Wednesday 17 December 2008

Blood Glucose, Insulin & Diabetes

Diabetes is afflicting an increasing percentage of the population as time goes by. Even athletes like Sir Steven Redgrave can get it. This article tries to explain the workings of the body's blood glucose (BG) regulation system and what can go wrong with it.


How does the body regulate blood glucose?

At any given moment, there's ~4.5g of glucose in your blood (5mmol/L x 180g x 5L). As the brain alone uses about 6g of glucose per hour in the absence of ketones, blood glucose (BG) level could fall to zero within an hour if we ate no sugary/starchy carbs. If we ate a mere 5g of glucose, BG level could double. As very low BGs are fatal and very high BGs damage proteins by a process called glycation (a bit like caramelisation), the body keeps BG levels within fairly tight limits by the use of a negative feedback (NFB) control system.


How does a negative feedback control system work?

NFB systems consist of a non-inverting (more in → more out) part, which in this case are the islet cells of Langerhans (a.k.a. pancreatic beta cells), as increasing BG level results in increasing insulin secretion. It's actually more complicated than that. Beta cells can store insulin and dump it into the blood if there is a sudden increase in BG level. This is analogous to the accelerator pump in a carburettor, which dumps petrol into the engine if you slam your foot on the accelerator pedal, i.e. it produces a rapid response. The dumping of insulin from beta cell storage is known as the 1st Phase insulin response. If this (or the accelerator pump) fails, there is a lag in the response; this will become significant below.

Increasing BG level results in increasing insulin secretion from beta cells and is known as the 2nd Phase insulin response.

The other part of a NFB system is the inverting (more in → less out) feedback part, which in this case is split into three parts, all working in parallel. They are:
  1. Liver - increasing insulin level results in decreasing Hepatic Glucose Production.
  2. Muscle cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.
  3. Fat cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.


What can go wrong?

There are three main types of diabetes:

1) Type 2 diabetes. This is by far the most common (about 95% of all cases) and is usually caused by abdominal obesity. Type 2 diabetes has two main mechanisms going on. The first is a progressive insulin resistance (IR) of target tissues, possibly caused by increased levels of saturated fatty acids being fed to the liver from abdominal fat stores, chronically-high BG and insulin levels caused by chronically over-consuming high glycaemic load carbohydrates, possibly accompanied by large amounts of saturated fat and/or large amounts of omega-6 fat. A sedentary lifestyle lowers the sensitivity of muscle cells to insulin. Insulin resistance also has a hereditary link. IR is reversible. See Insulin Resistance: Solutions to problems.

Insulin resistance weakens the feedback in the NFB system, resulting in increased BG level (hyperglycaemia) and increased insulin level (hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective. Increased BG level causes increased damage to beta cells by glycation. Increased insulin level gradually causes further insulin resistance as target tissues become increasingly insensitive (a bit like louder and louder music making you progressively deafer and deafer). Eventually, beta cells become too damaged to secrete sufficient insulin and insulin levels begin to fall. This results in a massive rise in BG level and this is now full-blown Type 2 diabetes. There are five main treatments for Type 2 diabetes:
  1. Lifestyle interventions - reduced intake of high glycaemic load carbohydrates and/or increased intake of omega-3 fats and/or increased intake of Vitamin D3 and/or increased intense exercise and/or loss of abdominal fat.
  2. Sulphonylureas - drugs which stimulate beta cells to secrete even more insulin. Unfortunately, that's a bit like flogging a dying horse as it doesn't address the problems caused by weakened feedback and eventual beta cell failure is inevitable, resulting in the need for insulin injections.
  3. Biguanide drugs such as Metformin - increase insulin sensitivity in target tissues. This strengthens the feedback in the NFB system, which results in reduced BG and insulin levels. This combined with lifestyle interventions can return the NFB system to normal operation.
  4. Thiazolidinediones - also increase insulin sensitivity in target tissues, e.g. muscle and fat, as well as possibly improving the secretory function of beta cells. Increases the number of new, empty fat cells.
  5. Insulin injections take the strain off beta cells, but may worsen insulin resistance.

2) Type 1 diabetes. This is much less common (about 5% of all diabetes cases) and is caused by an autoimmune disease. One possible mechanism is as follows: Due to an increase in Zonulin, the gut becomes more permeable than it should (a.k.a. Leaky Gut), which allows protein fragments to pass into the blood. These are locked-onto by antibodies, and destroyed by the immune system. However, if a protein fragment happens to have the same sequence of amino acids as a protein in your body, the immune system sets about destroying parts of your own body. Examples of this are gluten (proteins found in wheat, rye, barley and oats) producing antibodies in the blood that can destroy the gut causing Coeliac Disease, or skin cells causing Dermatitis Herpetiformis, or mucous membranes causing Sjogren's Syndrome, or brain cells causing Cerebellar Ataxia. As there's an association between the consumption of cows' milk and the incidence of type 1 diabetes (see here ), it's possible that, in susceptible individuals, casein protein fragments enter the blood, resulting in auto-immune destruction of pancreatic beta cells. Another possible mechanism is autoimmune attack after a viral infection. Once all beta cells have been destroyed, no insulin is secreted and insulin injections are required. If some beta cells survive, there's a possibility that normal BG levels can be maintained if sugary/starchy carbohydrate intake is reduced.

3) Latent Autoimmune Diabetes of Adulthood (LADA). This is a slow developing diabetes that is more like type 1 in origin (autoimmune with antibodies) but is often misdiagnosed as type 2 because of the age at diagnosis and the relatively slow progression of the disease (slow compared to type 1 but fast compared to type 2). It is believed that Sir Steven Redgrave has this. Whether or not his autoimmune disease was triggered by a huge intake of milk (to build those Olympic-winning muscles), we'll never know. To minimise your risk of developing autoimmune diseases, see Keep 'em tight.



What else can go wrong?

As stated earlier, loss of the 1st Phase insulin response can occur. This usually happens when beta cells are chronically over-secreting insulin due to a chronically-high intake of sugary/starchy carbs and are unable to store any. This results in a lag in insulin response. This isn't a problem if low glycaemic load carbs are eaten and BG levels change only a little or very slowly. However, if high glycaemic load carbs are eaten, this produces a rapid rise in BG level. If a NFB loop with a lag in it is presented with a step response change in input level, its output overshoots. This results in too much insulin being secreted (a.k.a. postprandial hyperinsulinaemia), which causes feelings of postprandial sleepiness and also down-regulates insulin receptors in the ventromedial hypothalamus (VMH), resulting in an eventual normal insulin level being interpreted by the VMH as rebound hypoinsulinaemia, which causes feelings of ravenous hunger (as insulin acts as a satiety/satiation hormone in the brain). The solution? Stick to low glycaemic load carbs.


Where does blood glucose come from if I haven't eaten?

When no sugary/starchy carbs are being digested, BG starts to fall. Adrenaline and noradrenaline (catecholamine hormones) are secreted by the adrenal medulla into the blood and also by sympathetic neurons. Like glucagon (see below), they stimulate the mobilisation of glycogen and triacylglycerols (stored fats) by triggering the production of cyclic AMP (adenosine mono-phosphate). Adrenaline and noradrenaline differ from glucagon in that their glucose-producing effect is greater in muscle glycogen than in liver. They also inhibit the uptake of glucose by muscle. Instead, fatty acids released from adipose tissue are used as fuel. Adrenaline also stimulates the secretion of glucagon and inhibits the secretion of insulin. Thus, catecholamines such as adrenaline and noradrenaline increase the amount of glucose released into the blood by the liver and decrease the utilization of glucose by muscle.

Pancreatic alpha cells secrete glucagon. This hormone mobilises the conversion of liver glycogen into glucose. The liver only stores about 70g of glycogen, but when combined with water, a larger mass of glucose is generated. Eventually, liver glycogen stores become depleted and BG level falls again. Glucagon also stimulates gluconeogenesis in the liver & kidneys, which is the production of glucose from non-carbohydrate precursors, like the conversion of glucogenic amino acids, such as glutamine, into glucose. This causes slow muscle wastage unless there is sufficient protein intake to provide the necessary amino acids. When BG falls to about 3.3mmol/L, the pituitary kicks-in and secretes ACTH (adrenocorticotropic hormone) which stimulates the release of cortisol from the adrenal cortex. Cortisol further stimulates gluconeogenesis in the liver & kidneys by catabolising (breaking down) muscle mass. When BG level falls to about 2mmol/L, the pituitary secretes GH (Growth Hormone) which has an anti-insulin effect.


What else does insulin do?

Insulin has many metabolic effects in the body apart from lowering BG level. It's a very anabolic hormone and an insulin spike is usually desired post workout to maximise the uptake of glucose and amino acids by muscle cells. There's nothing wrong with the occasional short-term insulin spike. It's chronically-high insulin levels due to chronic overconsumption &/or insulin resistance that cause long-term health problems like high blood pressure and clogging of arteries.

13 comments:

Unknown said...

Hi Nigel,

I managed to re-read this post because of the latest one that you have up on the front page.

Regarding the order of insulin resistance: liver -> muscles cells -> fat cells. According to CarbSane, that's rather Taubsian, and wrong, based on some studies she discussed in one of her recent posts.

Have a look if you're interested.

http://carbsanity.blogspot.co.uk/2012/06/insulin-resistance-iii-glucose-uptake.html#more

Would you consider revising your stance regarding the order of insulin resistance. Or is this one of those contextual things, where such an order of resistance only occurs when a person is sedentary?

Cheers.

Nigel Kinbrum said...

Hi Kade,

I did read CarbSane's post. I still feel that IR in a particular tissue depends a lot on the fullness of cells in that particular tissue, so IR could develop in any order, depending on carbohydrate intake (affecting liver IR), carbohydrate intake & activity level (affecting muscle mass IR) and fat intake & number of fat cells (affecting fat mass IR).

It looks as though an update to this ancient post is in order. But not right now, as I'm off out again!

Cheers, Nige

Nigel Kinbrum said...

I had a bijou tweak-ette before I went out!

Unknown said...

I myself am not fully sold on this static equation that it's always x cells followed by y cells, and so on and so forth - fixed order that no one can defy. This is due to some personal observations I've made of certain individuals. Nevertheless, the scientific view is interesting.

It does make more sense that any time a given tissue is full, only then would insulin resistance take place. This means that the order in which the resistance manifests is highly subject to each individual's case. We're all different, right?


And seriously, what's a bijou tweak-ette? Can it be hunted in a gruesome battle between man and beast, resulting in a primal backwoods barbecue?

Nigel Kinbrum said...

Exactly. A study on fat, active people would highlight fat mass IR. A study on thin, sedentary people would highlight muscle mass IR. A study on people consuming very high sugar/fructose diets would highlight liver IR.

RE bijou: I like to slip French words in every now & then! See Bijou (adjective). I emphasised the smallness of my tweak by adding the suffix -ette.

Pretentious? Moi? ;-D

Unknown said...

Shouldn't insulin resistance also prevent body fatness? Or does ASP take care of that side of the equation, thus keeping them fat?

And in the case of our sedentary slim friends, wouldn't muscle mass insulin resistance lead to hyperglycaemia issues since body fatness isn't increasing, and it's not going to the muscles either.


As for the high sugar and fructose diet-related liver insulin resistance. Well, that is something that I am very interested in seeing as the Peat-a-tarian school of thought argues that glycation-factors, glucose clearance, and metabolic rate should improve greatly on such a diet if it was made up of nutritious whole fruits. There's so much conflict at the moment over the question of sugar, but most of the arguments are the back and forth crap about body fatness as opposed to blood glucose stability.


. . .and French? Really, now? Damn, I should've paid attention in French class.

Nigel Kinbrum said...

Kade Storm said...
"Shouldn't insulin resistance also prevent body fatness? Or does ASP take care of that side of the equation, thus keeping them fat?"
Fat cells become increasingly IR the fuller they become, so IR stops them from exploding. Once fat cells are full, there are two possibilities. Both have good & bad points.
1) If there is further caloric excess, no pre-adipocytes are converted into adipocytes. There is no further storage capacity, so T2DM develops - bad.
If there is now a caloric deficit, fat cells empty and T2DM goes away if beta cells haven't been thrashed to death. The small number of relatively full fat cells secrete sufficient leptin, so metabolic rate is sufficiently high & appetite is sufficiently low - good.
2) If there is further caloric excess, pre-adipocytes are converted into adipocytes. There is further storage capacity, so T2DM doesn't develop - good.
If there is now a caloric deficit, fat cells empty. However, there are more fat cells than in case 1) so for a given fat mass, cells have to be emptier than in case 1). The larger number of emptier fat cells secrete insufficient leptin, so metabolic rate is lower & appetite is higher than in case 1) - bad.

"And in the case of our sedentary slim friends, wouldn't muscle mass insulin resistance lead to hyperglycaemia issues since body fatness isn't increasing, and it's not going to the muscles either."
Active muscle mass is a major glucose sink. Disabling that sink impairs the NFB loop stability & blood glucose control, resulting in overshoots & undershoots in BG.

"As for the high sugar and fructose diet-related liver insulin resistance. Well, that is something that I am very interested in seeing as the Peat-a-tarian school of thought argues that glycation-factors, glucose clearance, and metabolic rate should improve greatly on such a diet if it was made up of nutritious whole fruits. There's so much conflict at the moment over the question of sugar, but most of the arguments are the back and forth crap about body fatness as opposed to blood glucose stability."
An IR liver secretes too much glucose, resulting in some hyperglycaemia. Fructose can enter full liver cells, so too much can result in a fatty liver. The big question is: How much is too much? The answer depends on starch intake, as glucose from starches contributes partly to liver glycogen and partly to muscle glycogen.

". . .and French? Really, now? Damn, I should've paid attention in French class."
Mais bien sûr! I didn't know if you were joking about not knowing French. Bon nuit.

Unknown said...

Ah! Shit! Forgot about those other outcomes that can take place when pre-existing adipose tissues are at full capacity. Thanks for the detailed break down of the potential outcomes.


Yeah, about the liver and fructose. Well, the general capacity's around 100 grams of glycogen. Really, it's not that high when we take into consideration some of these radical high sugar diet regimens. Say, if one were to get all of their calories from fruit, even for maintenance, I think the individual would be cutting it pretty close.

So some of these people, especially those nut-sacks at 30 Bananas a Day, recommending hypercaloric intakes (minimal 3000 calories) of just fruit, are certainly setting people up for problems ahead. Even if they don't necessarily gain outward weight, or become obese, I wouldn't want to imagine the state of their liver, as well as the underlying blood sugar issues. It seems to be a common complaint among the people who fail on that programme -- hunger and mood issues, rapid change in body composition towards greater body fatness (especially around the abdominal region) rather than extreme weight gain, reactive hypoglycaemia and usually other hormonal issues.

Yes, the confounding variables are still at play on a diet that is so maddeningly restrictive. However, I think such a high level of fructose exposure, even in whole fruit form, is likely to bring its share of problems to the equation.


Heh. Sugar issues.

I'd be interested to know what your thoughts are on the present controversy surrounding Robert Lustig. Everyone's on his case for overstating the perils of fructose (alarmism and all), but having that acknowledged, don't you find that certain individuals have become so polarised by his agenda that they outright overlook some legitimate concerns?


"Mais bien sûr! I didn't know if you were joking about not knowing French. Bon nuit."


Vous avez raison, monsieur.

Heh, I was half-joking. I really was a major slacker in French class.

Nigel Kinbrum said...

Kade Storm said...
"Ah! Shit! Forgot about those other outcomes that can take place when pre-existing adipose tissues are at full capacity..."
I have a feeling that I've written the outcomes thing as a comment elsewhere, but not as a blog post. Hmmm...

"Yeah, about the liver and fructose. Well, the general capacity's around 100 grams of glycogen. Really, it's not that high when we take into consideration some of these radical high sugar diet regimens. Say, if one were to get all of their calories from fruit, even for maintenance, I think the individual would be cutting it pretty close."
Durianrider gets only ~22% of his total energy from fructose. See 30 Bananas a day Durianrider, an analysis of his 'paleo' vegan diet. Bananas contain a lot of starch & glucose. Heavy soda & confectionery consumers get a higher % of energy from fructose.

"So some of these people, especially those nut-sacks at 30 Bananas a Day, recommending hypercaloric intakes (minimal 3000 calories) of just fruit, are certainly setting people up for problems ahead. Even if they don't necessarily gain outward weight,..."
If they're not gaining weight, they're not hypercaloric. If they are hypercaloric, then they are asking for trouble. Durianrider burns a humongous amount of carb each day exercising, so he can get away with eating so much fruit.

"I wouldn't want to imagine the state of their liver, as well as the underlying blood sugar issues. It seems to be a common complaint among the people who fail on that programme -- hunger and mood issues, rapid change in body composition towards greater body fatness (especially around the abdominal region) rather than extreme weight gain, reactive hypoglycaemia and usually other hormonal issues."
Eating like Durianrider but not exercising like him is the problem. His diet really wouldn't suit me at all!

"Yes, the confounding variables are still at play on a diet that is so maddeningly restrictive. However, I think such a high level of fructose exposure, even in whole fruit form, is likely to bring its share of problems to the equation."
See above.

"Heh. Sugar issues. I'd be interested to know what your thoughts are on the present controversy surrounding Robert Lustig. Everyone's on his case for overstating the perils of fructose (alarmism and all), but having that acknowledged, don't you find that certain individuals have become so polarised by his agenda that they outright overlook some legitimate concerns?"
I'm sympathetic to Lustig's cause. I guess you've already seen The bitter truth about fructose alarmism? Alan gave me only a mild spanking, as I did try to support my opinions with some evidence.

Like Peretti, Lustig is targeting the general public. I think that Lustig & Peretti are overstating perils, but as I wrote in Evelyn's blog, the playing field is so tilted in favour of Big Food due to decades of biased & inaccurate propaganda that I can forgive some bias & inaccuracy from Lustig & Peretti.

"Vous avez raison, monsieur.
Heh, I was half-joking. I really was a major slacker in French class."
Lol.

Unknown said...

Re: Lustig

I read it when it was freshly published. I know he had a bit of a back and forth with Lustig in the comments section, but I don't recall seeing your name pop up, although I do remember Matt Stone joining the party with some commentary on the s(n)ide (herp! See wut I did thar?).


I agree with you on the bias factor. It's not like anyone's denying the bias on Lustig's part. It's just that the idea in itself, sans hyperbole, does have some merit. Unfortunately, with the political climate the way it is, these guys won't last. They've got the entire dietary paradigm so galvanised that even the more conventional folk such as Evelyn and co., seem to be erring on the side of a political thinking that is similar to that of individuals like Tom Naughton. For once, they all agree – no regulation. So, ya' know. . . democracy and all. What Lustig's tryin' to do there won't work. Appeal to Popularity stands firmly against him.

In pursuit of regulating something of dietary relevance, he has indirectly challenged the highly sensitive political ethos, and landed himself square in the middle of a culturally polarised arena. My father; a diplomat – who's made plenty of health cock-ups in his rather short-lived life – once said that the best way to kill a given matter or policy, if the opposition can find even one straw of exaggeration to it, is to exploit that opening, then politicise the matter and watch the whole idea crumble into oblivion. Well, I added the oblivion bit the rest was more or less what he said.


Re: 30BaD

Right, it isn't hypercaloric if they're not gaining weight. However, in the case of the fanatical 30BaD approach, I think it fosters the kind of physiological environment that alters weight homeostasis and fuel partitioning; the end result can be weight gain and substantial shift in body composition. Most of the experiences tend to be accounts of individuals who have endured the approach over many months, and in some cases, years.

Typically, the body weight drops in the initial stages. It seems to be largely muscle, but obviously, fat will go with that as well, so they start looking lean. After this, I would assume basic metabolic rate drops as well to accommodate the new body and lower muscle mass (glucose sinks) and so those same intakes result in increased adiposity. The end result: you don't get obese individuals, but get quite a few skinny fats, and just soft looking folk with deficiency symptoms.

Also, with regards to the ratio of fructose. Well, yes, I hardly think that anyone who criticises their approach buys into the idea that it's all fructose. Whole fruits favour a good amount of glucose, especially the starchy kind like bananas. However, 22% percent can be substantial given the context of the intake. Now let's consider 22% of a 2000-2500 calorie maintenance diet for an average individual who is moderately active and even lean. That's still around 110-135 grams of fructose on top of most else coming from glucose. So even if this average individual isn't gaining or losing weight, I'd be interested to know whether any internal changes are taking place, such as liver insulin resistance or poor glucose clearance.

In the case of Bob (DurianRider), I do believe that his high endurance life style helps to cope with such an extreme fruit intake, and he's possibly even hypocaloric at times. (By the way, if you look into their videos and programmes, they often recommended loads of blended fruit and dates in the form of sugar-loaded smoothies, so it's really not as simple as downing bananas – that'd make the caloric target rather tough.) It's also interesting that they extrapolate his experience as the solution to others who're actually having trouble on the programme. If people are having weight issues; noticing drop in metabolic rate or muscle mass, they're told to eat even more fruit by way of blending and what not else – hammer in as many of those calories as possible.

Nigel Kinbrum said...

Edited to meet 4,096 character limit.
Kade Storm said...
"Re: Lustig
I read it when it was freshly published. I know he had a bit of a back and forth with Lustig in the comments section, but I don't recall seeing your name pop up, although I do remember Matt Stone joining the party with some commentary on the s(n)ide (herp! See wut I did thar?)."
My 1st reply (#10) was after Matt's 1st reply (#9).

"I agree with you on the bias factor. It's not like anyone's denying the bias on Lustig's part...Unfortunately, with the political climate the way it is, these guys won't last. They've got the entire dietary paradigm so galvanised that even the more conventional folk such as Evelyn and co., seem to be erring on the side of a political thinking that is similar to that of individuals like Tom Naughton. For once, they all agree – no regulation...What Lustig's tryin' to do there won't work..."
Are you suggesting that the Yanks (and thus, the rest of us) are basically screwed?

"In pursuit of regulating something of dietary relevance, he has indirectly challenged the highly sensitive political ethos, and landed himself square in the middle of a culturally polarised arena..."
Big Food has also lied & exaggerated. I don't know if the Peretti documentaries will ever be televised in the US, but they do a good job of showing Big Food's shenanigans over the decades.

"Re: 30BaD
Right, it isn't hypercaloric if they're not gaining weight. However, in the case of the fanatical 30BaD approach, I think it fosters the kind of physiological environment that alters weight homeostasis and fuel partitioning; the end result can be weight gain and substantial shift in body composition..."
The message there does appear to be "Eat moar and moar fruit! (sponsored by Andrex)".

"Typically, the body weight drops in the initial stages. It seems to be largely muscle, but obviously, fat will go with that as well, so they start looking lean. After this, I would assume basic metabolic rate drops as well to accommodate the new body and lower muscle mass (glucose sinks) and so those same intakes result in increased adiposity. The end result: you don't get obese individuals, but get quite a few skinny fats, and just soft looking folk with deficiency symptoms."
I agree.

"Also, with regards to the ratio of fructose...Whole fruits favour a good amount of glucose, especially the starchy kind like bananas...Now let's consider 22% of a 2000-2500 calorie maintenance diet for an average individual who is moderately active and even lean. That's still around 110-135 grams of fructose on top of most else coming from glucose. So even if this average individual isn't gaining or losing weight, I'd be interested to know whether any internal changes are taking place, such as liver insulin resistance or poor glucose clearance."
I would guess that a lack of EFAs & B12 from eating only sweet juicy fruits will result in slowly-decreasing mental faculties unless they supplement like DR. I have no idea about their serum TGs or liver fat content. A lack of choline will adversely impact liver fat clearance.

"In the case of Bob (DurianRider), I do believe that his high endurance life style helps to cope with such an extreme fruit intake, and he's possibly even hypocaloric at times....It's also interesting that they extrapolate his experience as the solution to others who're actually having trouble on the programme. If people are having weight issues; noticing drop in metabolic rate or muscle mass, they're told to eat even more fruit by way of blending and what not else – hammer in as many of those calories as possible."
Oh, dear!

Unknown said...

Damn. I just went over the thread again and now I find your response. For some strange reason, relating to the site design, I find myself distracted from properly reading the comments on Alan's website.

Ahahaha! No, Mr. Kinbrum. I don't think that we're screwed. I am not that much of a pessimist. Yanks on the other hand. . . maybe for a short while. There's still a cultural difference at play that does separate us from America (public acceptance and subsequent thought-out expectations of Government role that at least resembles some vague state of connection between public and body), even IF we like to pay political tribute to their methodology (Cameron's repeated tendency to indulge in not-so-classy Victorian-class judgement of the vulnerable and the poor who rely on some level of welfare). So we're better off on that front in my opinion. Even for the America the beautiful, this should mellow down over once some trust between people and the very crap they create (government, business, organisation) is finally realised. . . [troll]or they go to another outright war (that stuff seems to dazzle people) [/troll].

I just don't think that with the present landscape the way it is, Lustig will succeed in that sphere. Priority through the popular consensus is against any kind of government expansion or intrusion, no matter how right or wrong. The fact that he's recommending a limitation by itself means that some people will dismiss him without even hearing the idea. Kinda' reminds me of when Jamie Oliver went over to that side of the pond and suffered the ridicule of his career. For once, I actually felt a little sorry for him, despite the fact that I have a hard time tolerating his wimpish demeanour in general (personal taste thing; nothing big). It is for this very reason that I don't think the Peretti documentary, even if aired, will have much of an impact.


Re: The Banana Kingdom

Eat moar fruit!
Eat moar sugar!
Mayte, it will fix everything!
Blend it all and drink it down – pack on those calories and you'll be fit, mayte!


http://30bananasadaysucks.com/2012/06/yet-another-fruit-based-failure-story/


Just an example of the common complaints amongst most of the drop-outs of the programme. I believe there was a similar story about that young lad named Harout, courtesy of FreeTheAnimal (joy).

Anonymous said...

Nice post. I was checking continuously this blog and I am
impressed! Extremely useful information particularly the last part :) I care for such info a lot.
I was seeking this certain info for a very long time. Thank
you and good luck.

Here is my blog post สกรีนเสื้อ