Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Thursday, December 27, 2012

9 times less atherosclerosis now than 60y ago!


Bryant Webber and colleagues analyzed autopsy reports and available health data from 3,832 service members who died of combat or unintentional injuries in Afghanistan and Iraq and compared their findings to similar studies performed during the Korean and Vietnam wars. 8.5% of the newest group had evidence of coronary atherosclerosis, compared with 77% in the Korean War group and 45% in the Vietnam War group.

Any idea why? Less crisco/margarine?
And this is strange:

Surprisingly, cigarette smoking was not significantly associated with atherosclerosis in this study.



Galina L. said...

My wild guess, solders during Korean war were also leaner than now.

LeonRover said...
This comment has been removed by the author.
LeonRover said...

An interesting snapshot.

So, will the sociological/epidemiological/dietary narrative of sat-fat/cholesterol/atherosclerosis heart disease be changed in any way?

(I do not think so!)

I have noted proposals that would result in mass blood testing for teenagers for "cholesterol" and subsequent "statinising". This result ought to be road-block to same, but will it.
(I doubt it.)

I did not see whether the atheroslosed hearts showed any evidence of chlamidia pneu. bacteria.
(I am a sucker for the Helicobacter explanation of stomach ulcers as a narrative which ought to humble those in other clinical fields.)

(For "holiday" re-reading I dipped into Le Fanu's "The Rise & Fall of Modern Medicine" and then a review of LRC-CPPT. I noted (again!) that the proposed significance level of 1% Pre-Trial was altered Post-Trial to 5%. Ever since noting this, I have refused to accept that "epidemiological" results apply to ME unless results have significance of 1% - tho' preferably 0.1%. PS I spent a part of my professional life using stat methods.)

Peter said...

Stan, I haven't looked at the epidemiology well enough to be confident with time scales and consumptions but here are some thoughts:

I am coming to the idea that hyperglycaemia may be more problematic than hyperinsulinaemia. Hyperinsulinaemia may well have its own problems but insulin does have a number of benficial effects. Independent of weight we have sucrose as a primary driver of insulin resistance and so, on a carbohydrate based diet, of hyperglycaemia.

So rising sucrose intake produces rising hyperglycaemia and early onset arteriosclerosis.

Adding in corn oil or soya oil reduces insulin resistance, especially of adipocytes, and so moderates hyperglycaemia at the cost increasing fat mass through increased adipocyte insulin sensitivity. While ever adipocyte insulin resistance is blunted by PUFA hyperglycaemia can be controlled within the limits of insulin secretion from the pancreas.

Arteriosclerosis is then delayed until enough distention has been produced in adipocytes to re establish insulin resistance and subsequent hyperglycaemia.

The parallel is with the thiazolidinones, obesogenic effects blunt insulin resistance.

So the age of onset of arteriosclerosis can be delayed at the cost of obese service men. Or hungry non obese service men.

That's the logic.

I hate to have anything complimentary to say about PUFA but I see the logic pointing in that direction re hyperglycaemia. Of more concern is the failure to induce insulin resistance (by PUFA) when it is protective. Be interesting to see if this is why PUFA are so strongly associated with cancer.


Stan (Heretic) said...

Hi Peter,

I have been thinking about it but it seems that the mechanism you have described may equally apply to PUFA being protective against hype-insulinemia as well as hyperglycemia. R.W Stout's papers on rats from 1969 indicate that atherosclerosis is most likely the result of a conjunction of the two factors: hyper-glycemia simultanously with hyper-insulinemia.

From my observation of prediabetic people "progressing" into full diabetes, the main onset of diabetes t2 takes place not during the time when they put up weight but when they stop gaining weight!

It would agree with the idea of adipocytes expansion sucking out excessive glucose and while doing so, insulin resistance has to be reasonably low or normal, not too high. It is when the ir is beginning to rise when the problems arise because it leads both to hyperins. and hyperglyc.

One of my friend on the diet debate forum is a lady in her 60-ties who recently had a heart attack, after stabilising her diabetes maintaning normal glucose using a low fat vegetarian diet. A question is what has triggered her MI? Her glucose level has always been normal! My guess is that it was hyper-insulinemia, but I am not 100% sure. Other ultra low fat vegans are able to maintain heart attack free by completely avoiding any saturated fat. Again it would agree with your mechanism.

1940-ties and 50-ties was crisco (partially saturated fat) plus butter plus lard plus lots of bread and starches! Ideal condition for h.g. & h.i. What Kwasniewski refers to as a "pig trough" diet. When they replaced saturated fats with PUFA their heart risk has reduced somewhat but other chronic diseases like cancer went up, somewhat.

It also explains why most American medical "scientists" became hungup on the idea of cholesterol-heartdisease infecting the rest of the world with this sick belief system. Hyper insulinemia with hyperglycemia being a preconditions for anomalously high serum lipoproteins, in normal non FH people.

Best regards,

Stan (Heretic) said...


That may tie with Peters comments, they were leaner but possibly more insulin resistant because of that!

The highest CV mortality documented (30% death rate in 2 years) was among semi-starving concentration camp prisoners who once being released begun eating normal high carn medium fat type of diet and fully caloric.


Peter said...


Fully agree that insulin and glucose are very hard to tease apart. I keep going back to Veech's early work on ketones vs insulin/glucose, and their effect on the inner mitochondrial membrane potential. Ketones drop it, insulin/glucose doesn't, but insulin has "other effects" on the ETC which maximise muscle work in a similar manner to ketones. Using an isolated heart prep.

Then I picked up in an essay by Nick Lane that insulin phosphorylates ETC proteins, so I'm thinking this is another avenue to follow. And it may well be Veech's mechanism. His comment was that something "covalent" occurs in ETC proteins. Phosphorylation fits the bill.

What is wrong with hyperglycaemia is the ingress of glucose WITHOUT the modulation of ETC function by insulin because cells are insulin resistant.

Quite why glucose doesn't just abort to lactate under these conditions (neither fructose nor insulin free glucose would produce the insulin induced activation of pyruvate dehydrogenase complex), the way fructose tends to, is another avenue. Perhaps it does...


BTW I removed a comment from the first comment, adding that I suspect a simple switch from PUFA to sat fats WITHOUT carb restriction is a potential disaster. Replacing carbs with sat fats seems ideal. But this ties in well with your comments from the vegetarian fora.

Synthetic trans fats are another very interesting subject but I've not had the time. Just I've seen they increase fat oxidation. Now how do they do that...?

Galina L. said...

I your post I see a connection between the phenomenon you described and the prevalence of the obesity in US . I recently went to my native Russia for a two-month visit. It is astonishing how thin a general crowd looks there when I compare it with people in Florida, US, where I reside now. I know that Russians are not more healthy, their mortality rate is actually much worse. Your post about solders having worse atherosclerosis 50+ years ago made me think about people from another countries who do not suffer the same obesity rate as Americans, and whose example is often present in comments like "why Asian people thin?" , "why does French paradox exists?". In everybody's minds health equals thinness, and thin sufferers of maladies of Western civilization often got ignored.

Stan (Heretic) said...

There is a widespread view that pancreatic insulin is a benign accelerator of metabolism (under high carb diet) and promotes anabolism which also seems desirable, especially by athletes.

I don't think that insulin is as benign! I believe that tampering with it by means of ultra carbohydrate diet, by "pig trough" diet or by other means does shorten human life.

For example, your blog posts about mitochondrial metabolism seem to paint a different picture: that of a mitochondrion as an "engine" that has a certain maximal yield that should not be exceeded. Otherwise it will break. Insulin is an accelerator of glucose metabolism that may and probably does lead to "over-reving" of the mitochondrial "engine", which ultimately shortens mitochondrial live span and leads to a semi permanent mitochondrial degeneration that can only be reversed through total tissue rebuilt from stem cells. Which takes years.

Insulin seems like our stress or thyroid hormones - essential in small doses and only at certain times but deadly above certain limits!

There are 2 interesting articles by Dr. R. Rosedale, 1

and 2

that paint a bigger picture.


Stan (Heretic) said...


It is a fascinating thought - that perhaps our often vilified American nutrition "scientists" may have been right about saturated fats being bad - for the wrong reason!

I was born in Poland and while people there were generally thin or only mildly obese (only middle aged), heart attacks were the most common cause of death. Perhaps the reason was the "pig trough" diet high in saturated (animal)fats as well as high in starch, sugar and (ahem) alcohol.

Saturated fat protects against excessive obesity at the expense of triggering high insulin resistance (on the high carb diet) and thus leading to hyperinsulinemia and earlier heart attacks or early onset of arteriosclerosis, like in US soldiers in Korea.

Replacing saturated fats with PUFA a la infamous USDA "Food Pyramid", slows down an onset of atherosclerosis and heart disease due to lower insulin resistance and less hyperglycemia, at the expense of causing massive obesity epidemics!

Ultimately, an obese individual becomes diabetic, when his or her adipose tissue maxes out. A heart disease risk follows that, albeit at a later date. The recent American soldiers were too young for diabetic symptoms to show up, but they probably will later on.

Perhaps vegetable oils are indeed less bad than saturated animal fats, on the high carbohydrate diet?!


Galina L. said...

As I understand, you both follow the Dr.Kwashnevsky's diet advise,and the Optimal Diet is not ketogenic. Do you think that 200 grams of carbs are benign, or it is better to make a carbs- containing meal relatively low in fat? Or an intermittent fasting pattern of eating will put everything in place? The thought about my lean and muscular 20 y.old son inspired me to ask that question.

Stan (Heretic) said...


200g of carbohydrate (glycemic load) per day is OK on a high carb low fat diet (30% calories or less) but is not good on the medium or high fat diet. For middle aged people 200g of carb every day plus 40% or more energy out of fat will cause obesity and cause metabolic syndrome. For a young man who is physically active - I am not sure. Perhaps it might not do much harm but it is better to avoid that zone.

Maximum sporadic amount of glycemic load on a high fat diet is 1.5g per 1kg of ideal body weight per day. Maximum everyday carb load is 1g/kg per day. Recommended carb load, on the Optimal Diet, is 0.5-1g/kg.

Mixing versus not mixing. It is a similar question if one can do the high fat LC diet one day and the high carb LF diet the other day. Again I have no concrete data since I have never seen anyone being able to do it. I have seen people starting doing it and inevitably drifting towards and getting stuck in the "pig trough" (medium fat medium carb%). That is not good.

It took me more than 2 weeks to adjust to HF LC, and I heard it may take months to adjust from the high fat LC back to HC LF. Can a young person switch between HFLC to LFHC in a day? May be but I doubt. I suspect it will lead to problems just like a mixed fat+carb diet.


Galina L. said...

Thanks a lot, Stan,for your thoughts.
I will pass it on my son.
It looks like cabbage cooked with a lot of fat is better than potatoes as a side dish. Probably, monounsaturated fat is even better with higher carbs than O6, and Mediterranean diets seem to point into into such possibility.

Sorry, if I occupied too much of your attention.

Stan (Heretic) said...

No problem, I am always happy to do something useful like offering some information. I am having an impression that our mainly work and business focused attention is a mistake and there is probably more value in helping each other than we realized.

Stan (Heretic)

Peter said...


I'm still working at insulin vs hypeglycaemia. It's interesting that Nick Lane, although not a LC advocate, keeps moving (being pushed by the data) that insulin = live fast, breed now, die young.

I'm still very keen to follow his links on electron spillage from complex I (which is directed, not random) and then go looking for other sources of free radicals in the ETC and what they do differently from fatty acid input under LC.

I also want to go looking at electron transport through the ETC, which is a quantum mechanical movement, like a very complex tunnel diode. Lane keeps saying stuff which makes sense from our point of view.

But I still feel I'm at a very basic physiology level before moving on to pathology...

All the best to all


Anonymous said...

Forbes statement "Surprisingly, cigarette smoking was not significantly associated with atherosclerosis in this study." is peculiar.

The study is clear about the effects of smoking: "This 40% reduction in smoking prevalence within the military since the end of the Vietnam War likely contributed to our results."

Anonymous said...

Stan thanks for the further elucidation in the comments. You're very good at making complicated data make sense. Thanks for your blog.


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