No time to comment, but this is what happens to mice on a high fat diet, IF YOU FORGET TO ADD THE SUCROSE. I have the full text (thank you Luca via THINCS), high fat diet was about 42% of calories from LARD. Oleic acid plus PALMITIC acid (gasp and shiver, oh cardiologist). And cornstarch, no sucrose. Prof Yudkin: Yu wuz right, agin.
BTW fed and fasting plasma insulin levels and obesity were worse in the high fat mice, but at 35% of calories from corn starch that's not surprising. There was no suggestion of the massive hyperinsulinaemia seen in sucrose feeding, but levels were definitely up.
Peter
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35 comments:
Yudkin has a way of being eternally right about a lot of things. No T.L. Cleave perhaps, but definitely one of the best.
"Also, sugar has not been proven to cauuse obesity in the absence of fat, so it's the combination, not the sugar, that's to blame."
Er, no fat in the diet = death. Anyway the amount of sucrose or fructose in foods available to a European hunter gatherer or farmer was tiny and only there in summer until very recently in evolutionary time. Theoretically honey could be eaten in warmer climes if someone was good at finding it but think of the effect on teeth, abcesses would often kill those with a sweet tooth.
Bruce K,
Exactly what is high-sugar diet that both fat-free and starch-free?
A fruitarian diet or a diet of jaggery (as some poor Indians) or diet of sodas (poor Americans or sports drink diet?)
Or the Master Cleanse/lemonade diet...
re Bruce K;
A hunter-gather in a cold climate would have got barely 1% of his energy from fructose or sucrose.
Even in tropical rainforests wild fruit is not available all year round.
Sugar only became cheap and popular in the mid-19th century. Before that it was an expensive luxury.
How much fructose and other simple sugars *were* available to hunter-gatherers in tropical climates?
I'm just wondering, since a couple of commentators are emphasizing "cold-climate" or European hunter-gatherers, which have not been the majority throughout human history.
Even though I'll happily accept that fruit (and therefore fructose) was much less available to our ancestors than it is today, I'd like to see more discussion of non-European and non-Inuit (who seem to come up a lot) forbears. I haven't studied the subject myself, so I just don't know.
Bruce K, I couldn't get into the main body of the study you linked, so instead I dug up something that rhymes with it.
http://jn.nutrition.org/cgi/content/full/136/3/582/TBL3
That's a table from this study;
--------------------------
Chronic Intake of High-Fat and High-Sucrose Diets Differentially Affects Glucose Intolerance in Mice
Intakes of some macronutrients can comprise risk factors for life-style-related diseases such as obesity, hyperlipidemia, diabetes, hypertension, and atherosclerosis. In this study, we examined the effects in C57BL/6J mice of consuming excess fat or sucrose for a long period of time (55 wk). Another group of mice consumed a low-fat, low-sucrose (LL) diet. Mice fed the high-fat (HF) diet gained weight and developed hyperlipidemia and hyperleptinemia. At 25 wk, but not at 55 wk, hepatic glucose-6-phosphatase (G6Pase) activity of the mice fed the high sucrose (HS) diet was greater than that of mice fed the LL or HF diet. Those fed the HS diet were not obese and had greater hepatic lipogenic and gluconeogenic enzyme activities. The HF and HS diets resulted in different types of glucose intolerance. In an oral glucose tolerance test, mice fed the HF diet had a delay in the clearance of glucose compared with those fed the LL diet, perhaps due to the peripheral insulin resistance that resulted from higher levels of circulating free fatty acids. Feeding the HS diet for 55 wk induced hyperglycemia 10 min after oral glucose administration, although blood glucose declined rapidly after i.p. insulin injection. This finding suggests that the effects of chronic HS diet intake may be due to the reduction in early insulin secretion from pancreatic islets and the increase in sucrase activity in the small intestine. It is important to consider the effects of macronutrients in lean as well as obese mice to clarify the pathogenesis of the metabolic disorders.
--------------------------------
The reduced insulin reaction to oral glucose in sucrose fed mice makes sense; fructose doesn't need insulin to be metabolized, so chronic consumption should reduce the cephalic response to other sweet stimuli. So what happens if you don't have an habitual diet, and constantly jump back and forth between sucrose and glucose?
The table I linked at top shows that fasting insulin in the sucrose fed mice is actually only half that in the low sucrose low fat fed mice.
If an animal is forced to make its own fat from sucrose, significant calories are expended towards that synthesis. Another possible factor in the study I posted is that the vitamins and minerals are given as grams per kg, and each diet contains the same g per kg; so the high fat diet is less micro-nutrient dense than the other two diets.
Are absorption of fat in the gut, and synthesis of fat in the liver, in competition with one another? Glycine or taurine are needed to conjugate bile... and both have been shown to reduce fatty liver in sucrose-fed rodents. Maybe the Kitivans, hitting their livers with glucose from tubers, fructose and other sugar from fruit, and medium chain triglycerides from coconut, benefit from a lessened competition by the gut for these, or other nutrients (choline, etc.)?
Once we're talking about combinations of foods, rather than not blaming particular foods-- we're still left with blaming particular foods, just within a particular dietary context.
Not to mention particular strains of mice. (Whoops.)
helen said:
"How much fructose and other simple sugars *were* available to hunter-gatherers in tropical climates?"
Far less than most people would imagine. Most wild fruits are small, bitter and low in sugars. They are also generally inaccessible to humans who are far too heavy to climb to the outer fruit-bearing branches.
Even in the tropics most plants only fruit for a few weeks a year with little or no fruiting during the six month dry season.
Humans would also have to share the fruit with vast numbers of other mammals. A troop of monkeys or flock of birds could easily strip a tree bare leaving almost nothing for humans.
Don't forget the tubers! Many tubers have surprisingly high sugar content. Most hunter gatherers use more tubers when meat/fruit/berries are in shortage. Even in Canada there are places with a high edible tuber output. You just have to look!
http://www.enotes.com/food-encyclopedia/tubers
http://www3.interscience.wiley.com/journal/122305572/abstract?CRETRY=1&SRETRY=0
http://www.swsbm.com/ManualsOther/UsefulPlants/Useful_Wild_Plants-1.PDF
Peter,
Pardon my ignorance, but as an engineer rather than a vet or bioligist, the link tht you posted appeared to be ambivalent about high fat low carb diets. Could you explain in laymans terms?
Cheers - Mark
Hi Incognito, nice link to an abstract for the Hazda, there's been a National Geographic piece recently. The observation that people are slimmest when meat is rare suggests they only eat tubers when there's nothing better! But that shifts the emphasis of of metabolism slightly. Starvation is obviously a fat based condition. If tubers are a routine fall back there would be a weight loss period supplemented by carbohydrate...
MarkD, there are many things in the full text that are not there in the abstract. But the main things to me are that in artificially induced heart failure a "high" fat diet preserves mitochondria enzyme levels where as a low fat diet decreases them. Heart failure is ultimately a mitochondrial failure with shift to glycolysis as a pre terminal event.
The leptin levels merely reflect the adiposity of the mice and the elevated insulin levels are why the mice are obese. If you allow mice to choose their own macro nutrient ratio there is a wide range of choices. The ones which choose >80% of their calories from lard/coconut oil do not become obese, so by definition are not hyperinsulinaemic. If they are not obese it seems a reasonable proposition that they will not be hyperleptinaemic either....
These mice look are not on a sucrose inclusive diet. Look at the trigs, fasting/post prandial glucose and fasting/post prandial insulin. These are all exactly what you would expect from a human on a mixed starch/fat diet. Not bad, but not perfect. The post pranial insulin would drop with dropped starch. The fasting insulin wouldn't. But basically these mice are doing OK within their experimenter enforced dietary choices.
The mice in Donny's link were eating 10% sucrose by weight in their high fat diet. Look at the trigs, insulin and leptin here. Sucrose is essential to produce this on a "high fat" diet.
I'll leave high sucrose diets for those people interested in the lemonade cleanse. Love the reminder Hans! But I'd agree with the other comments, a high sucrose diet is utterly artificial. Limiting your fat to de novo lipogenesis from fructose may be useful in terms of proving support for the idea that sucrose is an acceptable caloric source for humans, if that is your agenda (even the AHA have given up on this one!), but that's not enough reason to base your diet on it.
Helen, It's hard to cover all bases, the arguments for mixed diets are certainly out there but in here I'm looking here to defend the concept that fat is good. We're not bombarded with the message that mixed diets in moderation are bad for you. But "Fat is BAD" is ubiquitous. And wrong. Now if you consider fat plus sucrose... And even that's not as bad as it's made out!
Re equatorial food sources, I've not read a huge amount about this because of my biases but I do remember a poster on Dr Bernstein's forum who was familiar with the Brazilian rain forests. You don't walk from fruit tree to fruit tree and anyone expecting to do so will end up very hungry!
Peter
'Satan has a culinary weapon... cholesterol?' Thought you guys might find this article amusing...
http://www.yumasun.com/articles/cholesterol-54888-anthony-chef.html
incognito said...
"Don't forget the tubers! Many tubers have surprisingly high sugar content. Most hunter gatherers use more tubers when meat/fruit/berries are in shortage. Even in Canada there are places with a high edible tuber output. You just have to look!"
Tubers are also seasonal crops.
You don't need to defend fat to me, Peter - but then again, I've been influenced by your blog and others.
I know most of it was cultivated at some point, but there is a lot of fruit here in New England, just for the taking. It starts early and lasts a long time. Some of it is indigenous - wild blueberries and cranberries. On our property, from July through November, there are several apple trees - with more apples than a family of four, birds, rabbits, and a local bear, can keep up with. I know they are a human addition, but a modern hunter-gatherer here could definitely walk from tree to tree - and be positively stuffed.
Bruce, I remember you pushing sugar disguised as the High Everything Diet many months ago.
How did it work out for you? And since it must have worked so great, can you post your before and after blood panel please?
Well Bruce that really does make sense, the evolution of the large human brain with the shrinking of the human gut must definitely be from all that energy dense fruit that our paleo ancestors ate...
Seriously, how can you blame poor health on both high sugar and high fat?
Well, I'll stop hating on you and I wish you luck (you'll definitely need it)eating a diet where 5-15% of calories come from fat and the rest is high carb and moderate/low protein...
The C57BL/6J mice in Bruce K's linked abstract (http://www.ncbi.nlm.nih.gov/pubmed/7752914) are mice specifically chosen (from a spontaneous mutation apparently) and inbred to become obese in response to a high fat diet:
"C57BL/6J mice fed a high-fat diet develop obesity, mild to moderate hyperglycemia, and hyperinsulinemia "
(from:
http://jaxmice.jax.org/strain/000664.html)
So the results of that study are hardly surprising. Seems to me that medicos had the idea 'fat makes you fat' and bred mice to fit the idea and 'prove' it.
Bruce K said:
"Who cares about hunter-gatherers? Many healthy groups ate diets that included agricultural foods, dairy, etc. Where's the proof that hunter-gatherers were any healthier than the groups Weston Price studied or various tropical groups who ate lots of fruit for carbs?"
If you want proof just look at photos of traditional meat eating Masai or Sioux and compare them with high carbohydrate diet Okinawans or Kitivans. The contrast is absolutely staggering.
Kitivans and Okinawans are amongst the shortest people in the world. Okinawans have crowded teeth and very little skeletal muscle.
A Masai warrior is at least 30cm taller and at least 25kg heavier than a Kitivan male.
A traditional Masai warrior may have have an aerobic fitness level approaching that of an Olympic marathon runner. A typical Kitivan male has an aerobic fitness level not much better than a sedentary Swede.
Price noted that those peoples who consumed a high quantity of animal foods were healthier and had better physiques than those who had a mainly plant based diet.
Hi blogblog,
Do Okinawans and Masai have the same life expectancy?
Marco said:
"Do Okinawans and Masai have the same life expectancy?"
Their lifestyles are so different that no meaningful comparison can be made. Masai are extremely poor Third World pastoralists. Okinawans are rich people living in the First World.
The long life of the Okinawans is essentially a myth. They only live nine months longer on average than Amercians. If you account for homicides and car accidents Okinawans have a lower life expectancy than Americans. Other westerners such as Australians have a greather life expectancy than Okinawans.
okinawan women's life expectancy is the highest in japan - 85.75 y.; men's - 78.75 (25th place out of 47 japanese prefectures)*
however, okinawa has the highest prevalence of obesity in japan: bmi higher than 25 has 46.7% of men and 39.4% of women**
should we call it a "japanese paradox"? - the fatter you are the longer you live?
*http://www.mhlw.go.jp/toukei/saikin/hw/life/tdfk05/02.html
**http://www2.ttcn.ne.jp/~honkawa/7310.html
[the statistics are in japanese]
addition: or we can assume it this way:
the longer you live the fatter you are
We'd be making a gross error if we assume that the statistical differences in the measurements of different peoples is all attributable to diet.
Gosh, it could be so many factors: climate, lifestyle, other genetic predispositions (like the little isolated group with almost no incidence of heart disease), activity levels, tobacco usage, alcohol usage... on and on and on.
And, even then, the differences are so incredibly small, I don't find them at all appealing.
I think the attributes they have noted in really old folks living to be > 100 is that they are generally able to get beyond personal tragedies better, they tend to be smaller in size, they are rarely gym rats... or purists in terms of any dietary regimens followed.
Just some thoughts. My guess is an optimal diet, whatever that is, allows one to sort of maximize genetic age potential where the quality of life dominates more of its whole term.
Cheers! Brad
Bruce,
From your very blog: "Eat all the starch you want. If you eat refined starches, unbleached and unenriched would be best - sprouted breads, good sourdough, rice, potatoes, beans, pasta, corn, vegetables, etc." You later go on to recommend all sorts of desserts like tiramisu and butter cookies.
If recommending up to 60% neolithic carbs is not pushing sugar, then what planet are you on? Maybe you could rename your diet the SAD Lite.
You are being totally irresponsible recommending this to people here who are sick and damaged due to years on the SAD and are looking to make positive changes in their health. You're also extremely rude to dominate the comments sections of other blogs, sowing doubt amongst readers in order to convince them to go back to your slightly-more-organic SAD.
You've strangely ignored all commenters who request that you furnish proof of the healthiness of your regime, whether in blood panels or in photos, and you have no body of scientific evidence to support your claims.
Why not just spend all this time actually gathering results data for your own ideas? Better still, maybe read something (anything!) by Gary Taubes.
Peter,
I think you'll get a kick out of this, considering your stance on fruits and vegetables: fruits and vegetables could be healthy not because they're healthy to eat, but because they contain low levels of toxins which strengthen the body through HORMESIS...
http://www.ncbi.nlm.nih.gov/pubmed/17000014?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10
Hi Peter,
Please help wth the dairy issue- full double cream - natural and pure is a problem , causes knee pain and running nose- autimmune caseing = response I guess, Help- what other option is there - I eat this alone, no carbs, gluten, only protein and fat diet, no addded milk proteins. Other suggestions for my whipped coffee/cream combo/ I guess raw is the only one... or abstinence and occasional indulgence. soy is awful.
Thanks for any help,
Elizabeth Jay
Hi gn,
That smacks of BMI between 25 and 30 having best all cause mortality over the next 5 years on the SAD. I think the mortality nadir is around BMI 26, and fat, not muscle, is the protective factor. For those of us with BMI around 20 and 12% bodyfat I hope that this only applies to the SAD! Or carb based diets.....
Uh, you mean yet another Japanese paradox!
And re fat and longevity: GAINING weight protects you from hyperglycaemia at the cost of modest hyperinsulinaemia. When you cannot get any fatter your blood glucose rises and you become diabetic and massively hyperinsulinaemic, until your pancreas dies. The better you gain weight the longer you put this off for. Think lipodystrophes, where total lack of fat gives very early onset diabetes.
Brad, yes, maximising quality years is what matters. Getting some extra is a bonus. I have yet to see anything to make me change what I do in terms of well being or life quality. High fat suits my personal genes. And whatever I eat is compounded by all sorts of other complicating factors. Thinking I'm correct is probably a big one!
Gunther, yes, bit of a giggle. If we draw the parallel with radiation hormesis maybe the American Dietetic Association feels we should all move to Chernobyl. Makes you amazed at the minimal damage done by of all of those fruit and vegetables in WHEL and PPT!
Peter
Hi Elizabeth,
If you really have casein issues you might be stuck with abstinence. It's possible. Also I think going gluten free is never simple and it is very, very hard not to get stung occasionally. My wife's experience suggest about two weeks for gut recovery after a single exposure. Also Jenny Ruhl has commented on soy saponins damaging gut intergrity. Unless you have genuine normal gut function you are not really in a position to decide if your cream intolerance is primary and genuine or secondary and potentially transient if you sort other issues.
I think Mark (http://www.marksdailyapple.com/) does have dairy free drink recipes but as I'm (apparently) casein tolerant and cream addicted I've not chased them! I have tried making cocoa with clarified butter or coconut oil but neither hits the spot!
Good luck
Peter
Peter, egg yolks cooked or raw? I saw an argument for cooking meat and human evolution supporting this throug Eades, I think.
But egg yolk in its raw form is like the soul of the chicken lol. Full of nutritional goodness. And the chick would use it raw. Are the proteins and fats and whatever is in egg yolks better absorbed than meat when raw?
Also, eggs have some quantity of thyroid hormone. I did some math a long time ago comparing it to units of armour thyroid and it doens't stack up to armour.
Free full-text:
http://icb.oxfordjournals.org/cgi/reprint/37/6/553
"Thyroid hormones of maternal origin have been measured in eggs of two galliform species, chickens (Hilfer and Searls, 1980; Sechman and Bobeck, 1988; Prati et al., 1992) and Japanese quail (Wilson and McNabb, 1997). The yolk thyroid hormone concentrations measured by the last three of
these studies are in agreement (concentrations of about 4-6 ng T4/g and 1.5-2.5 ng T3/g of yolk). These studies extracted/separated thyroid hormones and measured them by radioimmunoassay (RIA). In contrast,Hilfer and Searls, who attempted to measure hormones in unextracted yolk directly by radioimmunoassay, reported hormone
concentrations 2-4 fold higher than
the other studies. It seems likely that their values were inflated due to lipid interference with antibody binding in the RIAs,
and it should be noted that no information about validation of their assays was provided."
So I picked up .67 ounces of yolk from here: http://wiki.answers.com/Q/How_many_ounces_are_in_one_egg_yolk
Hope that's right. to convert to grams, http://wiki.answers.com/Q/How_many_grams_are_in_one_ounce
Take the 23.85 grams in an ounce and multiply by the .67
I can round it up to 16 grams per yolk.
So using 16 grams per egg yolk, and the numbers given for thyroid concentration, 16x5 T4 and 16*2 T3 (I took the average for the 5 and 2).
And we get 80T4 and 32T3. ng.
That's for one egg yolk.
For 8 egg yolks, it's 640 ngT4 and 256ngT3.
Let's compare that to Armour:
From: http://www.rxlist.com/armour-thyroid-drug.htm
Armour® Thyroid (thyroid tablets, USP) for oral use is a natural preparation derived from porcine thyroid glands and has a strong, characteristic odor. (T3 liothyronine is approximately four times as potent as T4 levothyroxine on a microgram for microgram basis.) They provide 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) per grain of thyroid.
Let's compare mcg with ng.
1000ng = 1 mcg. So... we have .64mcgT4 in eight egg yolks and .256mcgT3.
So... woefully inadequate compared with armour thyroid, but better than nothing. You have SOME hormone, and especially some T3 coming out of the yolk.
Mark.
Hi all,
Sorry to remove Bruce. He does have a blog somewhere of his own, this isn't it! I don't actually read his posts so there's not a lot of point leaving them around. As most of you will know I consider him to be unwell.
Peter
I have a question. Why is it desirable to do a period of gluten-free after having eaten gluten? (Peter, you mentioned your wife does this.) What exactly does it do to your gut?
On another note:
I think it's a shame to remove anybody to be honest ... I had a look at Bruce's blog and you might not agree but it's sensible compared to most 'diet advice'.
I don't know about the Masai vs. Okinawa argument ... it seems to be correct that a lot of peoples have grain/carb/potato based diets and are not at all stunted in their growth and live to eighty-something ... Germans for example ... ;-)
Heike,
Yes, it's unfortunate. Over the years I have tolerated Bruce's rants about the miracle man Ray Peat, then his manic phase at the start of the HED, but his degeneration in to opinion about my poor health and my diet "phobias" is unacceptable. I would consider it no more acceptable for myself to rant at Dr Eades about his imagined poor health based on his appearance and his carb "phobias" than I would consider it acceptable for me to berate Dr Kwasniewski for including gluten in the Optimal Diet. It's an issue of politeness, not correctness. Bruce interest me not at all, hence I've never read his blog. Others may differ. The mouse click is under your own control, play safe.
My wife and myself are full long term gluten avoiders, the two weeks mentioned is my wife's time to recovery from gut cramps after gluten exposure. If I followed Bruce this is clearly a mark of a "poor metabolism". Personally I take the point of view outlined here and here. It's a mark of immunology.
It is theoretically possible, but highly unlikely, that people can consume gluten with impunity. If people wish to try this, so be it. To me it is a brave and probably foolhardy action.
I discuss what interests me, when I get the chance, and answer what queries people come up with as best I can. I'm not up to save the world or become a guru. That's for others promoting a miracle diet.
Mark,
I've not seen specific data for egg yolks but the protein in egg white is more digestible when cooked. Quite why denaturing it aids digestion is beyond me but that's what happens. The thyroid is interesting but it has a way to go to help someone who is seriously thyroid deficient...
Peter
aw , you're way too modest.
Face it, you're a guru, dammit!
Now please continue to enlighten those of us on the path of fat (i.e., post something new f'gads sakes! The suspense is killing me!)
And kick off whomever you please.
Hi, it's a very great blog.
I could tell how much efforts you've taken on it.
Keep doing!
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