.. to prove that cholesterol and eggs were supposed to be harmful, in the most recent Finnish study:
Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study
I respect persistence, dedication, efforts and resources devoted by the world medical establishment to their long term goals. I believe that no civilian scientific project ever, in the history of science, commanded more time, efforts and money than attempting to prove Ancel Keys' cholesterol theory of the 1950-ties! Probably more so, if we include the R&D efforts by the pharmaceutical companies, than even the space programs.
Quote:
Conclusion: Egg or cholesterol intakes were not associated with increased CAD risk, even in ApoE4 carriers (i.e., in highly susceptible individuals).
(Thanks JC for the link alert)
14 comments :
In the highest control group, the study participants had an average daily dietary cholesterol intake of 520 mg and they consumed an average of one egg per day, which means that the findings cannot be generalised beyond these levels.
Not exactly HIGH cholesterol.
Hi Charles,
I didn't see the full paper, it is paywalled so I cannot comment on the methodology. Interestingly, similar null or inconclusive results regarding direct effects of dietary cholesterol vs risk, were obtained even in the earliest studies (Framingham, 1960-ties) and they still haven't learned anything from them. There is nothing preventing any of the nutrition research team equipped with these kind of financing to pick a wider dietary range or even conduct an active intervention study rather than observational statistics. Even after half a century, for some strange reason, that has not yet been properly done (there are only very few minor partial intervention studies).
Regards,
Stan (Heretic)
Hey, let's be fair to poor Ancel. He's got a lot to answer for, but not this.
"The evidence—both from experiments and from field surveys—indicates that the cholesterol content, per se, of all natural diets has no significant effect on either the serum cholesterol level or the development of atherosclerosis in man." -- Ancel Keyes, 1955
So the knuckleheads who did this study have no excuse.
(I'll post the link to that if you want, but too often it causes comments to go to the spam filter.)
You are correct, he may have backtracked indeed by the end of 1950-ties from blaming dietary cholesterol specifically, when it became untenable, but he still remained animal fatophobic. He remained one of the main obfuscator of cardiovascular research during his long life by deflecting public attention away from refined carbohydrates and vegetable polyunsaturated oils, and using his considerable ranking in the medical establishment and US government to squash any research into that aspect.
Coincidentally, major turning point of the public opinion in favor of lower carbohydrate nutrition begun after his death in 2004.
Regards,
Stan (Heretic)
Yeah, agreed. But credit where it's due, no matter how small!
I've been doing a little reading on veggie oils of late. Have you looked into the cardiolipin/4-HNE axis? It appears to be the smoking gun of the metabolic syndrome.
Thanks for the lead. It looks interesting but the papers I googled on 4-HNE seem to concentrate on how to block the pathway rather than figuring out what kind of feeding triggers. There is a mention of Western diet" fed to the mice triggers 4-HNE pathway through excessive radical oxidating species (ROS) generation, which then leads to cellullar and/or mitochondrial apoptosis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4099507/
It seems they are concentrating on a reasearch to find a drug that would suppress the channel rather than finding the primary cause of the process. I am curious as to what exact aspect of the "Western diet" is the main oxidative stressor, excessive carbohydrates? Polyunsaturated fats? Hydrogenated fats or other?
There is an interesting quote:
...This mechanism is further substantiated by the observation that the presence of only one un-oxidized fatty acid (such as oleic acid) in some minor cardiolipin species significantly decreases the formation of this characteristic bioactive lipid and other oxidation product...
Oleic acid is mono-unsaturated, I wonder if there is a benefit derrived from stearic acid a saturated precursor of oleic acid?
Yes, that "interesting quote" is the money quote.
"It seems they are concentrating on a reasearch to find a drug that would suppress the channel rather than finding the primary cause of the process."
LOL. Yeah, of course. No money in giving advice, right?
"I am curious as to what exact aspect of the "Western diet" is the main oxidative stressor, excessive carbohydrates? Polyunsaturated fats? Hydrogenated fats or other?"
Omega-6 Linoleic acid, only.
I did several posts on this recently (full-text links to research where available), when I really started looking into cardiolipin oxidation. The first post discusses what kind of feeding triggers. 100% regression in NAFLD in humans by blocking the pathway through dietary modification, on a high-carb diet! Other things got better too. The smoking gun is in the second paper, where they go through the exact pathway and what causes it, and what happens if you block the pathway (in vitro, in vivo is in the first post) through modifying cardiolipin.
"The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria"
http://yelling-stop.blogspot.com/2016/02/the-cause-of-metabolic-syndrome-excess.html
"How To Prevent Oxidative Damage In Your Mitochondria"
http://yelling-stop.blogspot.com/2016/02/how-to-prevent-oxidative-damage-in-your.html
There are a bunch of other posts looking into some of the other effects. 4-HNE is produced through the other metabolites, the HODEs if I remember correctly.
Although, while LA is the primary cause of this excessive oxidation and free radical generation, since the primary site of oxidation is complex 1, consuming carbs increases the rate of normal ROS generation in cokmplex 1, and increases the rate of CL oxidation, increasing the production of 4-HNE.
But the NAFLD study in the first post demonstrates that that's a secondary mechanism, as it resolved even on a high-carb diet.
It makes a lot of sense! It may explain a curious adaptation phenomenon I observed on myself and on may people who went on a low carb high animal fat nutrition. Initially, our carbohydrate tolerance went way down, we were not able to consume more than 70g or in some cases even less (total glycemic load per day) without hitting some unpleasant side effects.
However after about 5-7 years into it, I noticed I was able to tolerate about twice that amount of carbs with no problems! It is counter-intuitive that the body adapts to tolerate carbohydrates better after a few years without them, but the mitochondrial re-modelling (purging LA out) theory may explain this. The time-scale seems also to be about right since it takes that long to completely regenerate entire tissue (including new mitochondria) from stem cells. Lets check - mitochondria live about 2 weeks times 150 replications per cell makes 300 weeks or ~6 years total lifespan.
It is interesting that it must take growing entire new cells immersed in the new nutritional regime with the new genetic mitochondrial program in them, in order to have mitochondrial cardiolipins (CL) free of excessive Linoleic Acid.
Dr. Jan Kwasniewski of Optimal Nutrition wrote about that in his book "Homo Optimus" saying that in order to have a population completely free of metabolic disease, pregnant women must consume Optimal Nutrition because the adaptation takes place early in the fetus. It would work to some extent if adopted in adulthood but not as well. He did not elaborate on the exact mechanism (probably because it was not back then, in the 1970-ties, yet known...). Very good example of epigenetics!
Best regards and thanks for the links,
Stan (Heretic)
"It makes a lot of sense!"
Glad to hear. I felt like I was going out on a limb in the first post, but the more I read the less I felt that.
People who got LCHF by necessity cut out processed foods, which does reduce a lot of the LA consumption, as the definition is pretty much refined carbs + LA. I think we're looking at a simple function of changing two variables unwittingly.
The adaptation process isn't as bad as you make out: LA concentration in cardiolipin changes rapidly based on dietary changes, in the order of weeks. This may be because it's so rapidly oxidized, that it's rapidly replaced. Haven't found any studies looking at that phenomenon. We don't have to build new mitochondria for the changes to happen. Although I suspect that if you combine LA restriction with an exercise program geared towards mitochondrial biogenesis, you'll see things improve more quickly.
But we do have a big reservoir of LA in adipose tissue, and the half-life is apparently about 600 days, which would get us to that window that you're describing. I also saw a difference after 5 years, and cutting LA out was the first change I made in fixing my diet, and I've been diligent in it.
The biggest change for pale me was that I got much more resistant to sunburn. I used to burn severely in 45 minutes. Now I can go for days at high altitude (I ski) with no sunscreen, and I tan.
Turns out UV oxidizes LA, and 4-HNE is a pretty good marker for skin damage.
http://www.sciencedirect.com/science/article/pii/S0891584903000704
LA is so fragile that 4-HNE production can be triggered just by impact: it's associated with traumatic brain injury, of all things, where you see a surge in OXLAM production. I've become dramatically more tolerant to pain & injury; as I do a lot of sports where I get hurt, I've noticed a literally mind-boggling difference from ante. I know get minor injuries that I don't even notice. It's enough of a difference that I was actually concerned that I might be getting peripheral neuropathy or leprosy. LOL.
Interestingly, I also got much more resistant to sunburns since 1999 when I change my nutrition eliminating most plant based products (including vegetable oils). I experienced many other improvements, too many to list here. I used to think it was due to the low carb aspect but now I suspect it could have been due to both factors: - reduction in La and less carbs. Also much less wheat!
I would like to figure out thattime scale factor - why does it take so long to incur the damage before thee first metabolic syndrom symptoms show up, and why does it take equally long to reverse them. I suspect epigenetics - mitochondria are probably programmed in ("one time programming" OTP) in a new cell once it differentiates from a stem cell. Even if one has body fat storing a lot of Linoleic Acid, most people do not use their own body fat unless they fast, so in most cases if the mitochondrial fat flush theory were true, metabolic syndrome would reverse very quickly from the moment consumption of vegetable oils were curtailed but it does not.
Stan
"...metabolic syndrome would reverse very quickly from the moment consumption of vegetable oils were curtailed but it does not."
It's fairly quick:
"Following the six-month dietary intervention, hepatic steatosis resolved completely in all patients."
http://www.ncbi.nlm.nih.gov/pubmed/26408952
Obviously healing takes time, and some things heal faster than others.
No doubt there's some damage that can't be undone: dead neurons from Alzheimers, for instance; those memories are gone.
They don't mention it in the paper, but since it is a Polish paper, I wonder if they perhaps used Kwasniewski's "Optimal Diet" in the study? Did you read the full text?
I have a friend who cured his liver cirrhosis also in 6 months on Kwasniewski's diet, that was 17 years ago. However, reversal or liver disease,(6 months), or other diseases such as Crohn's and IBS (1-2 year) as per Lutz' data, cardiovascular disease (~2 years, by Kwasniewski's records), asthma (about 1 month) - does not automatically mean that the metabolic syndrome defined as glucose/carbohydrate intolerance would reverse in such a time. That takes about 7 years (based on my observations).
Stan
"They don't mention it in the paper, but since it is a Polish paper, I wonder if they perhaps used Kwasniewski's "Optimal Diet" in the study? Did you read the full text?"
I did. The diet they used was > 50% carbs. Definitely not the "Optimal Diet"!
"...does not automatically mean that the metabolic syndrome defined as glucose/carbohydrate intolerance would reverse in such a time."
While I think there's pretty clear evidence that metsym is a function of mitochondrial function, I don't think that limiting LA alone is enough to completely resolve it. I think in order to do that you'd need to increase mitochondrial function, and not just stop the damage. The best way to do that is exercise, specifically exercising while in a fasted/ketogenic state. Mitochondrial biogenesis (creation of more mitochondria) doesn't happen absent stimulation. (I don't know that this is guaranteed to increase carb tolerance to a "normal" level, btw, but it's certainly been my experience that my carb tolerance has increased a lot while doing this.)
This study shows that lack of fitness alone is a risk factor for diabetes:
"Physical Fitness Among Swedish Military Conscripts and Long-Term Risk for Type 2 Diabetes Mellitus"
http://annals.org/article.aspx?articleid=2499473
I doubt they controlled for LA consumption, which could be an obvious confounder, but it's pretty consistent with what we know about mitochondrial function and health.
Inability to metabolize fat as indicated by high RQ predicts both obesity and ability to loose weight. So fixing that along with reducing LA intake would seem to be the optimal strategy. Of course a LCHF diet is an excellent way to shift RQ.
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