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EventsHigh insulin precedes obesity, a new study suggests
A new study published in JAMA Network Open reports that insulin levels rise first, and then people develop obesity — not the other way around.
Why is this important? Traditional teaching is that obesity is related to dangerous health outcomes, including premature death.
However, as the study’s authors point out, the association between obesity and premature death is not strong and fails many criteria to suggest a cause and effect relationship. Perhaps the risks linked to obesity have more to do with poor underlying metabolic health than obesity itself.
Additionally, traditional medical belief is that people become obese first, which then triggers insulin resistance and hyperinsulinemia. If that is the case, any weight loss technique, including liposuction, should be equally beneficial for improving insulin sensitivity.
But if the opposite is true — if insulin resistance does lead to obesity — then only weight loss strategies that also lower insulin resistance and improve metabolic health will successfully address the underlying metabolic dysfunction and reduce the risk of future health complications.
While the current study does not prove that insulin resistance causes obesity, it makes a strong case for it.
The authors reviewed 60 studies — randomized trials and observational studies — with over 5,600 participants. They concluded that subjects had elevated insulin levels before they had a rise in their BMI. But the converse was not true. They did not start with elevated BMI and develop elevated insulin levels later. (caveat, these were subjects engaged in some sort of weight loss program including bariatric surgery for many).
Considering the number of people with metabolic dysfunction who are not overweight and the number of people with obesity who don’t have metabolic dysfunction, the paradigm of insulin driving obesity makes sense.
The so-called TOFI (thin on the outside, “fat” on the inside) or “skinny-fat” population tends to have visceral fat (fat around the organs) and insulin resistance, but they don’t have the traditional amount of fat to be considered obese.
Consider the patient with type 2 diabetes or polycystic ovary syndrome (PCOS). They are often overweight, and their diagnosis gets “blamed” on their excess weight. But, perhaps it has more to do with rising insulin levels than the weight itself.
If the disease state is more related to elevated insulin levels, then preventive measures and treatment strategies should focus more on addressing insulin resistance and metabolic health — and focus less on the number on the scale.
It’s true that many different weight loss strategies can help lower insulin levels and improve metabolic health — but not all.
Low-carb diets that focus on reducing carbohydrates, getting adequate protein, and adding fat for flavor have demonstrated significant benefits for weight loss, reducing insulin resistance, and improving blood sugar control. Low-carb diets aren’t the only approach, but they certainly are an effective one.
It is also true that this study is not “proof” that insulin resistance always causes obesity, and obesity never causes insulin resistance. In fact, the association between hyperinsulinemia and future obesity was greatest for those undergoing bariatric surgery, and it is unclear how this might apply to the broader population.
So, don’t take this study as proof of the “carbohydrate-insulin model of obesity.” Instead, we can see it as more evidence that metabolic health plays a critical role in weight management and the health repercussions of obesity.
If you are interested in getting started on a low-carb diet, try starting with our two-week Get Started Keto Challenge or our 10-week Weight Loss for Good course. You can also experiment with our personalized meal planner to find which of our 1,000+ premium recipes will fit your health goals.
Thanks for reading,
Bret Scher, MD FACC
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10 comments
"The authors reviewed 60 studies — randomized trials and observational studies — with over 5,600 participants. They concluded that subjects had elevated insulin levels before they had a rise in their BMI. But the converse was not true. They did not start with elevated BMI and develop elevated insulin levels later."
You are misrepresenting the study. Or maybe you just didn't bother to read past the abstract. The study was by and large about people actively losing weight (dieting or having had bariatric surgery). It was not observing people who gained weight.
From the abstract:
"... participants in most studies experienced decreases in BMI, fasting insulin level, and C-reactive protein level."
From the Results section:
"The 60 studies included 112 cohorts: 40 cohorts contained participants who had undergone bariatric surgery, 33 cohorts contained participants who were receiving diet therapies (all except 2 designed for weight loss or weight maintenance)..."
If you are losing weight, it means you are in a calorie deficit. A calorie deficit leads to a decrease in insulin faster than it leads to a decrease in weight. This study says nothing about obesity onset or progression.
The background study is not so good, they omit incretin effect, viscera etc., but they stumble and fall to the right direction.
"if insulin resistance does lead to obesity" no it does not. As long as you are insulin sensitive, you can add energy to fat cells and stay protected from metabolic mayhem. Insulins major task is to keep 100 000 kcal of fat energy away from blood. The moment storage is full, and fat energy (lipolysis + FFA release) leaks into blood despite insulins efforts to keep it locked, you have everything in abundance in blood -hormones, fats, glucose. If insulin has been a bit highish en route, the viscera has been accepting energy -because it is 4 times more active metabolically (4*GLUT4 e.g.) than normal WAT. Add to this macrophages finding visceral fat similar to a protruding stick... inflammation releases more fat into blood... you insulin is useless, this is when insulin resistance reaches pathology.
I do like the concept "energy poisoning" much rather than the final red flag of it -hyperglycemia. It way too late...Add to this intensive blood glucose therapy :(
JR
False. See https://www.medrxiv.org/content/10.1101/2020.10.27.20220202v8 and https://www.medrxiv.org/content/10.1101/2021.02.22.21252026v1
Losing weight means wishing to loose fat mass. Means replacing eaten energy with inside energy. Means looks like you are in "calorie deficit". But it has to come from hunger signal; you do not want to eat. It never (98%) works long term the other way around: you start with fixed calorie deficit (cheese knife: a little bit of less of normal diet). There is macro adjustment needed: cut the fats or cut the carbs; if you stay on "sweet spot on both fats and carbs", the body never gets the idea. It kind of a tells you to eat more (by moderating resting energy expenditure down, making you cold and hungry). I do not get it why fasting works the other way around (body turns on the "turbo" for a couple of days; run faster for your prey).
This mass-in mass-out model is quite interesting (Peter's refs). It is brand new. So, let's wait the opinions to settle on it, the creators have already made bold and all-knowing claims about it. Actually, I do concur with their point, that caloric balance only coincidences with mass balance. Studies never count the energy from inside directly... nor the wasted energy e.g. heat production. They should have a thermometer with those feeding trials... the simplest thing. But if your mass-intake is less than your oxidised-mass-output (+loo), you are loosing mass, clearly. Hopefully fat mass not muscle mass.
JR
Peter, your reference is a preprint (i.e. not accepted for publication) about a mathematical model/simulation. I don't know what you think it proves.
I admit there may be a way to provoke fat gain and greater muscle loss during a calorie surplus, or fat loss and greater muscle gain during a calorie deficit. Those far-fetched scenarios, if achievable, would make my initial statement false, but I don't think they are relevant here.
@Dr Scher, your title and your opening statement are still inaccurate.
"High insulin precedes obesity, a new study suggests"
"A new study published in JAMA Network Open reports that insulin levels rise first, and then people develop obesity — not the other way around."
The study is actually about weight loss. It suggests low insulin precedes weight loss.
I like to think about calories like this: Cal from inside + Cal in = Cal out + increase of storage (fat).
If you manage to reach your inside fat as energy, then you need to eat less to achieve balance with Cal out. Seldom someone wants to increase the fat mass. For eating Cal in, rely on your hunger.
We all know what it requires to effectively reach fat storage i.e. favor lipolysis first... less carbs less often. And educate and obey your hunger.
Counting exactly ins and outs is rather hopeless (and unnecessary).
Peter, I did read the papers and more and I especially liked the picture with mass flows and calorie flows with neogenesis. As Valerie points out, this is only a model (predictions of which went quite well) and we are waiting for peer and other reviews. It provoked a thought: if you need 1800 kcal, then 200g of fat satisfies this, as well as 450g of carbs (or protein). You also need more oxygen to burn long -CH2- chains than C6(H2O)6 carb molecule, to create the same amount of H2O and CO2. What ever it may mean...
Does insulin precede obesity? Dr. Kraft certainly showed, that a hidden imbalance (excess) on insulin precedes any measurable effect in blood glucose. So, if you have higher peaks AND longer duration of insulin secretion (IUC many times of "normal), you certainly end up with a "part-time insulinoma". Storing more and lettin less free fatty acids into cirkulation, and starting to disturb visceral areas (which have ca. 4 times faster metabolism than WAT). To me, even part of this is mechanistic formula to weight gain. The study at hand has nothing to do with this.
JR
https://www.medrxiv.org/content/10.1101/2020.10.27.20220202v8
https://www.medrxiv.org/content/10.1101/2021.02.22.21252026v1
We have seen that you are able to send links (same and repeatedly) to this debate.
What is your take on this, apart from that you have found a new prophet which you blindly believe in?
No need to answer, they may be on correct trail, I'll stand by, over and out for me in here. This is useless.
JR