Thermodenyics in the Incestral Health Community: It Began with Atkins
For the past couple of months, I've been somewhat obsessing about thermodynamics having written the AARR piece and a few blog posts, not to mention revisiting several dating back to near the beginnings of this blog. I began this a while ago as a single lengthy post, but it's gotten out of hand and finding time to tidy up such a post vs. publishing shorter chunks in parts became impossible. Not sure how many parts this will have. This series will put several members of the IHC "on the record" so to speak. While I've done so in the past, the hope is to have it all in one place.
Robert Atkins the Calorie Guy!
Surely Atkins is an honorary member of the IHC, even though he passed away over a decade ago before this community reached the level that it has. Most of the "greats" have learned something (perhaps essentially everything) they know about low carb diets and tangentially about thermodynamics/calorie theory from the "late great one" himself.
In 1972, Atkins came out with his first book, Dr. Atkins' Diet Revolution, with the subtitle "the high calorie way to stay thin forever". I have the paperback version of this from Bantam Press (1973) though it went through many reprintings. Atkins never intended to be a calorie guy. After all he titled Chapter 8: To Stay Fat - Keep On Counting Calories, wherein he attempted to debunk the "calorie hoax" and repeatedly blasts this as failed. Interestingly, he even states that we'd been counting calories for 60 years, which would put our national obsession with such dating to the early 1900's ... an odd claim to be sure. On page 94 in that chapter, Atkins wrote:
The calculation of calorie outflow is based on the assumption that fat, as it is burned in the body, is completely degraded (biochemically broken down) to yield all the potential heat (energy) that it contains. (The end products are the basic substances, carbon dioxide and water.) If a portion of the fat molecule were to leave the body in another form containing potential energy, the calorie theory would be proved wrong.
In actuality, this is not true! Atwater and others have always taken into consideration what was excreted unabsorbed (feces) and incompletely metabolized (urine, breath). Atkins goes on to make this rather exciting claim:
We already know about our wonderful friends those ketone bodies and how they are being excreted in the urine. We measure them with our "turning-purple" sticks. Dr. Kekwick and Dr. Pawan, in their pioneering research, were the first to point out that a significant amount of latent energy is excreted in this form. On a low-carbohydrate diet nearly three times as much energy is lost in the urine and stools, mainly in ketones, as on a high-carbohydrate diet. (italics are Atkins')
Atkins goes on to exaggerate the additional ketones lost in breath. The above (highlighted) claim is probably factually accurate, perhaps even a conservative estimate. But it is misleading as the amount of ketone energy lost to the urine is minuscule and three times minuscule is still going to be pretty minuscule! Atkins sought to replace the existing calorie theory with what he called The Diet Revolution Calorie Theory. I snapped a picture of this on my cell phone and augmented it a bit for effect.
This was over 40 years ago. Atkins merely misrepresented the First Law or Calorie Theory or whatever you want to call it, (noting that calories in are chemical potential energy of absorbed molecules):
Calories In = Calories Expended + Energy Stored
Calories In = Calories Expended + Energy Excreted + Energy Stored
It's not really anything groundbreaking or different. Atkins just grossly misrepresented the magnitude of the energy excreted as being quantitatively significant (which it is not). A formal complete accounting of energy in the human body -- no gimmicks required -- would include energy excreted. Most don't because this has been measured to be on the order of less than 1% of total energy in the low carb dieter.
Atkins version 1.0 = First Law of Thermodynamics or CaloriesIn-CaloriesOut energy balance. That's the bottom line. Ketones were simply a "magic" CO term in the CICO.
Atkins Said Something Really Dumb!
... but Dr. Mike can forgive the man as a doctor, not a scientist. In 2007, the co-author of Protein Power, wrote a blog post entitled: Thermodynamics and weight loss. Seven years ago now, he wrote:
Probably no laws of physics have been so over invoked and less understood than the laws of thermodynamics. Everyone it seems is using the laws of thermodynamics to justify every position imaginable in the field of weight loss. Journalists often throw out the laws of thermodynamics to prove or disprove dietary regimens they’re writing about. Authors of various blogs and other online sites rabbit on about how the laws of thermodynamics are aligned with their pet theories. And even worse, research scientists – who really should know better – more often than not misquote the laws of thermodynamics, especially when talking about the possibility of a dietary metabolic advantage. ‘It can’t be valid,’ they sniff, ‘it violates the laws of thermodynamics.’
So, I figured is was time to delve into these mysterious laws so that readers of this blog at least can know thermodynamic nonsense when they see it.
Snicker. That second paragraph can be read as if Eades is about to serve up a load of thermodynamic nonsense. Heck ... can I snicker again? :-) I'll get to the thermo per se in a moment, but first ...
And it helps to understand the vituperation heaped on Robert Atkins who wrote one of the most hubristic and outright ignorant statements imaginable showing a total lack of understanding of the laws of thermodynamics when he said:
- When I make this claim, that you can lose more weight on a higher number of calories, I seem to be breaking the law—one of the hallowed laws of thermodynamics. Many powers-that-be get terribly provoked when I repeal their laws. But the calorie theory is a false law that is meant to be broken, and ketosis/lipolysis is the instrument for breaking it.
Actually, it's only Atkins' schtick that got him in trouble when ketosis was the instrument, he just meant the "simple calorie law that ignores excreted ketones" was a hoax. After all, IF excreted ketones were of a quantitatively significant caloric amount, his original claims didn't violate any inviolable laws after all!
Lipolysis, Ketosis and Breaking the Law
One of the things I love so about internet search engines, is that when someone like Eades quotes someone without sourcing the quote, it's not all that difficult to find it. As it turns out, Atkins wrote the above in Dr. Atkins' NEW Diet Revolution. DANDR is like the low carb Bible of the IHC. It turns out what Atkins put forth in that book did violate the First Law, but also a more fundamental concept that one barely needs to understand any science to accept. I'm talking about conservation of mass, which boils down to: what goes in must come out, or it adds to the number on the scale. It is important to understand that all absorbed fatty acids make their way out of the body in only one quantitatively significant manner:
Fatty Acid → [ β-oxidation + Krebs ] → CO2
The β-oxidation + Krebs part is the "metabolism" of fatty acids resulting in production of some heat, some ATP, and a large number of so-called "reducing equivalents" that will produce much more ATP (cellular energy currency) in the Electron Transport Chain. You don't see mass escaping your body, but the carbons that were originally contained in the larger fatty acid molecules are exhaled as carbon dioxide. Atkins' original claim was that enough molecules escaped the Krebs cycle and were excreted before being fully metabolized for their caloric content. The vast majority of β-oxidation to burn fat for energy occurs in organs like the heart and skeletal muscle. Once a fatty acid is committed to the β-oxidation pathway they are oxidized completely down to carbon dioxide.
The definition of lipolysis sounds like Nirvana to a person longing to lose weight. It means "the process of dissolving fat." Isn't that exactly why we're all gathered here today? Now I will tell you the "secret" to unlocking the latent power of lipolysis. When you burn fat, it breaks down into glycerol and other fatty acids. How does the process actually work? Are there any drawbacks? There are plenty of laypeople and even physicians who think there must be.
So it would appear that confusing lipolysis with β-oxidation is yet another common gimmick that can be traced back to the "late great one". Gone from the new book was the Diet Revolution Calorie Theory as Atkins instead threw calories completely out the window as there were even grander claims to be made!
As for the weight loss phases of Atkins, they are simple and overwhelmingly effective. I don't see any reason why I should understate the facts. Lipolysis is one of life's charmed gifts. It's as delightful as sex and sunshine, and it has fewer drawbacks than either of them!
Wow! Sign me up for unrestrained lipolysis right away!!
In the earlier editions of this book ... I said: "The term `ketosis,' when it applies to the benign, diet-induced type we're talking about, is really a shortening of the term ketosis/lipolysis, which is enough of a tongue twister that you can see why it is commonly referred to only by the name ketosis." ... The Atkins Nutritional Approach stimulates the process of lipolysis, a state I hope you are always in: burning your fat for energy. A secondary process of lipolysis is ketosis. Ketosis occurs when you are taking in a low level of carbohydrates from the food you eat, as you will during the Induction phase of Atkins. Lipolysis results in the creation of ketones (that's ketosis), a perfectly normal and natural function of the body.
Lipolysis does not make the index of the original book. Perhaps its in there, but I have neither the time nor inclination to even drudge back through the entire sections on ketosis. In the end it doesn't really matter if he equated ketosis with lipolysis back then, he did it here and "now" with DANDR first copyright in 1992. And in that book he also coined the term "Metabolic Advantage" ... a term that has come to mean different things to different people in the 20 or more odd years since. This next and last paragraph cuts to the core of the scientific bankruptcy of advocates of LC diets. I'll break it into bullet points in order to make comments directly to each issue:
- How does lipolysis work? Lipolysis simply means that you're burning your fat stores and using them as the source of fuel they were meant to be.
WRONG: Lipolysis is the breaking apart of triglycerides into fatty acids and glycerol. Fat burning is the breakdown of the fatty acids into CO2.
- The by-products of burning fat are ketones.
WRONG: Ketones specifically produced, mostly from fatty acids, by the liver. Most fatty acids are "burned" completely to CO2 in the heart, other organs and skeletal muscle.
- When your body releases ketones -which it will do in your breath and your urine- it is chemical proof that you're consuming your own stored fat.
WRONG: Medium chain triglycerides have been known to generate ketones without carbohydrate restriction. Further, on a high calorie high fat diet, there is no evidence that stored fat is the source of those fatty acids, nor that even if burned, there is a net loss of body fat in the process. Also, see Jimmy Moore in 2014 :-)
- Once more, for emphasis: When a person on a safe, controlled carbohydrate plan such as mine is releasing ketones, he or she is in the fat-dissolving state of lipolysis. This process is simply the most efficient path ever devised for getting you slim. And the more ketones you release, the more fat you have dissolved.
|From Guyton & Hall |
Textbook of Medical Physiology
GIMMICK & HYPE: (Also wrong.) Ketones in a state of ketoacidosis are indeed the result of unrestrained lipolysis and excessive fatty acid delivery to the liver. Those fatty acids are "released" from their proper storage depots (fat cells) but not released from your body.
The plot at right is for glucose, FFA and ketones after removal of the pancreas (in dog). Both glucose and FFA level off at an elevated level because glucose eventually exceeds re-uptake thresholds and is excreted in the urine (CO!) while FFA diffuse into non-adipose tissue such that the maximum level of fatty acids is roughly double the usual circulating amount. Note that the ketones keep rising.
Another way to look at this is that ketoacidosis would not be possible if the body had an efficient way of ridding itself of these molecules. Yet another way of looking at this is that if carbohydrate restriction "unlocked" your fat in the manner claimed, you would be looking at ketoacidosis instead of the mild ketosis observed under even the most stringent of conditions.
- Lipolysis is the biochemical method of weight loss -the alternative to using glucose for fuel, the very process that has made you heavy.
WRONG: Using glucose for fuel doesn't make you heavy so long as your total caloric intake doesn't exceed expenditure.
- Lipolysis can be your life raft, giving you both slimness and health, and distancing you from the obese person's perils of diabetes, heart disease and stroke.
WRONG: Lipolysis -- or unrestrained lipolysis accompanied by inadequate recycling within the adipocyte -- is what leads to the "perils of diabetes" associated with obesity. Most of the obese have long ago used this "life raft" unwittingly, as most obese have elevated circulating levels of free fatty acids.
- Most of all, of course, it is the key to achieving your goal to use up the fat stored on your body.
WRONG: To repeat, lipolysis is not fat burning, and therefore not a route out of your body for stored fatty acids.
- The phenomenon of lipolysis or fat burning being the major alternative fuel system has been so well researched that it is simply not disputed in academic circles. It is scientific fact.
THIS CANNOT BE MORE WRONG: Yes, these metabolic pathways are well researched. Yes, they are a matter of scientific fact at this point. But -- to repeat once more -- lipolysis is NOT fat burning.
The Thermodenyics of Atkins:
To sum up this first installment then, Atkins didn't really begin as a First Law denier or what I'll call a Thermodenialist. He merely misunderstood the process of constructing a valid equation based on the principle of conservation of energy. However in DANDR, Atkins earned his full PhD regalia from the school of Thermodenialism. While he still hung his hat on ketosis, the new calorie balance equation that factored in ketone energy losses went missing, replaced by the magic of lipolysis and the flat-out erroneous notion that lipolysis is synonymous with fat burning.
Once you absorb the molecules=calories, any explanation of what comes next must comply with the laws of thermodynamics (most specifically the First Law, or more broadly the Law of Conservation of Energy). Even Dr. Eades stated this point blank. Lipolysis, the breaking down of triglycerides (storage form of fat) to free fatty acids (transport/usage form of fat) and glycerol, is not the rate limiting factor in what comes next: the breaking down of fatty acids to CO2.
Furthermore, one might ask themselves why, if ketones are evidence of body fat burning, they are not present at similar levels in all humans who are actively losing body fat?!
Stay tuned ... A Thermocraptastic exposé of the mirdled low carb guru is in the queue.
The implication that I was peeing out most of these luxurious foods via ketones was even more marvelous. I feel a bit embarrassed admitting this, but I actually even ordered some ketostix online via ebay at one stage.
ketones in the breath is the building 7 of these denialists; probably real fat burning beasts produce thermite in their stool ... imagine the amount of energy lost there.
And where do farts figure into the equation?
Where I think some of the low carbers go wrong is they see their weight dropping when their ketones go up and then they start to pay more attention to the number on the ketostick than things like portion sizes and whether or not they're actually losing weight.
Near as I can tell, a ketone meter will respond either to: A) someone losing weight or B) someone eating lots of coconut oil or butter. So the person might start out restricting their carbs, restricting their protein and inadvertently restricting their calories and losing weight. But then they get addicted to the number on the ketone meter and wind up just eating a lot of butter.
It amazes me that some of these people will prick themselves with a needle 6 times a day and pee on a ketostick and count carbs and count protein grams and monitor the omega 6 to omega 3 content of every nut and seed on the planet, and parse the difference between a grass fed cow and a grain finished cow or a pastured egg vs a free range egg, but they can't be bothered to simply measure their portions or count calories.
The argument as I understand it is that if you are in ketosis, it's because your body 'prefers' to be burning fat, and therefore will dip into your fat stores for fuel, while the body of a 'sugar-burner' will simply get hungrier and hungrier until the poor sod stuffs their mouth with every slice of bread, bowl of cereal, and bag of sugar in the house.
The farts, as I understand it, are mostly generated by bacteria in the lower gut who eat the food that the bacteria in the upper gut won't touch. In Atkin's day, this was 'dietary fiber', and he gave that stuff a free pass. It didn't count toward your 'net carbs', and you could eat it freely.
This led to quite a few low-carb junk food products where the "net carb" count was manipulated or even flat-out fabricated. Plus, it turned out that a lot of these carbs actually were being converted into calories by the bacteria. So, some of the low carb clinicians started using "total carbs" again.
Recently, the low-carb community has discovered that resistant starch, which naturally occurs in things like navy beans, and is also formed when foods like potatoes are cooked and cooled, has similar benefits. But instead of, you know, deciding that maybe beans and potatoes aren't really that bad after all, some of them took to eating spoonfuls of uncooked potato starch with their coconut oil and butter. Which in turn has led to a lot more discussions about flatulence than one usually associates with optimum health.
Hey Snarks! I hope you stopped the vitamin D. My mom just told me she stopped vitamin D at the beginning of October and has been pain free for almost a week now, off all medication. She started the D two years ago, developed intractable radiculopathy attributed to spinal stenosis about a year and a half ago and had two subsequent laminectomies which provided little relief. Whoops! She has crazy good bone density, spends hours outdoors every day, lived below the 38th parallel at high altitude in sunny Santa Fe and has absolutely no reason to take oral vitamin D, but, hey, it's good for you, right?
The role of vitamin D in curtailing the development of obesity and comorbidities such as the metabolic syndrome (MetS) and type 2 diabetes has received much attention recently. However, clinical trials have failed to conclusively demonstrate the benefits of vitamin D supplementation. In most studies, serum 25-hydroxyvitamin D [25(OH)D] decreases with increasing BMI above normal weight. These low 25(OH)D levels may also be a proxy for reduced exposure to sunlight-derived ultraviolet radiation (UVR). Here we investigate whether UVR and/or vitamin D supplementation modifies the development of obesity and type 2 diabetes in a murine model of obesity. Long-term suberythemal and erythemal UVR significantly suppressed weight gain, glucose intolerance, insulin resistance, nonalcoholic fatty liver disease measures; and serum levels of fasting insulin, glucose, and cholesterol in C57BL/6 male mice fed a high-fat diet. However, many of the benefits of UVR were not reproduced by vitamin D supplementation. In further mechanistic studies, skin induction of the UVR-induced mediator nitric oxide (NO) reproduced many of the effects of UVR. These studies suggest that UVR (sunlight exposure) may be an effective means of suppressing the development of obesity and MetS, through mechanisms that are independent of vitamin D but dependent on other UVR-induced mediators such as NO.
Deng et al.  used two large National Health and Nutrition Examination Surveys data sets to assess interactions between Mg intake, vitamin D status and outcome. According to the Institute of Medicine (IOM) classification, circulating 25-hydroxyvitamin D (25OHD), the generally accepted indicator of vitamin D status, was within the deficit range (<12 ng/ml) in 12% of participants and the insufficiency range (12 to 20 ng/ml)  in 30%. Mean energy-adjusted total Mg intake (dietary and supplemental) was clearly below the recommended daily allowance, which is between 310 and 420 mg depending on age and gender . High Mg intake was associated with reduced risk of vitamin D deficit or insufficiency. ...
a) Asking your advice?
b) Asking her MD's advice?
c) Getting an independent serum 25(OH)D test?
I do not believe she wanted to be doing that!
How much Vitamin D was she taking? Everything is bad for you in excess, even water (where consuming a mere 10 x RDA is fatal).
Steenbock, 1955), beryllium, barium, zinc and cadmium (Worker & Migicovsky, 1961 a, b), cobalt and caesium (Wasserman, 1962) and iron (Masuhara & Migicovsky, 1963). It has also been suggested that a relationship exists between vitamin D and manganese (Ministry of Agriculture, Fisheries and Food, 1963), a slight deficiency of either being counteracted by a larger intake of the other ...'
T(min) , BG(mmol/L)
0 , 5.8
30 , 7.9
60 , 9.3
90 , 10.3
120 , 8.7 (<7.8 = O.K. >11.1 = Diabetes)
150 , 7.1
180 , 5.3
210 , 4.3
240 , 3.9
270 , 3.9
300 , 4.4
The nadir occurred at 4-4.5 hours post-glucose, and I wasn't technically hypoglycaemic, as 3.9mmol/L doesn't count as hypoglycaemia.
The results from the 2-hour OGTT in 2008 were:-
T(min) , BG(mmol/L)
0 , 5.0
120 , 3.7
My endocrinologist said that I still had Metabolic Syndrome, even though I had a print-out of Chiu et al (http://ajcn.nutrition.org/content/79/5/820.full ), which stated that Insulin Sensitivity was inversely proportional to 2-hour BG value. My endo' said that I didn't need to see him any more, as I had got my serum TG's down to 1.4mmol/L without medication (it was 4.95mmol/L), and BG was no longer on the high side. I haven't seen him since.
N.B. To convert BG from mmol/L to mg/dL, multiply by 18.
All three of us live well below 38 degrees in latitude where we are exposed to adequate UVB year round and have no other need for D supplementation (i.e. we go outside most days which a nursing home resident, for instance, might not). My mom was also living at high altitude. Someone living further north might benefit from judicious D supplementation, but right now it's being promoted as a magic cure-all for whomever and whatever. Unlike the UK, a good portion of the US lives in a location where D supplementation should not be necessary.
Sorry to hijack your blog, Evelyn, but I was in a lot of pain and now it's gone and it's hard not to be a crusader. I've been arguing alternative medicine topics on-line for 20 years now and diet claims are just a subset for me. I do believe that conventional medicine has it's flaws, particularly a lemming like need to adopt "alternatives" that are even slightly plausible....
What was your serum 25(OH)D level, pre-Vitamin D?
What Vitamin D dose were you prescribed?
Was it D2 (ergocalciferol) or D3 (cholecalciferol)?
What was your serum 25(OH)D level, post-Vitamin D?
It's annoying when something is touted as a "universal panacea", as it's like "the boy who cried 'wolf'". When the health problem is caused by a lack of Vitamin D, someone might refuse therapy on the grounds that Vitamin D has become "woo".
I started taking ~400mg/day of Mg (also 15mg/day of K2) in 2003, after the osteoporosis diagnosis. I'm on the same dose of Mg, but I'm taking 5mg/day of K2 as a maintenance dose.
I jumped on the Vitamin D bandwagon b/c of some improvements folks were seeing and "it can't hurt". I didn't notice joint pain, but I developed high blood pressure. Granted this was one data point, but even at my heaviest my BP was only high normal. This reading was taken after losing around 100 lbs and the nurse looked at me askance -- do you have high blood pressure? I was also having strange "dizzy" spells. I don't know how else to describe that but when I would roll over in bed my head would spin. All of this went away when I stopped taking VitD. So not everyone is deficient and there can be negative outcomes.
To all: I've been reading all comments but dealing with a ton of family issues for the past couple of weeks. Trying to keep a trickle (for me) of blog posts going and phone is good to keep tabs but no good for typing out replies.
I googled to find the dose of the TJ D3 I was taking and up popped numerous blog posts singing the praises of vitamin D for the treatment of everything. The top post was Seth Roberts on the use of vitamin D for the treatment of insomnia. I can not even find negative reports on Medline, because I'm too impatient to search theough all of the laudatory small studies.
I can believe that vitamin D causes hypertension. It's part of the renal axis. I had BPs elevated to "pre-hypertension" levels for the first time ever this past winter. I had assumed weight (BMI 25) genetics and age, but the BP post Weight Watchers (BMI 22) and vitamin D cessation is now 110/70.
Note that in California anyway, the only legal rat/mouse poison is D3. Warfarin is no longer available.
Low Carbohydrate Diet From Plant or Animal Sources and Mortality Among Myocardial Infarction Survivors
The healthiest dietary pattern for myocardial infarction (MI) survivors is not known. Specific long‐term benefits of a low‐carbohydrate diet (LCD) are unknown, whether from animal or vegetable sources. There is a need to examine the associations between post‐MI adherence to an LCD and all‐cause and cardiovascular mortality.
Methods and Results
We included 2258 women from the Nurses' HEALTH STUDYand 1840 men from the Health Professional Follow‐Up Study who had survived a first MI during follow‐up and provided a pre‐MI and at least 1 post‐MI food frequency questionnaire. Adherence to an LCD high in animal sources of protein and fat was associated with higher all‐cause and cardiovascular mortality (hazard ratios of 1.33 [95% CI: 1.06 to 1.65] for all‐cause mortality and 1.51 [95% CI: 1.09 to 2.07] for cardiovascular mortality comparing extreme quintiles). An increase in adherence to an animal‐based LCD prospectively assessed from the pre‐ to post‐MI period was associated with higher all‐cause mortality and cardiovascular mortality (hazard ratios of 1.30 [95% CI: 1.03 to 1.65] for all‐cause mortality and 1.53 [95% CI: 1.10 to 2.13] for cardiovascular mortality comparing extreme quintiles). An increase in adherence to a plant‐based LCD was not associated with lower all‐cause or cardiovascular mortality.
Greater adherence to an LCD high in animal sources of fat and protein was associated with higher all‐cause and cardiovascular mortality post‐MI. We did not find a health benefit from greater adherence to an LCD overall after MI.
Im interested in this comment, can it be explained in more details, ......where does it come from? ..... and from what references does it gain support?
I seem to have "postprandial syndrome" or whatever it's being called now - my blood glucose peaks shortly after a meal (usually no higher than around 140), and then crashes pretty quickly, but never drops lower than 70s (according to the meter I picked up). I get jitters, massive headaches, difficult focusing, and heart racing kind of effects from it.
Fat seems to blunt this effect quite a bit (I can eat potato chips, for instance), low-fat starch with protein is the worst possible combo (6 oz chix breast with 2 cups of rice and a cup of squash nearly finished me).
Initially I figured I had nuked my glucose sensitivity and that I had too much glucose in my blood, but it seems like that's the opposite of the issue now. Aside from "give up - starch is not for you - hope you like veggies" I'd like to figure out if there's something better I can do, besides eat an ounce of potato or rice at each meal and see how badly things go.
It seems the Vitamin D story is incredibly complex.
I thought you might mean, that rodents are nocturnal so they don't normally get their vitD from sunlight. I've been puzzling about that. Then I remembered I used to have very nice little mice living in my garden, and I'd see them during the day. They would come to collect bits of peanut dropped by the birds from the bird feeder. They could have come at night, and maybe they did, but not always.
Yesterday I found out that plants can make D3. Until recently it was thought they could only make D2. Some plants make such a lot that animals grazing on them get calcium intoxication.
So I suppose, rodents deal with vitD much like we do. Some comes from the sun, and some from their food. And they can tolerate large doses just like (some) humans. But really huge doses kill them, and maybe they kill humans too. I told you about my friend and her mother who both died not long after starting on high dose vitD.
A couple of weeks ago I posted a long list of "miracle" supplements that have been touted in my life and which have, on closer inspection, proved to be useless. I suspect that D falls into that same category for most healthy people and that, except in very specific cases of renal disease, supplementation may be useless to harmful.
Then there are the fringe woo-tastic nutters who take anything and everything (Null again), the more bizarre the better, and there's plenty of bleed over between life extensionists, vegans, paleos, etc that what may have started off as "hey, this may be worth more study" in a study abstract soon gets a few billion google hits on "mainstream" health blogs or fitness magazines and is reposted in a few hundred alt health mommy blogs. See above for affiliate $$$ as well here.
There's the obvious issue with supplemental XYZ most likely not being nearly as valuable as XYZ as a dietary component. There's also the folks who see "500 mg of vitamin c per day may be good for [heart health|longevity|immunity|cognition|etc]" in some study and extrapolate that to mean that 50 grams of vitamin c per day would make them immortal.
The internet has made all of this *much* worse. It used to require direct marketing to bilk folks. Now there's a universe of folks actively searching for wonder crap online.
insulin secretion and overshoot. Your beta cells are not sensitive
enough to glucose, so they don't secrete insulin at once when glucose
starts to rise. Later they secrete too much, and blood sugar plummets.
Then you get counter regulatory hormones which give you the nasty
Your beta cells probably need repairing. If you look up 'beta cells autophagy' you will find what I am talking about. They should normally be going through cycles of breakdown and re-synthesis of cell components, and this process needs micronutrients. Especially the ones found in whole grains and legumes, which of course give you the nasty symptoms. I don't know what to suggest.
Thanks for the reply and for the info. Whatever the issue is, my body seems to be learning how to produce the effect more efficiently, and there definitely seems to be a tie in with protein + carbs. I just produced the effect with 6 egg whites cooked in a little olive oil and a large apple for breakfast. I guess that kind of points towards all carbs rather than just grains (beans don't seem to be an issue, other than the usual "musical fruit" effects).
The highest my meter has even gone is low 160s, and the lowest has been low 70s, checked at 15 min intervals. Unregulated highs and lows of BG doesn't seem to be the issue. I'm wondering if the issue is adrenergic, honestly - I feel, if this description makes any sense, like I had *way* too much coffee and just narrowly avoided an auto accident, plus I have a splitting headache.
All the pseudo-hypoglycenia info I have read has been very cursory, and often suggests it's all in the head of the patient, using words like nervous or anxious to describe the person. I'll admit to being somewhat of a hardass IRL, but I'm neither nervous nor anxious, generally speaking.
Thanks again for the input. I'm clearly going to have to do more work to figure out what my issues are.
It sounds as though you don't have much, if any, first phase insulin response. The $64,000 questions are:-
What can be done to fix it?
For a few ideas, see http://nigeepoo.blogspot.co.uk/2011/02/insulin-resistance-solutions-to.html specifically, also http://nigeepoo.blogspot.co.uk/search/label/Insulin%20Resistance generally. Hope that helps.
Thanks a lot for the reply. If I eat a high carb, high protein meal (say, 2 cups of rice and 6 oz of chicken breast) and track my BG every 15 min using a store bought meter, the highest I've ever seen would be around 8.8 - 8.9 mmol/L anywhere from 30 min to 45 min PP, and the lowest reading around 3.9 - 4 mmol/L shortly after that (60 or 75 min PP). My understanding (based on consulting Dr. Google, not based on any medical consultation) is that these readings are neither very high nor very low, is that correct?
Based on that assumption, the next thing I've seen referenced that makes any sense to me is that sometimes the rate of the BG drop can be problematic, even when the actual peaks and valleys are not extreme. Most of what I've seen is "in passing" though, and in reference to people using fast acting exogenous insulin. Have you heard or read anything similar?
The only other thing I've seen referenced that makes any sense is adrenaline response to BG spikes or drops. Lots of the very cursory descriptions of this kind of issue I've seen mentioned seem to imply that it's maybe make-believe, or possibly just psychosomatic. I suppose it's possible, since at the onset, I almost feel vasovagal, but OTOH, I'm very keen to be eating more carbs and less fat/protein, so it's not like I'm in fear of food here.
My Dr is very pro-paleo/low carb, so I doubt that I'll get a lot of good advice from him, but he'd probably be willing to at least send me for a glucose test if there's any point in it.
Thanks again for your input.
I'm a cico believer, but I can't argue with reality.
One cause of your type of response may be that you are MODY (2 I believe). This person has all the machinery working but the glucose sensor is not so good. What happens is that it takes higher glucose to finally elicit the insulin response, by which time some glucose is already on the way into cells without the insulin and/or the insulin secretion is in excess of what it should be leading to a "hypo" that may or may not be medically hypo (but who cares, I've known lots who feel shaky in the low 70's and 60's including myself in the low 60's).
There is not dietary cure for MODY so you can manage with LC or low glycemic index, but there is a med for this type of MODY called Prandin that will trigger your insulin release sooner. May be worth the genetic test to find out or see from an OGTT if this is what's happening.
Out of curiosity, I've tested myself a few times when I notice that I'm feeling reasonably good, and I am always just a little over 100. On rising, I'm usually upper 80s to low 90s.
Yes, I think at this point I'm going to have to ask for a glucose test. I've more or less exhausted what little I can determine with a cheap meter and sore fingers.
You tolerate legumes because they have a super low glycemic load (Beano, man, Beano! ... one of the few supplements that actually work). You're still eating a weird, restricted diet. Egg white omelet? Two cups of rice and some chicken? Ick! The only reason to ever eat two cups of rice is risotto, rich with olive oil, butter, and parmigiano which will considerably lower the glycemic index of the rice. I still think you should start with the starchy vegetables and introduce grains slowly. Since you can tolerate legumes (2 Beano tabs with the first bite will eliminate the music), eat those in conjunction with a small serving of rice and see how it goes.
It was just egg whites, not an omelet, and I was using them up as a quick breakfast this am since I spent a good bit of my morning helping my kid finish a project for school. All I can say about the rice is that I like rice, and may have gone a little overboard.
It's been a very long time since I've just eaten for pleasure, so I guess what I eat might seem weird to people regardless of what the macros look like. Not that I never eat for pleasure, but "hmm, what sounds good today?" is almost never a consideration. This is for monetary as well as intolerance reasons, but basically, food is just fuel most of the time. In that instance where I had chix with rice, I replaced greens with rice, since I usually eat *tons* of greens and veggies, but I had some dental work done recently and eating crunchy stuff is a challenge.
I only know this 'cos I used your graphic in http://nigeepoo.blogspot.co.uk/2013/05/impaired-glucose-tolerance-also-between.html :-D
I don't know how Glu-T1 transporters work, but if it involves enzyme up & down-regulation, there may be an issue with rapidly-falling BG starving the brain of glucose (due to slow up-regulation), resulting in a "panic response" of ACTH secretion & possibly also vagal nerve stimulation (I'm guessing, as I don't know) resulting in high serum adrenaline & cortisol, and ravenous hunger.
Some of your symptoms sound to me like magnesium deficiency.
Nigel eats white rice and takes extra Mg. He does not take extra manganese as far as I know, although he has updated the blog post he linked to include a recent paper showing Mn deficiency causes diabetes. White rice has very little Mn. I am waiting for him to ditch the Mg and eat brown rice.
Jane, take your OCD about copper, manganese & magnesium elsewhere, or get it treated. Hell will freeze over before I ditch the Mg, or eat brown rice. Now, GIVE IT A REST.
You might be in the top 2.5% of subjects who suffer problems above a certain serum 25(OH)D level. Do you eat much fermented foods?
Thanks - I'm working on it (and have been working on it). Fiber, both insoluble and soluble, is going to be a priority for me going forward. TBH, I was shocked to learn how little I was getting from eating several lbs of veggies each day, but I guess "roughage" doesn't equate to dietary fiber.
Thanks again for the response. The results I have in front of me from the most recent experiment (potatoes, squash, greens and chicken that I ate in about 10 min) are:
pre-test, fasting - 89
15 - 164
30 - 166
45 - 153
60 - 107
75 - 103 or 98 (had a lot of trouble with first test)
90 - 89
105 - 84
120 - 88
This is fairly typical of the tests I've done. My notes indicate that I started to feel pretty lousy between the 30 and 45 min tests, and really bad between 60 and 75 min.
I'm going to return to my paleo-esque diet for a while and get an OGTT that focuses on hypo rather than hypergycemia (or try, idk what's available here). I really screwed myself with that stupid egg whites and apple breakfast (which, again, isn't something I'd consider tasty, or a normal part of a diet, but sometimes we can't be picky, especially when it comes to leftovers).
Thanks again for the links to your blog posts - they were interesting.
Thanks for the reply. While I disagree with you about what I've shown (those were just examples, and maybe poor ones, since you seem to have fixated on the rice or egg white aspect of them), I agree that I'd probably be doing better with more moderate loads eaten with more fat. Hunger isn't really an issue for me unless it's making me grouchy.
My issue is not that I have a problem with that, it's that I *really* wouldn't expect to get sick sometimes, and still do. While an egg white and apple breakfast (again, the eggwhites were leftover from making hollandaise) might be gustatory blasphemy, short of actually being allergic to one of those things, I would not expect to get sick from that meal. Instead, it totally torpedoed my entire day. Unlike true hypo, whatever my issue is, I cannot seem to fix it by eating a little sugar or a little fat or a little protein.
In any case, thanks again for you input.
a. Assuming you'd like to continue to enjoy your carbs, I'm sure
you do know that the higher your post-meal insulin level rises, the
greater the likelihood that you'll "overshoot" on the return to a normal
BG level. The biggest factor in avoiding this overshoot is to maintain a fully functioning intact & robust Phase-1 insulin response [so do not mess around with VLC diets!—i.e., be sure to have enough daily carbs to avoid "obliteration" of your Phase-1 insulin response]
The other major factor is the way you put your meals together. For the reason why your lean protein + low-fat starch meals result in your post-meal BG "crashes", compare the insulin and glucagon and liver glucose production (HGP) levels in the following various metabolic states:
Meal...................Insulin level.........Glucagon level.............HGP
Carbs (small)......... ..++............................ ± .........................0
Carbs (large)....... ....+++.......................... ± .........................0
Protein................. ... ++............................++........................+
Protein & Carbs......++++......................... ± .........................0
Prolonged fast..... .... ± ...........................++.........................+
You can see that no meal or meal-combo provokes a larger insulin response than does Protein & Carbs.
[from: George Cahill. Physiology of Insulin in Man. (1971) Diabetes. Vol 20, No. 12. (p.791)
b. Do you think it's a good idea to have TWO cups of rice with your 6 oz chicken breast? That's ~88g of net carbs! (if long grain white)—and if you prefer brown rice that's still ~42g net carbs. If your aim is avoid these post-meat BG crashes you will benefit by paying attention to all the factors that provoke especially large insulin
responses. You will not want to, for example, be drinking milk when having a big plate of spaghetti! Doing so will provoke "unphysiologically" high levels of insulin in healthy individuals—and chronic exposure to
such levels may reduce insulin sensitivity and predispose you to the metabolic syndrome.☞
c. I recall reading in a book about children with Type-1 diabetes
that researchers were surprised to find that Type-1's could indeed
have a serving of potato chips and not experience the expected disastrous hyperglycemia—despite NOT injecting the typical insulin
dose calculated to "cover" the carbs. The reason, they found, was that unlike putting butter on potatoes or olive oil on pasta, the modern methods of producing regular commercial chips results in a near "bonding" of the potato starch to the fat, such that we have to first work on breaking down the fat before our guts can have access to the starch that is locked-up inside that fat. Resulting in a much slower release of BG raising starch. Just be sure to have the regular high-heat processed chips (Lay's regular, for ex.) and not the lower-heat "kettle-cooked" chips—which do not have the same fat-starch "bonding."
Thanks for the information. Two things come to mind.
1. I think that you haven't lost your 1st phase insulin response, due to the speed at which your BG returned to baseline level (only 90 minutes).
2. You ate the entire meal in only 10 minutes! Does eating more slowly make a difference (in terms of reducing the magnitude of BG fluctuations)?
I can't correlate your feelings with your BG levels.
In what way did you feel lousy @30-45 minutes? Hot? Nauseous? Sleepy? Headachy? Something else?
Ditto @60-75 minutes?
Snarks, I generally agree with Stella here in that there may not be a "problem" at all here.
The thing is that there can be a number of scenarios that can produce the same blood sugar responses. So an OGTT with insulin levels can help sort that out. If your doc is willing, perhaps you can do one with white rice and egg whites rather than a sugar solution. There are enough medical mysteries where it is difficult to pinpoint a cause, but this need not be one of them. Insulin hypersecretion is a real thing in some. If you are the type of MODY I described then you may want to induce an insulin response and then eat most of the meal later, or go with the "manual start".
Lots of great advice here on things to try but everyone is just brainstorming and you can save yourself some time and perhaps trauma by knowing exactly what is going on.
Best of luck and let us know how you are getting along!
Brown rice tastes like licking the devil's taint, or as Bris said in a different post, like "dog shit."
I think it is nit picky if one is only eating a small portion daily or not even that to concern over this. I love Trader Joe's white basmati rice for dishes involving rice - which is maybe twice a week if that? Otherwise give me wild rice mixed with white (1:1 is good) and I'm a happy camper :-) Wild rice is best in soups or on its own as a side, not a base for something like an Asian stir fry.
I also had a lot more energy, and I slowly realised my mitochondria had been starved of minerals. To my mind, eating food which should have high levels of minerals and doesn't, is insane. But then, people who have not had my experiences will be unaware of these things. I hoped for years that I could help people avoid the nasty experiences, but I have given up that hope. People like Nigel and Wooo have convinced me that all I will get is insults and abuse if I try.
You've gone waaay beyond nit-picky, Jane.
"I also had a lot more energy, and I slowly realised my mitochondria had been starved of minerals."
According to your theory, my mitochondria must be completely starved of copper & manganese, as I don't eat whole grains. As I'm not suffering from chronic hunger or a lack of energy, that indicates that my mitochondria are not starved.
∴ Your theory is dis-proven. Q.E.D.
"To my mind, eating food which should have high levels of minerals and doesn't, is insane."
To my mind, constantly repeating that copper & manganese deficiencies due to not eating whole grains are causing illness in many people, is insane.
" People like Nigel and Wooo have convinced me that all I will get is insults and abuse if I try."
Wuchtamsel and Sanjeev also "insulted and abused" you, on this blog. Anthony Colpo "insulted and abused" you (backed-up by evidence), on http://anthonycolpo.com/the-whole-grain-scam/ . People like Jimmy Moore, Fredrick Hahn, Jack Kruse, ItsTheWoo and you have convinced me that the internet world of Diet & Nutrition attracts delusional people.
If our (and other animals) guts weren't so efficient at absorbing minerals and our kidneys so efficient at retaining them, we'd have long since gone extinct.
56g long-grain brown with 226g H₂O; bring to a boil in the top section of a double boiler, then set that covered top-section atop the already gently boiling water in the bottom-section, let it cook for 60 minutes, voila. Yummy rice [that would even satisfy Ms Karlsson!]
I think he's frustrated because he has tried reading the literature on these metals and found out how impossibly complicated and contradictory it is.
I have only this to say to you Jane, from now on:- http://anthonycolpo.com/the-whole-grain-scam/ :-D
Jane Karlsson refuses to take one single bite of white rice or any other refined carb. That's Disordered Eating (a mental illness), not nit-picking. As Anthony Colpo demonstrated in http://anthonycolpo.com/the-whole-grain-scam/ , there's not that much difference in mineral content (in absolute terms) between brown rice & white rice.
Stop mentioning my name on-line and stop interacting with me. In other words, GO AWAY.
Oh, and everybody should read http://anthonycolpo.com/the-whole-grain-scam/ :-D
Everyone should read http://anthonycolpo.com/the-whole-grain-scam/
It speaks volumes that I have blocked you from emailing me & leaving comments on my blog, but I haven't blocked Razwell.
Now LEAVE ME ALONE.
I'm aware of some testy exchanges from time to time, but this isn't your blog and nobody has flagged any posts as inappropriate so I generally let things go and presume that we're dealing with adults.
Let's all take a deep breath ... engage when it's productive ... and just step back when it gets heated. OK?
They are on tissue regeneration, which is roughly the same thing as maintenance and repair, the process which goes wrong in degenerative disease. After this work was completed I spent many hours (actually years) in the Biochemistry library trying to find out what enzymes were important in these processes. I found that a number of the key enzymes were activated by manganese or copper, and I realised with shock that these metals are removed from a large part of our food. Then I read about the Hunza, who did not have our diseases and did not remove the metals from their food.
Many years later I tried to tell Anthony Colpo about these things, in the email conversation Nigel has linked, which Colpo published on his blog under the heading The Whole Grain Scam. He did not realise I was trying to help, he thought I was attacking him. He thinks I am a 'government shill' trying to force people to eat whole grains, and he is protecting them from me.
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