. Surprising, no. (Not to some of us anyway...) :wink:

This group of researchers were not seeing if they could make mice diabetic with a fatty diet or the 'right' proportions of fat/protein/carbs to prevent the onset of T2 diabetes.
The paper is very hard going for the non specialist and I only got the gist of it, not the detail.
They were looking at what is going on in the pancreases of mice who have had diabetes induced by such a diet and comparing theit islet cells with those of non diabetic mice and those of people with T2 diabetes.
They found high concentrations of free fatty acids in the diabetic mice.These fatty acids interfered with two proteins – FOXA2 and HNF1A – involved in the production of GnT-4a, a protein which is involved in the pancreas for sensing glucose levels and responding to them.
They seem to have found a similar situation in donated islet cells from humans with T2. (though I got lost at this point in the paper so I'm not clear on what they did here)
They also engineered mice to have enhanced levels of GnT-4a and found that those mice , despite getting fat on a high fat diet were less insulin resistant. They repeated this with another type of mouse that was engineered to have higher levels of another glucose sensing protein , Slc2a2, these mice had improved sensitivity on a high fat diet but not as much as those engineered to have enhanced GnT-4a
Having struggled with the paper, I found that this NHS choices article discusses the article in plain English.
http://www.nhs.uk/news/2011/08August/Pa ... betes.aspx

So is it relevant that these mice were made obese on an high-fat diet as opposed to a high-carb or high-protein diet? Did they test these scenarios?

Are we to assume that these internal changes result from the fat in the diet or from the excess stored fat mass?

Do high levels of FFAs in the blood correlate to an high intake of dietary fat? What about an high intake of refined carbohydrates?

What kinds of fats did they feed these rodents? Pro-inflammatory vegetable oils or naturally occurring fats?

What did they eat along with the dietary fats?

So many questions but it's oh so much easier to jump to conclusions :?