Type 2 Diabetes as a Simple Condition of Excess Fat
Research of recent years has shown that the triggering mechanism for type 2 diabetes is specifically excess fat in the pancreas. The only way to place that fat into the pancreas, in the normal course of affairs, is to become very overweight - to overload the body with fat to the point that it cannot find places to safely store it. Losing this excess fat through a low calorie diet, and then maintaining a lower weight going forward, is a cure for type 2 diabetes, as demonstrated in clinical trials.
For the first time, scientists have been able to observe people developing type 2 diabetes - and confirmed that fat over-spills from the liver into the pancreas, triggering the chronic condition. The study involved a group of people who previously had type 2 diabetes but had lost weight and successfully reversed the condition as part of the DiRECT trial. The majority remained non-diabetic for the rest of the two year study, however, a small group went on to re-gain the weight and re-developed type 2 diabetes while monitored by the study organizers.
"We saw that when a person accumulates too much fat, which should be stored under the skin, then it has to go elsewhere in the body. The amount that can be stored under the skin varies from person to person, indicating a 'personal fat threshold' above which fat can cause mischief. When fat cannot be safely stored under the skin, it is then stored inside the liver, and over-spills to the rest of the body including the pancreas. This 'clogs up' the pancreas, switching off the genes which direct how insulin should effectively be produced, and this causes type 2 diabetes."
"This means we can now see Type 2 diabetes as a simple condition where the individual has accumulated more fat than they can cope with. Importantly this means that through diet and persistence, patients are able to lose the fat and potentially reverse their diabetes. The sooner this is done after diagnosis, the more likely it is that remission can be achieved."
Link: https://www.ncl.ac.uk/press/articles/latest/2019/12/type2diabetesstudy/
So this means as long as I work out (both weight training and aerobic) and control my weight, that my chances of getting type II diabetes should be zero. Is this correct?
@AL, no, but it will reduce probability of you getting type2 by about 75% (off top of my head). Tom Hanks has type2, and he has never been overweight.
Hi Abelard, just a 2 cents.
John is correct, that no it will not reduce your probability to zero; but it will lower, nearly sure. There are many factors to this, besides visceral fat - visceral fat can accumulate thin or obese; I have known people who were thin and had diabetes type 2. Most likely, internally, there was havoc going on - they had accumulated visceral fat mass around their pancreas and 'choked it'; even if from outside they were thin. It takes very little (if I remember removing just 20 grams of fat around pancreas already allows it 'to breathe' again..and produce insulin from its beta-cells); thus yes, you can be thin your wholelife - with no belly fat - and Still die of obese-person diseases. I was one of them but thahnkfully survived. Thus, all we can do, is stack the deck of cards/odds in our favor by doing exercice, eating low calorie/more nutrient dense per cal food...etc..There is also genetic heritability component (if your (grand) parents have/had diabetes, you have chance that is comes to you - obese/thin or not). My father has type 2 diabetes, he had it first at 35-40...my age basically and now my body is saying the same thing - if I contine with sweets/crap food - I Wiill become (pre)diabetic (like dad...) no matter how much exercice I do (it goes to show there are intrinsic inherited genetic elements susceptibility/pre-dispositions and extrinsic environmental elements..both matter to the later outcome). There is always a probably, you can reduce as best as you can; but not to true 0.
Just a 2 cents.
Isn't the type II all about the cells being less sensitive to insulin whole your I is about having deficiencies of producing insulin?
Cuberat, I tend to agree with you. It is not uncommon to see diabetes 2 sufferers having uncontrollable and wildly fluctuating glucose levels throughout the day (hypo / hyper) and at the same time having extremely high insulin levels. Reducing fat, especially abdominal fat, reduces insulin resistance. This is a known fact. It makes diabetes 2 a condition that is hard to treat. Insulin jabs are not a solution. Lifestyle changes and medication that works on PPARx to modulate insulin sensitivity are the only way
Tom Hanks says he was overweight at times and ate poorly, so not a counter-example.
https://www.independent.co.uk/news/people/tom-hanks-diagnosed-with-diabetes-after-being-an-idiot-with-food-and-weight-when-he-was-younger-a7033681.html
Diabetes is manifested by high fat levels- but those are caused by high insulin levels, in turn caused by high blood glucose levels.
And how do you get high glucose levels? By eating carbs. Cut the carbs, cut the glucose, cut the insulin, cut the fat. It's that simple. You can enjoy savory fats and proteins in your diet to your heart's content because your appetite goes down when you don't have the blood sugar zigzag going on all the time. Even though fats are 9 kCal/g vs 4 for carbs, fats make you feel full sooner- and you end up eating fewer calories because you stop eating sooner. And you're not hungry again an hour later.
Cut the carbs.
In the last 15 months, I've shed 70 pounds of flab, eliminated arthritis that made the balls of my feet hurt all the time, my rotator cuffs are near-normal, and I fit into size 32 pants for the first time in 40 freaking years.
Cut the carbs, ignore the calories, and add intermittent and extended fasting if you're in a hurry.
But first, cut the damn carbs.
It's not just diabetes that makes a high-carb low-fat diet a bad idea, there's a whole array of bad consequences to metabolic syndrome, which is the underlying root of diabetes. From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191378/
"Insulin resistance is a common metabolic abnormality underlying type 2 diabetes mellitus and is also an independent risk factor for cardiovascular disease. Although ATP III identified cardiovascular disease (CVD) as the primary clinical outcome of the metabolic syndrome, we now have evidence that metabolic syndrome is associated with type 2 diabetes mellitus, polycystic ovarian disease, nonalcoholic fatty liver disease, and possibly some cancers. This review summarizes evidence in support of the relationship between metabolic syndrome and various cancers and possible underlying mechanisms and therapeutic interventions."
If you cut the carbs, metabolic syndrome goes away. And it takes all these lovely things with it:
"The prevalence of obesity in the general population continues to rise at alarming rates regardless of age, gender, or cultural differences. In general, the risk of comorbidities increases as the degree of obesity increases. Numerous health consequences have been linked to obesity, including metabolic syndrome, cardiovascular disease, and cancers, as well as many other chronic conditions. Metabolic syndrome (MetS) is a complex constellation of chronic illnesses associated with central obesity, including insulin resistance, type 2 diabetes mellitus, hypertension, atherogenic dyslipidemias, and chronic inflammation, and it is a known risk factor for cardiovascular disease. While not all obese people display the typical findings associated with MetS, all obese people appear to be at increased risk for negative health effects. Of great concern are the potential long-term health effects on the pediatric population."
(https://www.nurse.com/ce/health-effects-of-obesity-and-metabolic-syndrome)
It's heartbreaking to see little kids so fat that they _waddle_ and all it takes to cure them is to cut the goddamn carbs.
@Doug
I (and more importantly Dr. Greger) think you are on the wrong track advocating for low-carb over low-fat in this context (or most contexts).
Though Reason's linked article triggering this post is from late 2019, Dr. Greger posted that fat is the cause of T2D in 2016: https://nutritionfacts.org/2016/11/17/fat-is-the-cause-of-type-2-diabetes/
And just 2-3 months before the paper Reason cite's here, Dr. Greger explained that low-carb/keto diets don't cure T2D in this podcast (click the transcript tab if you'd prefer to read the text): https://nutritionfacts.org/video/does-a-ketogenic-diet-help-diabetes-or-make-it-worse/
"The reason keto proponents claim they can "reverse" diabetes is that they can successfully wean type 2 diabetics off their insulin. That's like faith healing someone out of the need for a wheelchair by making them lie in bed the rest of their life. No need for a wheelchair if you never move. [...] A true diabetes reversal diet is practically the opposite of a ketogenic diet; diabetics off their insulin within a matter of weeks, eating more than 300 grams of carbs a day."
Obviously, low-fat with high refined carbs is bad. Most low-carb/keto advocacy is reacting against that all-too-common but nutritionally poor version of low-fat, but the majority of the evidence suggests (as Reason has hinted here many times) that the optimal diet for healthy longevity is predominantly whole plant-based carbs and low in both fat & protein. (And note that a human calorie-restricted diet that provides sufficient micronutrients is necessarily of that type rather than being low-carb.)
The difference between really optimal lifestyle & typical western lifestyle makes only 10-15 years difference in lifespan (based on much epidemiological work), and that includes things like exercise, sleep, & smoking in addition to diet. Standard American diet vs. optimal version of low-carb or WFPB is a bigger difference than the latter 2 are from each other, so this low carb vs. low fat debate probably makes no more than 5 or so years difference to lifespan on average, and therefore as Reason (& Aubrey) like to repeat, this is perhaps not the most important thing to debate relative to the more common topics of this site (like how to push senolytics R&D faster).