TypeOneGrit membership?


I recently requested membership to the typeonegrit group on Facebook, but was rejected. I’m a type 1 diabetic and I follow Dr. Bernstein’s diet and program, and answered their questions.

I assume either I answered something incorrectly or they don’t accept anyone outside the USA? Can anyone illuminate me to a possible reason?

It’s not that it matters that much, I was just curious to read about other people’s challenges and how they overcome them, and see what other people on this diet eat and so on. :slight_smile:

You’re not missing much. It’s essentially a dr berenstein cult. I suspect if you said anything other than chanting and regurgitating exactly from the book or asked any questions they probably blocked you


It’s a strange group.

In a place like TuD, you can have reasonable discussion and debate about carbs. People can agree or disagree, but realize there are a lot different approaches and people choose what works best for them.

But with that group, there is no debate.


I suspected it was something like that… Their “about” information seemed really intense, lol.
I think it was my answer to the question of how he treats low BG’s that got me rejected. The current version of his book is from 2011, as far as I know, but I watch Dr. Bernstein’s monthly Youtube videos, and he is much more nuanced there, and I answered the question in such a way.

But yeah, I’m very happy on TuD, and I was more interested in their diets than anything else. :slight_smile:


I am curious, because I do not know that they do for that, but what is your version of treating low BG vs. their version?

I don’t really have a single answer for myself, because every low is different. But I prefer to make it tasty. :yum:


I’m a member of that group but rarely visit. I joined back in 2015 when I started to use Afrezza. A relatively non-controversial comment, I thought, about my Afrezza use brought a dismissive and negative comment from a site leader. Afrezza is not embraced by Dr. Bernstein, as far as I know, but doesn’t seem to conflict with his value system. At this site, disagreeing with Dr. Bernstein is a serious breech of their culture.

I admire the glucose results they get; their community was used as the basis for a study of low-carb adherents and their A1c results. I don’t admire their lack of tolerance for dissenting views. But they built their community and used this intolerance as a widely public value. Their house, their rules – my choice is whether to participate or not.

I think that frank discussion of any philosophy or set of rules benefits that philosophy if it is built on fundamental truth and value. I don’t get why any group would reflexively expel any who criticize.

I think humans can coarsely and generally be divided into authoritarians and those who question authority. Authoritarians and their much more numerous followers become uncomfortable with any challenges to their belief system. They often cheer when a challenger receives summary justice – in this case denying your entrance to the group but often when members are expelled for simply questioning the basis of the belief system.

This group does good work, especially for the frightened parents of young T1Ds who find this safe harbor to work out a way forward that’s healthy and sustainable for their children. I do think that good glucose control is much healthier than poor glucose control.

I wouldn’t take undue offense, @Lemonz. The core principles of Dr. Bernstein are shared by many outside of this group. I’m one of them but I do disagree with some of Bernstein’s philosophy. For example, I choose to follow a low-carb, high-fat diet while he espouses low-carb, high-protein, not a huge distinction. Dr. Bernstein is not a fan of insulin pumps either, although I know many of his followers do use insulin pumps. I wouldn’t volunteer to give up my automated insulin dosing system based on an insulin pump.

The internet is a big place. While people often like exclusivity, there are plenty of online communities to provide a forum for you to learn, exchange information, and provide support.


In his book, he only wants us to use pure glucose to treat lows, so as not to cause overeating. He calculates a hypothetical BG rise for 1 gram of glucose for a certain bodyweight. The book uses a 5 mg/dL rise for 1 gram of glucose on a 140 pound body. He only talks about glucose tablets in this case.

In his youtube videos, he talks about the beneficial use of liquid glucose as a subsitute, especially when exercising, due to reduced digestion and spit production during strenuous workouts, making the absorbtion of tablets slower. This isn’t mentioned in his book, as far as I know.
I answered typeonegrit’s question of “how does Dr. B treat low BG” with glucose tablets or liquid glucose depending on preference and circumstances. It’s probably too ambiguous for their liking… I don’t know.

I usually treat my lows with glucose tablets when at home, but I take a sip or two of (sweet) soda during work, because I’m pretty tired of glucose tablets, to be honest, lol. :stuck_out_tongue:
This is a “no-no” according to Bernstein (and thus, the “grit people”).


I totally agree. I guess that community isn’t right for me anyway, because I don’t do everything the way Dr. B would.

I find it difficult to eat the same amounts at every meal, like Berstein does. I keep my carbs the same at every meal, but the protein changes a bit, so that is something I do “wrong”. I also use an insulin pump, a MiniMed 670G, with the SmartGuard system, which is also “wrong”.
I’m a bit disappointed by the pump, because it comes with a pre-set BG value it moves towards which is too high in my opinion, but it works well for me and does help keep my migraines at bay. I have very BG sensitive migraines, so the SmartGuard system is good at keeping hypo’s at bay and my migraines at bay as a consequence. This is also an “incorrect” way of treating diabetes according to the book.
But for me, it’s either a choice of having an elevanted A1c or very frequent migraines, making my daily life unbearable. My A1c is usually between 5.8% to 6.2%, which is too high for Dr. B, but makes my life liveable.

So I guess I’m ineligible for typeonegrit anyway, because of my personal circumstances, lol. :stuck_out_tongue:


Would be interesting to follow these kids into later adolescence and adulthood and see if, on average, their good control continues, or if it’s doing more to address parental anxiety than lay a good foundation for a lifetime with diabetes. Extremely dogmatic, rigid practice seems not sustainable for most. Sure seems like a recipe for raising kids at high risk for developing disordered eating and other issues functioning as a flexible, adaptive adult…


we are delighted you found us.



I don’t think the Dr. B low carb regimen, by itself, places children at risk for later disordered eating. Raising children well can be tricky business and I suspect that other factors including family dynamics, the personality of the child, the quality of their parent’s marriage and more play important roles.

Driving a T1D child hard with a disciplined eating practice can certainly backfire and amplify an already dysfunctional family dynamic. But if the family communicates well, flexibly incorporates the child’s preferences, and is done with an abundance of love, then the follow-on risks can be reduced.

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I followed The Bernstein diet for 11 yrs. There were many good things to eat and lots of food that would appeal to a child. I no longer eat any of the high fat food, like nut butters, and I miss them. There were some great cheese cake recipes. I think a lot would depend on the child and how much time the parents could take to make really appealing food.

I sometimes wondered how I would have done with that way of eating when I was a kid. I would probably have done ok with it as long as I had plenty to choose from. Most teens are going to eat what they want no matter how they were raised, but at least the child would have had several years with more stable glucose levels.


I guess my answer of “margarita’s” wouldn’t let me join the group. :joy:

I think I have had 1 glucose tab in my 48 year career of T1D.


Glucose tablets go Moldy. I live in a very arid climate but every time I go for a glucose tablet, they have spots on them. However I have had carb gels in my glove box still good after 2 years. So I just gave up on glucose tablets.
I don’t see the point and they taste like sweet tarts which remind me of a sad Halloween experience when you run out of the good candy and are left with freaking sweet tarts!!!


Maybe. But I think that vastly oversimplifies how eating disorders work and develop. Plenty of largely functional and caring families raise kids with disordered eating, and pushing kids really hard in an over-restricted and highly perfectionist way can be a factor. (It seems like the degree of adherence in the T1 grit groups doesn’t really leave that much room for flexibility…) Also, in kids who were T1 back in the days of regimented meal plans to fit R/NPH or L insulin, eating disorder rates were high for a reason. It’s a very real risk. It also fails to teach key skills of how to engage in moderation and flexibility that most of these kids are going to need someday especially if as young adults in college they decide to experiment with other ways of eating/functioning and then find themselves woefully unprepared.


Thank you! :smiley:

Yes! I’ve probably thrown more glucose tablets away than I’ve eaten. As soon as I’ve opened a roll/package they turn soft and yellow within a week… Really unappetizing.

For what it might be worth, Lemonz, I don’t eat the same meal every day either and I don’t think this degree of rigor is necessary. But it helps. Everything in life is a tradeoff, and Bernstein is not a tradeoffs kind of a guy – he is a black-and-white kind of a guy.
My guidance, based upon the endocrinology of the prandial hyperglycemia/hyperglucagonemia, is different.
Islet insulin is the primary regulator of glucagon secretion by alpha cells, with islet blood glucose being a distant secondary regulator. Glucagon is regulated inversely to islet insulin. So an insulin deficiency, as in almost (but not quite) all forms of diabetes, will generate portal hyperglucagonemia and hence whole-body hyperglycemia, via hepatic artery from hepatic glycogenolysis.
But portal glucose and portal AAs (amino acids) stimulate insulin/glucagon secretion in completely different ways. Glucose (from dietary carb) acts almost exclusively on the beta cells, with alpha cells only indirectly inversely stimulated by local/islet blood insulin. AAs (from dietary protein) act directly on BOTH beta and alpha cells, stimulating a balanced and increased amount of both hormones insulin and glucagon, respectively, in such proportion as to keep whole-body/peripheral (to portal axis) BG unchanged. The increased insulin is the driving evolutionary force, because protein is the most valuable and precious macronutrient but also has little to no storage depot – it must be driven into the cells or it will be lost. The glucagon keeps the BG from dropping dangerously, so that the brain fuel supply (in the fed state) does not become suddenly inadequate. The brain cells, uniquely, are not differentiated to use FAs (fatty acids) as fuel.
Portal/islet glucose is a powerful stimulant of insulin secretion by beta cells – several times more powerful than most of the AAs. In the non-diabetic this shuts down glucagon secretion to zero. However, in the insulin-deficient (but not insulin-dependent) diabetic it INCREASES glucagon secretion – this results in POSITIVE feedback rather than negative feedback or regulation. That is WHY dietary carb CANNOT be reliably compensated for by ANY insulin – it has nothing to do with speed of action. During the prandial period the biological regulatory system is unstable wrt portal glucose / dietary carb’s. There is NO predictable ratio of insulin units to grams of carb that will work consistently, and due to the oscillatory system response both hyperglycemia and hypoglycemia will be observed with optimal titration.
Dietary protein from animal sources delivers AAs in fairly fixed proportions, even though the different AAs stimulate beta and alpha cells independently and differently. So a consistent ratio of peripheral insulin (from any non-portally located pump or subcutaneous injection) units to grams of animal protein can be derived, and it will behave consistently from meal to meal.
My rule is to keep carb’s low enough so that dietary protein dominates required insulin titration – i.e. so that prandial portal AAs dominate over prandial portal glucose wrt beta-cell stimulation.
But most T1Ds have virtually no functioning beta cells, as I do (I have unusually small or tiny beta cells underexpressing insulin due to HNF1-alpha mutations). For most T2Ds, still producing significant insulin endogenously, I think my rule should be adhered to.
For diabetics producing virtually zero endogenous insulin, which includes almost all T1Ds, the islet insulin signal has long since been gone. I think this is why T1Ds can arguably better compensate for dietary carb’s with some consistency or predictability. Because there is no insulin signal at all, the positive feedback is also at least attenuated or eliminated. But hyperglucagonemia is still the cause of hyperglycemia in T1DM. Maybe one can say that the balance of bolus vs. basal insulin is shifted toward basal being much more important than in diabetics still producing significant endogenous insulin. And the contribution of dietary carb’s to hyperglycemia is probably relatively greater in comparison to the hyperglucagonemia too, as Bernstein’s rules of insulin units to BG lowering imply.
These same rules make absolutely no sense whatsoever, endocrinologically, in anyone producing endogenous insulin. And not surprisingly, they don’t work at all in me. My beta-cell function is about 40% and completely stable. It will never change, and never has.

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P.S. Having seen Bernstein myself in his office for three full days (that is a requirement for a new patient who can travel to NY), I know his discipline. He measures his BG every hour, and is usually low and never high. When low he compensates with liquid glucose. When weightlifting he must do the same in between every set!
So Bernstein overcompensates with primarily basal insulin, and then compensates every hour to correct with oral glucose. He doesn’t explain this, but that is what he is doing for himself.
He has CVID and had an episode after an Ig infusion of hypoglycemia that caused him to pass out just before leaving the hospital. The infusions can stimulate some survival of regenerating beta cells so that significant endogenous insulin is produced transiently – this is not something that most insulin-dependent diabetics need worry about, including myself (I also have CVID, and a much more serious case – I produce essentially no antibodies whatsoever). Anyway, this is why he corrects BG every hour – it is a hypoglyemic event he is worried about.
An awful lot of Bernstein’s methods have been derived using his own unique case. He overapplies a lot of this to patients and others, not necessarily legitimately IMO.
Any kind of dextrose is pretty fast-acting, and generally adequate, for most diabetics IMO. Bernstein is an MD, and a bit paranoid (understandably, because they can get sued) about hypoglycemic events. But epigenetic degradation of alpha cells makes hypoglycemia more likely and more dangerous for all but early T1Ds (that still retain some working beta cells).
I myself feel absolutely nothing if my BG drops to fasted-state levels (20 to 30 mg/dL lower than fed-state) iatrogenically (i.e. due to excessive subcutaneous insulin). Brain fuel transitions seamlessly to ketones from glucose – alpha cells work normally. There is no secondary response (adrenaline) because primary response (glucagon) is flawless. But T1Ds cannot expect this, and each individual diabetic must understand his insulin response thoroughly wrt to meals and titration and so forth. The diabetics in this forum seem savvy and experienced enough not to be likely to experience dangerous hypoglycemia.

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As someone else here remarked, the Dr Bernstein of the 2011 book has mellowed now, as seen in his monthly Q&A sessions on Youtube. He will often say, "As Yogi Bear says, “‘What works works’”. Dr B comes across as someone for whom food is pretty unimportant, whereas maintaining what he considers a normal bg is vital. So, for him eating the same food at each meal is a great solution. However, if a patient could show that they were keeping perfect bgs while varying their meals, I really don’t think he would object.