Notes from the T2 Diabetes SummitPublished 4.20.2016
The Diabetes Summit for 2016 is this week— really, the title should be Type 2 Diabetes (T2D) Summit, because T2D is what they're talking about. I did not register this year and am not listening to any of the talks as I was unimpressed with the line up of speakers— too much woo, not enough science. However, I did listen to several talks given in the 2015 summit last March and never wrote up my notes, so I thought I'd take the opportunity to do that today.
Actually, I'd decided to write about Dr Roy Taylor again before seeing this article in the New York Times about his results, but I was happy to see his work garner more attention. The low carber comments about the article were hilarious though. No, going low carb does not reverse diabetes. People who control their diabetes by limiting carbohydrate intake do not have a properly functioning pancreas because they cannot pass an oral glucose tolerance test (OGTT) without prepping for it. That's not cured. That's barely controlled.
The short term low calorie treatment developed at Newcastle University reverses T2D in people whose body responds— and not everyone does. Even people who've had T2D can reverse the disease using the Newcastle protocol AND maintain the reversal if they follow a healthy diet afterward (not necessarily low carb, but it can be). The non-responders tend to be T2D sufferers of long duration who are on multiple T2D drugs. However, for those who do respond, the treatment offers genuine cure— as in they can pass an OGTT without prior preparation. None of this is new to you if you've read at this site previously. I am a big fan of Dr Roy Taylor and his work.
Fuhrman and MooreThe notes and commentary from Dr Taylor's talk follow, but before I begin I wanted to note that I listened to two other talks that I will not be providing notes for. One was given by Joel Fuhrman, who distinguished himself by advocating that T2 diabetics should eat carbs, especially beans. The strong bias in the T2 Diabetes Summit is for low carb as the only treatment for T2D. That's nonsense, of course. First of all, as noted above, people do NOT reverse T2D with a low carb diet, at best they control it. Second, people have reversed T2D using other low calorie diets, including a vegan diet. Dr Fuhrman tried his best to make his points, but I don't think the host or many of the audience listened to what he had to say.
The other talk a listened to was given by a blogger named Jimmy Moore. How he is considered an expert in anything health related, let alone T2D is beyond me, but his message of shoving your gob with fat was certainly more acceptable to the host than Dr Fuhrman's. It should be noted that though he is obese, Moore is not a T2 diabetic (at least not yet, he seems to be doing his best to make himself into one). The comments underneath the link for Moore's talk were telling. The Summit provided Moore an audience beyond the small low carb sphere, and commenters were not willing to turn a blind eye to the irony (hypocrisy?) of a fat man lecturing them on how to eat to lose weight and improve their T2D. At least Dr Fuhrman was thin.
As those comments will make clear, I do expect anyone giving me diet advice to "walk their talk" and not be obese. And now having sufficiently buried the lede…
Roy Taylor's 2015 Diabetes Summit presentationThe presentation, as is usually the case in these "webinars" was really a conversation between the host and Dr Taylor. No slides were presented. These are notes and commentary made during the talk while I watched, by know means are they an exhaustive representation of information imparted by Dr Taylor. This was actually early days in my infatuation with Taylor's results and their implication, since then I have done much more research on the topic. However, I've decided to keep the editing of these notes to a minimum and present my reactions as they were on that day.
- T2 can be reversed. It happens with bariatric surgery.
- This presentation was part of “The Diabetes Summit” which I chose not to register for because I didn’t want to weed through the woo.
- BUT Taylor is an actual MD and the Newcastle Diet is extreme but it works.
- Taylor states definitively that if you are huge you HAVE to be eating a HUGE amount of food. So if you suddenly eat much much less, then the body will take the fat from the liver.
- He did his studies on people who had T2 for under 4 years (that was to avoid complications of long term disease)
- The diet is 600-800 calories for 8 weeks. And the subjects were motivated and did it. And they were not hungry (after the initial adjustment I would think). The diet VERY severe.
- Subjects did lose weight, AND glucose went back to normal. Within 7 days.
- Used MRI to measure the fat and glycogen levels in liver in real time.
- Over the rest of the time, the insulin response recovered. Meaning that the beta cells recovered. At the same time the fat level in the pancreas returned to normal. If the beta cells are surrounded by fat don’t respond well.
- It’s a revolution in the understanding of T2, Taylor says. It sure as hell is.
- It’s not a one off study, he’s repeated it.
- This can be done by anyone. You do NOT need to go to a program. People doing it on their own had a 60% success rate. And if they kept the weight off, they didn’t relapse.
- And he makes the point explicitly that you do NOT need doctors to do this. You just need to DO it. But hell for 2 months?? I can do that.
- Taylor thinks composition of the diet is over emphasized. Low carb or high carb doesn’t matter it’s the ENERGY BALANCE!
- When the liver makes fat, it stores it. Excess energy = liver makes fat =lipogenesis. Some people can have lots of fat in the liver, others wind up with livers that lose the ability to respond to insulin.
- Liver exports excess fat =VLDL and sends it to whether it can be stored. If the outer fat cells are filled, then it gets stored viscerally and then into the organs and specifically into the pancreas and around the beta cells.
- The host focused on carbs, but that’s NOT what Dr Taylor did. He just bottom lined it as TOO MUCH FOOD— or DRINK. It's too many CALORIES that's the problem.
- Hyperinsulinemia (elevated insulin release because the liver isn’t responding) lipogenesis is stimulation by elevation insulin. Insulin resistance is the starter motor he says, NOT the engine. It’s about fat in the liver and pancreas from TOO MUCH FOOD.
- The brain needs GLUCOSE. Liver puts out glucose to feed the brain and body. And it’s a rapid process. Glucose is always getting made and being used up. Glucose turn overs very fast. Fasting glucose level is due to the liver. So Insulin resistance means that the liver is making too much. After the fat leaves the liver then the liver makes the correct amount of glucose.
- Triglycerides are stable from of fat, but to use it cells have to take off fatty acids, and that leaves it in a dangerous form that can inhibit the the function of insulin (it then has two not three fatty acids on it) That’s the free fatty acids Carbsane is often on about.
- The host asks about the Dawn effect- it is related to rise in cortisol— the stress hormone— that makes us a bit more insulin resistance. If your pancreas is normal, it’s not a problem. But your liver is making too much glucose, then the cortisol effect is heightened. So glucose is higher. And carbs can increase it. That’s an evolutionary physiological response. The overnight fast means the body is preparing just in case there isn’t food right away. If you don’t eat, the brain still needs fuel, so it makes do with other fuels (ketones?) Thus when you eat, the body has to adjust to food it didn’t expect. it’s known as the “second meal effect” Fatty acids are high in the blood in the morning, which means glucose can’t be stored. So a small snack first thing in the morning can mitigate this effect.
- Does it matter what the first snack is? The research used LC snacks. They used soy protein. High protein low carb snack is what he suggested.
- You can’t tell the fat where to go. If you’re unlucky and it goes to to organs, that means you’ve got to reduce the amount of fat in the body. Subcutaneous fat (under the skin, not a problem) Visceral fat = in the organs. = ectopic sites (outside the usual spot) Calls the Omerta (??) relatively harmless.
- Man, this host does not want to say that people with T2D need to EAT LESS FOOD.
- The host asks are there surrogate marker for fatty liver? Taylor says the trousers you wore at 21. People should NOT put on weight as they age. There is NO biological reason why you should. Waist circumference is what he points to. No expensive tests required. “Ok great” is the only response the host can muster. LOL
- What did the 600-800 diet were structured. Wanted no uncertainty how long people were eating, so they did liquid replacement meals. Each packet was 200 calories. Had 3 per day + unlimited low calorie vegetables “to keep the bowels working”. So basically 600 calories + vegetables (lettuce and cabbage is what he mentioned). This made it easy for people to do. The liquid diet is for people who can’t just cut back to those calories.
- Exercise? His papers say it can speed the process. Exercise isn’t for weight loss, (fatties can’t do it enough to use enough calories) It’s ALL ABOUT FOOD INTAKE. Can exercise for an hour and undo it in 2 or 3 spoonfuls. So exercise because it’s good for you, but not for weight loss. Exercise can make you hungry and you need not to eat.
- But exercise is important in preventing weight GAIN. Once weight is gone, then you should exercise (and maintain a slight calorie deficit to what you ate previously to become a fatty).
- Exercise is important for maintenance. Hmm.. Says nothing about NEAT (non-exercise activity thermogenesis. NEAT doesn’t increase appetite, but EAT (exercise activity thermogenesis) or TEA can. Ha. I just noticed that EAT, might be the exactly perfect acronym for it.
- Patients have been enthusiastic from the start. And it’s worked for many. Diabetes UK has been spreading the word— but with caution. The caution is that diabetes can be reversed, but we don’t have any controlled diet over time. Diabetes UK is funding a random control trial for two years. Will be 140 people in each arm. The research has just started.
- Not all T2 diabetics are fat, though most are. Genetic differences explain the rest. There are different liver susceptibility. Everybody has a personal fat threshold. It explains why obese doesn’t mean diabetic BUT it still means you’ve eaten too much. You’ve eaten more than your subcutaneous fat levels can handle.
- So it’s the “personal fat threshold” that is the hypothesis (I think).
Search this site: