Unfortunately Excel doesn't do nice sweeping curves, so I've mangled it by eye to a straight line thus:
Which is still very convincing. Slightly less convincing is when the choice of different countries from the same data bases suggests that dietary fat has nothing to do with heart disease and that heart disease is very rare anyway:
Of course choosing a few other countries might have given a negative correlation:
And, with a little effort, we can see that if only we could just get everyone's fat intake above 40% of calories heart disease would be a thing of the past, just so long as we chose the correct countries to look at:
So let's stop playing and look at the whole database from which Keys carefully selected his six countries:
OK, there IS a correlation. It's pathetic, especially compared to the original line swept in by Keys. Of course things get worse if you add in the Masai, the Inuit, the Rendile, the Tokelau and a few others, shown as red dots:
At this point you would have thought that the name Keys would have become a joke and people would simply have ignored him as a self publicising evangelist with scant respect for the truth. But Keys was nothing if not determined. In 1958, the year after Yerushalmy and Hillebo had shown him to be a charlatan, out came this paper explaining the mechanism by which the high fat diet apparently caused heart disease, even if it didn't. Serum total cholesterol!!!!!! Picture credited to Dr Ravnskov (couldn't get the original).
Of course adding a few data points, which Keys had conveniently forgotten, gives this plot, again credited to Dr Ravnskov:
Anyone for a straight line? These studies are the core of the lipid hypothesis. They are where it all came from and the "science" is total junk.
As a final comment on between nation studies this figure, credited to Dr Kendrick, shows the rates of death from CHD plotted against the percent of a given population who are frankly hypercholesterolaemic. He extracted the data from the little discussed MONICA study:
Obviously living in Russia, Northern Ireland, the Czech Republic or Lithuania is bad news for CHD. Forget cholesterol.
That's as much as there was time for on between nations studies. Essentially they provide absolutely no support for dietary fat or serum total cholesterol as causes of coronary heart disease. It seems impossible that they should have spawned the current climate of cholesterol psychosis, but they did.
Within nations studies comes next.
Peter
OK, time to knuckle down to five very long days at work...
Thank You Peter! Very informative post!
ReplyDeleteBetween 30-40 % dietary fat seems to give highest CHD and TC numbers. Is there any information on their HDL levels? I'd expect them be to be quite low in those high CHD mortality countries.
Peter/All,
ReplyDeleteOff topic...
A short little video clip on why we get fat... just scroll down a bit on this page to view it. It is called "Why You Get Fat."
Simplistic, yes, but an effective manner to promote any topic... just explain it in a cartoon format.
http://conditioningresearch.blogspot.com/
Cheers! Brad
P.S. I made African Stew last night and will eat it today.
Peter,
ReplyDeleteNice. I've never seen the data graphed out. I'll have to go photocopy that paper.
How do I find Key's original data for this?
ReplyDeleteHI Peter,
ReplyDeleteThanks so much for your earlier response with the suggestion for amines etc. Have researched this and think it could well be part of the whole issue.
Off topic I am afraid: On the whole issue of insulin release and sensitivity: I have been testing blood sugar and is always low at 3.1 in the morning and maybe 4.8 at other times. Does this mean I am insulin sesnsitive, or does it mean I have masses of insulin coming in and lowering the sugar? Which way do you look at these things - because of course, this is no indication of the insulin, just the blood sugar.
Also, If I am eating 1500 calories a day and 10g of my food are PUFAs is that OK? Too much?
Thanks, Elizabeth
Great post! I'm just wondering (not being a mathematician) what the trend line does look like for the original data.
ReplyDelete(I'm talking about the picture under which you write 'OK, there IS a correlation. It's pathetic, especially compared to the original line swept in by Keys.')
A quick glance does still seem to indicate in a general correlation between higher fat consumption and death rate, but is it considered to be statistically insignificant? Is there any chance you could add the same graph with the trend line through it? :)
Very informative, and great to read through. It's always amazing how statistics can be twisted to produce whatever result one likes.
I'm very much a layperson in all of this, having been sent here via a Facebook link. So, this is all very intriguing, but I'm also finding it very complex. Is there a (relatively) authoritative source someone can point to that covers the basics of these concepts?
ReplyDeleteThanks!
Peter/All,
ReplyDeleteI found this article interesting, a bit long and general in nature, but worth a reading. Here goes:
http://www.bestlifeonline.
com/cms/publish/health/
Omega-3-Nutrient.php
It suggests that modern humans developed owing to a new nutrient exposure allowing brains to expand in size.
The article is pretty "pro-fat" and laments the loss of Omega 3 fats in our grazing animals, those that no longer feed on grasses and forbs.
Cheers! Brad
Forgive me for being argumentative (as usual, right? ha) but it does appear as if there is a general trend toward higher cholesterol and disease. When all data is included the relationship is not as neat as was originally presented, but there is still definitely an upward general trend between disease and fat.
ReplyDeleteThere is plenty of scientific evidence to support the notion that some fats are inflammatory (saturated, omega 6). Inflammation causes heart disease. Inflammation also leads to insulin resistance, which increases insulin levels and heart disease a second time. Dietary fat itself will prevent carbohydrate from being metabolized effectively, if mitochondria are oxidizing a dearth of fat glucose uptake is reduced, requiring compensatory hyperinsulinemia and all of the effects (further inflammation and vascular/cardiac diseases).
While it's apparent dietary fat does not cause heart disease in isolation (as evidenced by cultures with extremely high fat intakes and no HD), it is true that dietary fat will promote hyperinsulinemia when consuming a higher carb diet, especially if the fats are omega 6 or saturated fats... and hyperinsulinemia mediated inflammation definitely causes heart disease.
The point of my post is that "fat is good" can be just as much of a problem as "fat is bad".
Fat can and does cause hyperinsulinemia, unless one is eating an extremely low carb or low cal diet, and the point at which this happens is dependent upon sensitivity to glucose/insulin disease, which is determined by genetic and acquired metabolic damage.
I've noticed it doesn't seem incidental that those who report being able to eat huge amounts of fat with moderate amounts of "paleolithic carbs" like tubers are those who are naturally thinner even when eating a normal diet. People like me, fatties by birth, numerous carb diseases at early age, could never get away with that crap.
For optimal control of all symptoms I must watch fat, especially if carb and protein intake and calories are higher.
Peter
ReplyDeletei was wondering about one thing conserning the ON. When you count protein, should the protein in the potatoes be calculated? like from 400g there is 15g protein.
Hi Stephan and Anna,
ReplyDeleteI've emailed the Y and H paper.
Elizabeth, you can't say, you could either be very sensitive with low insulin levels or producing more insulin per unit carbs than you need, which salicylates can cause. Provided you feel ok with a glucose of 3.1mmol/l I would just get on an sort other issues before worrying about it. You know your total insulin exposure per 24h will be low if you LC compared to anyone on SAD like food...
PUFA at 10g/d would be difficult to reduce while still eating food!
Jedidja and ItsTheWoo,
Can't remember what the correlation coefficient was but even Keys noted that there was a similar correlation for sucrose, but he knew it was fat that was the problem. He and Yudkin argued this out in public. Keys was listened to, Yudkin was correct.
Keys moved the fat goal posts several times before eventually deciding that omega 6s were good and animal fats bad, because omega sixes drop TC and he had decided TC was the problem. Re correlation, to go back to Eades' illustration, long belts cause obesity and CHD. All we have to do is close down the men's department of Marks and Spencer to end both obesity and CHD, no obese person wears a 28 inch belt... make them all shop at GAP or River Island.
Mark, everything is a bit spread out. You could try
http://www.thincs.org/
http://www.cholesterol-and-health.com/
http://www.westonaprice.org/
and work outwards from there. It's also useful to keep thinking, none of us has all the answers or agrees completely. That would be boring!
Hi Brad, I think most of us who visit here are fairly pro omega threes in moderation, and anti omega 6s too. Need to have a read there. I feel there are a few other factors thrown in...
Mr S, Nutrition Data gives 2g/100g boiled weight, so about 8g/400g fresh weight, slightly less for peeled. I've generally ignored the protein in spuds, probably quite incorrectly, but I try and relax about a few grams of protein here and there. I try to relax full stop. Difficult with a long ops list and a practice secretary who calls you Tigger!
Peter
The correlation coefficient for all the data (excluding the added red dots) is about 0.5. The weak association is there, I would guess for the reasons ItstheWoo says, but that's all it is an association... not a cause.
ReplyDeleteThere is a brilliant paper (I have it somewhere) by a statistician who worked for the UK dairy board in the 1970s where he showed mathematically that the probability of Keys having chosen his 6 or 7 countries 'by chance' (e.g. with a pin and a blindfold) and thus getting such a strong correlation was very very small. In other words, he was very politely trying to imply that Keys had chosen his data deliberately - seems obvious to us now, but maybe in those days, they were more reticent about making such accusations. Also, he did work for the dairy companies...
The thing is peter that the relationship between fat and heart disease has a real physiological mechanism. It is not simply "correlation" like the association between plus sizes and obesity. I outlined them, but I'll do it again.
ReplyDelete1) High fat intakes promote hyperinsulinemia when eating carbs with the fat, and hyperinsulinemia promotes inflammation which promotes heart disease.
2) Omega 6 and saturated fats promote inflammation, and inflammation promotes heart disease.
3) High fat intakes promote high calorie intakes which promotes hyperinsulinemia thus inflammation thus heart disease.
I am on board with you here, I agree that a fat-based metabolism is the way to go, but my point is it is a mistake to say "fat is good". Fat is only good if you are eating next to no carbs, if you are eating a moderate calorie intake, if you are not eating excessive protein. For the general population, fat is not good... fat is only good if it is displacing carbohydrate calorie for calorie.
I'm being anal and argumentative I suppose but it seems significant to at least mention that there is a grain of truth to the hypothesis that fat promotes heart disease (thus the positive correlation exists even if not as strong as once thought when all data is considered).
Re: elizabeth:
ReplyDeleteA low morning glucose might suggest adrenal insufficiency, not hyperinsulinemia. Hyperinsulinemia and diabetic-like conditions will usually have sugar lower in the evening time and higher in the morning. If sugar is lower in the morning, this suggests glucose output is insufficient during fasting overnight due to a weak morning cortisol response, which suggests adrenal insufficiency.
Do you have changes in skin pigment, weakness, dizziness/faintness especially when standing, poor appetite?
Elizabeth I just found the post you wrote earlier about the inflammation reactions even on an elimination diet (just fat/meat)... amines could be a possibility but it is also possible that insufficient corticosteroids makes your inflammation response hyperactive. Eating produces inflammation and without sufficient cortisol this may account for streaming bloodshot eyes and other bizarre reactions to food. The immune system goes into overdrive when there isn't enough cortisol. Given your low morning blood glucose, and perhaps fatigue, maybe this is something to investigate.
ReplyDeleteWoo,
ReplyDelete"Saturated fat causes inflammation"
What's the source for this?
Isn't body fat mostly saturated? If I'm supposed to live off it when food is scarce, and it's bad for me, then mother nature screwed up big time. Which it does sometimes. But I don't thinks so in this case.
"High fat intake promotes high calorie intake"
Probably more like tasty food promotes high calorie intake. Eat a stick of butter by itself. Fuel. Nothing more. Drop it on a big stack of pancakes with warm maple syrup. Good eatin'!!!
"High fat intakes promote hyperinsulinemia when eating carbs with the fat"
ReplyDeleteItsTheWooo, can you point to
where you got this from?
After seeing last graph I have to comment from Czech Republic. It's true that consumption of fats, especially saturated fats, is and always has been relatively high, but I would guess that the cause of high incidence of CHD here is the wheat and refined sugars.
ReplyDeleteTypical Czech daily menu looks like this: breakfest - wheat bread with something, lunch - meat with something based on wheat (alternatively potatoes or white rice), afternoon snack - bread or cake, dinner - there you go again, bread.
Given the amount of diseases connected with gluten and high carbohydrate intake I would blame wheat and refined sugars (you can find prospering sweetshops even in small towns) rather than fats.
I remember that when I was eleven or so, I was wondering why almost every old person is so fat, and that was still during communist regime before we started eating western processed unfoods.
Hi ItsTheWoo,
ReplyDeleteThe production of pathological insulin resistance is quite straight forward, you just need to replace starches in the diet with sucrose.
Yudkin found (he doesn't give the refs in Pure, White and Deadly) a significantly better correlation between CHD and sugar than Keys did for fat and this was confirmed in an independent analysis of 20 countries by a Japanese group, without Keys style selective data choice. Yudkin then went on to intervention studies replacing starch with sucrose and leaving everything else as unchanged as possible. About 30% of his volunteers gained weight (5lb in 2 weeks), raised their insulin levels and developed hypersticky platelets. In two weeks you can start metabolic syndrome in 30% of apparently healthy men using sucrose. The situation almost, but not quite, reverses in a further two weeks of normal eating.
You cannot do this with fat, saturated or otherwise, under isocaloric intake. In the real world fat and sucrose intakes are usually associated together and rise in parallel. You have to decide if it is the fat or the sucrose which raises insulin as it is the raised insulin which stores the fat. Sucrose is a fat better candidate for chronic hyperinsulinaemia than any sort of fat.
The normal physiology remains that fat does regulate insulin levels but humans eating real Food consume relatively little sucrose (compared to sucrose/HFCS being the primary caloric source in a percentage of USA populace nowadays) and random ratios of fat to starches, from the extremes of Kitava through Tokelau to the polar regions, appear to be healthy. None of these populations become obese, hyperinsulinaemic or hyperglycaemic. Sucrose changes that, with the added extras of omega 6s and gluten thrown in I guess.
But real humans, eating real fat and real starches have been doing this for significant evolutionary time periods without developing metabolic syndrome. I can't see fat as the explanation for CHD, particularly not saturated fat. Sucrose has been around in freely available amounts for just over 100 years, it makes platelets sticky and it raises insulin. I don't like that.
Peter
Hi JC,
ReplyDeleteNot so good, but what about the poor Ukraine, about 10% of calories from fat, lowest saturated fat intake in the developed world and I can't remember if the CHD death rate is 1,000 or 1,500 per 100,000. Off the top of the scale in Kendrick's graph anyway.
Peter
OK fixed the worst of the typos! any more I missed?
ReplyDeletePeter
About Ukraine and CHD death rate. As we've discussed earlier ethanol has same impact on metabolic health than fructose in sucrose. According to "WHO Global Status Report on Alcohol 2004" Ukraine has alcohol consumption of 8.0 litres pure alcohol per capita for population
ReplyDeleteolder than 15 for the years after 1995. Could this high alcohol consumption explain part of high CHD death rate?
L - There is a lot of information about how saturated fat promotes inflammation. Obviously metabolism isn't as simple as "eat saturated fat and you will have higher inflammation", it's not that simple because other things a person does can outweigh that... for example, a lower calorie very low carb diet is going to slash inflammation, even if fat consumed is heavily saturated. This is because a very potent inflammatory hormone is insulin, and if saturated fat helps a person reduce insulin (by eliminating carbs) then obviously the net effect of satfat is beneficial.
ReplyDeleteBut for regular people not minding their diets, sat fat IS inflammatory, because they make no other steps to reduce the carb load of their diet.
Fats promote higher calorie intake not because they "taste good", it is because inflammation increases insulin resistance which increases insulin level which makes us hungrier. Do deep ketosis for a few days, and magically food looks disgusting and eating feels unnatural, even if it is delicious pancakes with butter, they will look repulsive. The pancakes with butter only make us ravenous when we are actually eating them, screwing up our metabolism.
Since fats promote reduced uptake of glucose (again, do a search about it, high fat intake will slow clearance of glucose and require more insulin and subsequent inflammation) it is logically true fats promote higher calorie intakes in the context of mixed (carb-filled) diets.
Kiwi, when scientists want to make a lab rat fat and diabetic they feed it fat, and they do so because fat will make their cells resist oxidizing their normal glucose chow, which increases average blood sugar, which increases insulin & promotes metabolic changes that cause obesity and diabetes. There is lots of information about the relationship between fats and insulin resistance, this research is where the myth that fat causes obesity got started. You can search it out anywhere.
Peter - I agree completely that sucrose has a much stronger relationship with obesity and heart disease than does fat, or any kind of fat. My point was to say it is not black or white, just because sugar is the biggest problem doesn't mean fat has no role in this epidemic because it does.
Which is more disease causing... feeding a hypercaloric diet containing high fat with high carb, OR feeding a hypercaloric diet containing carbs with lower fat? Everything is equal otherwise. Over and over it is shown the former is more fattening diet, if you want to get fat and sick, eat a hypercaloric diet of both fat and carb. Even if eliminating the carbs makes fat benign (if fat increase is proportional to adequate carb decrease) it still is significant that fat PLUS carb is more disease causing than carb alone.
The correct interpretation is "carbs are worst, but don't overdo fat either unless you are specifically on a diet that contains borderline ketogenic carbs if you are at all vulnerable to metabolic disease".
Instead we are doing this 180 saying "fat is not the problem" when its just as untrue as saying "fat causes HD"... it's fat with carb with lifestyle (sleep, stress) and all these dynamic factors mixing together.
I don't know if it is correct to blame sucrose either, I know I could mightily get fat on a diet of potatoes, starchy tubers, and beef / butter...
I don't think it is any one thing.
Very interesting analysis. Just for your knowledge, there is a lot of this type of data available in Excel format at http://www.heartstats.org/atozindex.asp?id=8 I think it would be quite interesting to do the same analysis with more current data. Thanks for your website and work.
ReplyDeleteHi ItsTheWoo,
ReplyDeleteI know it's just observational but Dr Garemo found that (based on 7 day food diaries) 4 year old children with BMI >25 ate 52g/d fat and 204g/d carbohydrate of which 48g was sucrose. The BMI <25 children ate 55g/d fat and 191g/d carbs of which 44g were sucrose. I find it difficult to see how eating more fat within a free choice situation could be responsible for the incidence of BMI >25 as the fat intake was highest in the slimmest children. Rat studies are notoriously difficult to dissect out and the rats usually have no choice about eating what they are given. When give a choice they are usually better than swedish children at making pro fat choices if they are going to stay slim or avoid diabetes.
I think we have to look further at what influences food choices and satiety. Obviously the overweight children were eating less protein, so may have been driven to eat more empty calories to get adequate protein for growth through poor food choices.
Interestingly absolute energy intakes between heavy and light children were the same and energy intake per kg bodyweight was significantly lower (p<0001) in the overweight children compared to the slimmer ones.
The paper is a bit difficult to pick apart but I find it interesting. Might put it up as a post some time now the full text is available.
Peter
But yes, keep kicking the ideas around... Personally I do find it interesting that adding 20% lard to a high sucrose rat diet is worse than the high sucrose diet alone. This is real and may have implications for humans if we are going to continue to maintain the essential profitability of Kraft and Unilever while supporting the amazing profitability of Astra Zeneca and co.
Ricardo,
ReplyDeleteGoldmine!!!!!!!!!!!!! HUGS (blushes, we don't do that sort of thing in England). I've been wanting this sort of data for ages. Always too busy to go hunting, and until you find something you have no idea it's worth looking for!
Peter
Westie,
ReplyDeleteYes, but think of all of that marvellous HDL they must die with! They are probably beaten by the Australian aboriginies who apparently have LDL to die for and masses of HDL (alcohol again?). And one of the highest CHD rates in the world.
Peter
Speaking of aboriginals...
ReplyDeleteAnyone know the source for Kendricks aboriginals lipid values? There was none in the book and values that I found from the net did not support what Malcom said in his book.
Dear Petro, some more Excel data: http://www.fao.org/es/ess/yearbook/vol_1_1/site_en.asp?page=consumption and also here http://ers.usda.gov/Data/FoodConsumption/spreadsheets/nutrients07.xls
ReplyDeleteNow we can't complain we don't have freely available statistical data. Please see http://faostat.fao.org/site/609/DesktopDefault.aspx and http://faostat.fao.org/site/610/default.aspx
ReplyDeleteIts TheWoo:
ReplyDelete"Fats promote higher calorie intake not because they "taste good", it is because inflammation increases insulin resistance which increases insulin level which makes us hungrier. Do deep ketosis for a few days, and magically food looks disgusting and eating feels unnatural, even if it is delicious pancakes with butter, they will look repulsive."
You're mixing facts and conjectures here. SFA's definitely not causing inflammation. Your mitochondria prefer it. Your body can desaturate it with enzyme as necessary. Moreover, when you fast (in deep ketosis) it's the fuel that the body burns. Peter made a point sometime ago (with my full agreement) that there's no difference between fasting and eating fat since in both cases the same stuff is being consumed whether coming through the stomach or from the body reserve.
The pre-occupation with insulin-sensitivity has less merit when considering the fuel you burn, if it is SFA/NEFA, needs no insulin for consumption. A much better yardstick for health would be achieving the low baseline insulin when your body at rest and/or needing a minimal amount to process a meal. Guess what kind of food can deliver those twin goals?
Best regards,
John
ItsTheWoo said:
ReplyDelete"There is lots of information about the relationship between fats and insulin resistance"
Think I'll rely on Gary Taubes' massive tomb for confirmation that rats don't count for much. He put in the time (five plus years), reached his conclusions, and saved me the bother.
Yes, good reading for the after-life :)
ReplyDeleteHi Quelle,
ReplyDeleteI had a quick pubmed on aboriginals and it seems they have minimal HDL and any LDL they have is of the small dense type, so I assume they are consuming a diet closely related to what a rat gets given to give it metabolic syndrome, ie fat with sucrose and possibly not a lot else. I was surprised at the low HDL in view of their reputed alcohol consumption...
BTW I would still stick with the diet being the problem and the lipid changes reflecting the diet, rather than the lipids being the problem per se. Impossible to seperate the two aspects though.
Peter
Its the Wooo stated that saturated fat causes hyperinsulinemia. No, it's the high amount of carbs in our western diet that causes hyperinsulinemia. Hyperinsulinemia leads to inflammation, which leads to heart disease, among others.
ReplyDeleteHi Michelle,
ReplyDeleteI think we have to be very careful here. High carb intake undoubtedly leads to severe hyperglycaemia/hyperinsulinaemia in the face of insulin resistance, but in normal insulin sensitivity circumstances a high carb intake still allows normoglycaemia with physiological levels of insulin. The nitty gritty is what, in the Western diet/environment causes insulin resistance per se. The Kitavans eat 70% of calories from carbs and do not become insulin resistance. Flooding someone's physiology with artificially raised FFAs immediately induces insulin resistance. The assumption that triggering a normal physiological mechanism explains a pathological state is where medicine is going wrong here. What we need to know is what is disturbing our physiology to upset what billions of years of adaptive development that has worked well until very recently, evolution-wise.
It is very very complex (to me anyway) and it does all have to fit together. Ideas are for kicking around, so everyone is, of course, very welcome to comment. I wish it were as simple as carbs are bad!
Though that is certainly true if your metabolism is damaged enough for you to be insulin resistant...
Peter
ItsTheWoo...
ReplyDelete"High fat intakes promote hyperinsulinemia when eating carbs with the fat..."
Read what you said again. WHEN EATING CARBS. Why does this matter? The nutritional definition of carbohydrate is sugar. All carbs are sugar. Even fiber is sugar, but you can't digest it, so it does nothing to you. Every one that you can digest, though, raises insulin levels.
Why would fat not raise insulin levels in the absence of carbs, which is the reverse implied by your statement? Because fat doesn't raise insulin. Therefore, fat does not cause hyperinsulinemia.
By the way, I'm a fattie too. If I drop the grains and sugar and eat lots of fat, I do lose weight and experience far fewer inflammation symptoms. (I'd go so far as to say the inflammation disappears, but I don't have access to a CRP test to say for sure.) Yes, even saturated. For Pete's sake, I cook with butter and bacon fat. If I forego the carbs, I thrive on this stuff. If I re-introduce them, I start swelling up again and my hands and joints bother me again and life is generally unpleasant.
It isn't the fat. Period.
Hi Dana,
ReplyDeleteAgain, you have to be very very careful about the data you are using. There is absolutely no doubt in my mind that a high level of free fatty acids in the blood stream will divert metabolism from glucose to fatty acids and that this phenomenon can be described as insulin resistance. Eating a high fat meal will invariably raise free fatty acids in the bloods stream and produce this perfectly natural selection of fats for the metabolic substrate.
The problems occur when it is impossible for the body to get the balance of fatty acid consumption aligned with glucose utilisation.
From here you have to go in to the causes of the metabolic syndrome, MS.
But while pathological failure of energy control (MS) is a disaster when you consume but cannot use glucose, it is no problem at all when you consume fat. You may well have a slightly higher fasting blood insulin than a healthy carb eater, but it will be miles below an insulin resistant carb eater.
Living on free fatty does not fix insulin resistance, it side steps it by making the energy source suit the injured metabolism. Ketone bodies do an even better job. Trying to live on carbs when you have broken your metabolism is very difficult. Going in to exactly what breaks your energy control system is very complex, but it is notable that the manouvers which ameliorate metabolic syndrome best, ie moderate ketogenic diets or fully paleolithic non ketogenic diets both control appetite spontaneously. Energy through put seems to be very important.
How well a given person responds to ketogenic or paleo diets probably depends very heavily on where you have been metabolically in your earlier life. I know full well that ItsTheWoo has a very interesting life history and does not find anything metabolically works particularly well without specific planning/control from herself. That's a very interesting situation that very few of us are (hopefully) ever likely to experience...
But the upshot of all of this is that I would expect that a healthy well fed Kitavan would probably have a lower fasting insulin than an equally healthy northern hunter gatherer living through late winter on plentiful cariboo fat, not by much but by some. The area under the curve for insulin and glucose would be lower in the HG over 24h, but both individuals would be functioning within normal physiology and be healthy.
Peter
Hi Peter,
ReplyDeleteThank you for this eye-opening post (for the neophyte).
You mention that you think a moderate amount of supplementation of Omega 3 fish oil is good to do, but moderate the comment if one drinks a fair amount of alcohol.
As background, I was told my FBS was in the pre-diabetic range last January (checked old blood tests and it has been around 100 for over 10 years) and that I have reactive hypoglycemia. This led me to the Blood Sugar 101 website and a whole new world of information that contradicted everything I thought I knew about diet and exercise. Linking to Jenny's blog list led me to many others, including Whole Health Source (I sit at his feet!) and Stephan's blog list and you. All of the thinking and information is new to me and jaw dropping.
I am now LC with no grains and supplement with D, A (cod liver oil), and K2(butter oil). I also take 4000 IU Omega 3 fish oil. I still drink about 15oz of red wine each evening. I do not eat organ meats.
Now I am curious to hear what amount of fish oil you consider safe, given my alcohol intake?
Sorry for the long post, and I hope you don't mind the personal nature of my question in your comment section.
Hi Nick,
ReplyDeleteI'm not sure that I, or anyone else, can set exact limits on what you can and can't do. As you are well aware, alcohol intake decreases the risk of CVD. You have to appreciate that there is no decrease in all cause mortality, the lower CVD deaths being roughly replaced by cancers, primarily of the digestive system. But this is in the context of eating the SAD, which ever country you live in... If you are eating a LC, low omega 6 PUFA diet then no one has researched your risk factors for anything, as there are currently no populations eating this way in a study-able manner.
If you eat a largely animal fat based diet where the predominant fats (and total caloric sources) are either saturated or monounsaturated fats you will cope far better with alcohol that if you eat to the ADA food pyramid homicidal diet. Under a low PUFA diet I can't see 5g/d of high omega 3 fish oil doing any harm, merely because it is such a small percentage of your total fat intake. You don't need very much DHA each day unless you are drinking vegetable oil as if it was a health food.
A few things I have noticed since LC eating re alcohol: I don't crave it much, I get very drunk very easily, I get minimal hangover. Richard, over at Free The Animal (http://www.freetheanimal.com/root/) has discussed a moderate alcohol intake and might have looked at the literature rather better than I have...
HTH
Peter
Hi Peter,
ReplyDeleteThank you for your thoughtful response. I'm new to the LC diet - since February of this year, so I am still trying to sort out all the changes. I am still having cognitive dissonance with regard to eating any kind of fats beyond a certain amount, which means I am likely eating more protein than I need (8-10% carbs from dairy, nuts and vegetables). I don't eat any PUFA oils unless unwittingly when I am in a restaurant.
My experience mirrors yours with regard to alcohol, except I have to be very careful to eat when I drink, as alcohol can send my blood sugar very low, which I originally mistook for feeling under the influence.
I recently read Cordain's book after browsing Stephan's nutrition hall of fame. Other than his dated opinion of saturated fats, I noticed two pieces of information that I have not seen on any of the LC blogs -- that testosterone is reduced on an LC diet and that highish salt intake disturbs sleep.
Both topics are interesting to me and I wonder if there has been much discussion about each, though sleep is a very complicated subject. I would swear that my libido has decreased with the LC diet (though I suspect simultaneously giving up my 3x weekly three mile sprint/jogs may be more telling in this regard).
Thanks again.
Hmmm, I was unaware of any lowering of testosterone on LC unless it is accompanied by a fall in testosterone binding protein, which then increases free testosterone. I think I read this somewhere, maybe 5 years ago. I think if loss of libido was a routine feature of LC eating the Ornishes and his like would have made very sure we all knew about it! I have to say it's not an effect either my wife or I have noticed.
ReplyDeleteAs LC fixes PCOS I don't see why it should fix one problem and cause another....
Cordain is the weirdest guy. If he says something is so, I want to read the studies myself, in detail. He is undoubtedly being rehabilitated on the net after his idiocity on saturated fats, but he still has his name on some pretty unsavoury pro statin papers.
Personally I'm eating about 10% of calories as protein (my diet is adequate protein, lowish but not ketogenic carbs and high saturated fat) and because I eat real food my only real sources of salt are cheese and bacon. Obviously, I'm not paleo, but I listen to what paleo tells me. I doubt I'm high salt or low enough carb to have problems (phew).
Why dairy and not full paleo? The gifts to humans from plants are accidents or poisons. The gifts from cows are health giving to a calf, it's own genes. I steal that health....
Peter
The loss of libido was also something I noticed personaly when I went LC. But, it was only transitional, after some time it got again as it was before. I suppose it has to do with the change in metabolism, not with the food itself.
ReplyDeleteHmmm, maybe like the hair loss that some people get. Can be spectacular but transient...
ReplyDeletePeter
Hi, where can I get the original data used in this post? Could you send me the articles you used in the post.
ReplyDeleteThanks
miguela71@yahoo.com
@ the first graph: Excel will do a smooth line. Choose Scatter Data with Smooth Line.
ReplyDeleteOnly a naive person would look at that last graph and assume that there's no connection between high cholesterol and heart disease. There are simply other factors at work here. Russia, Northern Ireland, Lithuania, and the Czech Republic have very high rates of alcoholism, and countries like Iceland, Belgium, and Switzerland have excellent health care systems. The Swiss also live at a high altitude which is said to confer cardioprotective benefits. And a time lag explains the famous French Paradox, in addition to the undercertification of heart disease deaths in France:
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115846/
Some words on Ancel Keys:
1. Keys selected the six countries because they were the only ones with reliable data which conformed to international standards. (http://www.youtube.com/watch?v=unH-AEDKV8s)
2. You reference Yerushalmy and Hilleboe. Why do you fail to acknowledge the crux of their paper, that other factors correlated with ischemic heart disease better than total fat consumption, chiefly animal protein?
3. Where did you get your data showing low rates of CHD deaths in the Inuits, Masai, Rendille, and Tokelauans? And since these are isolated hunter-gatherer populations, how can you be sure they're not succumbing to heart disease because they simply die of other causes first like infectious diseases and malnutrition?
I've come back to all your posts because of Denise Minger's recent backflip on AHS14, "What we can learn from the vegans". I was quite concerned after viewing her performance because for a few days I was worried about my high fat intake. I'm currently going through your data because when I dropped my fat intake my hunger skyrocketted and my weight has increased 5 kg, practically 1 kg per week.
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