Is there any such thing as "safe fat" for diabetics?
So some of the AHS12 videos are now online, HERE. I'll have some comments on particular presentations, though by no means a majority. Still, I had to, of course, watch the Safe Starches panel. For the record, I think Paul & Chris did a good job, especially considering the circumstances, but this thing was an abomination in the making from the get-go. I'll have more on that in another post.
The whole "debate" goes back to Jimmy Moore's "data dump" post on safe starches. You remember that one, right? Is There Any Such Thing As ‘Safe Starches’ On A Low-Carb Diet? As I said, I'll have more to say on this follow-up, but as one would expect Jimmy expresses his concerns over the safety of starches, and around the 5 minute mark essentially tries to take Paul to task for using the term "safe"! Citing Webster's Medical Dictionary
SAFE: not causing harm or injury; especially : having a low incidence of adverse reactions and significant side effects when adequate instructions for use are given and having a low potential for harm under conditions of widespread availability
First of all, this is a medical definition that refers to treatments and drugs ... not food! But the definition of "harm" is where the LC community takes great liberty. No doubt rampant hyperglycemia leading to significant and persistent glycation does harm. But we're talking only a segment of the population for whom carbohydrate ingestion is even a small part of the picture. I post this here from time to time in case new readers have not yet seen it: Insulin: understanding its action in health and disease. Yes it's a peer-review journal review article, but it is not overly jargon-laden and technical. The bottom line is that the glucotoxicity of untreated diabetes is due to the lack of insulin and thus failure to suppress endogenous glucose production. Yes, insulin facilitates glucose clearance, but the problems in a T1 are far more complex than hyperglycemia, and even on a zero carb diet, the untreated T1 will still be hyperglycemic. In the pre-insulin era, a 10 year old diagnosed with diabetes had a life expectancy of under 18 months. Further:
Before the introduction of insulin, a person with acute-onset diabetes had a short life expectancy and died in ketoacidosis.
Regardless of the various myths swirling as to the etiologic cause of T2 diabetes, nobody (hopefully) would suggest that T1 is caused by eating too much glucose. Starch is a food. Nobody is suggesting it as a treatment for T1's, but to suggest fat is really much better is folly -- after all, it is ketoacidosis (due to unchecked NEFA levels) that is truly lethal for T1's.
So anyway, the knock against starch (spoken or implied) is that for "some people" it is not "safe" ... those "some people" being those who are diabetic. So because "some people" will experience soaring glucose levels for a few hours after ingesting starch, it is somehow irresponsible to consider any starch safe. Nonsense!! And further nonsense if some of those "some people" are folks like Fat Head (I consumed around 100 grams of carbohydrates per day during my fast-food diet and still lost weight.... my glucose level is usually around 90 to 100 mg/dl. If I eat a white potato, it shoots up to 175 or so and stays elevated for two hours or more.) who have turned themselves into glucose-intolerant functional diabetics. Doing so doesn't make starches unsafe for you, you've made yourself dysfunctional. In addition, that there are those for whom certain foods are indeed legitimately unsafe, e.g. those with Celiac or peanut allergies, doesn't make those foods unsafe to recommend to the general population.
Let's switch things up a bit to demonstrate the folly of demonizing large classes of food. As everyone knows, if you take the carbs out of the diet, you must replace it with something for calories. Enter the high fat meal. You want "harm" ... I'll give you harm: Acute Elevations of Plasma Asymmetric Dimethylarginine and Impaired Endothelial Function in Response to a High-Fat Meal in Patients With Type 2 Diabetes.
Asymmetric dimethylarginine (ADMA), a compound detectable in human plasma, is an endogenous inhibitor of NO synthase. Endothelial dysfunction is an early event in atherogenesis, and large-vessel atherosclerosis is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus.
The study involved 50 T2's (34M/16F, 42-75 yo, avg 62) that ingested a liquid meal (75% fat/15% carb/10% protein, 1265 calories with 105 g fat/52 g saturated fat, 48 g carb, 32 g protein, 300 mg cholesterol, Vitamin A (100 000 IU/m2 added.) and were assessed for TC, LDL-C, HDL-C, TGs, VLDL TGs, and ADMA at baseline and 5 hours post-meal. Controls were some patients who ingested a comparable sized non-fat meal on another visit, and some patients who repeated the high fat meal following nitroglycerin-induced vasodilation. Results:
- Plasma ADMA increased from 1.04±0.99 to 2.51±2.27 μmol/L
- Brachial arterial vasodilation after reactive hyperemia, a NO-dependent function, decreased from 6.9±3.9% at baseline to 1.3±4.5%
- These changes occurred in association with increased plasma levels of triglycerides and very low density lipoprotein triglycerides, with reduced low density lipoprotein cholesterol and high density lipoprotein cholesterol, and with no changes in total cholesterol.
- The increase in plasma ADMA in response to a high-fat meal was significantly and inversely related to the decrease in percent vasodilation.
- In 10 of the subjects studied with a similar protocol on another day, no significant changes in the brachial artery flow responses or in plasma ADMA were observed 5 hours after ingestion of a nonfat isocaloric meal.
Conclusion: The data suggest that ADMA may contribute to abnormal blood flow responses and to atherogenesis in type 2 diabetics.
This is but one study, and there's nothing definitive in all of this biomarker stuff, but there are lots of studies out there discussing detrimental effects following high fat meals. By lots, I mean an enormous amount of peer-reviewed scientific literature looking at the immediate impact on vascular function in response to high fat meals, and these changes in "at risk" populations such as those with diabetes and dyslipidemia. One of the ways folks dismiss studies like this one is that the "high fat" meal is often a mixed meal with high carbs. This was a large "meal" but it wasn't particularly high carb by percent (only 15%). Another way folks dismiss such studies is that "nobody eats like that". Which, outside LLVLC-land is a valid point upon which to dismiss them! Who eats 100g of fat in one meal? That's over 3/4ths of a stick of butter. Ahhh, but we do know someone who eats this way, and has been eating this way for quite some time now. We know that someone has seen deterioriating lipid profiles despite consistent carbohydrate restriction.
Is it safe to romanticize super high fat diets and promote "nutritional ketosis" in diabetics and the dyslipidemic? Crunched down further, we can ask, "Is There Any Such Thing As A Safe Fat?". The answer, by carbophobe logic, would be no. Because if a lot of fat causes problems, then fat = poison, and a little fat = a little poison, and you wouldn't advise that, right? Yet Paul Jaminet is suggesting a rather modest intake of starches. If you cannot process PHD levels of carbs, it might be time to consider your activity level, overall caloric intake, and/or if changes there fail, having your insulin response evaluated and addressed. And let's not put this entire onus on Paul's shoulders as there are lots of paleos out there who advocate eating whole starchy foods, and many who would advocate eating even more of them (and less fat) as part of a healthy diet. I don't know of any proponents of low fat diets who encourage unrestrained consumption of refined carbs. That's the biggest strawman of all, because sugar was always up there on the very tip of the pyramid, and never given a pass. Whole grains as the starch source at the base may have been misguided, but this never meant Wonder bread and donuts. Meanwhile, Volek and Phinney are advocating very high fat intakes, and Jimmy Moore is encouraging others to follow his lead down the tallow brick road. Safe? I'd say the potential for this advice to be harmful to others is high, while the potential for following PHD or Voight's potato diet to be harmful is quite low.
Comments
I have pondered that question before.
But I thing you meant "Is there any such thing as "safe fats" for diabetics?"
As to safe fast for diabetics? I would think fasting is not likely a good idea for your T1 or any insulin-dependent diabetic.
I appreciate you questioning the safety of "heart healthy fats" that are eaten in this quantity. The blogosphere is a potentially dangerous place to be getting one's nutrition advice.
should have been called the "safe wife and child abuse" panel
His point (I think. There was a lot of ranting.) was that since glucose is the endpoint that is measured, carbs are what diabetics should limit. I suppose it really is no wonder that people have started freaking out over their glucose numbers. I want to see fatty acid meters! I would seriously buy one.
I have no idea what's the best diet. All the debate just confuses me further it seems. I do know I will not trust any diet that says don't eat fruits and veggies. End of story. I won't trust any diet that says JUST EAT ONLY PROTEIN or JUST EAT ONLY FAT or JUST EAT ONLY POTATOES. Come on. Imbalance simply cannot be the real way for humans, omnivores to eat.
I'm a Christian, like Jimmy. Some might call me moderte, others fundamentalist, depending on how to the skeptical side they stand. Last time I checked my Bible, the very first thing we were given to consume was produce--fruits, veggies, seed-bearing... Then outta the garden and into the thorny world, where the Noahic covenant gives us free rein to eat insects, animals, birds. Produce and animal protein. Gee, sounds like the Paleo diet. :D I don't recall God advising us to just douse a lot of good cow fat on everything. And while Christ's last supper would have included lamb, bread, herbs, maybe honey and fruits, certainly wine, I don't think the sacred bread--no doubt lower in gluten and whatnot than our rejiggered bread-- got slathered in 3 inches of butter.
Paul tells us not to make our stomachs our god. Not to obssess about food.
But looks like we're doing just that. We want to be healthy, and we throw both theology and common sense sometimes right out the window.
I really wish Jimmy would give a solid year's shot to a diet radically different than what he eats. Radically. Focus on fruits and vegetables and lean protein with some healthful fats in caloric restriction for a man his size. Maybe a mediterranean style diet. One year. Let's see how he would emerge after a year like that with exercise.
I'd like to see that n=1. I think it would be a revelation after the months of initial adjustment (where doubtless his body would freak).
But doing something non-low carb would destroy the structure he's set up and invested in. He can't be objective. But I wish he would, because he might have a revelation. Maybe not. But MAYBE.
I come here to read you because YOU actually can be more unbiased. You lost weight on low carb, but you're not a fanatical adherent. You see the evolutionary arguments and don't immediately dismiss anything. You look to find the science behind the blather. Studies can be poorly designed, and most of us layfolks can't figure out if a study is a good one, bad one, promising, ridiculous. I come here to see how you sort through it for us.
For that, thanks.
The isocaloric nonfat meal contained whey protein, skim milk (250 g), evaporated skim milk (63 g), syrup (40 g), and granulated sugar (2.4 g).
Oh, come on!
(and it looks like more protein in the low-fat meal, which would be cheating)
The only way of increasing that 10mth life expectancy in DM1 back in the day was via Dr Allen's "starvation diet". This was what kept Elizabeth Hughes alive. Very low carb (only a little oatmeal for breakfast) very low calorie (only 800/day). Glucose in urine was the endpoint.
There were no 1,200 calorie meals of icecream.
You can treat diabetics of all stripes with a high-fat diet if you keep an eye on the calories. Why not? It happens all the time. You can take this insulin denialism too far.
You have to ignore a great deal of medical and personal experience and focus on unusual, indeed bizarre, experimental diets to keep it afloat.
Yes, the carb-insulin explanation is oversimplistic, over-eating fat may sometimes be as bad as over-eating carbs, we get that, but does everyone who diets for a disease now have to take a degree in advanced physiology and get so confused they don't know what they're doing anymore?
Good to see a mention of assymetrical dimethylarginine in a nutrition blog.
(FOX01 is the transcription factor for gluconeogenesis)
Diabetes. 2011 Jul;60(7):1872-81. Epub 2011 May 20.
Suppression of FoxO1 activity by long-chain fatty acyl analogs
OBJECTIVE:
Overactivity of the Forkhead transcription factor FoxO1 promotes diabetic hyperglycemia, dyslipidemia, and acute-phase response, whereas suppression of FoxO1 activity by insulin may alleviate diabetes. The reported efficacy of long-chain fatty acyl (LCFA) analogs of the MEDICA series in activating AMP-activated protein kinase (AMPK) and in treating animal models of diabesity may indicate suppression of FoxO1 activity.
RESEARCH DESIGN AND METHODS:
The insulin-sensitizing and anti-inflammatory efficacy of a MEDICA analog has been verified in guinea pig and in human C-reactive protein (hCRP) transgenic mice, respectively. Suppression of FoxO1 transcriptional activity has been verified in the context of FoxO1- and STAT3-responsive genes and compared with suppression of FoxO1 activity by insulin and metformin.
RESULTS:
Treatment with MEDICA analog resulted in total body sensitization to insulin, suppression of lipopolysaccharide-induced hCRP and interleukin-6-induced acute phase reactants and robust decrease in FoxO1 transcriptional activity and in coactivation of STAT3. Suppression of FoxO1 activity was accounted for by its nuclear export by MEDICA-activated AMPK, complemented by inhibition of nuclear FoxO1 transcriptional activity by MEDICA-induced C/EBPβ isoforms. Similarly, insulin treatment resulted in nuclear exclusion of FoxO1 and further suppression of its nuclear activity by insulin-induced C/EBPβ isoforms. In contrast, FoxO1 suppression by metformin was essentially accounted for by its nuclear export by metformin-activated AMPK.
CONCLUSIONS:
Suppression of FoxO1 activity by MEDICA analogs may partly account for their antidiabetic anti-inflammatory efficacy. FoxO1 suppression by LCFA analogs may provide a molecular rational for the beneficial efficacy of carbohydrate-restricted ketogenic diets in treating diabetes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121436/
As I said, I will have some general comments on that panel, but you are right, it was an embarrassing spectacle for the AHS folks. Poor Chris is also so tall he looked like he was under KGB interrogation the whole time ;) Not to mention, WAAAAY too much time wasted on introductions, this should all be in the program. It is unfortunate, because I do think that the role of starch in human nutrition is a valid discussion that should be had, but not this way.
Apparently, quantification of FFA is tricky which is why it seems to mostly be evaluated specifically in diabetes studies. That is an important observation if you ask me. The diabetologists have known that NEFA play a crucial role -- if not always the exact mechanism(s) -- for decades now. In any case, it's doubtful home-meters for them are anywhere on the horizon.
I would love to see a comprehensive post prandial metabolic profile, OGTT and OLipidTT. It should look at insulin, glucagon, perhaps other hormones and factors like IGF, GLP, GIP, glucose, total triglycerides, VLDL-TG and NEFA. No idea how much this would cost, but man oh man would it give all the possible answers in one swoop!
Jimmy has backed himself into a corner like no other. He literally cannot alter course, and whatever bridges out he could have taken in moderating his carb intake he pretty much burned over the past couple of years. Everyone else that I can think of has something outside of their internet diet-related presence ... for most, their IDRP is only a fraction of their total worth/income. That can't be a financially comfortable position to be in in any environment, let alone today's economy coupled with his unstable weight. This instability is nothing new and it must be super stressful.
I too would love to see him do your experiment for a year. It would be difficult, but I think it would be worth it for the rest of his life.
The current LC diabetes diets tend to go out of their way to avoid caloric restriction.
Yes, protein may be a confounder here.
I'm not sure what you're talking about with insulin denialism, unless you are referring to those who deny the crucial positive roleS insulin performs in the body.
Gut insulin from Foxo1 loss.
Neuroendocrine cells, including those in the gut, have a vast array of functions. A new study shows that conditional inactivation of the gene encoding Foxo1 in mouse intestinal endocrine cells converts them into cells synthesizing and secreting insulin. Ectopic gut insulin production was sufficient to ameliorate glucose control in mice with conditional pancreatic β-cell loss and diabetes mellitus.
http://www.ncbi.nlm.nih.gov/pubmed/22456735
There is a theoretical basis here for a ketogenic diet supplying some non-pancreatic insulin.
"FoxO1 suppression by LCFA analogs may provide a molecular rational for the beneficial efficacy of carbohydrate-restricted ketogenic diets in treating diabetes."
Elizabeth developed diabetes in 1919 at age 11. She was treated initially by Dr. Frederick M. Allen at his special clinic, the Physiatric Institute in Morristown, New Jersey. Dr. Allen put Elizabeth on a strict diet and continued to monitor her condition over the next three years while she lived at home with a private nurse. The diet was typically as low as 400 calories per day, and was restricted to a point below which sugar was detected in the urine. It caused a gradual weight loss from 75 pounds to a mere 45 pounds from 1919 to 1922 when insulin became available.
By the winter of 1921/22 her health was deteriorating seriously; she was 14 years old and weighed 52 pounds.[2] In 1922 her mother contacted Canadian doctor Frederick Banting in Toronto. Elizabeth came to Toronto with her mother in August 1922 and began receiving insulin from Dr. Banting.[3]
Elizabeth's health continued to improve with insulin treatment. She returned to school in 1923 and graduated from Barnard College in 1929.
Avoiding calorie restriction is not the same thing as overeating. Appetites vary naturally, and are often easier to control on LCHF diets. LCHF diets for diabetes are not high-calorie diets in trials.
http://en.wikipedia.org/wiki/Richard_K._Bernstein
In 1946, at the age of twelve, Bernstein developed type 1 diabetes. For more than two decades, Bernstein was what he calls, "an ordinary diabetic"—one who dutifully followed doctor's orders. Despite his diligence coping with the disease, the complications from his diabetes worsened over the years, by the time Bernstein reached his thirties, many of his body's systems began to deteriorate.
Bernstein began to measure his blood sugar about 5 times each day and soon realized that the levels fluctuated wildly throughout the day. To even out his blood sugars, he adjusted his insulin regimen from one injection per day to two and experimented with his diet, notably by reducing his consumption of carbohydrates. Three years after Bernstein began monitoring his own blood sugar levels, his complications were still progressing and he began researching scientific articles about the disease. He discovered several studies on animals suggesting that complications from diabetes could be prevented, and even reversed, by normalizing blood sugars. This is in contrast to the then extant treatment of diabetes which focused on low-fat, high carbohydrate diets and on preventing hypoglycemia and ketoacidosis.
Bernstein set out to achieve normal blood sugars; within a year he had refined his insulin and diet to the point that they were normal throughout the day. After years of chronic fatigue and complications, Bernstein felt healthy and energized. His serum cholesterol and triglyceride levels were now in the normal ranges, and friends commented that his complexion was no longer gray. He is believed to be the first individual to self-monitor his blood sugar and was an early advocate for such monitoring by diabetics.
In 2008, at 74 years of age, Bernstein has surpassed the life expectancy of type 1 diabetics. He attributes his longevity to the low-carbohydrate dietary approach and lifestyle changes he developed for diabetics. As of 2006, Bernstein had an HDL cholesterol of 118, LDL of 53, Triglycerides of 45, and average blood sugar of 83 mg/dl.
I guess, being a professional doctor, he's making money off his diet so needn't be taking seriously. Surely that kind of criticism really belongs in the U.S.S.R., not the U.S.A.
I'm sure someone with better 'Google' talents than me could find the information.
http://www.nytimes.com/2006/02/05/nyregion/05diabetes.html?pagewanted=all
http://www.youtube.com/watch?v=mdxVfi632Xw&feature=relmfu
Same Debate Topic.... Different Conference....Different Cult ... but only 7 years apart.
Uncanny similarities between these two communities... (paleo and vegetarian)
Bernstein has proven his case by living to 74 - that makes his lipids acceptable whatever they are.
Dr. Bernstein has normal lipids, HDL a bit high but it's working for him. He also uses insulin and I believe metformin.
I want to make clear I'm not anti-LC for diabetes. However, given the varying and invariably beneficial actions of insulin in the body, if it were me or a friend or relative who asked my opinion, I'd say normalizing insulin levels and action in the body is a better goal than just managing glucose levels. The thing is, if one focused on insulin, the glycemia will follow, but not vice versa. So if I'm wrong, there's not really much of a downside, if the LC'ers are wrong, well ...
Let's have a look at PHD.
2500 calories required.
800 calories from non-toxic carbohydrate starch and protein (mix and mingle).
That leaves what? 1700 calories from fat with a restriction to SFA and MUFA. Yeah. That's high fat, if not, very high fat.
Somehow, I am having a very hard time overlooking the dichotomy between the premise and spirit of this blog post and the conclusion that PHD's potential for harm is substantially low.
Cheers.
I have seen the high-HDL low-LDL in LCHF people who work out. I wonder if metformin mimics this.
1. I was asking above about 2500 cals b/c I was not aware there was some caloric requirement.
2. There have been some tweaks since earlier editions and I've asked Paul on his blog about protein -- I tend towards higher protein so the general guidelines can be for up to 1000 cal from protein and carb.
Now ... I am not 100% onboard with everything in PHD. Most specifically, and I hope to outline some of this in coming months, that the rest of the energy is preferred to come from fat. Paul mentions 30% carb which, btw, is specifically from starch, and there are more carbs from veggies that aren't really counted. If you are adding up all piddly veggie carbs like Mark Sisson does in his sample menu, total carbs are closer to 200-250g. Or, if one is using the 2500 cal benchmark, 30% = 750 cal = 187 g starch.
So as regards this post, and Kade's concerns, yeah, I guess I should say that as PHD goes, there is likely more to be concerned over the fat than the carbs. The insulin-sensitizing properties of protein are under-addressed in PHD by my memory (it's been a while since I read the book in full, and I recall more concern w/overdoing protein than I believe is supported by the literature.
If PHD level carbs are "unsafe", one should address the reasons why -- INCLUDING insulin therapy. That is my considered opinion.
Now, to be fair, I am not all that familiar with the PHD's details and the changes that it might be undergoing. So correct me if I am wrong, but wasn't there some statement at AHS '12 by Paul Jaminet during that 'safe starch debate' that glucose should be capped off at 150 grams? As you say, he prefers fat as the optimal fuel with carbohydrate being a side-essential macro nutrient. Again, I could be wrong. For all I know, Paul may have used that figure in the context of a 2000 calorie diet, but I am not certain.
Also, you'd be correct about the protein concerns in that paradigm, Evelyn. Paul's quite straight forward about the matter on his blog. I mean, he doesn't condemn or endorse, but states simply that for the athletic types looking for a certain physique, protein limits can be eased in order to get the job done but for longevity and long-term health, protein should be minimised to just the required level, ditto for proper starches (they should be taken). I believe there's the recommendation of getting about 50-100 grams from protein, and depending on the amount of protein, carbohydrate should be in the range of 100-150 in the form of safe starches; the rest is fuelled by fats with a preference for MUFA and SFA with minimal PUFA.
I certainly think that a more detailed post addressing this subject would be worthwhile. Yes, the PHD approach is a much more reasonable and non-aggressive model within the low-carb paradigm, but speaking frankly, it's still low-carb seeing as it promotes fat as the primary and optimal fuel.
So the question in my mind is 'Does a low-fat vegan diet suppress a normal and healthy elimination of excess cholesterol or is it therapeutically keeping cholesterol in a healthy range?'.
Is it possible to have a pathologically high HDL?
It seems that there's a lot of recent findings coming out bringing into question just how protective HDL is after all. As Dayspring pointed out in his podcast with Jimmy, HDL-C may turn out to be the new LDL-C.
I don't know what it means when someone goes LCHF and sees lipids like Bernstein's.
@George, I think it's important to look not just at percent fat in the diet, but absolute amounts. Bernstein doesn't look very tall or large, so I suspect he's not a big eater. A jumbo egg contains 6g of fat. If one eats 2 jumbo eggs fried in 1T butter, you're under 30g fat. Said meal may be a high % fat, but it's not really all that high fat in terms of what the body can effectively clear and process. This is what I think is Jimmy's problem more than anything -- he's consuming 5X that amount of fat in a sitting.
http://www.ncbi.nlm.nih.gov/pubmed/20808333
'The phytosterol-abundant diet resulted in lower cholesterol absorption (54.2±2.2% (95% confidence interval 50.5%, 57.9%) vs 73.2±1.3% (69.5%, 76.9%), P<0.0001) and 79% higher fecal cholesterol excretion (1322±112 (1083.2, 1483.3) vs 739±97 mg/day (530.1, 930.2), P<0.0001) relative to the phytosterol-poor diet.'
How does this apply to vegans?
http://www.ncbi.nlm.nih.gov/pubmed/19942022
'The total phytosterol content of the experimental phytosterol-deficient diet was 64 mg/2,000 kcal, with progressively larger quantities in Atkins, American Heart Association, vegan, and the high-phytosterol Dietary Approaches to Stop Hypertension diet (163, 340, 445, and 500 mg/2,000 kcal, respectively)'
The vegan diet is only topped by DASH for phtosterol content.
When fasting, you take away that benefit.
Jimmy never engages with interviewees who advocate higher protein levels - most notably Dr Donald Layman, tho' others have been similarly ignored.
Absent gms(macro)/Kg/day, there is too much scope for TwitTrolls to bully Les Naifs as being Wrong or Stupid.
As for what a safe consumption of protein is, I think that ceiling is far higher than is generally discussed. Many studies have looked at high protein intake and it's all been nothing but positive that I've seen (the LoBAG diets replace carb with protein in one version, pro+fat in others) except in people with pre-existing kidney conditions.
In the modern context, I bet one could live on 90% protein for years. Have a kilo of salmon per week and even the putative rabbit starvation (which I accept reservedly) won't happen - a little fat's supposed to stave that off.
There was the stuff Don Matesz put up around the time of his vegetarianism recidivism; micro-mechanistic reasons to think high protein's bad but no controlled trials and whole-body end-points.
If I remember correctly Alan Aragon tracked down some studies that were purported to show adverse kidney effects but the actual studies only found higher blood flow through the kidneys, which really can't be spun as any kind of toxic overload effect.
http://www.ncbi.nlm.nih.gov/pubmed/22365371
A kilo of salmon per week - piffle, that's not so much!
I do not know the percent fat in a rabbit, but I imagine if it were eaten whole animal style, rather than as drummets, one might just not starve on one. There's fat in brains and intestines, and likely good nutritive stuff in that cecum. At least one paper outlining the Inuit diet puts their protein intake rather high at 45%, and I hope one day to get around to discussing the very high protein low fat diet of an Australian aboriginal population.
It seems to be a total myth that ancient humans evolved on fatty fish BTW. The cold climate humans ate cold water mammals because these came up on land to breed and sometimes feed where humans could kill them! It is mostly warm climate coastal areas or regions with rivers/streams/tributaries where fish were easily trapped where humans consume a lot of fish. Such fish are quite low in fat indeed.
Unless there was some sort of mistake, the LC leg of that JAMA/Ebbeling study involved around 250g protein/day on average in maintenance. Yikers!
http://www.nutritionj.com/content/8/1/41
http://www.ajcn.org/cgi/reprint/90/6/1674?ijkey=e0ee007436a689d8b34f60723508d58845074ada
http://www.ajcn.org/cgi/content/full/82/5/921
mineral deficiencies other than calcium may be as important
http://jasn.asnjournals.org/cgi/content/abstract/17/11/3213?ijkey=ddecde551b9011044147ca256fd4034c72e46b9f&keytype2=tf_ipsecsha
protein and osteoporosis, that is
Doing this chronically over one's lifetime overloads osteoblasts, eventually killing them.
If I remember some search terms I'll post a link
dietary protein on the skeleton appears to be favorable to a small extent or, at least, is not detrimental. However, the long-term clinical importance of the effect is unclear, and a reduction in fracture risk was not seen. More research is required to resolve the protein debate. In the meantime the protein intakes and balance of different protein sources as indicated in the current healthy eating guidelines (eg, Balance of Good Health) represent appropriate dietary advice.'
(from http://www.ajcn.org/cgi/reprint/90/6/1674?ijkey=e0ee007436a689d8b34f60723508d58845074ada)
'For Americans and peoples of industrialized countries to achieve the combination of a high-protein diet and a net base-producing diet, a considerable change in food consumption patterns would be required. This change would involve the consumption of greatly increased amounts of bicarbonate precursor–rich plant source foods—such as leafy green vegetables, stalks, roots and tubers, and fruit—and the consumption of greatly reduced amounts of energy-dense, nutrient-limited foods—such as fats and oils and refined carbohydrates—and net acid-producing cereal grains. Such a diet would resemble that of prehistoric hunter-gatherers. How to become a 21st century urban hunter-gatherer requires considerations beyond the scope of this review'
(from http://www.ajcn.org/cgi/content/full/82/5/921 - roots, tubers and fruits, oh, my!)
'It generally is not appreciated that the acid load that is induced by the Western diet typically is on the order of 25 to 125 mmol/d protons and is present for the entire lifespan. Quantitatively, this “normal,” diet-induced acid load is large and can approach 50% of that induced in short-term (1 to 3 wk) human mineral acid-loading studies'
(from http://jasn.asnjournals.org/cgi/content/abstract/17/11/3213?
ijkey=ddecde551b9011044147ca256fd4034c72e46b9f&keytype2=tf_ipsecsha)
The conclusion in that study states:
'This study establishes that bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as Kcitrate and that this effect is independent of reported in vitro skeletal effects of co-administered K. The magnitude of the effect is large, and the safety profile was found to be excellent, albeit based on a limited sample size. The results strongly support the thesis that neutralization of the modern Western diet will promote skeletal health.'
'In a further study to complement these findings it has also been shown in a group of thirty young women that in Ca sufficiency an acid Ca-rich water has no effect on bone resorption, while an alkaline bicarbonate-rich water leads to a decrease in both serum parathyroid hormone and serum C-telopeptide.
Further investigations need to be undertaken to study whether these positive effects on bone loss are maintained over long-term treatment. Mineral-water consumption could be an easy and inexpensive way of helping to prevent osteoporosis and could be of major interest for long-term prevention of bone loss.'
Eat a diet of 90% protein the rest of your life if you want, but make mineral-water your friend. Wait... no, are you a woman? If not, you're on your own!
http://www.ncbi.nlm.nih.gov/pubmed/8198060
'On the basis of food tables, the four nearly isoenergetic diets (one lacto-vegetarian and one high- and two moderate-protein diets) were estimated to yield the following NAE values: 3.7, 117.5, 62.2, and 102.2 mEq/d, respectively. The analytically determined urinary NAE (24.1 +/- 10.7, 135.5 +/- 16.4, 69.7 +/- 21.4, and 112.6 +/- 10.9 mEq/d) corresponded reasonably well to these estimates, suggesting that the calculation model is appropriate to predict the renal NAE from nutrient intake and anthropometric data.'
NAE= Renal net acid excretion
Yes, your pee will be acidic!
Yikers = 250g = 8oz is high?
'Habitual diet and estimated NAE calculations indicate the probable ranking of urine pH by dietary groups, and may be used to determine the likely acid-base status of an individual; EAA calculations were not predictive of urine pH.'
My comment about acidic urine had to do with the hypothetical 'In the modern context, I bet one could live on 90% protein for years.' I don't think anyone expects that ever to happen!
A year of fasting, or 2 years of semi-fasting ... not much diffrence IMHO. For really high protein using real food the biggest difficulty would be getting enough calories.
I think it's doable ... that 10% leaves room, after the chicken and turkey breast for some beef liver, fish and vegetables - a kilo or 2 of spinach per day ... those 3 items should take care of most possibilities for deficiencies.
http://www.columbia.edu/cu/news/07/08/bones.html
I'm also wondering about 'protein' drinks. I like Muscle Milk, but I just checked the box and saw that it is 20 grams of protein but also has 7 grams of fat and 7 grams of carbohydrate - plus a ton of supplemental vitamins (the usual suspects).
Do they actually make pure protein drinks and people drink them? IMO, drinking egg whites would be quicker and cheaper!
I'm skeptical that 90% protein wouldn't cause some serious problems. You're right in thinking it would have to be fat-free chicken breast (no fat, no skin - and it still contains fat, 3 grams in 100 grams of chicken!) A kilo of spinach per day would be a lot of spinach and the oxalates alone would give you some discomfort, eventually.
http://www.ncbi.nlm.nih.gov/pubmed/17538185
' For participants in the highest compared with lowest quintile of dietary oxalate, the relative risks for stones were 1.22 (95% confidence interval [CI] 1.03 to 1.45; P = 0.01 for trend) for men and 1.21 (95% CI 1.01 to 1.44; P = 0.05 for trend) for older women. Risk was higher in men with lower dietary calcium (P = 0.08 for interaction). The relative risks for participants who ate eight or more servings of spinach per month compared with fewer than 1 serving per month were 1.30 (95% CI 1.08 to 1.58) for men and 1.34 (95% CI 1.10 to 1.64) for older women.'
Ouch.
35 ounces (1 kilo) of raw spinach would give you 35 grams of carbohydrate. You'd be getting 5,915% of your daily requirement for vitamin K every day, which is an interesting experiment in itself.
'I bet one could live on 90% protein for years.'
How many year are we talking about, here?
I think 2 years is a reasonble compromise - if a fast is survivable for a year, then with some food 2 year sounds do-able
Lyle Mcdonald and Alan Aragon have written about the medically supervised fasting for hyper obese subjects In one interview Alan (or Ian McCarthy) mentioned one woman did her PhD while supervising one case in a hospital where the subject fasted for a year.
For the hyper obese the claim is they could go longer but eventually they go off the (mineral/vitamin/EFA supplemented) fast when they reach a predetermined goal weight. Since the main length limitation is the calorie deficit, any macronutrient that fills in the deficit would lengthen the length of time the fast could be done
I'm very interested in the kidney stone issue- I've been personally been eating a lot of vegetables recently, often a half kilo of spinach, occasionally a kilo and a bunch of kimchi every day.
I've just been drinking a lot of water to prevent stone formation, I'll probably take a month or few off spinach completely several times a year.
NO issues with vitamin K that I can tell, I'm more concerned with hypervitaminosis A because of the beef liver PLUS the beta carotene in spinach PLUS a couple of other high carotene foods I"ve developed a liking for.
It's definitely Primal to over-eat fat, just not every day, let alone every meal.
I find there's a point where fat produces some kind of disruption, like high-carbs used to, but different. Maybe 60-90g.
Late in the day on an empty stomach, I can pretty much handle any amount, but not if having regular meals.
http://www.youtube.com/watch?v=y_swvt0CLsc
http://www.ncbi.nlm.nih.gov/pubmed/16376893
In this human study, linoleic acid impaired nitric oxide tone; high oleic control diet was not as bad, but inferior to baseline diet - of high SFA from butter.
http://www.ncbi.nlm.nih.gov/pubmed/9844997
The thing is, dietary fatty acids should not effect things much because they are supposed to be sequestered away in chylo, then taken up by either adipose or peripheral cells, or recycled by the liver into VLDL. Free fatty acid levels and composition is supposed to be governed mostly by release from adipose tissue. When someone is eating a huge fat load, I can't help but think there are more escapees of dietary FFA into circulation. In this regard, the PUFA would disrupt things more than SF or MUFA as it is not a large constituent in fat tissue.
'..Whole grains as the starch source at the base [of the food pyramid] may have been misguided...'
Could I ask you please, why might this have been misguided? I know there are many arguments against whole grains but I don't know of a single one that really holds water. All food contains things you could call toxins, which need to be excreted or made into something else. We have complicated metabolic pathways for this, and it seems to me that it's ignorance of these pathways that make people think grains contain 'toxins'. Gluten, for instance, should normally be broken down completely and cause no problems, but cannot be if it isn't accompanied by the micronutrients needed to activate the enzymes that do it. Ditto for lectins. As for phytic acid, our gut bacteria have the same enzyme for degrading it (phytase) that rodents have. Theirs is in their gut bacteria too. Nobody argues grains are toxic to rodents.
I don't understand how white rice could be called 'safe starch'. It's had nearly all its magnesium removed. Magnesium is needed for metabolism of the starch and without it starch is definitely not safe.
I also don't understand why people think grains must be 'properly processed'. The grain-eating people of northern India studied by McCarrison 100 years ago did not ferment their (wheat) bread and were probably the healthiest people on the planet.
(I realize that may be a topic for a whole other blog entry...!)
Read Spreadbury's paper for a nicely presented, albeit still hypothetical, outline that does hold some "water":
http://dx.doi.org/10.2147/DMSO.S33473
Spreadbury's paper deserves a wider reading.
I stir fried some water spinach recently. It tastes fine just gets wrapped around my braces and ends up being a choking hazard.
It's clear enough that more and more carb restriction and saturated fat intake increase makes the body more and more glucose intolerant. It's also clear that there's a thing like excess carbs and sugar. So if you ignore all the mumbo jumbo and hype of VLC eating groups, what's a good diet to control blood sugar?
as a result there are now 2 types of lower-SFA spreads
1) expensive ones with, say, olive oil and butter, or butter, water and emulsifier...
2) cheap ones with <1% trans fats - made from mixtures of soy or canola oil, with palm oil and/or beef fat.
I had to laugh when I saw that beef fat and high-SFA palm oil are now necessary for the manufacture of margarine, now that trans fats are fata non grata!
RE protein - I had a look at this - it seems we cant very easily process more than 4 g/kg/day. http://paleozonenutrition.com/2012/08/07/how-much-protein-should-i-eat-protein-fat-amounts-in-fish-meat-eggs-poultry/
Rats are specialist grain eaters. They REQUIRE a diet that is very high in cellulose and extremely low in fat (2-4%). Rats have a totally different gut microbiota to humans.
There is no evidence that the North Indians were the healthiest people in the world. McCarrison merely noted that they were healthier than (extremely unhealthy) vegetarian South Indians.
The healthiest people in the world are those that eat starchy root vegetables such as the Kitavans and traditional Okinawans.
So now I'd invite you to go back to wherever "everyone" is hanging out and be careful the door doesn't hit you on the way out. Normally I would have invited you to repost your comment, but you are no longer welcome here.
"whole grain" means wheat and that means cereals and bread for the most part. Most "whole grain" products aren't/weren't 100% or even near that, and when you grind them to dust it makes for calorie rich, fiber poor starch.
The new My Plate is actually pretty darned good, IMO, if we just replace "whole grain" with "starchy veggie or whole grains". That potatoes are the "vegetable" Americans have increased consumption of most (in the form of french fries and variants thereof) is a problem, and this notion of having a whole grain requirement in the guidelines for school lunches? Huh? Granola bars and such being marketed as a way to "get a full serving of whole grain" or sugary puffy kids' cereals marketed as "whole grain" because that's the first item on the ingredients list. That's what I'm against. So that's why I think it's misguided.
There have been studies in one of the most diabetes-riddled populations out there -- the Pima in AZ -- and returning to traditional diet with staples like amaranth, mesquite and tepary beans. It's a very low fat high carb diet and it works for them. The LoBAG diets (search on that here for posts) show that high protein is effective for improved glycemic control.
LCHF works wonders over the short run, especially if accompanied by significant weight loss. But over the long run ...
Somehow it always keeps coming back to all of these higher carb lower fat consuming cultures being healthier and free of diabetes.
I truly believe that for most people, it ends up being about the calories and energy balance.
Help me out here blogblog. I am having trouble finding any literature for this.
Yeah, lots of the PUFA studies uses these types of oils. I'd be more interested in seeing studies with whole foods like avocados, olives, sunflower seeds and such.
Thanks for the protein link. Just to be clear, I'm not advocating a high -- by gram -- protein diet. But I was taught that the ceiling was around 250g/day and that appears to be one of those "facts" that somehow came to be common knowledge. Of course we have to eat something so in maintenance, there's got to be more than 250g carb or 100g fat in the diet if one is limiting the other macro severely. Looking around the globe through the ages and betting on the known, it seems the safer bet is more carb not more fat.
Your reply reads as an ignorant dismissal of Spreadbury's hypothesis. Perhaps you will reconsider.
The core of the hypothesis is this: Western diets present an evolutionarily novel gastrointestinal chime that is rich in high-density and largely acellular sugars and starches. The hypothesis is further that this chime promotes an inflammatory response from human gastrointestinal microbiota. The hypothesis is further that the products of this inflammatory response are absorbed from the small intestine into the bloodstream and lymphatic system, that such absorption is likely enhanced by dietary fat in the chime, and that the resulting microbiota-sourced inflammation interferes with satiety signaling in the human nervous system. Spreadbury's contribution is in the weaving of these emerging threads into a fairly explicit hypothesis that is readable, nicely presented, and likely testable.
Spreadbury's hypothesis may turn out to be incorrect, or if correct only marginally relevant, but it is way too interesting and specific to be dismissed as "just ... a sciencey case against processing".
If Spreadbury is correct, the Atkins-Taubes-style low-carbohydrate prescription for obesity is supported as useful but overly restrictive, however problematic and incomplete the original Taubes diagnosis may be. And if Spreadbury is correct, his hypothesis has clear relevance to Jane's comments relating to "healthy" whole grains at the base of a food pyramid.
Western diets may be novel in acellular fats, but that and the implications would be central to the Evelyn hypothesis, not the Spreadbury hypothesis. Please do note that the rendering of animal fats in heat is likely a pre-pre-pre-agricultural technology.
It's like the ten thousand news stories I've heard over the last 30 years promising a cure for cancer in 5 years, except many of those have a NEW bench study to talk up ... in this case there's not even that much.
Not true.
Hype - If an accusation, I plead innocent.
But I do apologize if my postings influenced your attention in a unproductive way. May you always find information that is more relevant and topical --- when reading in the comments section of this website named "The Carb-Sane Asylum".
Evelyn,
Yes the abstract, I presume in brevity, is missing the very useful qualifier "ad libitum", but the qualifier does appear nine times in the text of the paper.
Would you object even with that qualifier?
You did nothing to apologize for
Julianne, interesterification can be used to prevent alpha-linolenic acid from going rancid; it's a way of getting more omega 3 into spreads.
I know it can be used to harden fats, but surely that's an expensive way to do what the palm oil and beef fat are doing; do you know what products use it?
There's a variability of esterification in nature, which could explain some high-PUFA vegetable oils having lower smoke points than others.
"In most vegetable dietary fats, palmitic (C16:0) and stearic acids (C18:0) mainly occupy the 1- and 3-positions of the triacylglycerol molecule, whereas an unsaturated fatty acid such as oleic acid or linoleic acid usually occupies the 2-position. In animal fats, this is not the case. Interesterification of vegetable oils will enhance the amount of saturated fatty acids at the 2-position. Fatty acids at the 2-position are biologically different from fatty acids at the 1 and 3 position because they are handled differently during digestion and metabolism, and a relevant scientific question is whether there are health effects following from this."
http://en.wikipedia.org/wiki/Interesterified_fat
Margarine in New Zealand
To be called Margarine, it must be at least 80% fat. Anything less than that is an "edible oil spread." Margarine could not be sold to the public from 1908 until 1974. To get it before 1974, you needed a doctor's prescription. When the ban was ended, the dairy industry asked for another concession -- that Margarine manufacturers be forced to colour it blue. This time, Parliament told them to get stuffed. The gravy train for them had ended.
Read more: http://www.cooksinfo.com/margarine#ixzz2C9cadLvV
See butter rationing notice and link in the second part of my latest blog: http://hopefulgeranium.blogspot.co.nz/2012/11/hcv-replication-diabetes-main-roads.html
Slightly more nuanced writing than before thanks to this blog.
I just bought the book: The Art of Fermentation by Sandor Katz (2012 publication, Phaedon books). Gotta make time to read this. I make loads of kefir btw. Anyone in Toronto want kefir grains (my babies).
Amaranth is a lovely green. High protein, no oxalic acid, easy.
Actually, if you are eating loads and loads of greens, and I do it sometimes too, I cook them in whatever way I choose, then put them in the fridge to warm up for meals during the week.
I despair. I really did think you were doing your homework since the time you used to argue with me on Hyperlipid. Here is something about McCarrison.
"My own experience," [McCarrison] wrote in his book, "provides an example of a race unsurpassed in perfection of physique and in freedom from disease in general. I refer to the people of the State of Hunza..."
[he was their doctor for 7 years]
...The first object of McCarrison was to see if the rats in their small sphere of life could be made exceptional in physique and health. ...he chose as a diet for them one based on those of the three people of excellent physique, the Hunza, the Pathan, and the Sikhs.
...The diet given to the rats was chapattis, or flat bread, made of wholemeal wheat flour, lightly smeared with fresh butter, sprouted pulse, fresh raw carrots and fresh raw cabbage ad libitum, unboiled whole milk, a small ration of meat with bones once a week, and an abundance of water, both for drinking and washing.
...The result was very remarkable. Disease was abolished. This astonishing consequence, however, must be given in McCarrison's own words in the first of two lectures given at the College of Surgeons in 1931.
"During the past two and a quarter years there has been no case of illness in this 'universe' of albino rats, no death from natural causes in the adult stock, and, but for a few accidental deaths, no infantile mortality. Both clinically and at post-mortem examination this stock has been shown to be remarkably free from disease. It may be that some of them have cryptic disease of one kind or another, but, if so, I have failed to find either clinical or macroscopical evidence of it."
The Wheel of Health (1938) Chapter 2
This is just speculation on my part, I am not an MD and haven't got any expertise at all in this field. What I do have is the experience of actually being a thin person who is susceptible to IR.
My observation is that I can carry a higher fat mass by percentage than appearances would suggest pretty easily. Some of this may be and probably is intra organ. I experience the health effects one would expect from being overweight without actually being overweight.
It's interesting to me that Evelyn describes herself at 110 as underweight and visible abs shredded whereas I at 110 am decidedly neither even though I think we are of similar height.
What works for me in general is using a modest hand with both added fats and added sugars day to day and employing regular exercise [both moderate cardio and strength training].
I'll be lighter than people would expect me to be at what appears to be the optimal fat percentage range to keep everything functioning smoothly but even then my fat percentages won't be particularly low. I won't get collar bone thin or have visible abs for example.
The idea that appropriate, intermittently high insulin causes insulin resistance is majorly, bogusly, bollocks - misapplying as it does the lessons from things exogenous testosterone administration or the analogy of simple human control systems like the house thermostat.
It just doesn't happen with insulin the same way.
Insulin's more like stomach acid - produced as needed and not held at a controlled level. It (insulin and stomach acid) is controlled and measured so you don't over-produce, but not the same way as some other chemicals are.
True, I assumed that Leo was referring to ups and downs that were unpleasant rather than "I ate some carb and my blood glucose monitor said I went over 100". That's probably an important distinction.
Well, at least one reader was interested. (smile)
I converted from a low-fat/Mediterranean style diet with plentiful grains to a Lindeberg-style (and thus Spreadbury-conforming) diet eight months ago. In that time, I've experienced markedly reduced dental plaque (microbiota of the mouth), complete elimination of long-standing GERD (microbiota of the stomach), markedly improved satiety, sharp improvements in metabolic markers, and a needed weight loss of 50 lbs. Given this experience, I am quite congenial to the idea that a dietary response by microbiota in the small intestine may be related to these changes, and maybe too congenial.
For now, I am guessing that Spreadbury is correct - or at least quite close to correct - in identifying a typical seed of metabolic cascade.
I'm in no position to speak for Spreadbury (or for Ray Cronise, who apparently has some similar ideas that he may soon explain) but:
Look not at the starch. Rather, look at how it is packaged.
_________
Dunno why you address that to Jane. want to know how she'll respond?
http://anthonycolpo.com/the-whole-grain-scam/
> Tell me about other antinutrients, and I will tell you why they are not a problem.
she's "interested" in Spreadbury ... to the extent he's pro-whole-grains or thAT she can however remotely spin him as pro-whole-grain she'l love him.
Negatives? She'll minimize, dismiss, pretend they don't exist ... anything to try to get rid of them.
"tell me about the problems ... I'll show you where you're wrong"
these predictions are an iff-y thing - the person could change their behaviour specifically to falsify the prediction, but If it happens here, it will be a one-off thing.
for work safety copy and paste the below into your "url" bar
https://www.google.ca/search?client=ubuntu&channel=fs&q=%22nathan+thurm%22&ie=utf-8&oe=utf-8&redir_esc=&ei=NiukUMziAaqGyQG12YDQCQ
Hypothesis: bacteria control host appetites
Abstract:
To help investigate the relationship between inflammatory and other diseases and the composition of the gut microbiota, we propose that a positive feedback loop exists between the preferences of the host for a particular dietary regime, the composition of the gut microbiota that depends on this regime, and the preferences of the host as influenced by the gut microbiota. We cite evidence in support of this hypothesis and make testable predictions.
http://jb.asm.org/content/early/2012/11/05/JB.01384-12.abstract
Don't make me laugh. My university training as food scientist goes back to 1986. I've forgotten far more about food science and nutrition than you will ever learn.
I's sick of reading this ancient " primal nutrition" crap by people such as Cleave, McCarrison and Stefansson. The world of nutrition has well and truly moved on since the 1930s.
The Hunza health myth has been well and truly discredited. It is know known that they had exceptionally POOR health.
"...The diet given to the rats was chapattis, or flat bread, made of wholemeal wheat flour, lightly smeared with fresh butter, sprouted pulse, fresh raw carrots and fresh raw cabbage ad libitum, unboiled whole milk, a small ration of meat with bones once a week, and an abundance of water, both for drinking and washing."
Of course the rats were healthy. They were eating something very close to their natural diet.
Rat and human digestive phsyiology are polar opposites. Rats require a high cellulose diet and can't tolerate fat.
true, was talking about symptoms like blood sugar spiking to 200 and then after 1 hour crashing to 45 mg/dl
what kind of diet would you suggest? moderate or high carb?
what is a good macronutrient ratio generally to you?
I have read a lot on how LC is not that good but I haven't read anything about the alternative, so I am as confused as before.
I imagine you are trying to tell me you eat white rice. Colpo does, and that's why I emailed him. I was astonished when he posted our conversation on his blog. Why would he want the whole world to see an argument he lost?
The Hunza are certainly not particularly healthy today, and have not been since their population started to increase. Their land can support the 6,000 there were 100 years ago but not the 44,000 there are today. Episodes of starvation have been destroying their health for a long time.
I imagine your university training as a food scientist taught you the optimal diet for humans. Why then is it that when you and I first met, you were eating practically nothing but meat, and now are apparently a vegetarian?
I think g2sb wants an unbiased, unprejudiced discussion, I was pointing him to clues of what he's likely to get instead.
I'll admit I'm also rather jaded by the last fad blaming the gut -- Candida! Candida were calling out to the hosts to eat sugar and carbs ... feed me, feed me!! But there's little evidence to support this. If I recall Atkins claimed this in the original book but I could be confusing my gurus at this point. The reason I quoted what I did from the abstract was one of relevance.
To me any association with one type of microflora vs. another and obesity is basic microbiology -- got lots of extra starch that makes it further down the pike? Bacteria that likes starch grows and muscles out the other stuff. Feed the other stuff what it likes, it grows. Do the bacteria now demand more food from their host of a certain type, altering appetite/satiety?
But why not find out what's going on there?
Good points all, but a counter argument is that the obesity epidemic has a rather large correlation with the green revolution (order-of-magnitude improvement in wheat yield per acre) and the invention of HFCS. Such ingredients are now ubiquitous in fast foods and in the grocery store because they are historically inexpensive and people really, really like foods that contain them.
If I'm not mistaken, wheat consumption is actually down considerably from the late 1800's, so now we're in Wheat Belly territory blaming a particular strain to have any legs on that one.
I guess I always go back to thinking about the alcoholic and what they will drink. Alcoholics will resort to drinking cough medicines, mouth wash, horrible home made concoctions (my husband and his friends have brought back some of the most horrific liquor from the old country one can imagine -- smells like gasoline!), etc., to get their fix. And yet somehow never during even my binge days did I open a bag of flour and have at it. Same really for sugar, though in small quantities it can be appetizing.
As to HFCS, yeah it made the Big Gulps and such possible and liquid calories are killer. But I see the little bits of HFCS in processed foods being more about palatability and such. I doubt it has anything to do with messing with the gut flora. I think stabilizers and emulsifiers play a role too ... Keep fatty food from separating into a greasy mess, you can add more salt, add more sugar, play mind games with taste buds/satiety/etc.
But then we get back to gut bugs and leptin resistance. Does HFCS promote different gut flora vs. sucrose?
As far as new items introduced I am very, very skeptical.
Dr. Davis (aka "Wheat Belly") likes to blame Norman Borlaug with introducing the wheat that damages but celiac has been documented since the late 1800. 1888 was the first specifically identifiable case I believe.
so IMHO no corpses can be laid at dwarf wheat's feet that can't be laid @ any traditional wheat's feet.
And no, medical guesses and in vitro tests of whole wheat's Manganese and Magnesium helping digest gluten don't translate into real celiacs and those who don't tolerate gluten being able to eat whole wheat. Medical fantasies and proposals are one thing - quite a different thing tested in real people with well controlled trials.
as far as
new, novel proteins
or grossly large amounts of protein where before there were only trace amounts
These are the results:
Fasting bg 98
Fasting insulin 6.1
1 hour glucose 205
1 hour insulin 165
2 hour glucose 43
2 hour insulin 40.2
I will try eating some carb before and some later, thanks
Do you think starches like pasta, rice, bread, barley, quinoa are appropriate? Do you think I should remove sugar from the diet or eat a little? I'm thinking of trying something lik4 40/40/20 Carbs, Fat, Proteins. What do you think?
http://ajcn.nutrition.org/content/82/1/41/F5.medium.gif
Now this was to meals, not 75g glucose, but the increase is less than 10 fold. Presuming same units, your insulin response on the OGTT is roughly double that seen on average. Your 2 hr insulin seemed kinda high to me except that would appear to be normal. In that figure (baseline diet, high protein (30%),and ad lib HP - ate ~450 cal/day less) we see insulin stays elevated so perhaps your 2 hr mark is not all that out of the ordinary..
I'd be curious what your phase 1 (2-15min) insulin response is. I'm not a doc and don't know what is causing your reactive hypoglycemia. Here is one collection of possibilities: http://www.reactivehypoglycemia.info/articles/what-causes-reactive-hypoglycemia/
But I note they mention early stages of diabetes. But you clearly can mount a good insulin response (Perhaps that's exaggerated second phase b/c first phase is insufficient? I'm just guessing here!)
There was a reactive hypoglycemic person who posted quite a bit at Jimmy's forum a couple years ago. He had emailed me at the time that having small amounts of honey here and there helped him. I'm thinking the fructose doesn't spike the insulin, but enough glucose to keep the BG from crashing. He did not do well on VLC and he did try that!
What did your doc say about the BG over 200 at 1 hour? That's a diabetes diagnosis, or did they dismiss that b/c your BG had come down so low in the next hour? I'd pursue that if it were me.
I had no idea this is what you think of me. Well, I suppose I had SOME idea. You never talk to me on WHS and I suspected there was something going on. Please could you tell me exactly what it is? Do you find everything I say wrong/stupid/annoying or is this just about whole grains?
IME there is a lot of flexibility about how much protein one can eat, and higher protein intakes are often therapeutic. IME the difference between different proteins is more important the amounts. I have a clear limit on how much beef I can safely eat, but not lamb.
> Sanjeev, try tricolour amaranth instead of spinach. It's not an oxalic acid bomb.
Thought I should update you on this -
Hope you're still lurking here: I found some clues that Amaranth's oxalic content can be very high - the relevant papers that document actual analysis have never made it onto the internet but a couple of papers quoted from them.
I've gone over to seaweed as my main vegetable source, with spinach, amaranth, mustard greens or cabbage only occasionally
I'm avoiding Konbu for the high iodine, but I'm eating Nori, Wakame, and so on in unlimited quantities - the frozen bags for salad and I've been using the dried sheets the same way I used to use roti (a replacement for spoons, to scoop up soup & food chunks)
Post a Comment
Comment Moderation is ON ... I will NOT be routinely reviewing or publishing comments at this time..