Today we’re going to talk about changing the game on obesity. This is one of the underpinnings of why we question whether or not somebody should be eating carbs.
I just gave you a significant clue. It comes from a well-known obesity researcher at one of our better-known dispensers of “academic medicine”- Harvard. He’s a guy that does know his stuff at Harvard. He said, “be careful about those carbs.”
The well-known obesity researcher is David Ludwig. He is an endocrinologist. He ran the Obesity Clinic at Harvard. I’ve read his book Always Hungry. It’s a good book. I can’t entirely agree with everything he says, but it’s a good book.
One of my patients said he read the book. He said, “I don’t think he says what you say”. I asked him what that was. He said, “the author was talking about a Mediterranean diet”. No, I disagree with the Mediterranean diet unless you have a Mediterranean diet where you’ve taken out the grain products-one of the significant source of carbs.
It’s not a new book. It’s from when people were questioning the Mediterranean diet. I don’t beat up on any diet, whether it is Mediterranean, plants, or animals. My concern is whether or not you’re eating a lot of carbs.
I’m not concerned about where those macronutrients come from. You’ll see in the rest of this discussion why I say this and agree with his comment.
I compare his book and Robert Lustig’s book. Don’t confuse the two: They’re both endocrinologists; they both work in academic centers; they are both into the insulin mechanism of obesity; they are both researchers- one’s on the east coast at Harvard. One’s on the west coast at UC- San Francisco; they have very similar last names.
David Ludwig is at Harvard and wrote: “Always Hungry”.
Robert Lustig is at UC- San Francisco and wrote “Fat Chance”, he also wrote the introduction of the book “Pure, White and Deadly” wrote by John Yudkin. He has more books, too. His focus is on fructose.
Both of them have good content. I don’t agree 100% with either of them, just like I don’t agree 100% with anybody.
David Ludwig wrote an excellent article on the model explaining weight gain and obesity.
Here’s the thing- if you go back to Gary Taubes’ books, he says, “we think as we’re getting
older, we’re getting fatter because we’re eating more”.
One of his books is called, “Good Calories, Bad Calories”. It’s similar to a shorter book called “Why We Get Fat and What to Do About It”. His point is we don’t get fat because we’re eating more. We’re eating more because we’re getting fat.
The Question Is, Why Are We Getting Fat?
The new model on obesity by David Ludwig challenges the traditional obesity model based on energy balance.
He published an article in 2021 regarding the new obesity model. It is energy-based versus a carbohydrate-insulin model. It was published in the American Journal of Clinical Nutrition.
The traditional view is that the obesity pandemic is caused by overconsumption of modern, highly palatable (it tastes good), processed, energy-dense foods. A sedentary lifestyle exacerbates it. We sit around a lot and eat Twinkies despite the relentless focus on eating less and moving more.
Obesity rates remain higher than ever. It’s not just how much you eat and how many calories you’re getting. There’s something else happening. Conceptualizing obesity based on the energy balance model just hasn’t worked.
Image credits from Ludwig D. et. al. 2021
Take a look at the endocrine impact on the hormones: leptin and ghrelin to a large extent, but mainly insulin. The carbohydrate-insulin model proposes a reverse causal direction. It’s what you hear in Gary Taubes’ books.
We’re not eating or getting fat because we’re eating more. It’s that we’re eating more because we’re getting fat.
The relationship between energy intake and use is the same as the energy balance model. When you eat more, you will gain weight. The real issue the CIM (carbohydrate-insulin model) brings to the table is not questioning that we’re eating more, that is true, but the difference is the route to weight gain.
There are some qualifications that I am going to wait to review today because of the level at which we’re covering this. There’s an energy balance. There is truth to that fact. But it’s not the problem.
The Root Cause
The root cause of the problem is why we eat more-and and insulin resistance. The carbohydrate-insulin model proposes that hormonal and metabolic responses to dietary calories trigger the obesity pathway.
Suppose you eat a high-glycemic diet, and your blood sugar increases. To manage the blood sugar going up, you trigger insulin.
You get a big insulin load following a carb load and hyperglycemia; Hyper= too much glyce (glucose). emia= in the blood. Hyperglycemia = too much glucose in the blood.
You get a significant increase in insulin; then it starts taking it back down. This roller coaster effect of blood sugar causes the body to tell you that it’s hungry.
Number one- I want to sleep. An hour or so after carbs, your body tends to get fuzzy-headed. You want to rest, relax, and sleep. That’s what your body’s saying-we took on a big bunch of calories, and I need to sleep to put the calories in energy storage, the fat tissues.
You also tend to get hungry again soon afterwards. That’s because you’re on the carb and blood glucose roller coaster. Over the long term, a shift in substrate partitioning favoring fat
storage drives obesity. It is substrate partitioning favoring fat storage.
What does that mean? It means substrate is the energy our bodies are taking in – partitioning. The critical point is partitioning, favoring fast storage.
Over the long term, we can use the energy and go in this direction, or we can store the energy and put it in fat. That’s what the carbohydrate-insulin model is about. It’s for both of them.
The energy balance is accurate. But it’s what’s happening with the energy balance if you’re eating a lot of carbs that matter. If you’re putting all that energy into fat, and because you’re putting that into fat, you get hungry more, then you need to eat more.
If you’re not eating a lot of carbs, you’re not on that glucose roller coaster. You’re getting hungry less often. You’re using that energy instead of putting it into fat storage. You don’t have to eat as much because you’re not storing everything as fat.
The point is pretty simple. It doesn’t have to do with Apo B. This is the biggest issue we have worldwide regarding our health. Among the patients that I see are heavier people. It’s not just patients.
Walk down the street. Look at a picture of people on the street in the 1930s versus now. A BMI of 22 is too skinny and unhealthy.
We have been hammered as a population by eating high dietary glycemic loads. It’s put us on that roller coaster. We’re eating more. The average increase in body weight is attributable to the storage of less than one gram of extra fat per day.
You’re not going to pick up grams on your body scale. This is a very small amount. There are 365 days in a year. Less than a gram per day adds up.
The carbohydrate-insulin model only provides a partial representation of all causal mechanisms.
Here is an article from the Journal of American Medicine, 2018, from a U.S group talking about
The consumption of sugary foods.
This, in turn, affects substrate partitioning through calorie-independent mechanisms. They drive fat accumulation. It’s not about the number of calories but the type of calories.
Consuming sugary foods and carbohydrate-laden foods starts it. It goes to the partition and begins energy storage with insufficient energy burned. The energy storage makes you hungry again.
What about protein and fats? If decreasing carbohydrates is the solution, how many other macros should you eat?
The evidence could be more transparent. It doesn’t stop me from having an opinion. You have a few people who start a keto diet. They lose some body fat. It’s the most important thing we want to do to manage our cardiovascular health. Then they start losing too much weight.
Another question is, how do you maintain weight if you’re on a low-carb diet?
It’s a mixed story. I tend to get more protein than most folks. The U.S diet has a lot more access to protein. There’s more of a focus on protein. Some people think it helps manage your appetite. That’s true for me.
Is it true with everybody? You need to experiment to see what helps you the most. Some people, for example, Jason Fung, will say to be careful with protein because it stimulates insulin.
Fung believes it is less significant than it is. I’m a Jason Fung fan. But I don’t agree with everything he says, such as the importance of calorie intake. Calorie intake is very important. The keto crowd will say it’s not.
We discussed this in the calorie models—the energy balance model versus the insulin model. Energy balance is important for both.
When somebody goes on a keto diet, you tell them not to focus that much on the calories in the beginning. Once they get used to keto and get past the keto flu, calories and portion size become issues.
In the beginning, when someone goes on keto, most folks lose weight. It happens whether they think they’re eating a lot or not.
Why is that? We tend to go by our body’s signals. When you change your diet from 200 carbs to less than 100, you think you’re eating a lot because your hunger signals are turned off. The reality is you’re getting fewer calories than you think.
So, to summarize, carbohydrate metabolism is a complex process; plenty of evidence points out that it is not overeating that causes obesity; it is the impaired glucose metabolism that gets influence by excessive body fat and decreased insulin function.
REFERENCES:
1. https://prevmedhealth.com/is-a-low-carb-diet-related-to-coronary-artery-calcification/https://prevmedhealth.com/how-to-stop-ghrelin-the-hunger-hormone/
2. https://prevmedhealth.com/plant-based-vs-sugar-free-whos-right-how-to-use-food-labels-right/
3. https://prevmedhealth.com/new-risk-factors-for-type-2-diabetes-part-1/
4. https://prevmedhealth.com/can-type-2-diabetes-be-reversed-with-low-carb-diet/
5. https://prevmedhealth.com/inflammation-not-cholesterol-is-the-bigger-heart-disease-risk/
6. https://prevmedhealth.com/how-to-reverse-20-years-of-arterial-plaque-part-2/