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High-fat diets cause insulin resistance and oxidation/aging


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#1 kodi

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Posted 01 August 2009 - 02:30 AM


I've been practicing a relatively low-carb diet for over a year. Based on extensive research, I was reasonably sure that this was not only good for long-term health, but also better than higher-carb diets because of reductions in glucose and insulin.

So when I first saw the 2009 study below, my first reaction was, "NO WAY! This contradicts all my other research!"

Believing that the study must be flawed somehow -- or perhaps applied only to diseased animals -- I read the full text to try to negate its relevancy to healthy, lean humans. However, I was unable to do so. Maybe I lack the expertise, but this study makes things look bad for low-carb diets.

Below are some selected excerpts from this 2009 study, which is entitled "Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans".

...in skeletal muscle of both rodents and humans [even lean, healthy humans], a diet high in fat increases the H2O2-emitting potential of mitochondria, shifts the cellular redox environment to a more oxidized state, and decreases the redox-buffering capacity...
[My comment: H2O2 is hydrogen peroxide, which Wikipedia states is one of the most powerful oxidizers known.]
...
The response to carbohydrate ingestion, however, is likely transient, owing to the rapid clearance of glucose. By contrast, a diet high in fat generated a persistent reduction in GSH/GSSG [the ratio of reduced glutathione to oxidized glutathione] (i.e., evident even after 12-hour fast), suggesting that the clearance and metabolism of dietary lipids may elicit a more sustained elevation in H2O2 emission, shifting the cellular redox environment to a more persistent oxidized state."
...
[In rats on a normal diet (NOT high-fat)] glucose ingestion elicited an approximately 2-fold increase in GSSG [oxidized glutathione] and an approximately 50% reduction in the GSH/GSSG ratio presumably reflecting an increase in mitochondrial H2O2 emission in response to the insulin-stimulated increase in glucose uptake and oxidation..."
[My comment: in other words, the study shows that high serum glucose and high-fat diets both seem to damage insulin sensitivity by the same mechanism, which seems likely to create cumulative damage that may ultimately result in diabetes and other diseases.]
...
Total cellular glutathione content (GSHT) decreased by approximately 30% in high-fat diet-fed rats ...suggesting that high fat intake compromises total GSH-mediated redox buffering capacity in skeletal muscle.
...
[In lean, insulin-sensitive male humans] ...4 hours after consumption of a high-fat meal (35% of daily energy expenditure; 60%–65% fat), and after 5 days of consumption of a similar high-fat diet ...maximal mitochondrial H2O2 emission was increased by more than 2-fold ...Moreover, this heightened mitochondrial H2O2-emitting potential persisted through the 5-day high-fat diet regimen. Cellular GSH/GSSG ratio decreased by approximately 50% within 4 hours after consumption of the high-fat meal and remained at this level through the 5-day high-fat diet ...again indicative of a shift in redox environment to a more oxidized state.
...
Bonnard et al. (13) recently reported that deteriorations in mitochondrial structure and function in skeletal muscle of mice appear only after several months of high-fat feeding, well after insulin resistance has developed. The implication is that mitochondrial dysfunction, similar to insulin resistance, is a consequence rather than a primary cause of the altered cellular metabolism...
...
Koves et al. (36) have recently reported the presence of ketone bodies and the accumulation of partially oxidized fatty acids in skeletal muscle of rats fed a high-fat diet, implying that an oversupply of lipids overwhelms the beta-oxidation and TCA cycle pathways, generating metabolic intermediates that otherwise are not present. The generation of surplus reducing equivalents would in turn be expected to elevate the redox state of complex I and/or the ubiquinone pool ...even a small surplus of reducing equivalents would be predicted to elicit an exponential increase in the rate of superoxide production and H2O2 emission from mitochondria...


The full text of the study is at http://www.pubmedcen...i?artid=2648700

There's also the following study that shows negative effects when fat comprises as little as 50% of calories (rather than 60% like the study above); but this study seems lower quality: http://diabetes.diab.../1926.full.html

Also the following quote from Aubrey de Grey & Michael Rae seems relevant:

...the metabolic state that [low-carb] diets induce (the notorious “ketosis”) has the unfortunate side effect of causing a jump in the production of the oxoaldehyde methylglycoxal, a major precursor of AGE’s that is also, ironically, produced within the cells of diabetic patients when they are forced to take in more glucose than they can immediately process. A recent study tested the size of this effect in healthy people who successfully followed the first two phases of the Atkins diet for a month, and who had the ketones in their urine to prove that they were sticking to the diet. These previously healthy people suffered a doubling of their methylglycoxal levels, leading to concentrations even worse than those seen in poorly controlled diabetics. Like other oxoaldehydes, methylglycoxal is far more chemically reactive than blood sugar (up to 40,000 times more reactive, in fact), and is known to cause wide-ranging damage in the body, of which AGE cross-links are but one example. This potentially makes the Atkins diet a recipe for accelerated AGEing, not a reprieve from it.


Finally, perhaps someone will spot reasons why these findings don't fully apply to how low-carb diets are actually practiced. If not, the idea that low-carb diets are healthy for long-term use seems to have been dealt a major blow.

(Edit: Fixed "quote" tags.)

Edited by kodi, 01 August 2009 - 02:46 AM.

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#2 Skötkonung

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Posted 01 August 2009 - 03:57 AM

It is an interesting study and I have passed it to Dr Eades to see if he has any views on the subject.

That said, if a high-fat, low-carb diet did cause type 2 diabetes, we should expect to see high rates of diabetes in cultures with little to no carbohydrate consumption such as the Inuit. However, this is not the case. Type 2 diabetes was non-existent in these cultures until the introduction of western cuisine. Other diseases, such as osteoporosis, were much higher on a very-low-carb due to the acidic PRAL score of the traditional Inuit food until the introduction of Western foods.

Likewise, if a high-fat, low-carb does cause type 2 diabetes, why is it so effective in managing type 2 diabetes?

Has carbohydrate-restriction been forgotten as a treatment for diabetes mellitus? A perspective on the ACCORD study design
http://www.pubmedcen...i?artid=2315645

Carbohydrate restriction as the default treatment for type 2 diabetes and metabolic syndrome.
http://www.ncbi.nlm....pubmed/18609058

I think there is definitely more research to be done on this topic - especially in regards to the AGE production.

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#3 kodi

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Posted 01 August 2009 - 11:44 AM

...if a high-fat, low-carb diet did cause type 2 diabetes, we should expect to see high rates of diabetes in cultures with little to no carbohydrate consumption such as the Inuit. However, this is not the case. Type 2 diabetes was non-existent in these cultures until the introduction of western cuisine.

Maybe cultures like the Inuit always became insulin-resistant, but it never mattered (until recently) because they never needed to produce much insulin. If true, when their culture was exposed to high-glycemic foods, one might expect them to be acutely susceptible to diabetes, especially the older members of the population.

Likewise, if a high-fat, low-carb does cause type 2 diabetes, why is it so effective in managing type 2 diabetes?

Has carbohydrate-restriction been forgotten as a treatment for diabetes mellitus? A perspective on the ACCORD study design
http://www.pubmedcen...i?artid=2315645

Carbohydrate restriction as the default treatment for type 2 diabetes and metabolic syndrome.
http://www.ncbi.nlm....pubmed/18609058

The two studies you linked seem to cover only the reduction in serum glucose levels. Neither seems to measure insulin sensitivty or antioxidant status after restricting dietary carbohydrates. Also, it seems unsurprising that the studies found that restricting carbohydrates in diabetic patients not only alleviated their elevated serum glucose, but also other things that elevated glucose causes (higher inflammation, higher hemoglobin A1C, etc). In other words, maybe insulin resistance became irrelevant as long as they stuck to the diet religiously (just like the Inuits used to).

For better survival and long-term health, perhaps the optimal diet for most diabetes patients would be a diet rich in low-glycemic carbs (~50%) spread out over at least 4 meals a day. In addition, the diet might include mild calorie restriction (~5%) to minimize the times when glucose is flowing into the blood faster than cells can burn or store it. Unfortunately such a diet seems much harder to stick to than a high-fat diet.

I think there is definitely more research to be done on this topic - especially in regards to the AGE production.

Indeed!

#4 Mind

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Posted 01 August 2009 - 04:49 PM

Thus, the intracellular accumulation of lipid metabolites more likely reflects the simple consequence of fatty acid supply exceeding metabolic demand, regardless of mitochondrial content.


In fact, transitioning to a high-fat diet initially induces an increase, not a decrease, in mitochondrial biogenesis and fatty acid oxidative capacity in skeletal muscle


All rodents were housed in a temperature- (22°C) and light-controlled (12-hour light/12-hour dark) room and maintained on either standard rodent chow or a high-fat (60%) diet (Research Diets), with free access to food and water.


In the male humans:

**********************
Mitochondrial H2O2 emission was approximately 2-fold higher in obese versus lean individuals in response to titration of succinate (Figure ​(Figure5A)5
Figure 5
A) and nearly 4-fold higher during basal respiration supported by fatty acid (Figure ​(Figure5B).5
Figure 5
B).
***********************

It seems to me that remaining within your metabolic requirements while on a higher fat diet would ease some concern. Eating any macro-nutrient to the point of obesity is going to be bad.
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#5 kodi

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Posted 01 August 2009 - 05:43 PM

It seems to me that remaining within your metabolic requirements while on a higher fat diet would ease some concern. Eating any macro-nutrient to the point of obesity is going to be bad.

That is a good point and I was hoping the same thing. Unfortunately (if I'm reading it properly) the study seems to establish the following facts:
  • In lean, insulin-sensitive male humans...
  • eating normal-sized meals (not oversized) for 5 days...
  • and those meals contained 60-65% of their calories from fat...
  • H2O2 emission was increased by more than 2-fold [compared to normal diets]...
  • and the ratio of oxidized to reduced glutathione decreased by approximately 50% and remained at this level for the duration of the high-fat diet.
The last item above seems especially worrisome because, "the ratio of reduced glutathione to oxidized glutathione within cells is often used scientifically as a measure of cellular toxicity" [Wikipedia]. In addition, I seem to remember that glutathione and SOD are the body's first line of defense against free radicals, and that we'd die rather quickly without them. So reducing the amount of "available" glutathione by half seems likely to be very pro-aging.

Furthermore, this study and/or other recent studies indicate that although the number of mitochondria in muscle initially increases while on a high-fat diet, the mitochondria begin to malfunction and/or decrease after several months on the diet, at least in mice: "Bonnard et al. (13) recently reported that deteriorations in mitochondrial structure and function in skeletal muscle of mice appear only after several months of high-fat feeding..."

However, the above may be mitigated by the fact that these mice presumably ate as much of the high-fat diet as they wanted. If so, their intake may have been beyond their calorie needs, which wouldn't make it a fair comparison with humans maintaining constant weight on a low-carb diet.

Even so, it is troubling that lean humans who (presumably) did not overeat while on the high-fat diet suffered a sharp reduction in their antioxidant status and insulin sensitivity.

#6 rwac

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Posted 01 August 2009 - 05:57 PM

That is a good point and I was hoping the same thing. Unfortunately (if I'm reading it properly) the study seems to establish the following facts:

  • In lean, insulin-sensitive male humans...
  • eating normal-sized meals (not oversized) for 5 days...
  • and those meals contained 60-65% of their calories from fat...
  • H2O2 emission was increased by more than 2-fold [compared to normal diets]...
  • and the ratio of oxidized to reduced glutathione decreased by approximately 50% and remained at this level for the duration of the high-fat diet.
The last item above seems especially worrisome because, "the ratio of reduced glutathione to oxidized glutathione within cells is often used scientifically as a measure of cellular toxicity" [Wikipedia]. In addition, I seem to remember that glutathione and SOD are the body's first line of defense against free radicals, and that we'd die rather quickly without them. So reducing the amount of "available" glutathione by half seems likely to be very pro-aging.


It is fairly well known that it takes about 2 weeks for people to adjust to burning fat as opposed to glucose on an atkins style diet.
Most people feel lousy during that adaptation phase, probably due to the excess peroxide.
Very likely this is a temporary thing, since people are fine after the adaptation.

Furthermore, this study and/or other recent studies indicate that although the number of mitochondria in muscle initially increases while on a high-fat diet, the mitochondria begin to malfunction and/or decrease after several months on the diet,...


Mice are hardly evolved to handle high-fat diets, I don't think you can draw conclusions about long term human diet from mice.

Edited by Michael, 08 December 2009 - 12:04 PM.
Double quote


#7 Sillewater

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Posted 01 August 2009 - 06:34 PM

http://www.proteinpo...idative-stress/

Dr Eades covers this topic and he points towards a study done on humans.

Effect of short-term ketogenic diet on redox status of human blood.

Nazarewicz RR, Ziolkowski W, Vaccaro PS, Ghafourifar P.
Division of Vascular Surgery, Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
The present study investigated the effect of a ketogenic diet on the blood redox status of healthy female subjects. Twenty healthy females with mean body mass index of 21.45 +/- 2.05 kg/m(2) were provided a low-carbohydrate (55 +/- 6 g; 13% total energy), high-fat (138 +/- 16 g; 74% total energy), calorie-restricted (-465 +/- 115 kcal/d) diet. The followings were tested prior to and after 14 days consumption of the diet: Whole body, body weight and total body fat; blood, complete blood count, red blood cells, white blood cells, hemoglobin, and hematocrit; plasma, 3-beta-hydroxybutyrate, total antioxidative status, and uric acid; red blood cells, total sulfhydryl content, malondialdehyde, superoxide dismutase activity, and catalase activity. After 14 days, weight loss was significant whereas no changes were detected in body fat. No alterations were observed in blood count or morphology. 3-beta-hydroxybutyrate, total antioxidative status, uric acid, and sulfhydryl content were significantly increased. There were no alterations in malondialdehyde, or superoxide dismutase or catalase activity. The present study demonstrates that 14 days of a ketogenic diet elevates blood antioxidative capacity and does not induce oxidative stress in healthy subjects.
PMID: 17663642 [PubMed - indexed for MEDLINE]

Since the SH content increases doesn't that mean glutathione is higher?

Edited by Sillewater, 01 August 2009 - 06:34 PM.


#8 kodi

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Posted 01 August 2009 - 07:16 PM

Dr Eades covers this topic and he points towards a study done on humans. ...Since the SH content increases doesn't that mean glutathione is higher?

Dr. Eades writes:

SH is sulfhydryl group content, which is a measure of glutathione, a major home-grown antioxidant. Increased SH means the body is increasing its level of its own self-made antioxidants in the mitochondria where all the bad free radical activity takes place.

According to http://en.wikipedia....wiki/Sulfhydryl , Glutathione is merely one type of Sulfhydryl. Many other types are listed, which may indicate that measuring total Sulfhydryl is not an accurate method to detect Glutathione levels. This seems to be supported by http://en.wikipedia....ine_glutathione

Furthermore, there is apparently a crucial difference between oxidized glutathione and reduced (available) glutathione, which apparently wasn't measured by the study. However, the following study DID measure oxidized glutathione:

The ketogenic diet increases mitochondrial glutathione levels (2008)
http://www3.intersci...l...=1&SRETRY=0

The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague–Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of ?-hydroxybutyrate (BHB). [ketogenic diet]-fed rats showed a twofold increase in hippocampal mitochondrial GSH and GSH/GSSG ratios compared with control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate-limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity was observed in KD-fed rats, as well as up-regulated protein levels of GCL subunits. Reduced CoA (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared with controls. As GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial H2O2 production and H2O2-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.


At first glance, the finding above seems to directly contradict the newer 2009 study. However, there is at least one big difference: the newer study didn't necessarily induce ketosis in its subjects, so those animals were probably burning both glucose and fat for energy.

So perhaps ketosis is a cleaner process during which fat is burned really efficiently. Similarly, the body seems to burn glucose really well on a typical high-carb diet. But if you're somewhere in between (say 50-65% fat), perhaps it can't efficiently burn both at the same time. Imminst member Edward has had similar thoughts:

The body likes one primary fuel be that carbs or fat and it doesnt do well with an abundance of both, tolerance varies depending on genetics and lifestyle


It would great to find out the answer because then we might be left with only a few choices: ultra-high-carb diets or ultra-high-fat diets, or perhaps a system in which we alternate day-to-day or meal-to-meal. (However, "alternating" might be disrupted by glycogen stores, which would keep you in a mixed state until all the glycogen is depleted. In addition, frequently switching between high-fat and high-carb might put wear-and-tear on the system.)

Edited by kodi, 01 August 2009 - 07:33 PM.


#9 JackChristopher

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Posted 01 August 2009 - 08:11 PM

Glycosis is proportional to lyposis.
Stephan doesn't care about macro-nutri ratios and seems well. That's anecdotal, but I've never felt odd on days I've ate similarly either. But the carb or fat sources matters. On the other hand the downsides of eating that way may be undetectable subjectively.
^^^^

But if you're somewhere in between (say 50-65% fat), perhaps it can't efficiently burn both at the same time.

The body likes one primary fuel be that carbs or fat and it doesnt do well with an abundance of both, tolerance varies depending on genetics and lifestyle


It would great to find out the answer because then we might be left with only a few choices: ultra-high-carb diets or ultra-high-fat diets.


That's the consensus. We still disagree with which diet is better. But I do expect one to be slightly better. And that shines a light on protein: What's better for longevity, more or less of it?

Edited by JackChristopher, 01 August 2009 - 08:20 PM.


#10 niner

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Posted 01 August 2009 - 09:12 PM

It would great to find out the answer because then we might be left with only a few choices: ultra-high-carb diets or ultra-high-fat diets, or perhaps a system in which we alternate day-to-day or meal-to-meal. (However, "alternating" might be disrupted by glycogen stores, which would keep you in a mixed state until all the glycogen is depleted. In addition, frequently switching between high-fat and high-carb might put wear-and-tear on the system.)

I can see the argument for ultra-high-fat, because that is necessary to maintain ketosis. I don't see why we would need ultra-high-carb, however. It looks like we need good quality (low GI) carbs, adequate protein, and modest amounts of fats. We need certain essential fats, and there are a number of "good fats" that are at least not harmful. It would seem that if we don't want to attempt to live in ketosis, then a relatively low fat diet where most fats are "good" is the way to go. I don't see the evidence that we want extremely high carbs. I don't think alternating is going to work out well, given how long it takes to switch over to ketosis.

#11 rwac

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Posted 01 August 2009 - 09:35 PM

I don't think alternating is going to work out well, given how long it takes to switch over to ketosis.


It doesn't take long at all. Infact most people go into ketosis every night.

What takes longer is to get the body adapted to handling a high-fat diet, the first time.

#12 kodi

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Posted 01 August 2009 - 11:02 PM

I don't see why we would need ultra-high-carb, however.

I should have been more specific. For ultra-high-carb diet, I had in mind 15-20% protein, 10-20% fat, and 60-75% carb (low-glycemic).


It would seem that if we don't want to attempt to live in ketosis, then a relatively low fat diet where most fats are "good" is the way to go.

That is also how I'm leaning, in spite of it being a radical departure from my previous diet of 80-120 carbs per day.

We need certain essential fats, and there are a number of "good fats" that are at least not harmful.

Yes. My current targets are for an omega 6/3 ratio between 2.0 and 4.0, and a monounsaturated-to-polyunsaturated ratio between 1.5 and 2.2 (this is mostly a guess based on vague things I've read). For saturated fat, my target is also uncertain; perhaps it should be no higher than your polyunsaturated fat intake. (The free nutritional software CRON-o-Meter makes it easy to determine how much of each type of fat you're getting.)

#13 JackChristopher

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Posted 01 August 2009 - 11:54 PM

. niner: I don't see why we would need ultra-high-carb, however. It looks like we need good quality (low GI) carbs, adequate protein, and modest amounts of fats.


Hearing healthy ultra-high carb, I think the Okinawan diet; high carb (rice) w/ adequate protein and fat. A few other cultures fit the pattern too. Just swap rice with plantains, potatoes, yams or your choice of high GI starchy food.

And Skotkung's made the point before: it's hard to separate diet from lifestyle. Both diets foul you if you're a) eating too much, b) aren't active, c) have a slow resting metabolism or d) the rest of your diet is so inflammed that you need a fire department to put it out.

A caveat I have with very high fat is too much sat fat might create fatty streaks—much like very high carb—via oxidative stress. I have no conclusive evidence for this. But I can dig up references if you want. The caveat is against my intuition. High fat seem to be long within our dietary niche.

#14 Shepard

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Posted 02 August 2009 - 01:25 AM

In studies, people that are naturally lean and classified as insulin sensitive always seem to do better on higher carbohydrate intakes. The same is true of the obese, insulin resistant folks when they are placed on low-carb diets.

That said, a prolonged period on a high fat diet is likely to show both insulin resistance and high fasting glucose levels in anyone due to the high levels of NEFA in skeletal muscle. The question is, is this a problem if one sticks to a low carb diet indefinitely? I doubt it.

Will read the full text and comment on the oxidation issue if anything sticks out. Although, I agree that rat models aren't the best when looking at fat (either dietary or stored).

Also, this is probably the diet that was used on the rats if anyone is interested: http://www.researchd...eets/D12492.pdf

Edited by Shepard, 02 August 2009 - 01:29 AM.


#15 JackChristopher

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Posted 02 August 2009 - 02:08 AM

Also, this is probably the diet that was used on the rats if anyone is interested: http://www.researchd...eets/D12492.pdf


Nice find.

If this is the diet, it's likely the lard is hydrogenated. Combined with soybean oil that confounds things a bit. Not to mention the maltodextrin and sucrose, sure to trigger overeat. The rats had unlimited access too.

#16 niner

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Posted 02 August 2009 - 04:19 AM

If this is the diet, it's likely the lard is hydrogenated. Combined with soybean oil that confounds things a bit. Not to mention the maltodextrin and sucrose, sure to trigger overeat. The rats had unlimited access too.

Industrial lard is often hydrogenated, so that's a possibility. The Research Diets people are very science-based though, and make a point of having chemically defined diets. This would be quite an error for them to commit, so I think the odds that they are using lard laced with trans fats is not high. However, after looking around their site, I couldn't find anything that said it wasn't hydrogenated, so it's an open question at this point. I have emailed them to ask if it is hydrogenated, and if they know the fatty acid composition. I'll post any response I get.

Edited by niner, 02 August 2009 - 04:21 AM.


#17 JLL

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Posted 02 August 2009 - 10:16 AM

Hmm, this is certainly interesting. I'm naturally lean and can tolerate a lot of carbs, but I still eat a high-fat, lowish-carb diet.

It just seems to me that increasing carb intake introduces a lot more problems than it solves. There's only so much salad you can eat. Beyond that, we have the fructose/AGEs problem, the starch/insulin problem, the grains/gluten problem, etc.

Anecdotally, I've been on a high-fat diet for a some years now and my fasting glucose hasn't changed at all.

#18 JLL

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Posted 02 August 2009 - 10:20 AM

In studies, people that are naturally lean and classified as insulin sensitive always seem to do better on higher carbohydrate intakes. The same is true of the obese, insulin resistant folks when they are placed on low-carb diets.


Do you mean that lean and insulin sensitive people do better on high-carb diets than on high-fat diets, or that they do better on high-carb diets than obese and insulin resistant people?

#19 Shepard

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Posted 02 August 2009 - 03:11 PM

Do you mean that lean and insulin sensitive people do better on high-carb diets than on high-fat diets, or that they do better on high-carb diets than obese and insulin resistant people?


They seem to do better on high carb diets than high fat diets. Even in obese women, insulin sensitivity plays a role in how they respond to high carb vs. high fat: http://www.ncbi.nlm....pubmed/15897479

Now, note the typical diet composition. It doesn't necessarily mean much when compared to what most of us are talking about with low carb, high fat. But, it does tell us something.

Cooling and Blundell have looked into the differences between the apparent high-fat and low-fat phenotypes. But, still talking about relatively low fat intake compared to ketogenic levels.

#20 Skötkonung

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Posted 04 August 2009 - 09:21 PM

This is Dr Eade's response to the OP's study:

I don’t think the study is relevant at all. The very first line of the abstract is a lie. It says: “High dietary fat intake leads to insulin resistance in skeletal muscle,…” I would love to see the proof of this. It doesn’t exist. I didn’t have time to read this study critically, but my quick overview tells me that most of the data is from rat studies, and rats aren’t just furry little humans. The didn’t evolve to eat a high-fat diet, so they don’t react the same as we do. The one study they did in humans, was a muscle biopsy study after a single high-fat meat (and we don’t know what the rest of the meal was – it could have been sugar), which causes a different reaction than would be the case in someone who was low-carb, high-fat adapted.

#21 kodi

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Posted 04 August 2009 - 10:00 PM

[Dr Eade's said] The one study they did in humans, was a muscle biopsy study after a single high-fat meat (and we don’t know what the rest of the meal was – it could have been sugar), which causes a different reaction than would be the case in someone who was low-carb, high-fat adapted.

One part of the study also kept humans on the high fat diet (60-65% fat) for 5 days and the results were poor like the single high-fat meal.

Anyway, I agree that more detailed studies will be needed to confirm these results. In the meantime, it seems best to remain open to the possibility that long-term, high-fat diets (at least ones that don't induce ketosis) might reduce insulin sensitivity and antioxidant status.

#22 Blue

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Posted 04 August 2009 - 10:09 PM

Regardiing the Inuits they had a short average lifespan so they should if anything be used as an argument against a high-fat, high-protein diet. That they did not develop age-related diseases is not surprising considering their short life.

Looking instead at the Okinawa diet, which has produced the longest or among the longest average lifespans in humans, it is a low-calorie, low-fat, low-protein diet.

Edited by Blue, 04 August 2009 - 10:10 PM.


#23 Shepard

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Posted 04 August 2009 - 10:31 PM

Come on Eades, you can do better than that.

Anyway, it doesn't necessarily matter if it induces insulin resistance if what you're worried about is the lifetime AUC of insulin.

#24 Blue

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Posted 04 August 2009 - 10:50 PM

http://www.proteinpo...idative-stress/

Dr Eades covers this topic and he points towards a study done on humans.

Effect of short-term ketogenic diet on redox status of human blood.

Nazarewicz RR, Ziolkowski W, Vaccaro PS, Ghafourifar P.
Division of Vascular Surgery, Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
The present study investigated the effect of a ketogenic diet on the blood redox status of healthy female subjects. Twenty healthy females with mean body mass index of 21.45 +/- 2.05 kg/m(2) were provided a low-carbohydrate (55 +/- 6 g; 13% total energy), high-fat (138 +/- 16 g; 74% total energy), calorie-restricted (-465 +/- 115 kcal/d) diet. The followings were tested prior to and after 14 days consumption of the diet: Whole body, body weight and total body fat; blood, complete blood count, red blood cells, white blood cells, hemoglobin, and hematocrit; plasma, 3-beta-hydroxybutyrate, total antioxidative status, and uric acid; red blood cells, total sulfhydryl content, malondialdehyde, superoxide dismutase activity, and catalase activity. After 14 days, weight loss was significant whereas no changes were detected in body fat. No alterations were observed in blood count or morphology. 3-beta-hydroxybutyrate, total antioxidative status, uric acid, and sulfhydryl content were significantly increased. There were no alterations in malondialdehyde, or superoxide dismutase or catalase activity. The present study demonstrates that 14 days of a ketogenic diet elevates blood antioxidative capacity and does not induce oxidative stress in healthy subjects.
PMID: 17663642 [PubMed - indexed for MEDLINE]

Unfortunate that a high-fat ketogenic diet AND strong calorie restriction was introduced as the same time. Calorie restriction and weight loss has strong health promoting effects so very difficult to know what the ketogenic diet contributed.

#25 Shepard

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Posted 04 August 2009 - 11:04 PM

Unfortunate that a high-fat ketogenic diet AND strong calorie restriction was introduced as the same time. Calorie restriction and weight loss has strong health promoting effects so very difficult to know what the ketogenic diet contributed.


Unfortunately, this is fairly common.

#26 Skötkonung

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Posted 05 August 2009 - 05:53 AM

Regardiing the Inuits they had a short average lifespan so they should if anything be used as an argument against a high-fat, high-protein diet. That they did not develop age-related diseases is not surprising considering their short life.

Looking instead at the Okinawa diet, which has produced the longest or among the longest average lifespans in humans, it is a low-calorie, low-fat, low-protein diet.


Comparing lifespan is useless without also factoring in culture and location. I'm guessing the temperate climate of Okinawa is much easier on the body than the long winters of the arctic. Likewise, an agrarian society is probably more accommodating to senility and middle age than a society based purely on hunting in frigid conditions.

Lastly, if high-fat diets did induce insulin resistance, a society based entirely on a high-fat diet would be showing signs of insulin resistance long before they reach middle age just Americans are now developing diseases of insulin resistance during childhood and in their mid-twenties from a high carbohydrate diet. As for other diseases of civilization such as CVD, while many of the Inuit may not have lived long enough to demonstrate the full onset of CVD, that doesn't mean signs such as arterial streaking wouldn't have appeared much earlier.

That said, the age argument you are using to try and discredit the Inuit is kind of a moot point because according to data collected by a Russian mission to the arctic during the years 1822 to 1836, about 25% of the Inuit lived past 60 (if we exclude infant mortality). It's possible that life expectancy would have been higher before contact with the Russians, since they introduced a number of diseases that the Inuit were not resistant to.

See the data for yourself.

Edited by Skotkonung, 05 August 2009 - 05:56 AM.


#27 TheFountain

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Posted 05 August 2009 - 08:29 AM

Comparing lifespan is useless without also factoring in culture and location. I'm guessing the temperate climate of Okinawa is much easier on the body than the long winters of the arctic.


Okinawa is at the same latitude as florida. Why aren't many florida residents living to 110? For that matter, what about Hawaii? The bahamas? No matter what contrived answers you give you cannot escape the fact the the Okinawan diet beats the Paleo diet in observable longevity stats. The Paleo diet is good for today (and maybe only today) but the Okinawan diet seems to be best for tomorrow.

I think it was Duke who proclaimed that there is no such thing as genetic variability where diet is concerned. That one diet is the best for all. I approached my previous comment sarcastically, from that angle. Because I always thought it was a silly assumption.

Edited by TheFountain, 05 August 2009 - 08:29 AM.


#28 Blue

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Posted 05 August 2009 - 08:34 AM

That said, the age argument you are using to try and discredit the Inuit is kind of a moot point because according to data collected by a Russian mission to the arctic during the years 1822 to 1836, about 25% of the Inuit lived past 60 (if we exclude infant mortality).

See the data for yourself.

" Based on these data, the approximate life expectancy (excluding infant mortality) of this Inuit population was 43.5 years. "

Edited by Blue, 05 August 2009 - 08:37 AM.


#29 JLL

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Posted 05 August 2009 - 11:43 AM

Do you mean that lean and insulin sensitive people do better on high-carb diets than on high-fat diets, or that they do better on high-carb diets than obese and insulin resistant people?


They seem to do better on high carb diets than high fat diets. Even in obese women, insulin sensitivity plays a role in how they respond to high carb vs. high fat: http://www.ncbi.nlm....pubmed/15897479

Now, note the typical diet composition. It doesn't necessarily mean much when compared to what most of us are talking about with low carb, high fat. But, it does tell us something.

Cooling and Blundell have looked into the differences between the apparent high-fat and low-fat phenotypes. But, still talking about relatively low fat intake compared to ketogenic levels.


And when you say "do better", do you mean just weight loss/gain or something else? In the abstract you linked to, the only thing that was reported was weight loss.

I'm not really worried about my weight regardless of what I eat; low-carb or high-carb. I would be worried if a high-fat diet caused other problems in insulin sensitive people (which I probably am). If you have other references that address this, that would be great.

It is surprising that some of the obese women actually lost more weight on a high-carb diet.

#30 Shepard

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Posted 05 August 2009 - 03:52 PM

And when you say "do better", do you mean just weight loss/gain or something else?


Off the top of my head, it's all related to weight loss. But just that bit of evidence makes a better case for individualized dietary approaches than the simplistic view of "one diet for all".

Just enjoy your McDonald's until nutrigenomics picks up and we get our government-approved optimal eats in plastic packages every morning.




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