Fatty foods can lead to diabetes, researchers say

[CheeseSand]

http://news.yahoo.com/s/nm/20051228/hl_nm/diabetes_dc

Fatty foods can lead to diabetes, researchers say

By Susan Heavey
2 hours, 22 minutes ago

WASHINGTON (Reuters) - Diets high in fat can disrupt blood sugar levels and trigger diabetes, researchers said in a study on Wednesday that helps explain the link between obesity and a disease typically linked to sugar.

Fatty foods can suppress an enzyme crucial to the production of insulin, which regulates sugar in the blood, according to scientists at the University of California at San Diego.

Obesity has long been linked to type 2 diabetes, the most common form of the disease in which the body does not make enough insulin, or cannot properly use it.

In the United States, two out of three adults are overweight or obese. Experts have said obese people are up to 80 times more likely to develop diabetes, and both conditions are on the rise.

The new findings, published in the journal Cell, offer another explanation of exactly how the two are linked.

"We have discovered ... a molecular trigger which begins the chain of events leading from hyperglycemia to insulin resistance and type 2 diabetes," said Jamey Marth, a professor of cellular and molecular medicine at the university.

"This finding suggests new approaches to the prevention and treatment of diabetes," said Marth, an investigator with the nonprofit medical research organization Howard Hughes Medical Institute, which helped fund the research.

Marth and his colleagues studied the glycosyltransferase enzyme (GnT-4a), which helps the pancreas sense how much sugar is in the blood and release enough insulin to help process it.

In a study of normal mice that were fed a fatty diet, researchers found that the enzyme was repressed, leaving pancreatic cells unable to sense sugar levels and leading to diabetes.

"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," said Marth, adding that people who inherit a faulty gene that controls the enzyme may also be vulnerable to diabetes.

It may also play a role in the early onset of type 2 diabetes in children and teenagers, according to the study, which was also sponsored by the National Institutes of Health.

The researchers are now looking at ways to boost the enzyme in hopes of staving off diabetes.

Earlier this year, European researchers said they found a gene, called ENPP1, that helps control how cells respond to insulin. In 11 different variations of the gene, six were linked to severe obesity, they reported.

Researchers at Beth Israel Deaconess Medical Center in Boston have also discovered a substance called retinol binding protein (RBP4) that is released by fat tissue and can cause insulin resistance. Their finding was reported in the journal Nature in July.

[tom sawyer]

OK but you don't need this enzyme if your body isn't on a sugar rollercoaster to begin with. So its not a fatty diet per se, that causes diabetes. Its a high fat AND high carb diet. And I don't see this research as so revolutionary, likely this is one of a multitude of enzymatic/hormonal changes in the cascade of events that occur over years of eating SAD.

[tom sawyer]

I guess if they can come up with a pill to elevate the GnT protein, we can all go back to eating Twinkies.

Cell is a big-time journal, somebody thinks this is hot stuff.

[ceberezin]

It is known that fat plays a role in the mechanism that leads to insulin resistance. Blaming fatty diets for insulin resistance is an enormous stretch from that conclusion. If the hormone is expressed by body fat, then it comes from visceral fat related to de novo lipogenesis from carbohydrate consumption.

Any time a researcher isolates an enzyme that is part of a metabolic pathway and tells us that this enzyme is the evil doer, you can be sure that they're wrong. Rather, something has gone awry with that pathway that needs to be straightened out. Usually, the metabolic pathway has been disturbed by too much insulin from you know what.

[Dodger]

The body is full on enzymes, hormones etc., all of which do not operate independently. Too much or too little of any of them is bad.

[LC FP]

"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," said Marth, adding that people who inherit a faulty gene that controls the enzyme may also be vulnerable to diabetes.

Sure, maybe this accounts for 0.5% of type 2 diabetics. Or maybe it only applies to mice.

[Michelle H]

Is there any information as to what type of fats the poor mice were fed?

Saturated? unsaturated? hydrogenated? oxidised?

[Azlocarb]

I've asked Dr. Eades to comment on this study on his blog, I will be checking to see if he responds.

[gryfonclaw]

This article makes me giggle.

[littlejohn]

I am totally confident the conclusions of this study are wrong. They may see an enzyme. But the conclusion that a high fat diet causes diebetes will not hold up.

[ceberezin]

The only reason for research in which you isolate an enzyme and claim it is the cause of some disease state is so that you can design a molecule to impede that enzyme, patent the molecule, and make oodles of money from a drug. It's the worst kind of bastardization of science.

[LC FP]

The only reason for research in which you isolate an enzyme and claim it is the cause of some disease state

I agree. Every enzyme in our genome is there for a reason. No normal enzyme "causes" a disease. Some enzymes may be expressed too much or too little in response to something abnormal that we are doing. Like HMG Co-A reductase, which increases cholesterol production in the presence of high insulin levels.

[CindySue48]

I am totally confident the conclusions of this study are wrong. They may see an enzyme. But the conclusion that a high fat diet causes diebetes will not hold up.There is nothing in other research, or our history to indicate that fat causes diabetes. Now too many carbs leading to high triglycerides? That's a different story. But fat? nope

[K Walt]

The conclusion of this article is rather odd, considering that a slew of studies have shown that high-fat (low-carb) diets dramatically improve the symptoms of diabetes -- with lowered blood sugar, improved lipids, and lowered BP. Higher fat (low-carb) diets routinely and consistently improve insulin sensitivity -- in living, breathing humans.

Mice? Who cares what happens in mice?

[Nando]

http://biosingularity.wordpress.com/2005/12/29/researchers-discover-how-a-high-fat-diet-causes-type-2-diabetes/

[Ayustar]

Aren't they talking about a diet high in carbs as well as fat...that, as well all should know, and experienced by now, is harmful.

[Samuel]

I always see something wrong with saying that Americans are more obese than others because they consume more carbs.

Americans far exceed the rest of the world in meat, eggs, butter and cheese consumption and if we assume that all people need the same amount of calories per day to survive, we must conclude that people in the US actually consume less carbs than others. Probably this does not apply to sugar, but it applies to rice, wheat and beans which most people in many nations eat a lot of.

Saying that over-consumption of fat causes diabete and obesity does not contradict with how low carb diets fixes the two problems. This is because eating low carb makes the insulin resistance problem irrelevant no matter what caused it.

However as a personal opinion, I agree with the ones who say that eating high carb and high fat at the same time is the cause. Probably if we ate enough fat to supply us with all the energy we need, our bodies don't know what to do with the additional carbs we ate and this may end with the insulin resistance problem.

[Abd]

the headline:

Fatty foods can lead to diabetes, researchers say


The article does not confirm the headline. The researchers speculated on a link, based on research with mice. But what they say about it doesn't make sense:

Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," said Marth, adding that people who inherit a faulty gene that controls the enzyme may also be vulnerable to diabetes.

Wait a minute! How could a faulty gene cause an epidemic? (Except perhaps that there has been some change in diet, and a certain gene does not allow the body to deal with it)

[LC FP]

Not only did you find an article which better explained the study in question, you found a rebuttal by Gary Taubes, my favorite NYT journalist!

Comments»
1. gary taubes - December 29, 2005
At the risk of sounding faddist, if, as the last paragraph says, ” too much insulin can also be harmful, and has been found to contribute to the pathogenesis of cancer, cardiovascular disease, ovarian diseases, and Alzheimer’s disease,” and if as Marth says, “It may be that suppressing insulin production to some degree could be beneficial in such disorders,” than why don’t they just tell people to eat less carbohydrates? That suppresses insulin. It doesn’t enrich the pharmaceutical industry, but it certainly shuts down insulin. It does it even better than simply eating less calories. See, for instance, the classic paper on the subject: Grey N, Kipnis DM. Effect of diet composition on the hyperinsulinemia of obesity.
N Engl J Med. 1971 Oct 7;285(15):827-31.

[CindySue48]

http://biosingularity.wordpress.com/2005/12/29/researchers-discover-how-a-high-fat-diet-causes-type-2-diabetes/
From article's comments:
1. gary taubes - December 29, 2005

At the risk of sounding faddist, if, as the last paragraph says, ” too much insulin can also be harmful, and has been found to contribute to the pathogenesis of cancer, cardiovascular disease, ovarian diseases, and Alzheimer’s disease,” and if as Marth says, “It may be that suppressing insulin production to some degree could be beneficial in such disorders,” than why don’t they just tell people to eat less carbohydrates? That suppresses insulin. It doesn’t enrich the pharmaceutical industry, but it certainly shuts down insulin. It does it even better than simply eating less calories. See, for instance, the classic paper on the subject: Grey N, Kipnis DM. Effect of diet composition on the hyperinsulinemia of obesity.
N Engl J Med. 1971 Oct 7;285(15):827-31.

Great comment!

[ItsTheWooo]

I think it makes sense that fat would encourage insulin resistance.

WILD AND CRAZY THEORY (warning :) ):
First lets assume something about human evolution. Let's assume that carbohydrate access was predicative of nutrient availability. This is a reasonable assumption considering that harvest times, times of plenty, starches turn to sugars, fruits are most ripe, etc.
Carbohydrate might be, in many ways, a "famine switch". Carbohydrate deprivation = leaner times; depriving human bodies of carbohydrate = famine adaptation. Deprivation of carbohydrate would immediately trip a switch to get the body adapted to famine; low carb diets mimic starvation in many ways.

However it probably does not work the same in reverse, meaning, carbohydrate plenty likely does not tell the body squander; I don't see an evolutionary advantage for the body not trying to capitalize to the fullest extent on plentiful times. There is a "famine program" but there is NOT a "spend like an idiot" program sadly.

Now to speak more of this vague "famine adaptation". Part of it most definitely includes using ketones, lipolysis, appetite suppression, etc. Perhaps part of it also includes increasing sensitivity to dietary sugars, i.e. insulin resistance. If we assume that the body is in a "famine state" it is reasonable to conclude that the body wouldn't want that. You survive af famine by conserving energy and body fat; you do that by increasing IR (as well as decreasing T3 and anabolic hormone output - both of which have been shown to decrease disproportionately on a very low carbohydrate diet).

So deprivation of carbohydrate would trigger famine adaptation (in theory), then what would trigger insulin resistance (a subset of this "resource deprivation")? I think expression of fat as an energy source (dietary OR body) as the trigger for IR makes perfect sense; it is a subset of the "famine adaptation cascade". Just as the body has evolved to think "uh oh famine" when it doesn't see carbs; it has evolved a complementary system of seeing lots of fat and associating this with famine as well. Increasing fat & decreasing carbs = famine. IR = way of surviving famine. In a natural environment this logic works; too bad it doesn't today because of our diets and the capacity for obesity.

Like I said this is a totally wild and crazy theory so don't get too mad or hate me too much for it :).

[TBoneMitch]

Woo,

well-explained and intriguing theory, however, fat is the body's preferred energy source, so it is quite content burning it all the time.

When plenty of calories and amino acids (protein) are entering the body it does not equate with famine.

Testosterone and growth hormone are higher on a low carb diet (if the diet is calorie-adequate).

[LC FP]

Wooo, I think I agree with TBoneMitch, that fat is the body's preferred energy source, and it's quite content to burn it. If that's true, why should high fat intake trigger insulin resistance?


You state:
Now to speak more of this vague "famine adaptation". Part of it most definitely includes using ketones, lipolysis, appetite suppression, etc. Perhaps part of it also includes increasing sensitivity to dietary sugars, i.e. insulin resistance. If we assume that the body is in a "famine state" it is reasonable to conclude that the body wouldn't want that. You survive af famine by conserving energy and body fat

As I understand insulin resistance, dietary sugar will be shunted to formation of new fat. This would fit your theory, to conserve body fat. But wouldn't that process be wasteful of energy? Turning sugar into fat, for storage, would cost more energy than just burning the sugar directly instead of using already-stored fat. I think if you just burned the sugar, you'd end up with more body fat in the end because your process is more direct and efficient.

Plus I'm pretty sure studies of insulin resistance show it decreases when on a LCD.

[Hybrid]

True or not, it's a good enough reason to eat a low carbohydrate diet. No one in their right mind would eat a low fat, high carbohydrate diet to prevent the onset, or progress, of diabetes. Very few people would willingly eat a low fat, high carbohydrate diet because of the hunger issues involved. As more research like this comes out, it becomes increasingly clearer that we owe it to our bodies to eat fat preferentially and carbohydrates sparingly.

[kebaldwin]

Gene links high-fat diet to diabetes
Saturday Dec 31 18:47 AEDT

A team at the University of California at San Diego has identified a gene that produces an enzyme that enables cells in the pancreas to recognise glucose and secrete insulin. Furthermore, a high fat diet suppresses the enzyme.

In a study published in the research journal Cell, Dr Jamey Marth and colleagues describe the gene that encodes GnT-4a, a glucose transporter enzyme. Without GnT-4a, beta cells in the pancreas fail to produce insulin when exposed to glucose and fat.

Marth's team studied mice that did not carry the GnT-4a gene and found that the animals initially had high blood glucose levels, which progressed to beta cell failure followed by the development of type 2 diabetes.

Normal mice that carried the GnT-4a enzyme but were fed a high-fat diet had reduced GnT-4a expression, followed by the chain of events leading to type 2 diabetes.

"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," Marth commented in a university release.

If further research confirms the findings, one possible clinical application would be the development of therapeutic agents that boost GnT-4a levels, and Marth is currently working on this.

Agents that inhibit GnT-4a may also be useful in preventing a number of diseases linked to too much insulin production, such as cancer and cardiovascular disease.

http://news.ninemsn.com.au/article.aspx?id=79505

[kebaldwin]

Here we go again.

They could just discover that eating low carb stops diabetes. But how would they become millionaires by discovering something natural? No, they have to go find some enzyme and then develop a drug to block it from happening so that they can make their millions of $$$.

morons.

[LC FP]

They could just discover that eating low carb stops diabetes

Not only do "they" want to sell a new blockbuster drug to the fattened sheep, they're not all morons.

There are powerful forces out there fighting for their livelihoods, their profit margins, and their friends who could lose them all if eating low carb becomes an accepted way to get or stay healthy. These people will stop at nothing to discredit fat and the low carb lifestyle. Faking or manipulating research may be the least nefarious thing they do.

If you think about the number of US Senators who represent states which have agriculture as their primary industry, you will see why official government agencies will never tell the truth about corn, wheat, soybeans etc. Just a cursory look at the map shows me about 20 states that are purely agricultural and 15-20 more that are greatly agricultural. Even a state like California which has a very diversified industrial base has huge agricultural interests which I'm sure the liberal senators don't want to offend. But the "heartland" states, with their lifetime senators, who end up chairing the important committees, will just smile at our feeble arguments. They have to protect their constituents -- if they want to keep their jobs.

[Duparc]

When I examine my own experience it is manifest that whenever I subscribe to low-carbing that my fasting BS level drops to either within the normal range or lower. Furthermore, I never suffer from indigestion nor unpleasant bowel motions which seems to indicate that something beneficial might be occurring within my body which, in turn, tends to contradict the tale that is being highlighted in this research text.

Samuel: a moot point here about comparing the US to the rest of the world; the US is a continent and whenever it is compared to other parts of the world, the comparison is usually (but not entirely) with other countries rather than continents. In my neck-of-the-woods (Scotland) its population is around 5m while in the State of Florida (for example) the population is in excess of 10m. I would guess that the land size of the UK could probably fit into the size of the State of Florida or just about, so hardly a fair comparison!

[ItsTheWooo]

Woo,

well-explained and intriguing theory, however, fat is the body's preferred energy source, so it is quite content burning it all the time.

When plenty of calories and amino acids (protein) are entering the body it does not equate with famine.

Testosterone and growth hormone are higher on a low carb diet (if the diet is calorie-adequate).

I agree that energy content is much more important than carbohydrate status at keeping the body in a high energy state (preventing "famine adaptation"). However, I have heard there are studies which show low carbohydrate diets, disproportionate to energy contents, cause endocrinological changes hallmark of starvation. The negative ones as well as the good ones, e.g. favorable blood sugar & insulin changes.

Searching for a few seconds in pub med I came across this study which compared an isocaloric high fat diet to a high protein diet; the study was intended to research the effects of various types of LC diets on T3, glucose, and insulin.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3900181&query_hl=1&itool=pubmed_docsum

I found this study interesting for two reasons. First it backs up my personal experience that, for the insulin resistant person, high fat is the money and I wasn't imagining less control with lower fat high protein. High protein DOES adversely affect sugar metabolism more than fat, and that people who claim that it's only carbs that are important (for controlling metabolic syndrome) are wrong. The HP diet was demonstrated as less effective for controlling metabolic syndrome (in that insulin & PP glucose & triglycerides were higher on it).
Seeing as on the glucose tolerance spectrum a HP diet is relatively more similar to a HC diet than a HF diet is (in that a HP diet is much higher glucose load)... these findings make sense. Insulin would be higher, as would sugar levels and triglycerides.

Now hold on I'm getting somewhere here. There is a second (more relevant) reason this study was interesting. An additional difference between the two groups was that the HF diet resulted in lower T3. T3 declined in both groups (relative to "normal diet"), but more in the "more low carb/less sugar" (high fat) group. The researchers said they did not know the significance of this difference. Other research shows that a disproportionately lower T3 level is part and parcel of carb-deprived (e.g. low sugar) diet. HF diets are lower glucose than a HP one; the difference makes sense. This reinforces the notion that glucose/sugar restriction is one trigger for "famine adaptation" and it explains why T3 levels would correlate with sugar state.

If I have time I'll try to find more studies which demonstrate that carbohydrate deprivation, secondary to energy status (which like I agree is the most overwhelmingly significant factor) is an additional factor which determines conservation state.

I'm not knocking LC diets, I will never stop believing they are necessary for people like me with these sugar problems. See, even if it IS true (that LC diets are more energy-deprived than higher glucose ones and trigger a "famine adaptation" independent of caloric content difference)... it may be a moot point. If one tolerates carbs and sugar poorly for whatever reason, then carb restriction would be a relative improvement.

It's like if you have a person with a broken leg, and someone with a healthy strong leg, the one with the healthy leg is going to run just fine on their own. The broken leg person will limp and barely be able to even function. Introduce the variable of a cast & crutches, and suddenly the broken leg person will find their mobility increases, and they can move about more like a normal person. Relatively speaking, this would be an improvement for them as their leg is damaged, and the tools allow them to bypass that. However for the normal-legged, a cast and crutches would decrease mobility depriving them of more efficient use of their healthy limbs.
I would not be suprised if diets are similar; being insulin resistant is like having a metabolic broken leg, and LC diets are our crutch that allows us to get around better with our disability. For us it is an improvement, but for someone who is very insulin sensitive and can use & regulate sugar well, it wouldn't be, and in fact, they would be depriving themselves of "more efficient' fuel that they can use just fine.
The theory would also explain why people who tend to tolerate sugar well find a decrease in well being low carbing (I used to not think it was possible but I've seen it for myself numerous times now). It would also explain those paradoxical studies which show how less insulin resistant people lose more weight on low fat diets, and more insulin resistant people lose more weight on high fat ones.

[Duparc]

On reading the article you drew to attention 'ITW' I was alarmed to note that the fat used in those trials was polyunsaturated. This seems incredible when it is known that PUFAs are a potent immune suppressant and that they also impair the flow-mediated vasodilation of the brachial artery and if my memory serves me correctly on other arteries too, making them less flexible and causing, among other problems, high BP. What other adverse problems do PUFAs cause that might, so far, be unknown to us? Why, indeed, use a fat that is known to have adverse side-effects? Don't those scientists read about the research done on the substances they are likely to use in their own research and, if they don't, how valid can their research findings possibly be?

What a crazy world in which we live!

[ceberezin]

Duparc, do you have some references for that information about PUFAs? I hadn't heard these things and would like to read something.

[Azlocarb]

Here is what I asked the Dr.

I did not see a contact link on your sight so I would like to ask a question here in the comments. I have been debating a guy on another message board on the causes of diabetes. I contend that it is an over-consumption of carbohydrates that is causing the large increase in diagnoses and he is arguing that it is fat consumption and the increase in obesity caused by fat consumption that is causing the increase. I have done a search of the web and can find no human studies that support the theory that fat consumption causes obesity or diabetes. Are there any such studies out there? I found many health sites that make the statement that fat consumption is the cause but they do not site any studies to back up there contentions. As far as non-human studies there is a new one out that I was wondering if you could comment on. Here is the link: http://news.yahoo.com/s/nm/20051228/hl_nm/diabetes_dc

Here is what Dr. Eades had to say about this

Without commenting on this link, which is a news report (and we’ve seen how inaccurate those can be) of a couple of animal studies that have very little relationship to what happens in humans, I can say that at this time most scientists believe that the root cause of insulin resistance and type II diabetes is a defect in the insulin receptor caused by an intracellular accumulation of fat. The question is, what causes the intracellular accumulation of fat? We know that one thing for sure does: fructose. Carbohydrates in the diet cause the liver to produce more VLDL, which in turn leads to increased levels of triglycerides and increased intracellular fat. I would put my money on the theory that overconsumption of carbohydrates, especially fructose, is the culprit.

[SadLady]

All I know is that for me to control my diabetes and bring down my blood sugars whithout medications, I need to be on a high fat diet. When I eat 80% fat, 15% protein and 5% carbs, my blood sugars are between 85 and 90 in the morning, just like a non diabetic. So for me, it controls my diabetes rather than make me a diabetic.

[GeorgeMead]

http://www.second-opinions.co.uk/fats_and_cancer.html

Polyunsaturated fats (PUFs) are greatly immunosuppressive, and anything that suppresses the immune system is likely to cause cancer. The first person to suggest that polyunsaturated fats cause cancer was Dr R A Newsholme of Oxford University, England. (6) What Newsholme wrote was that when our bodies get sufficient nutrition, our diet includes immunosuppressive PUFs which make us prone to infection by bacteria and viruses. When we are starved, however, our body stores of PUFs are depleted. This allows our bodies' immune systems to recover which, in turn, allows us to fight existing infection and prevent other infections. He was making the point that the immunosuppressive effects of PUFs in sunflower seeds are useful in treating autoimmune diseases such as multiple sclerosis, (7) and that the same fatty acids could be used to suppress the immune system to prevent rejection of kidney transplants.

It was during the early days of kidney transplantation that doctors first encountered the problem of tissue rejection as their patients' bodies destroyed the alien transplanted kidneys. If transplantation were to be a success, they had to find a way to suppress the immune system. Newsholme had said that there was no better way to immunosuppress a renal patient than with sunflower seed oil. So kidney transplant doctors fed their patients linoleic acid. (8) (Linoleic acid is the major polyunsaturated fatty acid in vegetable oils.) But the transplant doctors were then astonished to see how quickly their patients developed cancers: some cancers were up to twenty times as frequent as was expected.

This was in line with heart trials using diets that were high in PUFs which, reported an excess of cancer deaths from as early as 1971. (9)

By the early 1980s, we were being exhorted by doctors and nutritionists to eat more PUFs because they were 'good for us' despite the fact that Oncology Times carried a paper in January 1980 from the University of California at Davis that mice fet PUFs were more prone to develop melanoma. In May 1980, the same publication carried a similar report from Oregon State University which said that PUFs fed to cancer-prone mice increased the numbers of cancers formed.

In 1989 there was a report of a ten-year trial at a Veterans' Administration Hospital in Los Angeles. In this trial half the patients were fed a diet which had double the amount of PUFs as compared to saturated fats. In the half of the patients on the high PUF diet there was a fifteen percent increase in cancer deaths compared to the saturated fat group. (10) The authors of the report said that the PUFs had been the cause of the increase in cancer deaths. The British Medical Journal carried an editorial in its 6 October 1973 issue which asked if PUFs were carcinogenic. It came to the conclusion that they were.

Wayne Martin likes to tell a story which suggests just how cancer-causing are PUFs. In 1930 in the USA, eighty percent of men smoked cigarettes and the tar content of cigarettes was much higher than it is today. The death rate at that time from lung cancer was very low. In 1955 doctors decided that PUFs were good in terms of heart disease protection. After this lung cancer deaths increased so dramatically. By 1980 although the number of American men who smoked had dropped to only thirty percent, three times as much PUF was being eaten – and there were sixty times as many lung cancer deaths. (11)

In 1990, Martin called Newsholme's Oxford University office but by then Newsholme had retired. Martin spoke to his successor to find that they were still treating autoimmune diseases with PUFs. By then they were using fish oil. The doctor said the reason for the fish oil was that the degree of immunosuppression increased with the degree of unsaturation and fish oil was much more unsaturated than sunflower oil. Martin asked the doctor why they were not talking about PUFs causing cancer. The doctor replied that if he did that he would be run out of Oxford.

Carcinogens – background radiation, ultraviolet radiation from the sun, particles in the air we breathe and the food we eat – continually attack us all. Normally, the immune system deals with any small focus of cancer cells so formed and that is the end of it. But linoleic acid suppresses the immune system. With a high intake of margarine, therefore, a tumour may grow too rapidly for the weakened immune system to cope thus increasing our risk of a cancer.

.....

Saturated fats and animal fats are usually blamed for all manner of diseases in Western society. But look at the facts:

In the 19th-century, when animal fats were all that was available, cancers were rare (as was heart disease).
Polyunsaturated fats and oils are used to suppress the immune system, such immunosuppression is known to cause cancers to start and promote cancer.
In this last century there has been a change in favour of polyunsaturated fats and oils – and cancer rates have soared.
Unfortunately, as polyunsaturated fatty acids are also essential to the body; we must have some. So a proper balance must be struck. Whether the dramatic increase in the numbers of cancers in the last century was as a result of a similarly dramatic rise in our intake of polyunsaturated vegetable oils is not known – but the evidence strongly favours such a conclusion.

Under the circumstances, it seems prudent to get what linoleic acid we need from animal sources. Or to restrict polyunsaturated oil consumption so that linoleic acid is no more than three percent of the total fat intake.

[Duparc]

SadLady, I concur with your comment.

Ceberezin, here are a some references to 'kick-start' you on your own search.

Look-up Dr Mary Enig's many interesting articles on lipids but especially her 4 part article on the "Oiling of America".

Ditto with Dr Raymond Peat but particularly his article, "Unsaturated Vegetable Oils: Toxic" and his many other interesting articles including the one on "Coconut Oil". Regretfully, he has changed his original URL and so far I have not been able to trace his current one.

There is an article that should interest you too at:www.second-opinion.co.uk/fats_and_cancer.html (http://www.second-opinion.co.uk/fats_and_cancer.html), and another at the same site ".../fat-not-protein.html".

Checkout this one if you can: De Roos et al. Replacement of dietary saturated fatty acids by trans fatty acids lowers serum HDL cholesterol and impairs endothelial function in healthy men and women. Arterioscler Thromb Biol.2001; 21(7): 1233-1237.

Here are a couple of others unrelated but may be of some interest to you:

http://www.contactmusic.com/new/xmlfeed.nsf/mndwebpages/ANTHONY%20ANDREWS%20OVERDOSES%20ON%20WATER

http://news.bbc.co.uk/go/pr/fr/-/1/hi/england/cornwall/3709819.stm

If you have read the downloaded article below by GeorgeMead you will undoubtedly understand why the population is dying upwards! Regretfully, there won't be many GPs/MDs who are aware of this effect. If GPs/MDs were paid for their knowledge there would be lots of paupers among them! A little magic like PhD works wonders in this cockeyed old world of ours!

[ceberezin]

Thanks, George Mead, that's astounding information I hadn't seen before.

[Dodger]

The effects of omega-6 poly-unfats and the omega-3 poly-unsaturated fats are totally different on the body. Almost all modern diets contain massive amouts of omega-6 PUFAs. This is very unhealthy and the cause of numerous problems.

Eliminating the 'vegetable' oils from the diet would reduce numerous health problems. Adding fish oils would help balance the omega-6s with some omega-3s.

[zajack]

Sorry...going back to the OP and I gotta wonder about the science behind these theories. I mean...how can they attribute risk of diabetes to the high fat portion of the diet unless they've eliminated the impact of carbs? :rolleyes: The picture alone makes me fairly certain that carbs weren't reduced or eliminated during this study.... which in my mind, if true, makes the whole thing a completely useless bunch of bunk!

I looked it up in 4 or 5 different locations and it simply said the mice were fed "a high fat diet"...which makes me think "regular mouse food...add fat", right? So...just out of curiousity :D ...I went and checked out standard mouse food ingredients at petco...and these are the first ingredients listed:
Ground yellow corn, dehulled soybean meal, ground wheat, ground oats, ground peanuts, dehydrated alfalfa meal, corn gluten meal, dried cane molasses, lignin sulfonate, fish meal, corn sugar WOW!!! So... if they fed these silly little things this "top rated" rodent food and increase the fat content...I'm surprised the little buggers werent dropping dead left and right....and with more health issues than just diabetes!!!

I'd guess (take bets even) that with a high fat/high carb diet they'd find a whole lot more going wrong with the health of those mice if they took the time to look. Weight gain, high cholesterol, increased risk of diabetes, high blood pressure, increased risk of heart disease, etc. In short...nothing we didnt already know.

If they wanted to get my attention (or even make me think they had modicum of common sense) with this.... they would have done a scientific study which (um...hello?!?!) means effectively reducing/eliminating extraneous factors. Dopes.

[Duparc]

I hear what you are saying about the omegas Dodger but somewhere among Peat's research articles he states (something like) that the medical profession has known since around the 1940s that the body is capable of making its own omega 3s & 6s if they are absent in the diet and which is contrary to today's cherished beliefs. I do not take polyunsaturated fats (or fish oil) as supplements and I try hard to avoid them in my diet but it is almost impossible and I am not aware of any adverse health effect to this. Interestingly, however, my angina symptoms disappeared on ceasing to take polyunsaturated oils.

As some of you will already know, I was a vegetarian for almost 18 years and my diet included lots of (so called) healthy fish and oils (including grain products) and it ended with having to have an urgent quadruple by-pass. That was 1990. Since that occasion I have become interested in dietetics. Now in my mid 70s I am fit and healthy and do not suffer from any health problems whatsoever. I like to think that there is a message here, in this anecdotal tale, for all to hear.

[Abd]

WILD AND CRAZY THEORY (warning :) ):
First lets assume something about human evolution. Let's assume that carbohydrate access was predicative of nutrient availability. This is a reasonable assumption considering that harvest times, times of plenty, starches turn to sugars, fruits are most ripe, etc.

Wow! Someone with a wild and crazy theory who actually states the underlying assumption (which is exactly where it goes astray, in my opinion). Congratulations! As I could say, Woo! Woo! (sound of train whistles).

Humans evolved in multiple environments. If I'm correct, nobody really knows what the original diet was, but game was probably abundant. Quite clearly, we are adapted to use both fat and carboyhdrates for energy; but if we have any problem, it is with the carbs. The fact that we so easily overindulge in carbs probably indicates that high-glycemic-index carbs were not very common; finding that beehive was finding a treasure trove of energy. And it would even keep, so it could be stored up for consumption later, without any particular technology. (But meat can also be preserved, and humans have known how for a long time.) Most of the carbs available would have been much higher in fiber than our processed-flour nightmare of a diet, effectively designed to feed the craving for sweets. (We don't always think of it, but craving carbs *is* craving sugar, the conversion of starch into sugar begins with the action of pytalin in saliva, so easy carbs do taste sweet.)

And some humans adapted, quite early on, to environments where carbs were truly rarities, mostly the far north. Regardless of how much this happened early on (which would produce more widespread genetic nutritional adaptaions), a major European stock (and Asian Indians, largely) came from the far north, if I'm correct. (The Aryans originated, it's been thought, in Siberia). So Europeans, in particular, as well as other peoples who lived in the far north for a substantial time, would definitely be expected to do better on a high-fat diet than on one high in carbs.

As has been pointed out, the only reason we get fat eating carbs is that the body has adapted to storing energy for times of famine, and how does it store the energy? As fat. So the body *has* to have a decent fat metabolism, or storage as fat wouldn't make sense. (And, of course, storage as fat is more efficient, more energy per unit weight.) Apparently, though, the body can only handle so much fat intake at one time, hence the appetite suppressive action of fat (probably the major reason why Atkins works). It is *much* easier to overeat with carbs than with fat. If I eat too much fat, my body complains, and it may even try to get rid of it before allowing it to be fully digested. Too much carbs? No such nausea.

[zedgirl]

Ditto with Dr Raymond Peat but particularly his article, "Unsaturated Vegetable Oils: Toxic" and his many other interesting articles including the one on "Coconut Oil". Regretfully, he has changed his original URL and so far I have not been able to trace his current one.


Mary Enig says that Raymond Peat is wrong regarding some of his claims about PUFAs. She wrote this article:

‘A Reply to Ray Peat on Essential Fatty Acid Deficiency’. You can read it here:

http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html

[LC FP]

As has been pointed out, the only reason we get fat eating carbs is that the body has adapted to storing energy for times of famine, and how does it store the energy? As fat

Thanks, Abd. And I'm sure nutritionists would be horrified to know that we manufacture and store saturated fat, mostly C-16 palmitic acid, from all those "healthy" carbs. Somehow our metabolism isn't afraid of saturated fat.

So I guess WW has been recommending high saturated fat all this time, and we didn't think they got it!

[Duparc]

A fascinating article ZedGirl by an eminent lipid researcher and I am glad to have read it. Although it is an attack on the accuracy of Dr Peat's comments it seems to have taken Dr Enig a rather long time to subsequently dispute Dr Peat's views and one wonders why.

While I am not denying what Dr Enig has said I am also not yet fully convinced by her views. When reference is made to the body making mead to compensate for its lack of EFAs it sounds to me (as it seemingly did to Dr Peat) that the body knows what it is doing and presumably can survive on this stuff otherwise why produce it?

Dr Enig further states that Peat is wrong in saying that PUFAs become rancid in the body but then admits that it goes through various stages of 'oxidation', which is close to what Dr Peat said, so there is a kind of contradiction woven through her article.

We read elsewhere in literature that few foods, indeed, possess EFAs but Dr Enig states that it exists in nearly all foods and hence the reason for the body not making it, so where does the truth lie? She further says that it is needed in 'minute' quantities and can be obtained from meat products so why the need for massive toxic-doses of fish and vegetable oils etc?

She also touts the benefits of cod-liver oil as it contains in addition to PUFAs, monounsaturated fatty-acids, yet it is well-established that PUFAs are effective immune suppressants and as such will induce cancer (as other research has substantiated) so why encourage anyone to take the stuff?

Dr Enig further admits to the adverse health-effects of having too much EFAs! Presumably she is suggesting that, as it exists in most foods, and as the body requires only minute amounts, then there is no requirement for supplementation.

On reading the book Dr Enig wrote in conjuction with Sally Fallon 'Nourishing Traditions' (pgs 8, 9, 10 & others) it looks as if she may have 'shot herself on the foot' as she supports what Dr Peat has said in saying that PUFs and omega 3s are highly reactive and turn easily rancid. From half-way down page 10 she goes on to support Dr Peat's views although does not mention his name as such.

On reading this article it seems that Dr Enig has unwittingly supported Dr Raymond Peat's contentions!

[kebaldwin]

I try to eat zero carbs and eat half (by weight) protein and half fat

All of my type 2 diabetes symptoms go away

[Kristine]

Backtracking to the OP... I've asked Dr. Eades to comment on this study on his blog, I will be checking to see if he responds.

Here ya go. (http://blog.proteinpower.com/drmike/archives/2006/01/a_study_appeare_1.html)

[zajack]

Toooo funny!!!

[MyJourney]

I looked it up in 4 or 5 different locations and it simply said the mice were fed "a high fat diet"...

The article I read said they were fed a high fat WESTERN diet which to me, translates into high carbs and trans fats.

http://www.eurekalert.org/pub_releases/2005-12/hhmi-rdh122105.php

Howard Hughes Medical Institute researchers have discovered a molecular link between a high-fat, Western-style diet, and the onset of type 2 diabetes. In studies in mice, the scientists showed that a high-fat diet disrupts insulin production, resulting in the classic signs of type 2 diabetes.