Channelling Dr. Atkins here (though I don't really accept the concept of a 'balanced diet' or hold much to channelling for that matter)--but how about an 'unbalanced' diet? If they can't produce 'enough' insulin for the increased calorie needs of pregnancy, how about eating in a way that can provide those calories with less of an insulin requirement?

YES!!

I was given the standard american diet food list, of which I remember the snacks specifically: eat ritz with peanut butter!! OMG!!

I dropped all the literature from the dietitian in the trash and followed Atkins instead. Though he said not to diet for weight loss, as Im sure that was to stay out of trouble. I ate lots of OP foods and gained far too much weight. ANd I was plenty active with a farm to run and 4 dogs.

IMO "they" have missed the mark entirely on managing gestational diabetes so far. Including using Insulin injections.

I don't really understand this study. Thin women get GD, too.

That's all kinds of wrong. Here, diabetes means type 2 diabetes, where there's both hyperglycemia (BG too high) and hyperinsulinemia (insuln too high). How could anybody then conclude that there ain't enough insulin?!? They have no clue what insulin does. They have no clue what insulin resistance is. What they believe it is, is a resistance to insulin signaling, exclusively in the context of "pushing" glucose into those resistant cells, cuz that's exactly the absolute total full complete extent of their knowledge about insulin. What in fact happens, insulin is very well received and responded to by the liver, to wit there's zero ketones in the blood and the only way for that to happen is if ketogenesis in the liver is shut down by excess insulin. Furthermore, fat tissue responds exquisitely well to all that surplus insulin - it grows bigger, doh. Indeed, if it did not, BG would go even higher, since fat tissue grows bigger by taking in excess glucose, converting it into glycerol, forming triglycerides. In spite of this "protective" mechanism, BG remains higher than otherwise. I'm not a genuises, but Ima say, ya know, just for kicks, that maybe, just maybe, it's got something to do with that Holy Balanced Diet, Full Of Wholesome Good-For-You Grains And Other Refined Carbs, cuz ya gotta eat yar carbs, or we won't sell any.

Redman is a Big Giant Idjit.

I'm so pissed. Somebody please pretty please point me to a genuinely smart article about gestational diabetes.

Perhaps they should do a study where the women eat fewer carbs.

Insulin resistance causes fat gain, not the other way around. Therefore insulin resistant pregnant women are more likely to be fat. Pre- and full-blown T2 diabetes are insulin resistance. So I think is GD. Back in the day for GD we were given carb-reduced (but in no way low) diets, generally low-fat due to the era. I was on Atkins and told to get off to avoid harming the baby because that's what well-intending doctors thought. But even a diet that left me hungry and losing weight third trimester, normal looking blood sugars etc., didn't prevent a huge birth weight. Now that more is known about safety issues with low-carb during pregnancy, I'd advise that cutting carbs with GD is the way to go because insulin resistance (trouble processing carbohydrate) is happening.

That was me. Quite thin, but still got GD with 2nd pregnancy. But I had gone thru a couple of overweight/thin cycles before that. I did eventually get fat along with full-blown t2.

I don't really agree here. Overfilled subcutaneous fat cells leading to fat being deposited in liver and other vital organs, leading to insulin resistance is a pretty plausible chain of causation. After that, increased peripheral exposure to insulin due to central (liver, pancreas, brain) insulin resistance might drive fat gain further.

A thinner person might get type II diabetes, and there are situations where some difference in individual genetics etc. may cause this. But a lot of people who aren't all that fat, but who develop type II, may still be "fat" in the sense that their personal subcutaneous fat limit before fat trapping is compromised and fattening of the liver and pancreas becomes more likely to has been met--some Asian groups becoming diabetic at a lower bodyweight than people from a background more prone to fat gain is an example here.


From the side of weight loss--I do think insulin resistance (as long as it's not of the fat cells themselves) can certainly interfere with weight loss itself, since by definition the insulin levels will be much higher than they needed to be to stimulate most of the fat gain in the first place.

One Vietnamese lady who I have known for 15 years is very very thin and diabetic. She eats a ton of rice and very little meat. She asked me about not being diabetic and why am I healthy. I told her to cut way back on the rice and eat more meat. She doesn't like meat but maybe she listened and is replacing some of the rice for meat.

There was that weird Rice Diet which some people found helped their diabetes. Though that can't be working for her.

Even here, very very thin--there are mouse models of very very thin that result in fattening of the liver and insulin resistance. It's not the getting fat, there are models where increasing ability to trap fat subcutaneously decreases central insulin resistance. Central visceral obesity is something that can be measured with a tape measure, but fattening of the liver itself cannot--and in the case of the pancreas itself, levels of pancreatic fat supposed to cause insulin resistance and beta and alpha cell dysfunction is measure in grams, single digits.

teaser is it something like when Dr. Fung brings up gastric bypass curing diabetes. Is it the weight loss or the change in diet that cured their diabetes?

On the question of thin Asian diabetics, many, Asians I know eat tons of fruit. Filipinos eat 11 different types of round fruits for New Year's luck.

Good research is pointing to the flood of progesterone during pregnancy (important for the entire nervous system of the developing fetus) which can trigger gestational diabetes for those on high carb diets.

And we all know the solution to that.

The Newcastle people suggest that it's the reversal of fatty pancreas and liver that's most important. We do know that the diet they use there, that's similar to the early phase of a gastric bypass diet, where there is a very low calorie diet, reduces fatty liver and pancreas fairly rapidly. Of course, with gastric bypass, early on, most of the overall body fat hasn't been reduced all that much, and people reverse diabetes without becoming what you would necessarily call lean. But even on a standard macronutrient ratio, these people will be eating less carbohydrate, so into the mix goes the fact that it just takes less insulin to handle a smaller amount of food, and walking around with lower glycogen levels, tissues may be more insulin sensitive.

The fat in/fat out conundrum for organs--strategies for defattening the liver include increased export of triglycerides--this actually does happen for a lot of type II diabetics when they first go on insulin, that nastly VLDL that our liver puts out is also doing a good thing, transporting fat out of the liver. Another good strategy that occurs more in starvation or semi-starvation or on a low carb diet is increased oxidation of free fatty acids in the liver. Increase this and fatty liver could be reversed. It's not just because those fats are oxidized--also, the pathways for triglyceride synthesis tend to be reduced when fat oxidative pathways are upregulated and glucose pathways are downregulated. So, you can increase export of triglyceride, or decrease synthesis. Fattening occurs when synthesis outstrips export.

For synthesis--that's where subcutaneous fat and the personal fat threshold comes in. "Overstuffed" fat cells-->increased availability of free fatty acids from spillover for synthesis of triglycerides in the liver and pancreas. In starvation or very low carb, elevated free fatty acids is the physiologic norm. It's a pathological state when accompanied by a high availability of glucose. If the liver is glucose replete, and free fatty acids are elevated, that's a good recipe for fat accumulation in the liver. If free fatty acids are elevated, but glucose is scarce, it's not.

What I'm trying to say here is--I think yes, it's the diet, and yes it's the fat loss. In rodent models, just getting the animals very fat can get them diabetic--but concentrating on a high sugar diet is a more direct path to insulin resistance and diabetes, even though it might not get them as fat as some other diets.

Thanks, teaser.

I was stealing the thread, I will post my question on a new thread.