Dr. Roy Taylor's Diabetes Summit Presentation
I received some fanmail yesterday -- it was a nice email!! -- encouraging me to share Dr. Roy Taylor's presentation at the 2015 Diabetes Summit -- of Newcastle Diet aka "crash diet" for reversing diabetes. It's too bad he ended the talk encouraging the host to keep spreading good information ... sadly his is a rare inclusion in this event.
HURRY -- I thought these would be available through Thursday Noon, but it's saying 3 hours :( -- hopefully they'll extend that. SORRY!!
This summit is the second annual event put on by the director of Sweet Life Diabetes Centers, a chiropractor turned nutrition expert and other things, Brian Mowll DC. Last year he co-hosted the event with Jimmy Moore, and I dubbed it the Reversing Diabetes Knowledge Summit. There are more of the same chiropractors, naturopaths, and such spreading their views on how you basically should eat a very low carb diet and avoid this or that bad food that is killing your pancreas, etc. Mark Sisson was back spreading his misinformation on how diabetes develops, which is why it is all the more important to wonder why Taylor was not made THE keynote speaker?! But that diabetes expert Jimmy Moore ... is on deck tomorrow ....
If you scan down my article from last year, my main complaint with calling it the "Reversing Diabetes" Summit was that low carb diets rarely reverse the disease, and in the cases where they do, adherents are practically pummeled at every turn with the falsehood that they must eat fewer and fewer carbohydrates to continue in their remission. But therein lies the rub. Because while Tim Noakes downs 2000 mg of metformin a day as he runs (does he still?) around the globe spreading his #LCHF-cures-diabetes message, the difference in Taylor's approach is that at the end of the day, folks are actually non-diabetic! As in, they can eat carbs and not have blood sugar control issues. I believe the phrase he used in this interview was something to the effect of having an athletic insulin response.
I've blogged on this quite a bit:
Although I believe Taylor's take and mine disagree (and disagree with scientific evidence) in some places, the bottom line is spot on, and I believe he is more relying on older evidence than the LC schtick. Two points:
- There appears to be ample evidence that the source of fatty acids in VLDL is not from DNL (see the series on triglycerides beginning with Part I). However even if it is, Taylor emphasizes that this is due to overconsumption -- period -- and doesn't blame carbs per se. IOW, the source of the fat deposition is rather irrelevant.
- Some possibly outdated ideas on insulin resistance: though this is far from a settled case, the peripheral IR model has fallen out of favor, or is at best a late stage development, see for example: β-Cell dysfunction vs insulin resistance in type 2 diabetes: the eternal “chicken and egg” question. From the early days at this blog -- The Progression of Insulin Resistance -- to more recent discussions -- Insulin Secretion in the Progression of Type 2 Diabetes ~ First/Early Phase -- insulin action at the muscle cell level seems to be a symptom of things already gone awry if all that relevant in the end.
Taylor emphasizes that the source of glucose in hyperglycemia is the liver, a point made in this post, and a point, I might add, that is known, or should be, to every low carb researcher and doctor out there. Further, towards the end Taylor mentions that he has just submitted a paper regarding a personal fat threshold, which seems to be becoming more and more recognized. Here is a 2010 post on a decade old paper discussing a similar concept: Critical Visceral Adipose Tissue Theory.
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I have seen much derision in the low carb community both towards Roy Taylor's work, and the man himself. Indeed it may have been my blogging on his discoveries that got the attention of a particularly disgruntled diabetic in the UK. I suppose they see Taylor's efforts as a threat to the low carb way of life. Jenny Ruhl called his diet "idiotically dangerous", as if PSMFs haven't been used safely in various contexts for decades, and insisted the same results could be attained with moderate carb restriction. Every other blogger went on and on about it not being a sustainable diet -- ignoring the fact that it was NEVER intended to be! And if you really think that adhering to this is too far fetched, take it up with Dr. Eric Westman.
I believe the problem is one where diabetics seem to turn on one another. You see it in various communities of those with health/physical challenges -- somehow if there is the opportunity for someone in the community to "get out" -- this is seen as turning on their peers. I saw it in the deaf community several years ago when cochlear implants became more accessible and feasible. I have a deaf cousin (and another by marriage) who attended the very famous New York School for the Deaf (eons ago) which was at the center of this controversy early on. There were some contentious news stories regarding how to deal with a "cure" for many of the hearing impaired, and it was as if those who chose to embrace the technology were turning their backs on the others. They were viewed as turncoats who didn't want to be "like them", rather than perhaps just wanting to be able to hear like everyone else which was bad somehow? Anyway ... I see an analogy here in the behavior.
Ahh ... sorry folks. I went on there. Posting this up because I just noticed the clock is ticking on this. I recorded this so if anyone has specific questions, I'm happy to help.
Comments
http://www.wholefoodplantbasedrd.com/2013/11/dr-noakes-knows-running-but-not-nutrition/
In the “Lore of Running” Noakes recommended a high carbohydrate diet. He now tells people to rip out those pages. Noakes 64, changed his diet a few years ago after reading “Good Calories, Bad Calories” by Gary Taubes. Noakes came to the conclusion that his diabetes is caused by carbohydrate intolerance. Noakes writes:
“My biology is such that I am unable effectively to clear from my bloodstream, the breakdown product of ingested carbohydrate, glucose. As a result my pancreas must over-secrete the hormone, insulin, one of whose normal functions is to direct the glucose from the bloodstream into the liver and muscles. But instead, in my case, under the action of insulin most of the carbohydrate that I ingest is directed into my fat cells where it contributes to progressive weight gain, continual hunger, lethargy and, in time, pancreatic failure and the onset of the irreversible and universally fatal condition, adult-onset diabetes.”
Dr. Noakes has lost weight, improved his running and his irritable bowel syndrome and severe allergies have disappeared. He admits that these improvements may be the result of his eliminating gluten in his diet as he no longer eats grains. It’s possible that gluten intolerance may have been the cause of his symptoms.
Although Noakes is running well at the age of 64, he still requires metformin (glucophag) to help control his blood glucose which he claims still fluctuates wildly. He attributes this to his liver overproducing glucose. Dr. Noakes does not offer any scientific evidence to support his conclusion.
http://www.idiabetesblog.org/2013/09/carbohydrates-kill-a-conversation-with-tim-noakes/#.VRLCI_nF9op
"I subsequently decided I had type 2 diabetes and needed treatment, but my diabetes is quite well-controlled on Metformin and this low-carbohydrate diet"
This is pure BS!!
My sister was frightened into weight-loss surgery because she was having difficulty controlling her blood sugar with THREE meds. She began to have eye problems, and the specialist told her she could lose her sight. Her primary doctor assumed that weight loss would 'help' and encouraged the surgery.
Two months after her gastric sleeve, she was off all meds and running normal blood sugars--it's the AMOUNT eaten rather than the type of food because she's been stable for the past 2 years, and she eats a varied diet--carbs, protein, fats--although in very small portions. She still 'has' diabetes, but is able to maintain normal blood sugars with no meds.
Sorry, I keep coming back to this sentence and re-reading it. Is it mistyped, or maybe sarcasm and I'm just not getting it?
Anyway, I did watch the interview. I almost never listen to podcasts, because I much prefer reading to having information shoveled at me in an audio-visual format. Most of the information I knew already from your very excellent blog, but I did learn something. I didn't know (or maybe remember) that it's diglycerides specifically that interfere with insulin signaling. Would you say that's correct science? I was wondering when he said that DNL specifically causes fatty liver, and I'm glad you cleared that up in the text.
I guess I have one concern. I've read that gallstones are a common side effect of crash diets. Is there a way to prevent them, or are some people just going to get them, and tough luck for them? Honestly, crash diets scare me for this reason. I kind of wish he had some data on that.
I have talked about diglycerides here -- perhaps by a different name which I think he did use once: diacyl-glycerols or DAG. These ARE an issue and kind of what I was referring to in my webinar in general terms for things in fat metabolism that can "gum up the works". Ideally the fatty acids are plucked off and burned fully, but the overloaded cell the first FA can come off but the second doesn't and the DAG is reactive. This is current, but how much the DAGs effect the actual signalling of insulin has not borne out in a few studies I've come across over the years.
He didn't mention them, but ceramides are another thing that can be created from fatty acids and are implicated in what we call IR. Again there, the data is not always consistent.
What is, and this was his overarching message at the start, is that overnutrition leads to a "backlog" = stress in cells.
Hope that helps :-)
Question: If you have normal blood sugar with no medications, how is that diabetes?
Many of the 'cures' from gastric bypass were validated by the GTT. My sister had the "gastric sleeve' procedure, and she didn't bother taking a GTT because her goal was to control her BS. She actually never expected to be off all meds. She still checks her BG periodically because while 'controlled' now, her doctor has told her that her diabetes could resurface at some point. Although she can eat a lot more now than immediately post-surgery, she still can only eat very small portions, and it's the amount that seems to keep her BS under control because she eats carbs freely.
Shouldn't fasting blood sugar and HA1C be in sync?
The way most of these things work is they are marketing schemes to make money and grow mailing lists. That's why you're supposed to have to register to view, and there's the big sell. The person who sells the package through their link makes most of the money. The house gets a cut. The "talent" sadly usually gets squat (e.g. Roy Taylor) except for that carrot of "exposure".
Lysophosphatidylcholine as an effector of fatty acid-induced insulin resistance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090244/
This must be what you mean. Very interesting.
I'm sure there is a genetic factor as well relating to susceptibility, but why test it? I'll just stay lighter. So many benefits!
It is disturbing to me, that someone who embraced technology to some degree -- measure BG -- is so reticent to embrace the advances in diabetes control technology such as insulin pumps, etc. He seems responsible for a lot of the insulinophobia of many T1s in the diabetes community, many of whom are already drowned out by the T2s online.
I thought it was also interesting that T1 diabetics still produce glucagon despite having blown out Beta cells which produce no insulin. If nothing else, I'm learning some of the basics about the disease.
Bernstein's claim about normal BG's in the 80's throughout the day is based on his random samplings of pharma reps or somesuch?
Yes, a big part of hyperglycemia is the unchecked glucose production and glucagon plays a role in that insulin suppresses glucagon. There's been quite a bit of research on ways to suppress glucagon in T1s as combination therapy with insulin. I'm not sure why we don't have such a regime available yet.
In the 1950s, when diabetes was only diagnosed in very extreme cases (BS>300 causing glucose to spill into the urine) my obese but lifetime non-smoking grandfather had an MI in his mid-50s. He wasn't diagnosed with DM, but I bet that he would have been a few decades later. He went on the Rice diet, lost weight and maintained the loss for the next 25 years by eating regular food once a day and white rice with white sugar (no milk!) for his other meals before dying of a head injury in a bicycling accident. The criteria for DM was different then, but he probably reversed his disease adequately without statins or medications and with a nearly pure carbohydrate diet.
Sometimes, they're diagnosed when they actually become insulin-deficient T2s, long after their diabetes deepens for reasons other than hyperglycemia caused by carb consumption.
Then if they can control their blood sugars with the "LC Approved" metformin and avoiding carbs, it's the ONLY way to go.
http://press.endocrine.org/doi/full/10.1210/jc.2007-0692
Not so. You are confusing Bernstein with Taubes, Schwarzbein, et. al. I have every book in every edition that Bernstein wrote, as well as the written testimonies of some of his patients. Many of his patients at a first appointment with Bernstein are unpleasantly surprised when he tests their BG levels in the office and says he's going to give them an insulin injection right away—they're disheartened because they've been led to believe that if you ever need the needle—then it's basically all over for you. Bernstein has to then try to convince them that this needle right now is being given precisely to save their remaining pancreatic ß-cells. Saving and even restoring those which haven't yet been completely destroyed. Because to have even some ability to produce endogenous insulin makes one's life immeasurably easier than it is for those who've lost the ability to produce any insulin whatsoever. Insulin is not a demon, a culprit, etc., and even when elevated, Bernstein regards it as nowhere near the sort of problem that hyperglycemia is.
For Bernstein, chronic elevated blood sugar is the Number One physiological culprit. Insulin is not "something to be minimized", as it is for Taubes; on the contrary, by enabling you to maintain the anabolic processes that keep you in health,—that indeed keep you from melting away—insulin is marvelous, and maintaining the health of one's ß-calls is worth whatever effort it may take because one's endogenous insulin is especially precious ( being very much superior to any exogenous injected insulin). It's insulin that saves everyone from the pathologies of hyperglycemia. If anything, Bernstein regards insulin much as Elizabeth Hughes did:
Elizabeth Hughes—the first person person in the world treated with insulin,—a type 1 diabetic that Dr Banting injected with insulin in August 1922: She would turn 15 in 3 days. Banting's handwritten notes survive:
"wt 45 lbs. height 5 ft. patient extremely emaciated, slight aedema of ankles, skin dry & scaly, hair brittle & thin, abdomen prommt [sic], shoulders drooped, muscles extremely wasted, subcutaneous tissues almost completely absorbed. She was scarcely able to walk on account of weakness. Respiratory, digestive & cardio-vascular systems normal."
Banting began insulin treatment at once. The first injections cleared the sugar
from Elizabeth's urine. Banting immediately began increasing her diet. At the
end of the first week's treatment Banting had Elizabeth up to 1,220 calories—up
from the previous 889; another week and she was on a normal girl's diet of 2,200 to 2,400 calories....In her rooms at the Athelma Apartments, on Grosvener Street
next to Toronto General Hospital, little Elizabeth Hughes found herself slowly awakening from her nightmare of diabetes, diet, and starvation. [regarding this
magical new discovery of insulin] Elizabeth exclaimed to her mother:
"Isn't that unspeakably wonderful?"
I did not say avoided at all costs. Minimalized. Yes. I do believe that is accurate.
You are correct, however, that his rationale is not Taubesian.
Or as he put it: "Small inputs, small mistakes."
Why does this guy hate insulin pumps so much?
Q. "Why does Bernstein hate insulin pumps?"
A. 1. Pump failure, tubing coming out of the skin, insulin coagulation, tubing blockage, or kinking can occur in spite of sophisticated alarms and safeguards. As a result, ketoacidosis has occurred overnight in many Type 1 users.
2. There is a moderate incidence of infections at injection sites. Many of these have formed abscesses requiring surgical drainage.
3. Severe hypoglycemia is more common among pump users, posssibly because of mechanical problems.
4. All of the long-term (seven-plus years) pump users that Bernstein had seen (as of 2011) had fibrosis (scar tissue formation) at their injection sites. This had impaired
their insulin absorption so much that even high doses failed to control their blood sugars.
In addition, blood sugar effects of pump boluses appeared to be inconsistent in these individuals.
5. Many individuals are turned off by the idea of constantly having large-bore tubing sticking in their abdomens.
6. Users experience at least some inconvenience with the four S's—sleep, showers, swimming, and sex.
7. Over the past five years (as of 2011), the FDA has received reports linking 7,170 deaths to infusion pump problems...FDA officials believe that software and design problems underlie this situation.
8. Raising or lowering an insulin pump above or below the injection site can cause siphoning that will speed up or slow down the delivery rate by up to 123 percent if above the site, or 73 percent if below the site...The above variations in delivery rate can render blood sugar control impossible.
[AND]: "In our experience, insulin pumps to not provide better blood sugar control than multiple injections. Contrary to a common misconception, they do not measure what your blood sugar is and correct it automatically. Furthermore, most pumps are programmed to produce meal boluses that are computed to cover varying amounts of carbohydrate, totally ignoring both dietary protein and the Laws of Small Numbers."
There are more reasons, but I think these will give you his gist.
Your A1c is too high when compared to your FBG. That could be due to many things but you should look at your Hb and RBC. If you have anemia, your A1c will be too high. You might want Fructosamine in lieu of A1c. Keep an eye on WBCs and Globulin; they decline consistently if you've LCed for too long a la Bernstein and his blood sugar cult.
Got a link to this list of his?
>>>All of the long-term (seven-plus years) pump users that Bernstein had seen (as of 2011) had fibrosis (scar tissue formation) at their injection sites. This had impairedtheir insulin absorption so much that even high doses failed to control their blood sugars.<<<
Given this man's scientific basis for BG levels and HbA1c, I put little faith in his reporting. I looked briefly for some of the other statistics. Does he provide a link?
I've done LC on and off for the past 20 years, and continuously for the past 2.5, but have rarely gone below 50g CHO/day, so not exactly a NuttyK diet. And having come of age during the 60s and 70s, I've been conditioned to fear dietary fat (AHA), so have never quite been able to bring myself to eat the amount of fat the LCarbers ingest. I've also followed the training advice of Arnold S. and his ilk, and have always consumed as much protein as I could get my hands on, again, not a standard LC approach.
I do like keeping the weight off though, so it looks like it will come down to a delicate balance of the macros. I may do LC, but I'm certainly open to having my views changed, especially if it's for the betterment of my long term health.
Take a look at your Hb and RBC to see if they're low-normal. Then focus on your WBCs: you're probably around 4.0. Then look at your Globulin: many people fall from around 3.0 to 2.0. Those are probably the best health markers for those who've LCed for so long.
A-OK with me, and certainly no surprise, since of course the whole thrust of the website—name being CarbSane, after all!—is to elucidate the various errors of those who promote low carb diets, be it for weight loss or for general health and well-being, and Dr Bernstein does occupy a prominent position in that group.
If you don't see the the difference between advising low carbs in order to minimize damagingly high blood sugars [&/or large BG swings] and advising low carbs in order to merely keep insulin low,—a completely different target/goal!—then, just as you say, it's futile for me to labor the issue, and so I'll leave it there and not bother you further on that score.
Re the pros & cons of insulin pumps: I too wish that Bernstein had included the journal articles that support his various statements; I don't know why Little, Brown didn't regard the lack of such a list of references as a serious omission. But I've received courteous replies whenever I've phoned his office [usually to get his latest recommendation on blood sugar meters], perhaps you might call to ask for his links to these papers: (914) 698-7525.
I GET your point. I believe it's a distinction without a difference but I guess I'm wrong. That's OK, it happens sometimes. Bernstein believes diabetics should minimize any impact of dietary carb on blood glucose levels, but in doing that he is advising minimizing insulin therapy. See? But I do understand the man has pretty unscientifically based notions on what constitutes a normal blood glucose level.
Publishers don't care about referencing or the accuracy of references. This is abundantly clear, and Bernstein's publisher is no exception. Perhaps since you have a relationship with the doctor you can call him for the benefit of all readers here and report back.
Perhaps you could also ask him about the 7000 deaths. All I could find was this: http://www.fda.gov/ForHealthProfessionals/ArticlesofInterest/ucm295562.htm
Very impressive, indeed, Hello_I_Love_You.
Q: Did you severly restrict all dietary fat in order to get such excellent glucose tolerance?
Surprisingly, my WBC is 5.25 and Globulin is 2.7, however my RBC is 4.29 and my red cell width is lower and my corpuscular vol is large. This is what makes me think there's some anemia going on, but this may be the result of asthma. My TSH was 1.50, which is supposed to be normal, but I've read elsewhere that it's low. I didn't have a full thyroid panel run, so in isolation, I'm not sure how meaningful it actually is.
My body temp was 97.4F - this has me more concerned from what I've read about LC affecting core temp and cold sensitivity. It will be interesting to have these tests rerun in a few months after making some dietary adjustments. Apologies for posting personal test results - not sure if that's appropriate here, but thought it might help with the discussion. Your feedback regarding them has certainly helped me.
No, I don't take thyroid meds. Not sure where I read about the TSH
range - might have been an article on that non-condition: adrenal
fatigue. My hands are generally pretty cold. My wife refuses to allow me to touch her, but that's been the case long before I started LCarbing (sounds like a Rodney Dangerfield line).
Anemia can also be due to copper deficiency. I think someone who eats meat like Rich is more likely to have copper deficiency than iron deficiency. His doctor is unlikely to know about this.
Copper researchers have been trying to tell doctors for years that copper deficiency is very common. Some doctors are listening, and are starting to recognise it in patients they thought had B12 deficiency.
"Acquired copper deficiency has been recognised as a rare cause of anaemia and neutropenia for over half a century. Copper deficiency myelopathy (CDM) was only described within the last decade, and represents a treatable cause of non-compressive myelopathy which closely mimics subacute combined degeneration due to vitamin B12 deficiency."
http://www.ncbi.nlm.nih.gov/pubmed/20232210
I reject PHD's focus on micronutrient deficiency as an important and overriding cause of degenerative diseases, especially copper. It is possible but copper deficiency can't be that widespread. Certainly, PHD's focus on copper-high lipids isn't very convincing, although I find Paul to be one of the most reasonable and erudite voices in the Paleosphere.
Namely:
1. If your net carbs are up to ~150g/day, and you say that you're also having
about 15% calories from animal flesh, and supposing you're having ~2000kcal/day, that would make your protein + carb calories at 45% of total, which would mean that you must therefore be getting ~55% calories from dietary fat. If so, your case is even more remarkable, i.e., that you have such good BG values as a Type 2 diabetic while having that much dietary fat in addition to that 150g/day carb intake. [This would be supportive of Himsworth's conclusion that the sole dietary factor for improvement of glucose tolerance and insulin sensitivity is the presence of sufficient carbs, period—not the absence of dietary fat]. Something for which I'm always glad to see supporting evidence!
2. You mentioned avocados—which supply a pretty fair amount of fat for a plant food, but I think you can't be getting 55% fat calories from just avocados!
So then: do you use olive oil or any other bottled oils?
3. Do you drink milk or eat any dairy foods? If not, do you then rely exclusively on plant food sources for your calcium requirement, or do you use mineral supplements as well?
4. You mentioned lentils & beans, but I wonder whether you have them with their traditional accompaniments—rice, or pasta? If so, is it exclusively brown rice and/or whole wheat pasta, i.e., do avoid you avoid all fiber-free starches?
5. Do you eat any potatoes—a starch that has received such a bad rap for a long time due to it's purportedly damagingly high Glycemic Index?
6. Speaking of which—what is your view of the value of using Glycemic Index/Glycemic Load calculations for meal or snack choiceworthiness?
7. You mentioned cold-cuts as a typical lunch: as in a sandwich? If so, what kind of bread(s) do you use?
8. You mentioned 3 snacks, having ~30g [total] carbs each: would these be mostly fruit or starch snacks? Are these snacks exclusively carb snacks, or do you also try to "balance" the carbs with some protein & fat, as is frequently advised for reducing the subsequent impact of those snack carbs on one's blood sugar level?
9. You mentioned taking metformin @ 500mg every other day, but that "...you've never bothered to look for Glucophage" But Glucophage is metformin,—i.e., one particular commercial brand of metformin—isn't it? [And how does one go about getting one's pharmacy to supply free meds???!!!]
10. Do you regard exercise as being an important factor for maintaining good glucose control? If so, do you rate aerobic exercise higher than anaerobic?
11. Looking back on your past, what do you now think was the factor(s) that led to your developing Type 2 diabetes—any specific dietary culprit, or just excess total calories irrespective of the macros per se, or perhaps mostly due to genetic factors?
Wow,—I see my list of questions is going on and on, so I'll stop it here. I hope you won't mind taking a few moments to answer them. I'm sure I won't be the only visitor to the CarbSane website interested in blood sugar control who can benefit from what you have found that works [or not].
As Type 2 diabetic who has clearly found a strategy that has yielded such good blood sugar results without having to employ a low-carb diet, your personal example should resonate for those who are—as Evelyn puts it—"...seeking refuge from low carb dogma."
As Type 2 diabetic who has clearly found a strategy that has yielded such good blood sugar results without having to employ a low-carb diet, your personal example should resonate for those who are—as Evelyn puts it—"...seeking refuge from low carb dogma." <<<
WOW.
Wife to Rodney: "Take out the garbage!"
Rodney to wife: "You take it out,—you cooked it!"
Seems rather more invasive than various clinical trial backgrounders.
That's why you need carbs and fiber. Lots of fiber. The breakthrough came when I went from eating tubers to eating lentils. 3 different kinds of lentils: orange, green, beluga. But I'm at top 5% in discipline and don't eat more than 35 grams of net carbs in one sitting. That will maintain my BG and the low GL of what I eat will keep my BG rise very slow. 1H probably at 140. 2H I'm down to 90. Fasting is at around 85-95.
There're probably others who eat Fuhrman's way who keep around 5.0. But my endo refused to believe that I had diabetes and wanted to see all my records. He still thinks I'm misdiagnosed. But I know I have diabetes. I had neuropathy (gone now) from my undiagnosed days and I do go over 200 when I eat more than 100 grams of pure fast carbs.
Some other tricks: 4 cups of green tea in the afternoon -- keeps hunger at bay and lower BG, take some Chromium Picolinate (100 mcg), Gymnema Sylvestre (200), aged garlic extracts and raw garlic diced in water with a bit of apple cider vinegar, turmeric, kale/collard greens. Eat lentils, black eyed peas, chick peas, collard greens, kale, Bismatti rice, yams, yuca, green plantains (all microwaved), Lunch is 2 sandwiches with Ener G's gluten free tapioca bread. Avocadoes are mostly fiber; even Bernstein allows them in his diet. So avocadoes with cranberries, blue berries, and raspberries. Some Pinot Noir or Merlot mixed with Almond Breeze non-dairy coconut/Almond drink. For sweets, I take Stevia and about 2 squares of Lindt's 85% dark chocolate. That's about it. The macronutrient breakdown is probably 35% carbs, 50% fat, 15% protein. About 2400 kcal. 200g carbs, 90g protein, 135g fat. Some palm oil, 2-3 egg yolks similar to PHD, burgers or steaks every 3-4 days, etc.
"aggressive or invasive."
What H_I_L_Y—as a Type 2 diabetic—does and does not do to maintain such excellent BG control, is valuable information that I think cannot fail to be of benefit to others.
The questions represent my genuine interest in the details of the actions and food choices that have produced such excellent blood sugar results,—in someone who has a condition that typically makes getting such excellent results exceedingly difficult.
I've read papers saying UCPs shuttle fatty acids out of mitochondria and others saying they don't. Everybody seems to agree that UCP2 and UCP3 lower ROS, whether they shuttle fatty acids or not. UCP1 is different of course.
"The Western diet is often low in copper, [3] according to the pooled data from several articles on more than 900 diets chemically analysed. About 62 and 36% of diets of 80 randomly selected adults in Baltimore [4] were below the recommended dietary allowance and the estimated average requirement for adults, respectively, 0.9 and 0.7 mg daily."
http://eurheartj.oxfordjournals.org/content/27/1/117.1
So it looks like the diet of most Americans is below the RDA for copper. The RDA may actually be too low, because that level has been found to produce symptoms of heart disease in volunteers. In other countries the RDA is higher.
A recent study has shown that supplementation with B vitamins can slow
brain shrinkage in early Alzheimer's. The authors have pinpointed B12 as the
critical one, although none of the patients had B12 deficiency. The dose was astronomical, 500 times the RDA. Since the enzyme activated by B12 requires copper as well, one interpretation is that the patients actually had copper deficiency, which has often been suggested as a cause of Alzheimer's.
I'm reminded of ASP - acylation stimulating protein -- which is very similar to complement C3 that is involved in inflammatory pathways.
I hope to have more later.
"Weight loss averaging 15kg (2 stone 5lb) achieved over 8 weeks caused two distinct sets of changes. Within 7 days, liver fat had fallen by 30%, liver insulin sensitivity had returned to normal and fasting blood glucose had become normal. By 8 weeks, pancreas fat content had returned to normal and insulin secretion by the pancreas had returned to normal."
http://www.ncl.ac.uk/magres/research/diabetes/reversal.htm
http://www.ncbi.nlm.nih.gov/pubmed/21656330
In Newcastle, the complete reversion isn't seen immediately and the treatment lasts several weeks. In GBP, it is within the first few days, and while initial intakes are quite low, this isn't enough to explain it.
For me, my bets are on the incretins -- either GLP and/or GIP -- that are likely suspects as they either mimic insulin action on the liver and/or stimulate insulin secretion by the pancreas. I have a number of studies looking into these connections though I don't recall anything definitive.
Interestingly GBP outperforms other WLS like lapband, sleeve, etc. so there's something to the "shortcut". I would also add that one study I recall mentioning hypoglycemia following GBP requireing insulin suppression treatment. This would square with an incretin effect maximized by more direct delivery of nutrients to the intestine per GBP ... then the first weight lost is from the ectopic fat.
This isn't entirely a hypothetical for me (though I am actually not the one likely to be faced with this choice, rather it's a loved one). I've said before, but I say again: I very much appreciate your research and writings about T2 diabetes.
"In summary, weight loss directly influences thyroid hormone regulation, independently of the weight loss strategy used. The effects may be explained by a combination of decreased leptin levels and transient changes in peripheral thyroid hormone metabolism."
http://www.ncbi.nlm.nih.gov/pubmed/23811187
"These data indicate that deterioration of glucose metabolism in T2DM is associated with a decline of GLP-1 levels. Calorie restriction facilitates glucose metabolism and blunts hyperinsulinemia in obese (diabetic) humans. Additional duodenal exclusion through RYGB induces gut hormone release and hyperinsulinemia but does not improve postprandial glucose levels any further. Our data thus strongly suggest that calorie restriction underlies the short-term metabolic benefits of RYGB in obese T2DM patients."
http://www.medscape.com/viewarticle/825743
Actually, I didn't, and so I do apologize for having misunderstood that you meant that your mealtime portion size was ⅛ cup of rice, dry, i.e., before cooking;—I really did think you meant that you ate that much rice as uncooked!—Why?—I suppose because you had mentioned in several places that getting lots and lots of fiber [often referred to as unavailable carbohydrates] was something you regarded as quite important, and so I thought, hmm..., well maybe this is just another way you've found to increase your intake of undigested, unassimilated plant foods! And you had already mentioned your regular intake of some unusual [to me] substances—"Gymnema Sylvestre (200), aged garlic extracts and raw garlic diced in water with a bit of apple cider vinegar,...& something called "tapioca bread". Also, since I always portion out my rice by weighing it—as well as the water!—on my Acculab digital balance prior to cooking, it was a slip that I failed to remember that most folks do just measure their portions by volume.
(BTW, my own package of Trader Joe's Basmati rice [white!—product of India] lists ¼ cup dry as being one portion, weight 51g and having 40g carbs. I don't deduct the 1g of fiber, and just use the rule of thumb that 100g white Basmati = 80g carbs, which would make your ⅛ cup portion at ~25g = ~20g carbs.)
My "agenda"? I have no underlying ideological plan or program. I remain unconvinced by the research I've examined to become either a very-low carb enthusiast or a very-low fat enthusiast. I merely developed an interest in diet & health some years ago, with a particular interest in glucose metabolism & regulation.
My "métier"? Hmm...I suppose my vocation may perhaps be described as:
self-employed peasant, independently poor, hunting & gathering info wherever it may happen to lead.
As for tapioca bread, they're standard gluten-free alternatives made from powders of tapioca, white rice, brown rice, omega flax, millet-chia, etc. National brands like Udi's and Ener G make them and are carried by places like WholeFoods, Trader Joe's, Fairway, etc. You sound a bit like Brie Vegas, the half-wit from downunder who used to rant about cholesterol. This may be the second coming of Brie Vegas, who came back heavily medicated this time, possibly on tranquilizers.
a. You might have at least gotten his name right—I'm pretty sure it's Bris—not—Brie Vegas.
b. Now that you've started in with the personal insults, I see that it will no longer be worthwhile to continue this particular series of exchanges. Experience shows that once you start in with the personal insults, it frequently results in the situation where insult just begets insult, in an escalating series that ends up illuminating nothing, and boring both Evelyn and the readers of her website.
Further, my innate politeness and courtesy prevent me from returning your insults. I was raised to be considerate of others less fortunate. I have seen whole books devoted to the methods of coping with the depression and irritability that typically occurs in people who are compelled to live the unwelcome, restricted life
of a diabetic. Before you start insulting Bris Vegas or me as being "half-wits, you might remember that it wasn't he or I who ate ourselves into developing Type 2 diabetes and now have to spend the rest of our lives eating things like "gymnema sylvestre (200), fenugreek extract, and ersatz "bread."
I had hoped to learn something of value from your personal example, but it appears you have concluded that my real goal is to discredit you. Which is completely and absolutely false. Because Type 2 diabetes runs in my family, on my father's side, I am always on the lookout for proven strategies and actions that will help me to avoid the same fate.
So you see it's not just a matter of luck that I myself don't (yet) have diabetes—I take steps to help to keep it that way. I have the usual 3 meals a day, no snacks, and the meals are neither very low-carb nor very low-fat. Full fat milk and dairy foods are staples, and although gluten is the popular dietary culprit du jour, my investigations have led me to regard the current fear of gluten as baseless—similar to the past hyping of oat-bran as a being a dietary saviour. My own choice in bread is Bavarian Whole Rye [product of Germany]:
http://www.iherb.com/Bavarian-Breads-Organic-Whole-Rye-Bread-17-6-oz-500-g/31894
(Is it a hyperbole to say it's the most delicious bread in the world? Well, maybe so...)
In addition to rice and pasta, I also have potatoes—which Walter Willet will tell anyone to never touch with a 10-foot pole. [glycemic index, you see]. Yukon golds at last night's supper—the terrific traditional accompaniment to broiled buffalo cheeseburgers, big salad, and cabernet sauvignon.
I also place great value on aerobic exercise; I do believe it's one of the most important actions one can take to help prevent the liver and pancreas from accumulating fat: http://care.diabetesjournals.org/content/30/3/683.full.pdf
I recommend it,—that is, if you aren't already an aerobic practitioner. Before heading out for my regular pre-dawn 2-mile run this morning, my fasting blood sugar was 76mg/dl. Low-normal is what I like to see. I wish you good luck in managing your disease. Sincerely, not sarcastically.
[Final note: perhaps it's just an unfortunate and mistaken association, but the moniker "Hello_I_Love_You" immediately brings to mind the song of that name by
Jim Morrison [of the Doors fame]—i.e., "Hello, I Love You (Won't You Tell Me Your Name)". I say "unfortunate", because as an alcoholic who poisoned himself to death at the age of 27, Jim Morrison is, if anything, a paradigm of a genuine half-wit.
I'll close off this piece with the noting of a much better song—in the wonderful words of Roy & Dale: ♪♬♩"Happy trails, to you..."♫ ♪ ♬♭
Here's my problem in a nutshell: poor carb tolerance, despite being lean (waist size same now as when I was 19, since 2013) and never having done LC for more than a few months. 6 oz of potato by itself will send BG to 170. However it will be back down same as FBG levels of 80s-90s by 90 minutes. So I only have rice or potatoes 2x a day, and only about 3-4 oz so as to keep my spikes 130-140. Breakfast these days is usually a low-carb smoothie with avocado, kefir, eggs, yogurt, lots of prebiotic fiber (green powder, raw potato starch, inulin, glucomannan, psyllium seed, acacia). The rest of my food is paleo with dairy.
Seems to point to weak first-phase insulin response, with OK 2nd-phase. Recent 1-hr post-mixed-breakfast with 6 oz potato and butter test showed BG=170, insulin = 22, and c-peptide = 3.7.
Fasting insulin was <5.
I was never really a big SAD eater; lifted weights, was never fond of gulping big sodas and always liked eating a lot of meat and fat with modest amounts of rice or bread. Most I weighed was 30 lbs more, but for several years was 20 lbs. more. Back in 2005 I did an OGTT because I complained of reactive hypoglycemia. Starting BG was 98, at 1 hr was 89, and 2 hrs, 50 (but not feeling terribly weak). What happened to my robust insulin response? A recent OGTT got me to 217 @ 1hr and 101 @ 2 hrs. From 2005 to 2013 I first fixed my reactive hypo by going low-carb for just a few months with 3 square meals, then re-introduced carbs. Typically had burrito for lunch, and rice with dinner.
Here's another weird thing. In 2013 I discovered my poor starch tolerance and went LC Paleo for a couple months. Then started Potato Starch supplementation. After 6 weeks re-introduced rice and potatoes and discovered that I could eat an 8 oz potato with a BG spike at 35 minutes of only 130! Hooray, I was cured! I started eating "normal" amounts of carbs. It only lasted 2 months. Some spot checks revealed post meal spikes of 160-180. Chagrined, I dialed back my starches to limit spikes to 130-140. I also take 500 mg metformin 2x/day now, and this has lowered my FBG by 10 points. This is where I am now. I want that starch tolerance back.
Is there a NEFA blood test I can take? Should I do it 2 hours post meal with some starch to see if it's normal? Because fasting insulin is <5, I probably don't have insulin resistance, right? Because I'm lean, my liver and pancreas are probably lean, correct? How else can I check that? Aside from fibers, what else promises to improve first-phase insulin response?
Low-carb enthusiasts will say that reducing one's carbs will necessarily reduce the demands on your ß-cells, and thereby help to save them. But while this low-carb strategy will result in less bad postmeal BG levels, it won't correct the underlying problem,—that is, the insulin resistance secondary to accumulated hepatic and pancreatic fat. What we should want therefore is not just a less bad postmeal BG level, but a restoration of normal glucose tolerance. So that we can then have an ordinary, normal mealtime carb and process the damn thing normally.
It's definitely possible to be lean yet still some accumulated fat in your liver and pancreas. This is a fear I have too, which is why I try to minimize this by regular aerobic exercise: http://care.diabetesjournals.org/content/30/3/683.full.pdf
Check out the following—Richard Doughty's story of how a lean guy can have—and overcome—this problem:
http://www.dailymail.co.uk/health/article-2385179/I-reversed-diabetes-just-11-days--going-starvation-diet.html
There is a phenomenon of lean DM2s, but they're mostly Asian and they still have more abdominal fat stores and higher waist circumferences than similar weight, non-diabetic Asians. It's one of the reasons why people have suggested that current BMI standards should be revised for Asians. I'm of northern European heritage, but my A1C crept up into the pre-diabetes range when my BMI was 25 and change (but my body type is very thin). If you were to have an imaging exam to look for intra-abdominal fat, you would probably have some stores. A "Bodpod' or a more formal metabolic lab evaluation of body fat percent might be a useful guide. I know that this sounds terribly dated and old-fashioned, but you might do a bit better by losing a few pounds and monitoring calories rather than macronutrients.
A 6 oz potato has about 30-33g net carbs. That shouldn't take you to 170. Maybe to 140. But you have no starch tolerance because of wrecked insulin response in the 1st hour.
More intriguing though is your 2005 OGTT going from 98-89-50. You sure you took 75g of fast-acting glucose? You had 1st phase then but it's gone now --- that would be the interpretation. But you crashed to a ridiculous number after 2 hours, but you claim to be asymptomatic. How about now? Do you have any RH symptoms, although it's now 90, not 50.
You have issues, bud. You need to go see a good conventional endo who specializes in liver hormones hypoglycemia. If bottoming out at 50 was true, you may have had glucagon/liver issues. Because that's not Reactive Hypoglycemia but just hypoglycemia -- check your liver enzymes (AST/ALT/Alk Phos/Bilirubin/Albumin) and your endo might do a sonogram to check for any hemangiomas that could affect your glucagon. But that was 10 years ago.
What's happened in 10Y? Your BG control has slipped and there is something wrong there. It can't be fixed by VLCing or any conventional methods suggested by popular diets like Paleo, etc. I'm strictly going by your non-RH in 2005 and the RH now; who ever sees you must know your history of crashing to 50 from a non-peak of 89. You don't need naturopaths, back crunchers, not PCPs, GPs, not an endo who specializes in obese T2s, but an endo who can check you out based on your hypoglycemic history and current diabetes-level insulin resistance. Good luck. I'd look for someone affiliated with a university hospital. Trust me, no one in the Paleosphere can help you in that regard. They'll start their idotic VLCing protocol and you'll be worse off and have other unnecessary hormonal and immune ailments piggyback when you already seem to have a hormonal issue.
Liver and kidney numbers back in 2005 didn't raise any flags with my GP. He just "indeed you have reactive hypo, eat 6 meals a day". (instead I followed the leptin rules).
The recent fasting insulin <5 was with an FBG in the 80s. That means no insulin resistance, right?
From 2005 to 2013 my FBG was always in the mid-high 90s. It was only after someone told me that reactive hypo can lead to diabetes that I read up and checked my post meal BG and was shocked to find poor starch tolerance. I then went low carb paleo for a few months and lost 10 lbs to reach my current weight until I read about Resistant Starch in late 2013. I started on raw potato powder. My FBG went down to the 80s and my post starchy meal BG went down to 130. I was ecstatic but it was short lived. What happened during those 2 months of bliss? Why did it go away?
So the 3 LADA antibodies are GAD, Islet Cell, and Insulin? How about ZnT8?
Thanks a bundle!
Like I said, if you let your BG over 200 within the first hour and it's been like this for a while, you might already have minor diabetic complications like tingling, pins and needles at your bottom of your feet. That's why you need an MD who knows what he's talking about. Not a bunch of clueless Paleo docs or Paleo groupies who think great BG control is low fasting insulin.
I'll ask my gym to measure my bodyfat % (I know it's not perfect, but they have my numbers from like 2009).
Wondering out loud: I've often wondered if those ith reactive hypoglycemia might benefit from a pure carb load -- 10 grams? -- about 15 min before a meal. Then the delayed insulin is pumping when you eat the rest of the meal, no hyper and no overcompensation of insuin secretion. Seems an experiment worth a shot.
As to NEFA, my guess would be that this is not your issue as your problem isn't in the fasted state.
The drug Prandin is apparently used with those in your situation to stimulate insulin in a timely fashion.
What's your HbA1c?
I never bought into the "metabolic advantage" of the ketogenic diet and going long periods between eating, though I think it has some interesting implications for endurance athletes provided it's undertaken for short periods leading up to a competition - not as a on-going way of eating. Has to be better than getting a lifetime ban for using PEDs.
samples of drinking water were collected from a stratified random sample of 80 individuals as part of the National Human Exposure Assessment Survey in Maryland. The media were obtained from each participant in up to six equally spaced sampling cycles over a year and analyzed for copper by inductively coupled plasma mass spectrometry. Copper concentrations (μg/kg) and consumption rates (kg/d) of solid food, beverage and drinking water were used to derive average daily aggregate oral intake of copper (μg/d)."
What's the problem?
Here’s an interesting article that mentions genetics and Zinc:
http://usatoday30.usatoday.com/news/health/2008-03-18-3272226463_x.htm
“Collins points to one potential drug target: A gene with the sole job of getting zinc to insulin-creating cells. Zinc's a key part of the recipe; **too little or too much, and insulin isn't secreted.”**
I couldn’t find any more references discussing “too much or too little Zinc, and insulin isn’t secreted”
The 2 worst diabetes-correlated SNPs I have are:
7903146 (CT)
and
7901695 (CT)
The first one affects the ZnT8 “zinc transporter” protein.
Now here's an interesting twist in my case. A few months ago I discovered I needed Zn supplementation to bring my serum Zinc up from marginally low levels. Zn and B6 supplementation got rid of a slight lack-of-focus and concentration issues that started a few years ago. Perhaps there's a Goldilocks level of Zn that optimizes my first-phase insulin, but which is not enough for my mental performance?
A1c has varied from 5.2 when I was low-carbing, to a high of 5.8 when I was regularly getting >140 post-meal spikes.
I did try something like eating a plum 15 minutes before a 5-oz potato, and the effect on the post-meal spike wasn't measurable. Ditto some apple cider vinegar. What does help is a scoop of whey protein, potato starch and other fibers before a starchy meal, and eating rice that was cooked with some coconut oil and cooled in the fridge for 12 hours before reheating gently (see article making the rounds, it converts a bunch of the rice into resistant starch) and also lowers its GI.
The big mystery is, why did I have outstanding starch tolerance in a 2 month window in early 2014 after starting resistant starch supplementation? I had just lost a bunch of weight from low-carbing (and have lost slightly more since).
As I said, personal insults illuminate nothing, so I won't take up space on Evelyn's website by responding in kind.
You've concluded—mistakenly—that I'm out to discredit you, so you'll be surprised to hear that I forgot to mention that I did, in fact, derive some benefit after all from your personal example, namely seeing the importance to you of having legumes as your dietary foundation has persuaded me to reintroduce the addition of an old favorite to my morning scrambled eggs and bacon—beans & salsa, well-know down here in Arizona as the Mexican breakfast "huevos rancheros". The zing of a medium-hot salsa is a really nice counterbalance to the mildness of the buttery scrams.
Also, to place an order for another old favorite which I haven't had in quite a while,—these marvelous organic french lentils:
http://shop.goldminenaturalfoods.com/ORGANIC-FRENCH-LENTILS-HEIRLOOM-QUALITY-1-LB/productinfo/0207%2D1401/
"A Persian variety, they are tiny grey to green-black ovals. Many seeds are beautifully marbled in greenish-bluish-black hues."
If you haven't had these, I think you'll find them worth trying. In comparison to which, red lentils seem insubstantial and regular green lentils seem too mealy. These have just the right balance of texture, taste, plus the best visual appeal with their bluish-black seed coats. As you must know, boiling and turbulent cooking damages the seed coats and can cause the beans to disintegrate. So I've found the best method is to cook them, covered, atop a double boiler, for 40 minutes (wherein the water won't get any hotter than ~200ºF, which is still hot enough to get the job of tenderizing done, but not so hot as to do damage to the seed coats.)
Bon appétit!
So you can almost think of lifting weights as a sort of insulin substitute. In fact, a famous diabetes doctor [whose name I must be careful to whisper!] wrote in the 2nd edition of his
Diabetes Solution (p.204): "I have one Type 1 patient who keeps her blood sugars essentially normal. She still makes a little insulin and dislikes insulin injections so much that she works out—lifts weights—every day after lunch to save herself a shot to cover the lunch."
Lifting has other benefits—raises HDL, lowers TG's, and by increasing your muscle mass thereby reduces your need for insulin. But since you're not a Type 1 diabetic, you won't have the same primary goal of reducing blood glucose—what you'll want is to restore/maintain normal glucose tolerance, which means having the different primary goal of reducing accumulated fat. And it's sustained aerobic exercise that really gets this job done.
The moment his BG went above 200, that should've screamed diabetes. My old endo who passed away would've spotted this just looking at his OGTT. That 200 BG breach rule is still reliable. You spend the 1st hour of your OGTT over 200 and you pretty much have diabetes. It just confuses lots of GPs.
Well, since you already have a genetic profile, you could look to see if you also have one of the known MODY genes and that would help distinguish MODY from early type II (or you could have both conditions). The problem is that there isn't really any valid treatment, so what would you do with the information? Sulfonylureas will slow but not reverse the progress of both early diseases. I know that you are looking for a nutritional solution, but I'm sorry to say that I don't think there is one, at least beyond eating a moderate diet, regular exercise, controlling weight and avoiding cardiac risks.
HILY asked what the change was between 2005 and 2013 and I'm afraid that the answer is 8 years.
I've also started eating bread and pasta again, but prefer to make my own, lower-carb versions. I even use a bit of Bisquick to make the bread, again not worrying about the refined flour and what little trans fat comes through. Fortunately, I can tolerate gluten. I may give Ezekiel bread a shot, but not sure I'm going to like the taste.
I've been hearing a lot of good things about Lindt chocolates lately. I believe CarbSane has a preference for their truffles. Lindt could turn out to be the missing dietary link.
His method of choice for insulin are regular syringes. He prefers them even over insulin pens (which are inaccurate in dosage up to 10-15%).
Any opinions as to why I had a 2 month window of excellent starch tolerance in early 2014 when I had just started supplementing Resistant Starch? (which I'm still continuing, because the improved 90 minute post-meal BG is still there).
If by resistant starch, you mean RS in beans and lentils, I do follow Furhman's Eat to Live and am a big fan of his diet. After being in the mid-5s, my A1c dropped to the 5.0-5.2 range last 2 years after I introduced legumes to my diet.
Early 2014 I had 2 months of excellent starch tolerance when I had just started supplementing with Bob's Red Mill Potato Starch as a source of Resistant Starch. My theory is it got my gut flora in some (transient) state that improved my incretin response. I still take the PS, and recently added a bunch of other prebiotic fibers (inulin, FOS, GOS), to no avail. And most recently (months ago) my starch tolerance took a turn for the worse when I started taking Zinc and B6 which address a mild brain fog / lack of focus I started getting about 2 years ago.
I tried eating a plum 15 minutes before a meal and it had no effect on my post-meal spike. I'll try 30 minutes. Or, does it have to be starch and not sugar?
I searched in SNPedia for "MODY" and got over a dozen SNPs. If you click each SNP it goes to a page where on the right column there's a direct link to 23andMe and it goes to that SNP from your database. Most of the SNPs aren't tested by 23andMe. 4 were. I searched for each off them and none of them were conclusively linked to MODY.
The result suggests a slight improvement in the peak as compared to not having the "pre meal snack". Total carb load including the snack is greater than otherwise. It suggests that I can eat more carbs by eating them 30 minutes apart LOL. Maybe I can eat a bit of starch, then 30 minutes later eat a small dessert.
Here's the data:
time BG comment
10:00 83 just before eating 25g rice
10:30 98 started eating brunch
10:40 finished brunch
10:50 94
11:30 138
11:50 110
PPS I don't want to eat more than 3 meals a day because of the research that 4 hours are needed between meals to get insulin down to baseline, which allows mitochondrial DNA repair.. and that 12 hours between dinner and breakfast maintains leptin and insulin sensitivity. Learning to go 5-6 hours between meals back in 2005 is what cured my reactive hypo (where I had a robust 1st-phase, but hit 50 @ 2 hrs). Also, >4 hours between calorie intakes, helps prevent SIBO, FWIW.
https://intensivedietarymanagement.com/insulin-works-hormonal-obesity-vii/
When I showed reactionary hypo back in 2005 I used to eat 5 times a day. I quit that and went longer between meals and my shaking and crabiness before meals and sleepiness after meals went away. I also lost 20 lbs.
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