Fat-free Diets And Cancer In Rats

jyb

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So would humans with cancer benefit from a fat-less diet (if it were possible)? It's not clear, because some conditions can be reverted by saturated fat (RP mentions that liver disease).
 
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j.

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jyb said:
So would humans with cancer benefit from a fat-less diet (if it were possible)? It's not clear, because some conditions can be reverted by saturated fat (RP mentions that liver disease).

It depends on why that fat-free rats didn't have cancer. Was it because they didn't consume unsaturated fats, saturated fats, or both? And then there is the question of whether it applies to humans.
 

key

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jyb said:
So would humans with cancer benefit from a fat-less diet (if it were possible)? It's not clear, because some conditions can be reverted by saturated fat (RP mentions that liver disease).

Sugar can be turned into saturated and omega-9 series(oleic, mead, etc) fat. For example in this study eating refined sucrose to the point of fat deposition in the liver decreased oxidative stress-http://www.ncbi.nlm.nih.gov/pubmed/11018471
 
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j.

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High fat diet increases the weight of rat ventral prostate

In this study they found that rats with high fat diets (32%) had bigger prostates than those with a low fat diet (4%). What caught my attention is that they used saturated fats. Unfortunately I don't have access to the article to see what kind of saturated fat they used, and the rest of the diet.
 
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j.

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kranum

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I found the original, does anyone read german? My german is quite rusty

The conclusion reads something like:
1) When on a lipid-free diet carcinoma growth of white mice is extremely inhibited. The inhibition is not due to "atreptische" immunity. (Not sure about that word, not even a dictionary could help me)
2) The addition of cholesterol and lecithin reduces the growth inhibition, with the cholesterol proving more potent than the lecithin.
3) The contrasting behavior of cholesterol and lecithin cannot be determined in this experimental arrangement.
(Quite unsure about nr. 3, so maybe someone more proficient in german can correct me)
 

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Giraffe

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kranum said:
post 119303 The conclusion reads something like:
1) When on a lipid-free diet carcinoma growth of white mice is extremely inhibited. The inhibition is not due to "atreptische" immunity. (Not sure about that word, not even a dictionary could help me)
2) The addition of cholesterol and lecithin reduces the growth inhibition, with the cholesterol proving more potent than the lecithin.
3) The contrasting behavior of cholesterol and lecithin cannot be determined in this experimental arrangement.
(Quite unsure about nr. 3, so maybe someone more proficient in german can correct me)
(1) When they say the effect is not due to "atreptische Immunität", say mean: the effect is not due to an hypo-caloric diet. "atreptisch" is not really a German word, but they indirectly define the meaning in experiment B (Versuch B).
(3) They are saying that they could not detemine an antagonizing effect of lecithin and cholesterol. This is something to do with permeability of the "cell membranes" and water retention within the cell (explained in the preface).

The very same study was discussed here.
 
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Entropy

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I enjoyed his post, critical thinking instead of relying on authoritarian thinking which Peat is against.
 

Jarman

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Wow very interesting post! That entire site is definitely interesting!

I wonder what @tyw would have to say about this, not only about that particular topic but most of the claims the site makes.
 

tyw

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Wow very interesting post! That entire site is definitely interesting!

I wonder what @tyw would have to say about this, not only about that particular topic but most of the claims the site makes.

Can't draw too many conclusions based on non-human studies regarding PUFA unfortunately. Mice in particular have a lot more DHA on mitochondria membranes.

For comparison (from 'Human Longevity' by David Valentine):

Phospholipids from skeletal muscle, heart, kidney, and liver of naked mole rats contained an average 2.2 percent DHA (range 0.6 to 6.5 percent) versus 19.3 percent (range 11.7 to 26.2 percent) in mice.

The DHA content of membranes of heart cells in mice is about 10 to 15 percent of total fatty acids compared to about one-tenth this level of DHA in human cardiac cells.
ie: a "PUFA-depleted" rat still represents more membrane PUFA than an average human, with regard to critical organs.

Also, I don't know what kind of mice were used in the specific commentary. Depending on the strain, something like cancer susceptibility is going to vary tremendously. eg: A lot of the non-native EMF research used germ-free (gnotobiotic) mice, to "prove" that EMF-exposed and non-EMF-exposed mice suffered the same consequences. In reality, germ-free mice are horrible test subjects for that particular stressor, and the same goes for PUFA related stress.

----

I will be critical of Peat for using what I consider to be less than ideal studies to back his points up. To be fair, during the time in which he was formulating his hypothesis, the amount of studies specific to PUFA on membranes were very few, mostly because the effect of PUFA on membranes was still not appreciated.

That changed a lot in the 1990s to 2000s, with membrane PUFA now being seen as a critical component in aging, whereby the organism has to choose between faster potential metabolism, and higher potential for damage.

PUFAs in membrane will "enable more collisions between membrane components", which from a metabolic stand point, is a way to increase the potential rate of reactions between complexes. It also exposes the PUFA and other membrane components to much higher degrees of peroxidation, and Dr Valentine does a great job of showing exactly how excessive membrane-local peroxidation leads to aging and/or cancer.

NOTE: The keyword in the above paragraph is "potential". More PUFA in membranes increases the maximum possible rate of reaction. It doesn't mean that this is the rate that will happen all or even most of the time. eg: Hummingbird muscles need lots of PUFA in order to sustain their insanely fast rates of firing, but only during periods of flight. They then shut down their metabolic rate drastically during sleep (dropping their body temps dramatically as well, usually <25C in sleep vs 40+C during flight).

This is specific concentration of PUFAs, in specific parts of the body of that specific species of organism, which is all done in a controlled manner to exploit the natural properties of PUFA. This does not in any way mirror a PUFA overloaded situation, where PUFAs end up where they "shouldn't be" (based on how the organism is "meant to distribute PUFAs").​

NOTE: DHA is the "most powerful" PUFA, since it has the most double bonds. It presents the largest risk/reward profile, and organisms have selectively evolved to favour one side of the spectrum or the other. Small animals like Mice and Hummingbirds favour faster metabolism, at the expense of shorter lifespans. Humans and Whales favour less PUFA and relatively slower metabolisms, with longer lifespans.​

Sidenote: another quote from Valentine

Large baleen whales might be the longest-lived mammals, with life spans estimated to be as long as two centuries.

Gudbjarnason measured the levels of DHA in heart muscle tissue of various mam- mals ranging in size from small to large and from these data made two significant conclusions relevant to aging (Gudbjarnason et al., 1978; Gudbjarnason et al., 1989).
  • The first is that DHA levels rise in lockstep with increasing heart rates, suggesting a direct relationship.

  • Second, DHA levels in cardiac cells correctly predict life span, an inverse relationship.
It can be estimated based on the levels of DHA needed by the human brain (Chapter 15) that a whale requires about 25 mg per day of DHA to maintain DHA homeostasis in its brain.

Thus, a blue whale is estimated to consume around 1500 times more DHA than needed to maintain homeostasis of DHA in the brain.

Whale meat is lean and contains only a fraction of 1 percent of DHA, a proportion remarkably different than that of krill. Blubber contains DHA, but again, levels are far below those of krill.​


In other words, we have species-specific modulation of PUFAs up and down according to what that species determines is best for its environment.

It is then clear that in humans centenarians with genetic variants for longevity, that their adaptations / mutations are specific to dealing with lowering membrane peroxidation (through more uncoupling) and actually being able to respond to oxidative damage better.

We can make an educated guess, based upon observations of animals and humans, that reducing membrane PUFA levels, in large part through dietary manipulation, is the best we can do to approximate these centenarian mitochondrial conditions.

Personally, I believe that even in a fully PUFA-free diet, de-novo lipogenesis will produce some level of PUFAs, and have them incorporated into membranes of all forms. That is to say, a PUFA-free diet does not lead to a PUFA-free organism, since some PUFAs are necessary for function of the organism.

A PUFA-free diet will however, represent a local minimum of PUFAs, down to the minimum level of what the specific organism determines it needs for its own survival. Again, the educated guess is that this local minimum will positively select for human metabolism and longevity.

In that way, I will agree with Peat's conclusions, based on my own examination of his claims using whatever evidence I could find.

I do not like the methodology of debunking individual studies, and then calling that "debunking Peat".

.....
 

Luann

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@tyw thanks for your input, studies are often shrouded in jargon, half-baked conclusions, and bias, which make them a scary subject for anyone who seeks the truth
@Entropy agreed.
 
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