I've had this paper kicking around since it was published. There are a few things which grabbed me about it. I was initially a bit dubious; a diet containing 20% of calories as carbohydrate didn't really seem low enough to be seriously useful for a diabetic. But then I twigged that these people were using a calorie restricted diet, so the absolute amounts of carbs were actually down at 80-90g/d. That's just above Dr Lutz's suggestion of 72g/d and not hugely above Kwasniewski's recommendations. Of course it's WAY above Dr Bernstein's recommendations (30g/d), but he really is a perfectionist, a good one too. The 50% of calories from dietary fat under weight loss conditions was obviously being supplemented from stored adipose tissue (quite highly saturated I believe), hence the weight loss.
These are some of the sections of text I particularly enjoyed.
From the introduction:
"The objective of the present study, therefore, was to determine to what degree the changes among the 16 patients in the low-carbohydrate diet group at 6-months were preserved or changed 22 months after start, even without close follow-up. In addition, we report that, after the 6 month observation period, two thirds of the patients in the high-carbohydrate changed their diet. This group also showed improvement in bodyweight and glycemic control."
OK, it's a short study. A couple of years is way too quick to see changes in heart attack rate from eating all that fat. Isn't it? You know, fatty streaks to soft plaque to... (yawn)
The other feature here was the comment about "changed their diet" applied to the control group (low fat, ADA style diet). It's made clearer in the methods:
"Seven of the controls switched to a 20 % carbohydrate diet immediately after the follow-up period. For those we have data 12–14 months after the change. Three more have later sought information and have changed diet. We have no long-term data for those. Five of the original controls have not changed diet."
This was an open study by the look of it. You can't spend hours sitting in a diabetes clinic chatting to someone who is loosing weight, dropping HbA1c and binning their insulin without realising that the LC intervention diet works. Only an ADA diabetologist is stupid enough to miss this. Given the option to change, you change. Unless you really are as stupid as...
But of course, all of that fat will have the LC diet group dropping like flies from heart attacks. We all know that. We've been told.
So, from the discussion:
"We have examined the medical charts for both the original high-carbohydrate group and the low-carbohydrate group from 3 months after the initiation of the diet therapy – when an effect might be detected – and forward for episodes of cardiovascular disease. Three episodes of cardiovascular disease have occurred among the 5 patients that never changed diet. The 16 patients in the low-carbohydrate diet group (19 months observation time) and the 7 from the high-carbohydrate diet group that changed diet (10 months observation time) – totalling 23 patients – have been free of cardiovascular disease during the follow-up period (p < 0.03. Fischer Exact)."
So we have three out of five people with episodes of CV disease during about a year of ADA style low fat diet and zero out of 23 patients on Lutz style high fat.
Must be a paradox. Ha! (now think of the Queen launching a new ship) I name this paradox "The Swedish Paradox".
What, again? Ok, there are only a limited number of countries in the world and so many paradoxes looking for names...
Peter
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Very very nice! Thank you for yet another illuminating analysis of a piece of scientific evidence (which is so so oh-contrare to the estab)
Remember I luv eggs...
http://www.iloveegg.co.uk/
Volek et al strikes again... only (I'd guesstimate) 60-85 grams carbs daily (17% ad lib) and high % fat and protein. Guess what the results were in only 3mos? Similiar to your post (but not long enough to see CV events) improved adiponectin, dramatic increase in HDL, reduced CRP and TGs, and wt loss. Pretty plaque-busting if you ask me :)
As you've brilliantly said before, 'those 3rd rate receptors' determine our metabolic fates. And tell me who doesn't have 3rd rate receptors!?? Ummm... who could that be...
Nice benefits from vit A/lutein too, eh? Where else do you get your vitamin A, Peter? foie gras? pate?
Thanks as always, G
Nutr Metab (Lond). 2008 Feb 20;5(1):6 [Epub ahead of print]
Eggs modulate the inflammatory response to carbohydrate restricted diets in overweight men.Ratliff JC, Mutungi G, Puglisi MJ, Volek JS, Fernandez ML.
ABSTRACT: BACKGROUND: Carbohydrate restricted diets (CRD) consistently lower glucose and insulin levels and improve atherogenic dyslipidemia [decreasing triglycerides and increasing HDL cholesterol (HDL-C)]. We have previously shown that male subjects following a CRD experienced significant increases in HDL-C only if they were consuming a higher intake of cholesterol provided by eggs compared to those individuals who were taking lower concentrations of dietary cholesterol. Here, as a follow up of our previous study, we examined the effects of eggs (a source of both dietary cholesterol and lutein) on adiponectin, a marker of insulin sensitivity, and on inflammatory markers in the context of a CRD. METHODS: Twenty eight overweight men [body mass index (BMI) 26-37 kg/m2] aged 40-70 y consumed an ad libitum CRD (% energy from CHO:fat:protein = 17:57:26) for 12 wk. Subjects were matched by age and BMI and randomly assigned to consume eggs (EGG, n=15) (640 mg additional cholesterol/day provided by eggs) or placebo (SUB, n=13) (no additional dietary cholesterol). Fasting blood samples were drawn before and after the intervention to assess plasma lipids, insulin, adiponectin and markers of inflammation including C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-I+/-), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1(VCAM-1). RESULTS: Body weight, percent total body fat and trunk fat were reduced for all subjects after 12 wk (P < 0.0001). Increases in adiponectin were also observed (P < 0.01). Subjects in the EGG group had a 21% increase in this adipokine compared to a 7% increase in the SUB group (P < 0.05). Plasma CRP was significantly decreased only in the EGG group (P < 0.05). MCP-1 levels were decreased for the SUB group (P< 0.001), but unchanged in the EGG group. VCAM-1, ICAM-1, TNF-alpha and IL-8 were not modified by CRD or eggs. CONCLUSIONS: A CRD with daily intake of eggs decreased plasma CRP and increased plasma adiponectin compared to a CRD without eggs. These findings indicate that eggs make a significant contribution to the anti-inflammatory effects of CRD, possibly due to the presence of cholesterol, which increases HDL-C and to the antioxidant lutein which modulates certain inflammatory responses.
PMID: 18289377
Here's the thing. Low-carbers have their own paradoxes to explain like the Weston Price paradoxes and the Kitava paradoxes, and the Puka Puka and Japanese and Tokelau paradoxes. We should hold low-carb to the same standard of evidence. Has it met or exceeded those standards? As far as the scientific method is concerned, one contrary observation refutes a theory. OTOH, showing errors in low fat theory does not prove low-carb.
It might just be that certain types of carbs are bad. Or it might be a combination of those carbs and lack of nutrients in other foods. Or it might be a combination of all that, plus the junk fats being used now.
Here is a forum that explores these issues with another perspective. I don't agree with the website fully, but I think it's important to have as many sides of the argument as we can presented. And this one is very unique. The author eats a diet with mainly cheese, butter, coconut fat, non-omega-3 eggs (boiled), fruit/s, peeled potatoes, sugar, white rice (unfortified) and unbleached white flour (unenriched), gelatin, yeast, dark, chocolate, salt. No meat.
http://groups.msn.com/TheScientificDebateForum-
He recovered from serious problems caused by a vegan diet. The reasons for his diet are complex and he has given a lot of scientific evidence in essays and the discussion forum. There are many factors in his diet that might protect him, of course, like the low calorise. But he eats all he wants naturally.
He's a big proponent of restricting PUFAs and fiber severely.
Bruce K,
For the most part, I follow Low Carb and Weston A. Price, so what's the paradox? Not sure I understand what you are getting at. Not sure I understand your reference to a Japanese paradox, either, though I do think most Westerners, Western medicine, and Western media greatly misunderstand Asian diets (thinking it's lots of soy, always low fat, nothing processed, etc.).
I'll check out the forum you recommend.
Hi Chainey,
Very interesting link, thanks.
Cordain does his usual, much is excellent, I still struggle with the milk. You notice how interested he is in the glycocalix and the damage done by wheat germ agglutinin. This is new to me but most of my reading about IHD recently (sems like ages ago) has been largely focused on the role of proteogycan in IHD. Back in the days when there was cardiovascular research proteoglycans were realised to be crucially important. Then Keys and cholesterol took charge.
Back in the 1950s they were well aware that the initial lesion in arteriosclerosis was collagen damage and proteoglycan deposition in the arterial wall. Way before extra collagen build up and before any suggestion of fatty streaks. They come later.
The bits on milk are typical Cordain. No one would argue with casein (present in all forms of milk, cheese, yoghurt) is insulogenic. It's not hyperglycaemic. It is essentially absent from butter and is at low levels in cream. If it was indirectly carcinogenic via insulin this would be a feature of non western communities based on cheese, Swiss Alpine typically. It's not.
The beta cellulin idea surfaces again. But I note now he says that Beta cellulin can only access gut receptors if the glycoprotein coat of the gut is damaged. He never said it but I guess it is WGA damages the glycocalix coat of the gut as well as that of arteries, so this may be needed IF you believe beta cellulin is a problem.
The Alpine Swiss ate rye bread with their cheese, lactofermented. The WAPF suggest this gets rid of the WGA. Didn't work for me but maybe my first attempt at sourdough was not that effective!!!!!
Yourself and Bruce are right, you have to look at all aspects of nutrition. Changing macronutrient ratios does all sorts of things. Both Weston Price and Stefansson make it very clear that a wide range are potentially healthy. I've far more thoughts on this but it's a quarter to Squiggs wake up time...
Peter
PS Cordain drives me up the wall. He's so almost right so often.....
Peter,
Question on a different subject: you posted some time ago an information about Roy Walford (of CRON) dying of some peculiar disease, which I can't find now. Could you repost a link? Thanks,
Stan
Hi Bruce k,
Thanks for your comment, that's very true. I'm also a big fan of Weston Price's research. The thing to keep in mind though is that the outcomes Weston price studied were mostly developmental: width of the dental arch, straightness of teeth, facial structure. The big exception to this is dental decay of course.
He didn't look at obesity, heart disease, cancer prevalence, or longevity.
So anyway, I'm not disagreeing with you, all I'm saying is that the bread and oats may not have been optimal in every way and he wouldn't have seen it.
But I do think what his research pointed to (in my opinion) is that there are certain protective factors that can prevent disease in a large variety of diets. In the Swedish villages, whole grain bread without the rich milkfat would probably have been disastrous.
It's complicated!! It might take us another couple of days of brainstorming to figure this nutrition thing out...
This was the study I quoted when I told my HR department that, if they were really as concerned as they said about "fighting diabetes" and lowering their insurance claim rates, they should stop supporting the ADA.
(I'm in the U.S., where most health insurance is provided by your employer.)
Bruce K, ever heard of a guy named Roger Williams? He wrote an awesome book called Biochemical Individuality, which indirectly addresses the issue you describe.
However, let's be clear. The study Peter mentioned talks about diabetic individuals, i.e., people who by definition have disordered glucose metabolism and therefore probably have some genetic predisposition to the disease. Is it possible that some non-diabetics could thrive on an ADA-like diet? Sure - those non-diabetics who have no genetic predisposition to diabetes might do OK on it. My guess, however, is that the gene is pretty widespread.
I do think it is a misunderstanding of the scientific method to say "one contrary observation refutes a theory." The science of nutrition is never that simple, because it is impossible to alter one variable without altering at least one other. (If you reduce a specific nutrient, you've lowered the calorie content of the diet. You could increase another nutrient to restore the calorie content, but adding that additional nutrient introduces another variable - is the effect observed due to higher fat or lower carbohydrate?) So inherently all observations in nutrition science can be interpreted in at least two ways, making it harder to say that any observation supports or refutes a theory. Furthermore, a scientist who observes an apparently contradictory phenomenon also has to take into account experimental design, accuracy of the data collected, experimenter effect, placebo effects, reproducibility (can another researcher repeat the experiment and get the same effect?) and a whole host of other possible explanations for why an experiment appears to contradict a theory. What really contradicts a theory is not one contrary observation, but the accretion of many contrary observations made over time.
Hi Stan,
That would be this one. Pathophysiology looks pretty straightforward.
Peter
Peter: that's a good study to pass around. It's a compelling note to see 2/3 of the control group switch to low-carb.
One other comment:
Regarding: "one contrary observation refutes a theory."
That's precisely how scientific research is carried out - non-nutritional that is. Take the Fat/Cholesterol Hypothesis for example: numerous studies disprove the connection but it refuses to die.
The rural Chinese, the Okinawan, the Kitavan, etc. don't have unlimited access to bad/cheap calories that results in severe malnutrition.
There is no paradox if one ask the right questions. To paraphrase James Carville (for US citizens only): It's the Insulin...
Walford believesd that the low amount of oxygen in the 'bubble' for several years may have contributed to his ALS generation. (I think it was also likely initiated by Vit D deficiency which is affected due to glass blocking UVB... I believe the 'bubble' was made out of glass... but not certain).
g
Many tribes ate milk and/or grains, neither of which is low-carb. Is it fine to drink a gallon or three, as the Masai, Samburu, and Fulani did? Low-carb diets usually forbid milk, or put all sorts or restrictions on it (due to the carbs). I think many macronutrient ratios will work like Peter said.
migraineur: Scientific Debate Forum does not propose an ADA diet as you seem to be implying. The first page makes it clear that he believes the cholesterol theory is nonsense. He eats high saturated fat, low PUFAs, adequate protein, and carbs low in fiber. No whole grains, beans, or vegetables (except sauerkraut). he eats 3 meals a day, separated by at least 3 hours, with no snacking in between. He eats all he wants.
I agree that it's tough to control every variable, to prove a theory. There are always at least two ways you could interpret the data. When you change one variable, you often change another indirectly. That is the point. There are many ways you can interpret the data. It's not a low-carb vs. low-fat, but now many are raising the argument that it's the PUFAs causing diabetes and all sorts of other diseases.
http://raypeat.com/articles/articles/diabetes.shtml
Chris Masterjohn has written about how the low-fat diet is actually a low-PUFA and high-SFA diet. I feel like him there is a grain of truth to Dean Ornish's overall idea. The problem is that he's not isolating the reduction of total of fat from the reduction of PUFAs, etc.
http://www.cholesterol-and-health.com/China-Study.html
http://www.cholesterol-and-health.com/Campbell-Masterjohn.html
Usual nonsense from Cordain. Saying dairy is inflammatory, but most are eating PUFA oils and low-fat dairy. Dairy is very high in saturated fat (63%) and very low in PUFAs (3-4%). How can dairy be inflammatory? High PUFA oils are inflammatory.
Ghee has none of the issues Cordain mentions. No casein, no lactose, no bovine hormones. It's pure fat. You can melt butter on low heat, let it evaporate completely, then pour the melted fat through cheese-cloth (or a very fine strainer) to remove the milk solids.
All he mentions are epidemiological studies ("epi studies"), where most people are probably eating fat-free or reduced-fat dairy. There are all sorts of other confounding factors, too. Why doesn't he cite randomized controlled trials? Epidem-illogical studies (as I call them) can't ever prove cause-and-effect.
We should all have Chris Masterjohn's site bookmarked!
It's here.
Peter
The other technique is to melt and boil your butter for a few minutes, pour it in to a purex jug and stick it in the fridge. The casein/lactose/water settles to the bottom and can be washed off when the butter is solid. Flavour is fantastic, especially for egg yolks.
Peter
Hi g,
If Walford was detecting signs of ALS in the bubble then he had probably been in trouble for years before hand. I've not seen data for ALS but in Parkinson's you've got to have lost 70% of your dompaminergic substantia nigra cells before clinical signs show. Assuming ALS is similar, then he must have been having sub clinical problems well before this. ALS is strange in that a fair proportion of sufferers develop hypermetabolism in their skeletal muscles years before paralysis starts. If you accept that neuronal cell death in excitotoxin diseases is primarily an energy failure problem then caloric restriction on a carbohydrate based diet would be perhaps the worst thing one could do, muscularly and neurologically. As Parkinson's responds to ketogenic diet and Alzheimers and ALS are in the same family of problem, it looks like ketosis might be the way forward on all of these facets of the same problem.
Peter
Thank you Peter for your wonderful blog. I love the fresh ideas and controversial studies that you bring up.
A little off-topic:
I read that you had psoriasis way back. Am I correct? Do you have any particular advices for it? Do you think it's the 80% fat + gluten free diet that got you symptom-free?
Hi, Bruce K - before I address the ScientificDebateForum, I should emphasize that the bit about people thriving on the ADA diet was a minor point compared to my major one, which was about the notion that a single contradictory observation refutes a theory. That grave misunderstanding of the scientific method is what allows the likes of Gina Kolata to suggest strongly that the discontinuation of the ACCORD trial means diabetics should settle for A1c levels that many other studies have concluded are dangerously high.
But, since you have called ("re-called"?) my attention to the ScientificDebateForum - I just followed your link, and there's a daunting amount of information there that I don't have time, at the moment, to wade through. So for now I'll go by your description, which unfortunately doesn't tell me the relative proportions of, say, white rice to coconut oil in his diet. But it raises a big question for me. I usually refer to my diet as a low-carb diet because that's a recognizable term that most people immediately get, but by the Two Factor rule we've already agreed to, it is also a high-fat diet (not quite as high as Peter's, maybe 60% to 70% of calories). And I sometimes wonder if the high-fat part isn't more important than the low-carb part. I have done some digging to find out if anyone uses ketosis as a treatment for migraine, spurred by the notion that epilepsy can be treated by ketosis, and some other treatments for epilepsy work for migraine as well. (Haven't found much, sigh.) I may be misunderstanding this, but I think you can get to ketosis two ways - restrict carbs severely and replace the lost calories with fat, or restrict carbs somewhat less severely and add a whole lot of extra fat calories. The second option allows you to eat more carbs (though not unlimited amounts) and still be in ketosis. It probably also prevents the usual weight loss that comes with more severely carb-restricted diets.
So I wonder if increasing the fat in our diets is the real healing factor. If the SDF guy has done that, perhaps that's responsible for his health improvements?
Please understand, what I'm doing here is simply ... thinking. Not trying to prove anything, just throwing out some possibilities that seem like good hypotheses. I'd love to hear any thoughts, especially if anyone knows of any studies on the subject.
Hi Bruce,
On thing to remember is that nearly all cultures that consumed milk drank/ate it in a cultured form. So there wasn't actually that much lactose in what they were drinking/eating. Fermented milk, cheese and butter are all low in lactose.
I don't know how lactic acid fits into carbohydrate metabolism. It must be metabolized though the same pathway (entering at a later step than glucose), but I don't know if it elevates insulin or contributes to weight gain. My guess is that it doesn't to the same extent as lactose.
Also, sourdough fermented bread is less insulinogenic than regular bread. So I think their diets may not have been quite as insulinogenic as they appear on the surface.
Hi siberian,
Psoriasis appears to be one aspect of metabolic syndrome. There's a recent discussion paper here. Reducing insulin should down regulate NF kappa B, which controls a host of pro inflammatory genes, so should reduce production of all sorts of cytokines, whole body, not just skin. Though it's not really tied to wheat I would suspect that grain elimination might help too. Saturated fats would be preferred, any inflammatory response will propagate much better in a PUFA environmemnt. I also found my scaly skin lesions tended to resolve with sun exposure. So vitamin D should help, or sun exposure.
The diet I eat is very anti inflammatory on all fronts but the one thing which still flares my skin is wheat/barley/rye, even as I am now. No beer. Whether it is genuine psoriasis I don't know. It looked like the pictures on dermatology sites on the net. I tend to avoid medics unless it's absolutely essential!
Peter
Hi Chainey,
Feel free, the stuff is all up on the net so I take that as a sign that both this blog and its comments are up for public scrutiny.
I'm amazed that you find the time for what you're doing. I've got about 6 posts in various states of thought from roughed out to "hey that's interesting" levels and none of it's progressing much at the moment!
Peter
Sasquatch: although fermented dairy foods are low in lactose to varying degrees, only butter and cheese are low in carbs. Straining yogurt also seems to reduce the carbs, but I am not sure. Sourdough breads probably are better, but I'm on the fence in regards to whole grains. There have been arguments for and against. I'm experimenting with Ezekiel sprouted breads, French Meadow sourdough rye and sourdough bagels (organic white flour, unbleached, and unenriched).
I know that Ray Peat argues against eating foods with lactic acid, like yogurt, sauerkraut, and so on. He's convinced lactic acid damages cells and impairs energy production. When lactic acid rises, CO2 falls, which causes hypoxia and acidosis. Doctor Buteyko has also stressed the human need for CO2. Too much emphasis has been on oxygen, ignoring CO2.
http://raypeat.com/articles/aging/altitude-mortality.shtml
http://raypeat.com/articles/aging/transparency-cataracts.shtml
migraineur: I am not convinced much by low-carb claims about A1C. There is very poor correlation between an individual's blood sugar and A1C. I think it is an ad-hoc theory, which doesn't really explain much. We can find people with high blood glucose and low A1C, or people with low BG, and high A1C. PUFAs contribute very much to so-called glycation.
We also know that things like HFCS, and refined sugar seem to be really good at causing lipid peroxidation, depleting Vitamin E, and so forth, whereas foods like honey and starch don't seem to do that. (And I would always recommend fresh honey, that hasn't been heated/strained.)
You asked about whether high-fat or low-carb is the most important part of healing. I don't think it's that simple. The fat should be higher in SFAs and MUFAs, lower in PUFAs too. I worry about increasing PUFAs with increased fat. I would try to avoid that as much as possible.
I also put natural foods like fresh honey in a different class than the refined sugar and HFCS. It may have none of the harmful effects of such highly processed sugars. I see good honey (truly raw) as more an animal food than a plant food. For all we know, maybe fruits and veggies are the worst carbs, while potatoes and honey are the best ones...
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