It's from
Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial
The lead author does not appear to be a LCer. In general his publications are rather pro plants and quite mainstream. To his credit he has published some negative studies amongst the pro plant stuff. Harvard, ultimately, is no hotbed of pro Atkins zealotry.
If we want to look at the macros we can check here:
A little arithmetic allows us to look at the carbohydrate intake on the first graph at differing time points for Atkins and Zone diets:
Of course the Atkins diet was an unrestricted calories diet, Zone has a caloric restriction applied.
I have the impression from the data of the A-Z study that low carb is good, slightly higher carb is acceptable, adding more carbs back in is a booboo and that the Zone is crap. Just an impression. From the graph.
As an aside, of course the unanswered question is what, exactly, would a sustained 54g carb intake have produced in terms of weight loss over 12 months? Or 20g/d over 12m?
It is very clear that carbohydrate restriction only works WHEN YOU RESTRICT CARBOHYDRATE. A low carb diet does not appear to be as effective as a low carb diet when it has morphed in to an ex low carb diet through added carbs. A similar pattern might apply to ultra low fat diets if anyone wants to go down that dark alley. They don't work when you add fat. Assuming you don't mind the biochemistry while you eliminate fat.
It is also very clear that when comparing an almost-ketogenic diet to a modestly restricted carbohydrate diet of around 133g/d carbs, something like the Zone diet, the modest carbohydrate diet is just as good, if not a little better, than a ketogenic diet. You know the graph:
My problem is trying to square the circle between these two studies. Obviously, no study is free of bias. I struggle somewhat with Dr Sears, of the Zone diet, being the group leader of the study which shows a diet with 133g/d of carbohydrate out performs a ketogenic diet. That is very strange and doesn't happen in Stanford.
People must make up their own minds.
Peter
53 comments:
"He just gave folks the books and told them good luck."
Not true
The FULL study
http://jama.jamanetwork.com/article.aspx?articleid=205916
Each diet group attended 1-hour classes led by a registered dietitian once per week for 8 weeks and covered approximately one eighth of their respective books per class. The same dietitian taught all classes to all groups in all 4 cohorts and was rated by participants at the end of the 8-week sessions for enthusiasm and knowledge of the material (rating scale of 1-5, from “strongly disagree” to “strongly agree,” respectively). The LEARN program is intended to be a 16-week program and, therefore, the 8 weeks of guidance through this book reflected an accelerated time frame, which was necessary to match the time frame given for the other 3 diet groups. Efforts to maximize retention in the study included e-mail and telephone reminders for appointments, e-mail or telephone contact from staff between the 2- and 6-month and between the 6- and 12-month data collection points, and incentive payments of $25, $50, and $75 for completing the 2-, 6-, and 12-month data collection, respectively.
Each group received specific target goals according to the emphasis of the assigned diet. The Atkins group aimed for 20 g/d or less of carbohydrate for “induction” (usually 2-3 months) and 50 g/d or less of carbohydrate for the subsequent “ongoing weight loss” phase. The Zone group's primary emphasis was a 40%-30%-30% distribution of carbohydrate, protein, and fat, respectively. The LEARN group was instructed to follow a prudent diet that included 55% to 60% energy from carbohydrate and less than 10% energy from saturated fat, caloric restriction, increased exercise, and behavior modification strategies. The primary emphasis for the Ornish group was no more than 10% of energy from fat. Additional recommendations given for physical activity, nutritional supplements, and behavioral strategies were consistent with those presented in each diet book.8,9,18,19 The guidelines for the Zone and LEARN diets incorporated specific goals for energy restriction, while for the Atkins and Ornish diets, there were no specific energy restriction goals.
I was diagnosed as type 2 in June, 2011. I cut my carbs to 75. I got no exercise due to DDD.
It took 4-1/2 years to lose 143 lbs., which is exactly half my starting weight.
Within 1 month, my fasting BG went from 200 to 94. My a1C went from 9.3 to 5.1 in a year, and has stayed there. The protein in my urine disappeared along with high blood pressure. Chronic diarrhea and daily mentrual bleeding went away too. No hysterectomy for me. I was 55 when diagnosed, and had gone through menopause. When my BG went way up, I bled every day.
I didn't follow anyone's diet, I correctly made the assumption that diabetes is a disease of carb intolerance, so I cut back quite a bit. It worked for me. I doubt I was ever in ketosis, but don't know for sure, I didn't test.
"diabetes is a disease of carb intolerance"
statement not backed by science
I don't get how any reasonable person can draw a strong conclusion from these studies. To me the diets and weight changes just aren't different enough, and food type/quality is also very important. I know "low-carbers" who eat skinless chicken with salad, mayonnaise, and diet coke. Some big-time low carb pushers seem to think low carb is sufficient for good health. Like-wise, anti-low carbers use the inactive, obese mayonnaise eater as an example of why low carb "doesn't work."
From LEARN, <10% energy as saturated fat--I may eat more sat fat than the group as a whole!
Sears' book, like Cordain's, like Rosedale's, would help many people, but it still contains a good amount of garbage.
There are more than these two studies. I think the carbohydrate picture - particularly postprandial BG levels are important - not only to losing weight, but many disease processes. I am particularly interested in the effects of PUFAs - which we now eat 5x more than in 1960. I think the carbs matter - but there is something else going on causing the obesity/Type2 pandemic. There are people in the third world that are getting fat once they start growing corn. There hasn't been a careful epidemiological study showing correlations between the introduction of modern monocotyledon plants and obesity in the third world. I am also curios if frost resistance is related(often by increased PUFA content).
I've been reading every study that comes out on this topic and there is a big problem. A lot of the studies are just junk. The Rodent studies where they call sugar + hydrogenated vegetable oil fat is just the start. My hunch is there are more than a few vegans/PETA nuts that are quite willing to twist the science in support of their agenda.
But there is even more - I see many papers where knowledge of the process of experimental science appears lacking. In real science, one needs to change only one variable at a time. When I see feed lots from multiple companies - not restricted to the same batch I see something one might expect from a high-school student - not someone with a PhD.
Peer review is broken to such an extent that I figure about 90% of the papers should be ignored - just noise to muddy the water. The need to publish - the pressure to get grants - has would-be scientists going through the motions of science, but it takes a lot more than a lab coat, title, office in a university to turn research funds into real science. Cargo cult science.
"diabetes is a disease of carb intolerance"
statement not backed by science
25 Mar 2015, 17:58:00
... but it worked for SuperCheese.
For the record, the lead author of the A to Z diet study, is at Stanford, not Harvard. He's a long time vegetarian and is now a vegan.
Hi Peter,
I noticed you are being debunked,
- congratulations!
8-:)
Stan(Heretic)
Paula, thanks, it's corrected. I'd looked at the author affiliations on the paper some time before getting to the end of writing the post and Harvard snuck in there somewhere along the way. If that is the main author's mindset then all the more impressive that he published a study where, in his hands, Atkins beat Ornish as well as Zone.
Peter
Karl, yes, white flour and white sugar were the culprits in Weston Price's day, certainly as regards illness rather than obesity. They are nearly indestructible and easily packable/transportable. PUFA, especially omega 6, might be viewed as protective, with the hyperglycaemia made easier to control at the cost of distended adipocytes. They have come later...
Peter
We should make ridiculously huge and shiny looking badges that say 'backed by science' so we can whip them out whenever we are questioned.
He's a vegetarian not vegan
http://integrativemedicine.arizona.edu/formalbio_cgardner.html
Christopher Gardner has been a vegetarian for more than 25 years, or, as he prefers to describe it, a plant-based diet. His four boys (ages 19, 16, 5 and 2) and wife Melissa, a political scientist at Menlo College, all follow a plant-based diet.
@karl
"I am particularly interested in the effects of PUFAs - which we now eat 5x more than in 1960. I think the carbs matter - but there is something else going on causing the obesity/Type2 pandemic."
Hypothesis: the human brain reads the dietary fat intake, if it remains too low for too long, taken as signal it's time of famine, down-regulate fat-burning enzyme. But here's the kicker: animal fat works (maybe fruit fat also - coconut, olive, avocado) to send signal that it's not famine, so ok to burn fat at high rate; but "veg oil" doesn't.
@Charles Grashow,
One's carbohydrate tolerance used to be determined by how much glucose you could eat before glucose appeared in your urine or, in excess, in the blood.
If your carbohydrate tolerance was too low, you had diabetes.
Carbohydrate intolerance was the definition of diabetes because of this simple and very useful observation.
I think they had science back then.
Science also showed that if a large enough portion of the pancreas was damaged, feeding carbohydrate would cause further damage to beta-cells, whereas fat would not, in fact it allowed normal metabolism.
This matched what happened to people told to eat a low-fat, high-fibre, low sugar diet for T2d.
"After 3 months on a low-fat, high-carbohydrate, high-fiber diet, patients were randomized to therapy with diet alone, insulin, sulfonylurea, or metformin.
MAIN OUTCOME MEASURES:
Fasting plasma glucose and HbA1c levels, and the proportion of patients who achieved target levels below 7% HbA1c or less than 7.8 mmol/L (140 mg/dL) FPG at 3, 6, or 9 years following diagnosis.
RESULTS:
The proportion of patients who maintained target glycemic levels declined markedly over 9 years of follow-up. After 9 years of monotherapy with diet, insulin, or sulfonylurea, 8%, 42%, and 24%, respectively, achieved FPG levels of less than 7.8 mmol/L (140 mg/dL) and 9%, 28%, and 24% achieved HbA1c levels below 7%. In obese patients randomized to metformin, 18% attained FPG levels of less than 7.8 mmol/L (140 mg/dL) and 13% attained HbA1c levels below 7%. Patients less likely to achieve target levels were younger, more obese, or more hyperglycemic than other patients."
Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies (UKPDS 49). UK Prospective Diabetes Study (UKPDS) Group.
Turner RC, Cull CA, Frighi V, Holman RR. JAMA. 1999 Jun 2;281(21):2005-12.
Well Stan, I suppose better late than never. Still feel aggrieved that I'm so late to be honoured.
Peter
SuperCheeseUS says "diabetes is a disease of carb intolerance"
Charles retorts...
"statement not backed by science"
How do you define "backed by science" Charles?
A major tool used in the diagnosis of Type 2 Diabetes, is the Oral Glucose (a significant carbohydrate) Tolerance Test or OGTT. In plain English: am OGTT result showing poor tolerance to dietary carbohydrate is diagnostic of Type 2 Diabetes.
Evidently many have discovered for themselves (myself included) that a significant reduction in dietary carbohydrates, makes a dramatic improvement to all the major symptoms of Type 2 Diabetes... slowing, stopping, or even reversing them.
There have been clinical trials which bear out these observations.
While this being the path to improvement may not necessarily show that carbohydrates were the cause, it is certainly suggestive of such a causal relationship... especially given that Type 2 Diabetes is characterised as a "Chronic Progressive Disease"... which of course is usually taken to mean you will inevitably get worse (if you follow the standard advice) BUT it also implies that you were already getting worse all the while (many years or decades) PRIOR to that fateful day when you were diagnosed with carbohydrate intolerance.
@FrankG
Diabetes is a disease of REFINED carb intolerance. White flour and white sugar, as Peter mentioned. And white rice for that matter, look up 'white rice diabetes'.
The idea that any old carbs cause diabetes is based on ignorance of what the minerals removed from refined carbs do. They prevent diabetes! OMG
Hi Peter,
Could the difference in weight loss between the two groups in the 2006 Johnston paper be due to the difference in resting energy expenditure (REE)?
There is a 12.65 % difference at the beginning of the study. The two subsequent measure points find the difference diminished but the ketogenic group's REE remains lower than the non-ketogenic group.
Is the difference significant? Any thoughts?
Thanks,
Jim
@Jane K
Sorry, does "is a disease of" = "is caused by"..?
As a person with Type 2 Diabetes, I can assure you that my body has a problem with tolerating dietary carbs... ANY carbs. There may be variation in speed and intensity of the BG rise but eat carbs and rise it will.
Once again, I'll point out that a diagnostic test for Diabetes, is a Glucose Tolerance Test. Glcusoe IS a significant carbohydrate in the human diet... right?
In terms of causality, I can surely agree that a diet of unprocessed, real whole food, is far less likely to lead to Type 2 Diabetes... but no amount of minerals will make my body more tolerant to carbohydrates.
Possibly interesting citation statistics :-
Web of Science
Gardner - 390
Johnston (Sears) - 42
Pubmed
Gardner - >100
Johnston - 13
Secondary peer review in action ?
@Jim I looked at the REE issue but can't make sense of the units - 7 kcal/kg resolves to <700 kcal per unit of time. Help !
If T2D can be reversed by a high carb macrobiotic diet then how can T2D be a disease of carb intolerance??
https://www.youtube.com/watch?v=eREuZEdMAVo
This is a talk by Chris Gardner. Around the 45 minute mark, he shows a graph showing distribution of weight loss in individuals in each group--you can see at a glance that in each of the groups, most of the weight loss occurs in a smaller portion of the group, Gardner suggests that those most compliant lost the most weight.
Mean weight change at six months in the Atkins group might be 6 kilograms or so, looking at the graph in Peter's post, and carbohydrate intake averaged over the whole group might be 100 grams at the same time point.
But um, what was the carbohydrate intake of the smaller (maybe 25 percent?) segment of the Atkins group that actually lost the most weight?
I've seen Barry Sears make the argument that the Atkins group was eating closer to a Zone diet, so of course they lost more weight. But they weren't doing so individually, necessarily, but only on average over the group.
If type II can be reversed through a very low calorie diet, how can it be a disease of fat intolerance?
Type II is a disease of fat/glucose intolerance, maybe, the two just don't get along. If a high fat or a high carbohydrate approach can improve blood glucose, should we say that it's not a disease of intolerance at all? Anything goes?
Denise Minger made a claim in a talk this year that if the Kempner Rice Diet allowed diabetics to tolerate glucose, while a low carb diet only gave diabetics normal blood glucose, which would become elevated again if carbohydrate was reintroduced to the diet, then the high carb approach was a cure for diabetes and the low carb approach was merely therapeutic. This is wrong. Because you can no more add fatty steak to the Rice Diet than you can add rice (sorry Paul Jaminet) to the Bernstein diet and expect good results. Maybe some people can have a good sugar metabolism, or a good fat metabolism. Choose one. I go with fat.
@CG "If T2D can be reversed by a high carb macrobiotic diet then how can T2D be a disease of carb intolerance??"
Prove it.
Where is even a single clinical trial... let alone one published in a peer-reviewed journal?
Please don't say you are relying on that loonie-toons Gabriel Cousens -- with his crocheted hat -- as a credible source?
What defintion of "reversed" are you using?
Sure, I can see how an heavily regimented (i.e impossible to follow in the long-term) diet of inedible, raw sprouts, might improve symptoms for someone whose baseline diet was the SAD, or even the diet reccomended to diabetics by the establishment -- at least in the short-term -- but at 6 months later, a year... 10 years?
@Susan REE units are kcal/kg of body weight per 24 hours.@Jim
@Susan REE units are kcal/kg of body weight per 24 hours.@Jim
Denise Minger also mentioned that Kempner's regiment for his patients included whipping for achieving a better diet adherence. While reading her post I was wondering about the same things as Frank mentioned - if a rice diet improved the glucose tolerance for diabetics - than for how long? It supposed to be a short treatment anyway, according to medical dictionaries.
Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.
"a diet consisting only of rice, fruit, fruit juices, and sugar, supplemented with vitamins and iron. Salt is forbidden. It is prescribed for the treatment of hypertension, chronic renal disease, and obesity. It should not be followed for any length of time, because the severe dietary restrictions may lead to nutritional deficiencies or imbalance. Also called Kempner rice-fruit diet."
Farlex Partner Medical Dictionary © Farlex 2012
"a diet of rice, fruit, and sugar, plus vitamin and iron supplements, devised by Kempner to treat hypertension. In 2,000 calories, the diet contains 5 g or less of fat, about 20 g of protein, and not more than 150 mg of sodium."
Since we are on a blog of a veterinarian, there is a question to more informed people than me - does somebody tried a very low fat on diabetic dogs or omnivores like pigs? It is only a curiosity question. Compare to others who have to follow a diet, my health and weights problems are minor.
@Jim REE doesn't work with those units - 700 kcal/24h at 100 kg ? No way.
@Angelina I have seen estimates of REE at 75% of total energy expenditure. So these numbers do not seem unreasonable. Does help explain why exercise is unhelpful in when attempting to lose weight.
@Angelina I have seen estimates of REE at 75% of total energy expenditure. So these numbers do not seem unreasonable. Does help explain why exercise is unhelpful in when attempting to lose weight.
@FrankG
"In terms of causality, I can surely agree that a diet of unprocessed, real whole food, is far less likely to lead to Type 2 Diabetes... but no amount of minerals will make my body more tolerant to carbohydrates."
How hard have you tried? Have you tried a Hunza-style (grain based) diet, with zero refined carbs and meat once a week only, for a year? No I thought not.
Your beta cells are shot. They can be repaired. It's called autophagy. Autophagy needs micronutrients, especially manganese. I expect your diet is rather low in manganese. Taking manganese pills is not going to help.
Again Jane I suppose you can point to human clinical trials which would convince me go against my own years of self-experimentation, documented on many spreadsheets of food logs and BG tests... sometimes up to 20 tests in a day?
Or should I just radically alter my diet on your say so?
As for my diet, what makes you so sure? I focus on real, whole food, high-quality, naturally raised/grown and locally sourced. I don't rely on supplements. Are you telling me that the only traditional diet which correctly nourishes the omnivorous human, was that of the Hunza?
Frankly you are stretching the bounds of credibility.
But nice deflection away from the point that Diabetes is a disease which is characterised by an intolerance to carboydrates.
@FrankG,
Your diabetes management with a LC diet is a fact, while a Hunza exceptional health is a human-made myth
http://biblelife.org/hunza.htm
"The Hunzakuts were not extremely healthy as many claim. The Mir told Renee Taylor that the people were free of all diseases. This was not true. The Hunzakuts were always disease ridden, and the death rate was very high as observed by John Clark 10 years before the arrival of Renee Taylor. Clark was met by hordes of sick people who were seeking medical attention in every village (oasis) he visited. He diagnosed many diseases and treated those whom he could help. The diseases he listed are: Dysentery, Ringworm, Impetigo, Cataracts, Eye infections,Tuberculosis, Scurvy, Malaria, Ascariasis (worms), Leucoderma, Staphylococcus, Dental caries, Soft teeth, Goitre, Bronchitis, Sinusitis, Chapped and bleeding hands, Beriber, Influenza, Pneumonia, Infections, Rheumatic knees of sub-clinical rickets.
John Clark made a survey of the Hunza boys in his school to ascertain how many of the students had lost family members. This shows the terribly high mortality rate of the Hunza people. They were not healthy and free of disease as falsely claimed. The results are shocking for these boys between the ages of 12 and 16."
Should you go keto, LCHF or neither? I say go for which ever espouses indisputable basics & carries little to no fluff.
Also, avoiding things based on vacuous principles like 'moderation' (aka 30/30/40 Barry Sears' Zone Diet).
So considering little things like, oh I don't know, Occam's Razor / Precautionary Principle / burdens of proof / basic biology, we might conclude that a diet of fats & proteins from complete (aka animal) sources is the only reasonable starting point in humans. Why? For the simple reason that there are essential fatty & amino acids but no essential carbohydrates.
Since medicine is all about FIRST DO NO HARM, this diet seems like the only universally safe & defendable starting point in our species.
Things still aren't working? You need more? Each addition has to be considered in terms of opportunity cost to any essential macros & micros you will be displacing. I think it's quite hard to make that change in a scientific manner although it's certainly possible.
If my bias isn't obvious, I see plants & their compounds of interest more as medicines than food calories per se...apparently this is not a popular position!
There is the book by John Clark on-line for free http://biblelife.org/Hunza%20-%20Lost%20Kingdom%20of%20the%20Himalayas.pdf.
@FrankG
Are you completely uninterested in knowing whether your beta cells can be repaired? Has anyone other than me ever told you that?
I am a biologist. I have degrees from Oxford and Cambridge, and I have published papers on tissue regeneration, which is exactly the subject you need to know about if you want to understand what's happening to your beta cells.
Is the problem that you think I am insane, as Wooo does, or a fraud, as Galina does? I am neither, as should have been obvious years ago to everyone.
@Serova
John Clark studied the Hunza long after their health had started to deteriorate. Your article does not mention Sir Robert McCarrison, who was their doctor for 7 years and found them to have astonishing health.
You are not the first person to tell me Hunza health is a myth. Every time, that BibleLife article is quoted and McCarrison is ignored.
Nobody wants to believe that people who ate grains could possibly have been healthy. Well, they were. McCarrison even did experiments on rats to find out whether Hunza health was due to their diet, and the rats were just as healthy as the Hunza.
@jane karlsson
I think the totality of evidence has to be considered here. You're right to point to contrary evidence, but the quality of evidence you point to remains poor and most importantly does not fit with higher quality evidence. Every time proper controls are used to assess then healthfulness of grains they fall short and when they do appear to show benefit, it is always relative to something that's already quite terrible (whole vs refined for e.g.).
Arguments of authority never advance the conversation in and of themselves. It's understandable to use them when frustrated but ultimately, they're bad habits.
Hi raphi
My evidence is poor and I have bad habits. Oh shit
@Jane Karlsson
My diplomatic attempt failed (obviously). Your summary will do just fine.
Yes diabetes is a disease of carbohydrate intolerance.
If a macrobiotic diet reverses diabetes, or a low carb diet, or a low calorie diet, or bariatric surgery, then carbohydrate intolerance is by definition reversed as well, because diabetes is a disease of carbohydrate intolerance.
Do macrobiotic diets reverse T2D?
Charles pointed out 4 papers to me which are the total of macrobiotic research so far, by the Ma-Pi institute.
Summing up what I've learned about the Ma-Pi studies:
Carried out by members of the macrobiotic movement.
Apart from Italian study take place in countries (China, Cuba, Ghana) with governments friendly to the macrobiotic movement. Likely because of its agricultural aspects.
Not controlled, randomised or blinded.
Not yet at stage of being tested skeptically by scientists not invested.
Plenty of scope for publication bias.
None of which means it's not legit, just that it's passed very few of the hurdles that one needs to clear to have a method accepted.
While living in a western world, it is easy to forget about the societies where food shortages are still the fact of everyday life. I remember how it was - starches were unlimited, but not animal products, and it didn't work as a prevention for modern deceases, diabetes included.
For that reason I think that the experiments with a macrobiotic diet are very important. However, there is no data that such diet is the better option/alternative than the diet recommended by Dr. Bernstein or similar.
@George
Why is it so difficult to believe that a diet full of micronutrients can cure diabetes?
Calling it a disease of carbohydrate intolerance implies it's caused by carbs, when it clearly isn't. If you want your lab animals to have diabetes you give them a high FAT diet, which causes oxidative stress, ER stress, iron overload, beta cell damage etc. What we really need to know is whether the diabetes could be prevented by giving them extra doses of the micronutrients known to prevent oxidative stress and iron overload. In the case of manganese, the answer is yes. Manganese can prevent diabetes caused by a high fat diet.
It was recently shown that obese people have iron overload in their brains, including the hypothalamus. This explains the inflammation found there by Guyenet's group. Obese people also have excess free iron in their urine. Everything points to iron overload, in both obesity and diabetes.
Saturated fat is known to increase iron absorption, and this is dangerous because unlike other minerals, iron doesn't get excreted. If like me you want to eat a lot of saturated fat, you MUST eat a lot of foods high in micronutrients which prevent iron dependent damage.
http://www.ncbi.nlm.nih.gov/pubmed/23372018
http://www.ncbi.nlm.nih.gov/pubmed/25125507
http://www.ncbi.nlm.nih.gov/pubmed/21189275
Is saturated fat known to increase iron absorption?
Really?!?
Where? When?
Saturated fat has been found in several studies to increase iron absorption. Look up 'saturated fat iron absorption'. It has the opposite effect on manganese, according to this study.
Abstract
There is evidence that manganese (Mn) metabolism may be altered by the form and amount of dietary fat. Also, iron (Fe) absorption is greater with saturated fats, as compared to polyunsaturated fatty acids (PUFAs). The absorption of Fe and Mn are interrelated in many aspects; therefore, the form of dietary fat may indirectly alter Mn absorption. ...Manganese absorption was significantly (p < 0.05) lower in the stearic acid group (0.9-4.8%) than in the safflower oil group (20-33.8%)...
http://www.ncbi.nlm.nih.gov/pubmed/11697763
For those on a ketogenic diet, here's a paper that might be of interest.
Memory impairment induced by brain iron overload is accompanied by reduced H3K9 acetylation and ameliorated by sodium butyrate
http://www.ncbi.nlm.nih.gov/pubmed/22067609
The point being that butyrate is an HDAC inhibitor like beta hydroxybutyrate.
I guess it's an old discussion, but in the paper you cite as Mike Eades would point out, rats are not just furry humans. Without human data these are just intriguing hypoewtheses. He also pointed out that the best way to reduce iron stores was to donate blood, which is a socially responsible act.
Donating blood is fine, I'm intending to re start now I have the time. But the rodent studies on iron overload are to the same standard as many nutritional studies and it is very hard to see exactly what was done to the rats used in many of them. It is very interesting to see if a high iron diet is able to produce insulin resistance in the absence of bulk PUFA. The trail dries up about three layers of references deep without giving an answer. I might get back to it one day...
Peter
I've been running across references to iron overload. Tucker's blog has a post about it.
"tl;dr: Oft-mentioned iron overload does not appear to be a problem in healthy humans, only in those with genetic defects. Iron is steadily lost through normal mechanisms and regained through dietary intake. Deficiency is the problem in healthy people."
http://yelling-stop.blogspot.com/2018/01/iron-overload-myth-in-healthy-people.html
Peter:
I struggle somewhat with Dr Sears, of the Zone diet, being the group leader of the study which shows a diet with 133g/d of carbohydrate out performs a ketogenic diet. That is very strange and doesn't happen in Stanford.
https://www.researchgate.net/publication/7096307_Ketogenic_low-carbohydrate_diets_have_no_metabolic_advantage_over_nonketogenic_low-carbohydrate_diets
From SUBJECTS AND METHODS:
Sedentary, overweight men and women [aged 20 – 60 y; body mass index (BMI; in kg/m2 )> 25] were screened for diagnosed disease and use of prescription medications. Participants (n 20) were stratified by age, sex, and BMI and randomly assigned to 1 of 2 experimental diets: the ketogenic LC (KLC) diet or the low-fat, nonketogenic LC (NLC) diet. All participants gave written informed consent. The Institutional Review Board of Arizona State University approved the study protocol. During the 6-wk feeding trial, all food and beverages were provided to participants, who remained sedentary.
From the Conclusions in the Abstract:
KLC and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was associated with several adverse metabolic and emotional effects
Why being sedentary was so important for the experiment, but the conclusions don't mention it?
May be when you have lost metabolic flexibility a high-fat diet is not a good idea (at least without strength training). What do you think of the Blood ß-hydroxybutyrate data in Table 3? Were the participants in ketosis?
Hi novuel,
Personally I think the caloric restriction is the crucial part. No one in their right mind would go Zone vs ketogenic without restricting the calories in the Zone Diet (but then the Zone Diet requires caloric restriction in excess of anything spontaneous). Anyone who was in ketosis was encouraged to get out of it well before the end of the study. I always puzzles me that people can be so clever to defend their ideas, which are dumb....
cave, yup, read the post. Not that I eat a terribly high iron diet. High frequency of red meat but still limited total amounts. Not something to worry about, methinks.
Peter
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