At first I was shocked by this studies claims, but then I realized that we've known for a while that eating a low carb diet can cause a little insulin resistance as the body reduces the number of insulin binding receptor sites as a result of lower insulin levels. It seems that they have the chicken and the egg confused. One of the researchers commented that it was okay to have high levels of BCAA's if your food intake didn't exceed your energy balance. Still it amazes me that the headline tries to indicate that protein and fat are the cause of obesity. I don't believe the study is really showing that, right? What are your thoughts?
asked byCaveman_formally_known_as_Dan (4303)
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on June 09, 2012
at 02:30 PM
First, this study is on rats. The rat model has long been known to be an ineffective model for human extrapolation, and results are often quite different when research based on rat models is done in humans. Even the authors state that before any conclusions could be drawn, the research would have to be repeated and would need to duplicate in humans.
Also important is that -any- piece of information like this, separated out of its natural system, becomes, in a way, irrelevant. If you are forcing a problem in a closed system, the results are going to be much different than in an open system with natural checks and balances in place.
Last, we know that when we impact the body's macronutrient ratios, each person has a very individualized response. I'd suggest that in a natural, biodynamic system, with healthy food raised in its natural environment, with humane treatment and humane slaughter methods for animals/sustainable harvest methods for plants, you're going to see a much different picture of how foods respond in the body's systems than you will with commercial, "plastic" foods full of chemicals and processed to death. I can extrapolate that since this has been the case with me, and with countless others, it is likely true with many, if not -all- humans... and further extrapolate that, if the rats were fed real food that was high in fat and protein from natural sources instead of processed rat chow (which, if you've ever read the nutritional breakdown, you'll find is EXCEEDINGLY high in empty carbohydrates from processed grain, malt, and corn extracts in addition to being high in fat) a more subtle and less incriminating pattern would emerge.
Then, too, papers are published to gain notoriety and advance scientific careers (and/or corporate and pharmaceutical interests), and right now, there is a huge emphasis on obesity, as if curing our fatness will right all the wrongs in our current civilization. We don't understand the true implications of 90% of the research we publish, and I say this as an academic with a number of papers under my own belt -- but NOBODY who publishes scientific literature is going to say too loudly "We simply don't know what this means"... because that will NOT get a paper published!
That's my two cents, for whatever it's worth (Probably not even 2 cents anymore. chuckles)
on June 10, 2012
at 05:40 AM
Rat studies are extremely fallible when trying to prove that something harms a human. Not just because it's another species, that is sometimes the reason why, but also because we humans aren't living as lab rats. Some humans are living like lab rats, and it impairs their metabolic machinery so otherwise beneficial nutrients become hazardous. It seems absurd to me to keep blaming the macronutrients when they can't be metabolized properly, as if it's their fault. Let me explain.
Metabolic syndrome: Wonky metabolic machinery and abnormalities of metabolic functioning. A nutrient needs to go somewhere, but it can't because the body is so dysfunctional, so it goes off track and damages something, going where it's not supposed to. Hyperglycemia is an example of poor glucose metabolism, the glucose reaches a concentration where it damages the circulatory system and everything in it. Lipotoxicity is where fatty acids can't be cleared quickly from the blood or the cells and it builds up, overloading the cells, causing them to downregulate insulin sensitivity, and causing the fatty acids to be metabolized to harmful things, because they metabolic pathways aren't overloaded like the normal healthy ones. Neither of these maladies is caused by the macronutrient in question but by the inability to metabolize it, and so why should we think that BCAAs are any different?
Some examples of high fat reductionism refuted:
The dreaded high fat rodent murder diet doesn't actually cause metabolic syndrome in rats! It only does if the diet is deficient in omega-3 fatty acids or other nutrients. http://www.sciencemag.org/content/237/4817/885.abstract The mechanism is likely that omega-3 fatty acids are PPAR a and g binding ligands and facilitate peroxisomal beta oxidation so that they can prevent lipid overload. The long chain saturated fatty acids need to be broken down in peroxisomes, this means that palmitic acid and stearic acid get a bad reputation because when the peroxisomes don't do their job PA and SA are the most lipotoxic (because they really really really can't be metabolized). Also lowering inflammation from the get-go would really allow the cells to activate thermogenesis of fatty acids because there would be less leptin resistance impairing uncoupling of fatty acids. This also helps to clear the excess fatty acids. Lowering inflammation would also allow for better AMPK action, which also governs fatty acid metabolism. All of this allows the fatty acids to be metabolized quickly and efficiently so they don't build up or spill places where they will cause harm.
And you could do this with a wide variety of nutrients, I'm sure. And exercise http://www.ncbi.nlm.nih.gov/pubmed/20631645 Anything that prevents inflammation, oxidative damage to important metabolic structures, activates gene expression in a pro-metabolic way, etc. If that "high fat" diet was sufficiently low in omega-6 fatty acids we could probably expect to see better metabolism of saturated fatty acids too. But oh no, "high fat" bad.
Even though all of this knowledge is available people still think that feeding rats processed goo with synthetic vitamins, keeping them cooped up in a cage and stressed is a reliable model for how fatty acids behave in humans. Give-me-a-break. I can't exactly refute the BCAA thing (in rats) right now but let's see them demonstrate the same thing in healthy, exercising, nourished humans. Except that the biggest sources of BCAAs in humans prevent insulin resistance http://www.ncbi.nlm.nih.gov/pubmed/20377924 So if the best source of BCAAs in the human diet fails to cause insulin resistance, in fact the opposite is true, how can we even think of trying to extrapolate isolated BCAAs in a malnourished rat's diet to humans?
Yeah, I don't know either :D
I really doubt that this finding is applicable to healthy humans. And it may indeed be a situation where rats are just the wrong species to study.
Edit: and what do you know, even pure BCAA supplementation in exercising humans has no effect on body fat or glucose metabolism http://www.ncbi.nlm.nih.gov/pubmed/9051392
on June 04, 2013
at 12:56 AM
I've been following hyperlipid for years. He's mentioned this before, definitely back when he did a series on palmitic acid.
The liver regulates blood sugar for the brain, so in an environment where the liver is the monopoly provider of glucose, and there is plenty of fat and ketones around for the rest of the body to run on, it makes sense that we become insulin resistant. It keeps the blood sugar available to the brain.
Now, if you have a diet with plenty of carbs for both your brain and your muscles, yet you have insulin resistance, then you have a problem.
So, yeah, the study might be crap, but the general premise is correct.
on June 03, 2013
at 11:57 PM
Interesting, I'm going to go a little against the grain and tentatively agree with that study.
on June 09, 2012
at 11:55 PM
plus, the right attitude towards medical papers to adopt is that they bring some clues on what is going on and that other independent research teams must confirm the previous results [for a drug say, generally you move from a study showing some effects but with a small group of patients to a double blind placebo controlled study with more statistical relevance some months or years later].