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dturney

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dturney
And yet, from the the American Journal of Clinical Nutrition:

 

Results: During 5–23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.

 

Conclusions: 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. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

 

Data is a dime a dozen on both sides....

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Tribbles
Data is a dime a dozen on both sides....

This is true. I found an interesting paper (Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States -- Ascherio et al. 313 (7049): 84 -- bmj.com) that basically asserts that although there is an increased risk in a high fat diet it is not a marked increase. Interestingly if you have a high fibre diet you can eat as much fat as you want!

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PinkRose
I don't have a gall bladder and eating a lot of fat definitely upsets my stomach, metformin has nothing on it! That said, I can't tolerate metformin either for the same reason.

 

This does raise an interesting and unrelated question. I wonder how the incidence of gall bladder disease correlates to Type 2 diabetes since weight, age, and rapid weight loss are all indicators.

 

I would say the incidence of gall bladder disorders are quite high in the general population & not just amongst those in middle-age. My close friend has hers removed from gallstones at the age of 32 - when I have her over for dinner it can be tortorous serving meals that are not high in fats. She has strong reactions. A colleague in her 20s had hers removed for the same reason. Another chap in his early 40s was telling me of his ordeal. He mentioned that many people go around only getting small niggly feelings of unease after eating certain fatty foods before mayhem strikes with a severe attack. My impression is that it is relatively common.

 

This may also not be entirely unrelated either to the central theme of this thread - which seems to be the relative merits of following a LC/HF diet. People with certain conditions may simply not be able to follow it & if they should read that the HF/LC diet is the answer may be severely disappointed.

 

My own case, as I've advised, is in relation to kidney function and the protein consumption link. The jury is out on this one. My nephrologist does not generally advise his kidney patients to follow a low-protein diet but in my case, given the dramatic rise in Urea levels, he did advise me to cut down on protein for now.

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samorgan

I think this has already been mentioned, but just to make sure it is clear - proteins have NOTHING to do with a LC/HF diet. You can eat whatever level of proteins you want or need while on a LC/HF diet - average, below average or above average. Nothing about a LC/HF diet precludes any of those. Although I don't think anything is proven, I'm wary of too much protein and only eat the average amount that people eat or slightly lower - about 15% of calories. Personally, I don't think anything over 20% is a good idea.

 

As to the gall bladder, the cause of this epidemic is the wholesale reduction of natural fats from our diet. When people eat very little fat, the gall bladder stays idle. When it stays idle, the bile in it solidifies. Then, when some fat is consumed, the gall bladder contracts attempting to secret bile to assist in digesting the fats which is its job. But, since after too much disuse the bile has solidified, the result is only pain. With a normal diet, the gall bladder contracts every time you eat, keeping the bile "fresh" and so does not fall into disuse allowing the bile to solidify and cause the stones.

 

People get confused because the pain shows up when you eat fat and so they think that is the cause. Actually it is eating too little fat before that which was the cause.

 

Yet another casualty of the most dangerous fad diet of them all - low fat. (Along with something even worse - substituting healthy, natural fats with franken-fats like trans-fats and hydrogenated (rancid) vegetable oils.)

 

 

I would say the incidence of gall bladder disorders are quite high in the general population & not just amongst those in middle-age. My close friend has hers removed from gallstones at the age of 32 - when I have her over for dinner it can be tortorous serving meals that are not high in fats. She has strong reactions. A colleague in her 20s had hers removed for the same reason. Another chap in his early 40s was telling me of his ordeal. He mentioned that many people go around only getting small niggly feelings of unease after eating certain fatty foods before mayhem strikes with a severe attack. My impression is that it is relatively common.

 

This may also not be entirely unrelated either to the central theme of this thread - which seems to be the relative merits of following a LC/HF diet. People with certain conditions may simply not be able to follow it & if they should read that the HF/LC diet is the answer may be severely disappointed.

 

My own case, as I've advised, is in relation to kidney function and the protein consumption link. The jury is out on this one. My nephrologist does not generally advise his kidney patients to follow a low-protein diet but in my case, given the dramatic rise in Urea levels, he did advise me to cut down on protein for now.

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NickP
Researchers from the Heart Research Institute in Australia studied the body response from eating meals containing good fats versus bad fats. Participants were fed with meals prepared with either coconut oil (high in "bad" saturated fats) or safflower oil (high in "good" polyunsaturated fats). After only 3 hours, researchers found the participants fed with the coconut meal high in saturated fat had a significantly reduced blood flow due to arteries' reduced ability to expand. After 6 hours, researchers found that the good high-density lipoprotein (HDL) cholesterol's anti-inflammatory properties had decreased after the saturated coconut meal, but improved after the polyunsaturated safflower meal. The results of this study were published in the Journal of the American College of Cardiology . This study once again shows how good fats may improve body functions while bad fats hamper our health. Despite its extreme high level of saturated fat, coconut oil supporters have been promoting coconut oil as a health food. They claimed that coconut oil can cause weight loss, lower blood cholesterol, and is a germ fighter. It is true the structure of some of the saturated fats in coconut oil is different from other saturated fats, but it is scientifically farfetched to claim it as health food to be eaten every day. Like any other foods, moderation is the key.

Saturated fats are mainly found in animal products such as meat, dairy, eggs and seafood. Some plant foods are also high in saturated fats such as coconut, palm oil and palm kernel oil. Although this study is small, it showed that just one "bad" meal can do damage.

 

 

Just one in millions Nickp>

 

Don, sorry - another flawed analysis. If you go to Chris Masterjohn's website (cholesterol-and-health.com), he wrote an in-depth analysis of this study, the introduction of which is quoted below.

 

If anyone wants, I will be happy to send you the link to the complete analysis. I thought about quoting this article, but it was too lengthy. The analysis is very in-depth, interesting, and to a certain degree, complex.

 

Basically, only 14 subjects, after an evening of fasting, were fed a mikshake and a carrot cake breakfast, and their lipids and flow-mediated dilation were measured. One group drank this "healthy" breakfast made with coconut oil, and the other ate it with "safflower oil" - The study claimed that there were less damaging results with the safflower oil than coconut oil, which "proves" that saturated fat is bad for you.

 

Does anyone else see any "logic violations" with this simple experiment, and the big press release that claimed this "proved" that saturated fat is bad for you???????

 

So, Don, I would agree with you that eating Coconut Oil as part of a "healthy" breakfast of a milkshake and carrot cake is a bad idea....However, this study did not prove that saturated fat is bad for you.

 

This has been the issue with nearly every study that tries to prove that fat (or saturated fat) is unhealthy. Nearly all of these studies place the fat in a high carbohydrate diet, and then try to say that it is the Fat that is making your unhealthy....not the sugar or the refined carbs.

 

Please take a few minutes to read the entire report....I think you would find it entertaining.....

 

Introduction only - quoted below from Chris Masterjohn's Article "Myth: One High-Saturated Fat Meal Can Be Bad"

 

Newspapers the world over have recently declared that a single meal rich in saturated fats will disrupt the functioning of your arteries and contribute to the inflammation of your blood vessels, following an Associated Press story by Joe Milicia.1 Milicia reported on a recent study2 published by a team of researchers led by Dr. Stephen J. Nicholls of the Australian Heart Research Institute in the Journal of the American College of Cardiology entitled, "Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function."

 

The news article quoted the Kansas City cardiologist Dr. James O'Keefe as claiming the study showed that "when you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward." Of course, the study showed no such thing.

 

Dr. Nicholls, the lead author of the study, was quoted in the article as saying the study showed the "need to aggressively reduce the amount of saturated fat consumed in the diet." The AP article then clarified for us that this meant reducing our intake of beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, and replacing them with safflower oil, sesame oil, sunflower seeds, corn and soybeans. Wow! This study had the power to make sweeping conclusions about over 15 different foods! But in reality, of course, the study showed no such thing.

 

…this was a well-designed and interesting study; the authors of the report, however, unfortunately made unjustified conclusions from their data in the report itself, and the press articles further sensationalized the story and distorted the study's findings, making rather hysterical claims, unfortunately with the support of the study's lead author.

 

You may be surprised to find out that arterial function was actually better after the coconut oil meal than the safflower oil meal! Or that, contrary to the claims of the Associated Press article, the authors never measured inflammatory components in the subjects' blood. Or further, that they provided absolutely no evidence that different types of fatty acids, such as saturated or unsaturated, had anything to do with their findings!

 

In fact, they completely overlooked an alternative explanation that has substantial evidence in the scientific literature to support it: the differences they observed between the anti-inflammatory effects of the different diets may have been due largely or entirely to the difference in vitamin E content of the diets rather than the type of fatty acids present in the oils.

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dturney

This is true. I found an interesting paper (Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States -- Ascherio et al. 313 (7049): 84 -- bmj.com) that basically asserts that although there is an increased risk in a high fat diet it is not a marked increase. Interestingly if you have a high fibre diet you can eat as much fat as you want!

 

 

I am going to stick to what I have been doing seems to work.

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dturney
Don, sorry - another flawed analysis. If you go to Chris Masterjohn's website (cholesterol-and-health.com), he wrote an in-depth analysis of this study, the introduction of which is quoted below.

 

If anyone wants, I will be happy to send you the link to the complete analysis. I thought about quoting this article, but it was too lengthy. The analysis is very in-depth, interesting, and to a certain degree, complex.

 

Basically, only 14 subjects, after an evening of fasting, were fed a mikshake and a carrot cake breakfast, and their lipids and flow-mediated dilation were measured. One group drank this "healthy" breakfast made with coconut oil, and the other ate it with "safflower oil" - The study claimed that there were less damaging results with the safflower oil than coconut oil, which "proves" that saturated fat is bad for you.

 

Does anyone else see any "logic violations" with this simple experiment, and the big press release that claimed this "proved" that saturated fat is bad for you???????

 

So, Don, I would agree with you that eating Coconut Oil as part of a "healthy" breakfast of a milkshake and carrot cake is a bad idea....However, this study did not prove that saturated fat is bad for you.

 

This has been the issue with nearly every study that tries to prove that fat (or saturated fat) is unhealthy. Nearly all of these studies place the fat in a high carbohydrate diet, and then try to say that it is the Fat that is making your unhealthy....not the sugar or the refined carbs.

 

Please take a few minutes to read the entire report....I think you would find it entertaining.....

 

Introduction only - quoted below from Chris Masterjohn's Article "Myth: One High-Saturated Fat Meal Can Be Bad"

 

Nick, this could go on forever.....I am to old to switch, and what I have been doing seems to work....I will eat some fat, some protine, some carbs...etc.....leave the HF diets to you folks....I was thinking about that eating lunch today...went to LOgans had their fried shrimp bake potato with butter...hot roll and a salad...I said to myself "this is about as HF as I get...."but it was good.

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NickP
I am going to stick to what I have been doing seems to work.

 

Hey Don....It's great that you are happy with your plan. No one is trying to get you to change. For yourself, you may have actually found the perfect balance.

 

However, your diet does not work for me! My BG would have blown past 200 eating what you did tonight.

 

All I am asking from you is to consider the fact that maybe we are different (although we are both "old" Navy guys), and are bodies are metabolically different. Therefore, a low carb/high fat diet might be the best diet that my body can handle. Is that such a stretch to accept?

 

Can't we all get along?????

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Tribbles

I am curious - would it if you used insulin? I understand you don't want to use any medication but I think that is the difference and less that his diet wouldn't work for you. If I ate that without insulin I would go hurtling past 200 but I am pretty certain I could keep it under 140 with insulin.

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PinkRose
I am curious - would it if you used insulin? I understand you don't want to use any medication but I think that is the difference and less that his diet wouldn't work for you. If I ate that without insulin I would go hurtling past 200 but I am pretty certain I could keep it under 140 with insulin.

 

Excellent point Tribbles! Using insulin really makes a big difference. As I was reading through the posts I was scratching my head at the fact that on the one hand you have T2s who do not use insulin trying to have good control versus those T2s who use insulin to help achieve good control. To me it's like comparing apples with oranges. Of course I am a T1 so my reliance on insulin is absolutely sacred & set in stone but I would have thought that insulin use would also have a strong imact on BG numbers of T2s as well.

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NickP
Excellent point Tribbles! Using insulin really makes a big difference. As I was reading through the posts I was scratching my head at the fact that on the one hand you have T2s who do not use insulin trying to have good control versus those T2s who use insulin to help achieve good control. To me it's like comparing apples with oranges. Of course I am a T1 so my reliance on insulin is absolutely sacred & set in stone but I would have thought that insulin use would also have a strong imact on BG numbers of T2s as well.

 

This is the fundamental question - do you control your BG with insulin or with your diet and lifestyle. Since insulin is a fat storage hormone, I would prefer to avoid injecting insulin (I lost quite a bit of weight since my DX, by following a diet that keeps my BG and insulin response low), especially if I can maintain an A1C of 5.5 without it!

 

So, yes, if my only concern is to manage my BG, then taking insulin is a great choice. However, excessive insulin in your body has been demonstrated to have other bad health impacts. This is one of the reasons why, even for Type 1's, eating a low carb diet is recommended - this keeps your insulin requirement to a minimum.

 

However, this is still a choice that everyone with Diabetes needs to make. If folks take insulin to "cover" their carbs, that is their call.

 

However, I don't appreciate folks telling me that my diet is "bad" and "unhealthy" - I have the blood work and results that clearly prove that my health is vastly improved with eating a low carb diet.

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Jan B

Nick,

While I do appreciate your strong dedication, I can testify that insulin doesn't have to make a person fat. It makes me uncomfortable that so many people who could benefit from insulin are scared into thinking they are bound to become fat if they go that route. But I can also understand the fear of gaining weight, especially if that person has worked hard and lost weight in the past.

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NickP
Nick,

While I do appreciate your strong dedication.... It makes me uncomfortable that so many people who could benefit from insulin are scared into thinking they are bound to become fat if they go that route. But I can also understand the fear of gaining weight, especially if that person has worked hard and lost weight in the past.

 

Hey Jan...I do agree with you on that point --many T1's and T2's manage their insulin very well and keep a good weight. However, the truth still is that excess Insulin will cause weight gain. Being prudent to properly manage insulin is the key to keeping your insulin level at the required amount. Many Diabetics who use insulin to "cover excess carbs" usually struggle with their weight.

 

By using diet and exercise to manage my BG level, I am also managing my weight at the same time. Again, it's a personal decision....

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Tribbles

I came across this paper when I was doing a different search. First - rodent model warning: their work is based on rats although the reference papers that are not rat based. The action of fats isn't my specialty so I may have got this wrong but it looks like they are linking high fat (specifically free fatty acids) with insulin resistance. The paper actually sets out to examine a different issue (the link between muscle mitochondria and insulin resistance) and this is a by product, but from the start of the Discussion section:

 

The major findings of the first phase of this study are that feeding rats high-fat diets results in an increase in mitochondria and in the capacity of muscle to oxidize fat concomitant with development of muscle insulin resistance.

 

The mitochondria part is a red herring from our view point since the paper proves that there is no correlation to mitochondria. I don't really know what to make of this paper.

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NickP
I came across this paper when I was doing a different search. First - rodent model warning: their work is based on rats although the reference papers that are not rat based. The action of fats isn't my specialty so I may have got this wrong but it looks like they are linking high fat (specifically free fatty acids) with insulin resistance. The paper actually sets out to examine a different issue (the link between muscle mitochondria and insulin resistance) and this is a by product, but from the start of the Discussion section:

 

The major findings of the first phase of this study are that feeding rats high-fat diets results in an increase in mitochondria and in the capacity of muscle to oxidize fat concomitant with development of muscle insulin resistance.

 

The mitochondria part is a red herring from our view point since the paper proves that there is no correlation to mitochondria. I don't really know what to make of this paper.

 

Hey Tribbles....Did you mean to put a link in your thread? I do not know where to go and see this paper.....

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samorgan

I went through a discussion of this about a year ago. As I recall, the study basically mis-cast something making it seem to mean something it isn't. When you eat more fat and less carbohydrates obviously what is desirable is for your cells to prefer to fuel on the fats (more on that below). So, the phenomenon being discussed is

 

a) short-term only (right after eating) and

B) a GOOD thing, since cells preferring the fatty acids to the glucose is exactly what you're after. If the cells don't do this, they will start demanding glucose which can trigger

 

1) re-conversion of glycogen to glucose in the liver and muscles (if available) and its dumping in to the blood, and/or

2) the "cannibalization" of the body's own proteins (muscles) for conversion to glucose in the liver via gluconeogenesis

 

So, to the extent any such "insulin resistance" exists upon eating LC/HF, it is "good" insulin resistance.

 

Sorry for my sketchy recollection, but it was a long time ago.

 

Mitochondria are what allow cells to metabolize fatty acids directly for ATP (their actual energy source) bypassing the entire glucose/insulin process. That is probably what was meant by mentioning them.

 

Since I live in ketosis most of the time, I WANT most of my cells to be insulin resistant. This helps assure me that they will continue to fuel on alternatives and not cause liver dumps or muscle wasting.

 

 

 

I came across this paper when I was doing a different search. First - rodent model warning: their work is based on rats although the reference papers that are not rat based. The action of fats isn't my specialty so I may have got this wrong but it looks like they are linking high fat (specifically free fatty acids) with insulin resistance. The paper actually sets out to examine a different issue (the link between muscle mitochondria and insulin resistance) and this is a by product, but from the start of the Discussion section:

 

The major findings of the first phase of this study are that feeding rats high-fat diets results in an increase in mitochondria and in the capacity of muscle to oxidize fat concomitant with development of muscle insulin resistance.

 

The mitochondria part is a red herring from our view point since the paper proves that there is no correlation to mitochondria. I don't really know what to make of this paper.

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Tribbles
Mitochondria are what allow cells to metabolize fatty acids directly for ATP (their actual energy source) bypassing the entire glucose/insulin process. That is probably what was meant by mentioning them.

 

Yes, when they fed the rats a HF diet the mitochondria increased however the muscle insulin resistance also increased, they had been expecting a mitochondria reduction to be the cause of the IR rise I think. So the question then was what caused the rise in muscle IR.

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samorgan

Wait, I though mitochondria were only involved in fat metabolism and a separate process involving insulin and a bunch of other things are responsible for getting glucose through the cell wall for conversion to ATP. Fats (fatty acids I guess and/or ketone bodies) are taken into the cells directly via the mitochondria and converted to the same ATP without the need for any insulin.

 

Did I miss something or get something wrong?

 

 

Yes, when they fed the rats a HF diet the mitochondria increased however the muscle insulin resistance also increased, they had been expecting a mitochondria reduction to be the cause of the IR rise I think. So the question then was what caused the rise in muscle IR.

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NickP

 

Hey Tribbles....Thanks for the link.

 

This was a pretty complicated study to read and follow. However, the biggest issue that I normally see from these studies is there are way too many confounding variables, and then the study author turns around, ignores all of the other variables, and says "see...it's the fat that is causing this"

 

For this study...see what was fed to the mice (this is quoted from the study...)

 

Animals were given ad libitum access to one of three diets, a standard chow diet (PicoLab Rodent Diet 20, 5053) or one of two high-fat diets. The standard chow diet (chow) consisted of 23.5% calories from protein, 11.9% calories from fat, and 64.5% calories from carbohydrate. The high-fat flax seed/olive oil diet consisted of 20% calories from protein (243 g/kg casein), 50% calories from fat (187.5 g/kg flax seed oil and 93.7 g/kg olive oil), and 30% of calories from carbohydrate (210.8 g/kg corn starch, 105.4 g/kg sucrose, and 59.6 g/kg bran). The high-fat lard/corn oil diet consisted of the following: 23% calories from protein (294.5 g/kg casein), 50% calories from fat (180g/kg lard and 100g/kg corn oil), and 27% calories from carbohydrate (347.4 g/kg sucrose). Both of the high-fat diets included 22 g of vitamin mix (Teklad Premier #40077), 51 g of mineral mix (Teklad Premier #170915), 5 g of methionine (Teklad Premier #10850), and 1.3 g of choline chloride per kg of diet.

 

Now...they simplify this by giving a macronutrient breakdown. It does not appear that the standard diet had any sucrose. So....was it the fat or the sugar that caused this increase in insulin resistance?

 

Further, unless we see a breakdown of what actual ingredients is in each diet, we cannot even begin to guess what caused this change. Is it really that hard just to take the standard rat chow and soak it in coconut oil to keep everything else in the experiment stable?

 

Another study tried to make a "fat is bad for you " determination doing the same thing with the Rat Chow. One was given standard lab rat food (made from natural ingredients), the other was given a high-fat lab food (made entirely of processed food and sugar). Again, this study tried to say the results demonstrated that it was the "high fat" that caused the metabolic damage.

 

Come on Folks.....if you are going to run an experiment, you need to vary only ONE VARIABLE in order to blame that variable for all of your issues.

 

Finally, while 50% fat content may not be high for a human diet, it is very unnatural to a rat's diet. Plus, our metabolic system is not very close to one of a rat.

 

So, I am sorry, at first glance, it appears this study appears to be flawed.

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Tribbles
Did I miss something or get something wrong?

To be honest I don't know which is why I haven't commented on the paper to much. Fat metabolism mechanisms aren't something I have looked at much beyond lipolysis.

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NickP
Yes, when they fed the rats a HF diet the mitochondria increased however the muscle insulin resistance also increased, they had been expecting a mitochondria reduction to be the cause of the IR rise I think. So the question then was what caused the rise in muscle IR.

 

See my post above...(IMHO) the simple answer is "The Sugar"

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Tribbles
See my post above...(IMHO) the simple answer is "The Sugar"

 

I think our previous posts overlapped! I am always wary of rodent models because they don't always map well to humans. From memory a rat can lose 60% of it's beta cells before it comes diabetic, a human can only lose 40%.

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NickP
I think our previous posts overlapped! I am always wary of rodent models because they don't always map well to humans. From memory a rat can lose 60% of it's beta cells before it comes diabetic, a human can only lose 40%.

 

I agree. They use Rats to see if an idea will prove out in the lab. Rats are cheap and can be bred to display certain characteristics (obese, diabetic, etc). Then, they should then go to another animal (more expensive, but closer to a human metabolic system....for example - pig, monkey, etc) to prove the research if the hypothesis holds true.

 

The other problem with rats (if my memory serves me correct) is that they eat very little fat in the wild and don't have a great tolerance for fat. So, when they are fed high fat (to prove an experiment), it is not normal for them, and their metabolic system is not accustomed to it. So, using Rats to prove any "Fat Hypothesis" is a really a stretch to begin with (again....IMHO).

 

Finally, and the most important point is that you must constrain your variables, so that you are only modifying one variable. This is so important when doing research. It is amazing how many research dollars are wasted because the experiments cannot be set up properly.

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