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Dr Robert Lustig on Pediatric Metabolic Health: “Sugar Is the Alcohol of the Child”

Author(s):

Robert Lustig, MD, MSL, explains how the US health care industry needs to shift from measuring body mass index and obesity to measuring cardiometabolic health, which affects 93% of Americans, including children.

A recent Institute for Value-Based Medicine® (IVBM) event hosted by The American Journal of Managed Care® (AJMC®) and University Hospitals in Cleveland, Ohio, focused on obesity treatment as a way to reduce the risk of diabetes and cardiovascular disease. However, “obesity is not the problem, obesity is a marker for the problem,” says Robert Lustig, MD, MSL, endocrinologist and professor emeritus of pediatrics at the University of California, San Francisco.

During an interview at the IVBM event where he presented, Lustig explained that childhood obesity is a marker of metabolic dysfunction rather than the primary problem, with 93% of Americans, including children, experiencing metabolic issues.1 According to him, the main environmental and dietary factor contributing to metabolic dysfunction and related diseases like type 2 diabetes and fatty liver disease in children is sugar, which acts similarly to alcohol in its detrimental effects on the liver. With this in mind, Lustig argued that health care professionals should measure cardiometabolic health using waist circumference and lab tests, particularly fasting insulin levels, which are crucial despite current recommendations against them.

This transcript has been lightly edited for clarity.

Transcript

What are the most significant environmental and dietary factors that increase children’s risk of obesity?

First of all, you have to understand that obesity is not the problem, obesity is a marker for the problem. Metabolic dysfunction is the problem and 93% of Americans today have metabolic dysfunction, and that includes children. Now, children are getting the diseases of adults, they're getting the diseases of aging, they're getting the diseases of alcohol. Type 2 diabetes and fatty liver disease were the diseases of alcohol, and now they're the diseases of 5-year-olds. So, the question is not what is causing obesity, but what is causing metabolic dysfunction, of which obesity is yet another manifestation. When you understand that, then you can start to piece together what the real problem is.

Now, there are 3 fat depots. There's subcutaneous fat, which is the fat you measure on the scale—the "does this bathing suit make me look fat?" fat. That adipose tissue is actually metabolically benign. That's where you want to put excess energy, that's where it's safe. But that's what you measure on the scale, so when you say somebody has obesity, it's because their BMI [body mass index] or their weight is high. But that's actually not the problem, because there are many metabolically healthy obese people, and there are also many metabolically ill thin people. So, getting it right is really important.

The second fat depot: visceral or big belly fat. Now, that is due to stress. That is not due to diet; that is not due to environment, per se, except as it causes you stress. And it's not stress, it's response to stress. How do we know that? Because you can take patients who are clinically depressed that have to be kept from themselves for suicide watch, admit them to the hospital, and they're not eating because they're anhedonic. They don't want to eat. They're losing weight, they're losing subcutaneous fat, but they're gaining visceral fat. That fat is due to stress, not due to food, not due to environment, per se.

And then finally, there's the third fat depot: liver fat. That is where diet does its dirty work. That's where the real problem is. So, what makes a liver fat? And, by the way, can you measure liver fat on the scale? No. Even a half a pound of liver fat will cause significant metabolic dysfunction, and you can't measure that on the scale. So, what does? Sugar and alcohol. But kids don't drink alcohol, so guess what, it's sugar. Sugar is the alcohol of the child. Sugar is the reason that children today get type 2 diabetes and fatty liver disease. Sugar is the one environmental stimulus that we could fix tomorrow, if we had the political will.

How would health care professionals go from measuring BMI to measuring cardiometabolic health?

The question is, how does one measure cardiometabolic health? The easy way, the cheap way, is waist circumference. Now, the problem with waist circumference is standards and different measures will get different answers, so it's not a great measure in that respect, but it is at least addressing the problem. The next level up: lab tests. So, what is the lab test that tells you the most about metabolic health? The answer is a fasting insulin level. The American Diabetes Association says don't draw a fasting insulin level; I say it's the most important thing to draw.2 Why do they say one thing and I say the exact opposite? Well, because they're wrong and I'm right, that's why. But why?

The reason they say don't draw fasting insulin level is for 2 reasons; unfortunately, both are specious. The first is, fasting insulin levels are not standardized across platforms and across assays; that is true. And all things being equal, that would be a big issue, I agree. However, if your fasting insulin is high, it doesn't matter. It means you have a problem, and you didn't know you had the problem before, and you need to do something about it. And as long as you send the blood to the same assay platform each time, it will have the same issues, so you can use it to monitor benefit. Second reason they say don't draw it: they say fasting insulin does not correlate with obesity. That's right, fasting insulin correlates with cardiometabolic health, because obesity is a marker, not the cause! But they don't understand that. I think a fasting insulin is the single best measure of cardiometabolic health, and it is not being done and it is not being covered by insurance today, and I think this is a major mistake.

Another thing we could do is an ALT, alanine aminotransferase. Now that's part of a standard chem panel, so that's not hard. That gives you a lot of information. The problem with an ALT is the reference range. When I started medical school in 1976, the upper limit for ALT was 25. Today it's 40. Same assay. How come it was 25 and today it's 40? Because the entire curve has shifted to the right because everyone has fatty liver disease today—45% of adults and 25% of children have fatty liver disease they never had before. This was a disease never even seen before 1980, and in the last 45 years it has become the biggest epidemic in the history of the planet, COVID bar none. So, the problem is, what do you use to measure the ALT? What's the reference range? Well, today, if you take 10,000 "normal" people and you run their ALT levels, you'll get a standard deviation curve and you'll say, "2 standard deviations, oh that's 40." No, 25, because that's before the problems started. So, if you use that, then ALT is extremely beneficial and very helpful.

References

  1. Grady O. Dr. Robert Lustig offers insights into connection between food choices and chronic disease. Elon University. September 22, 2023. Accessed June 21, 2024. https://www.elon.edu/u/news/2023/09/22/dr-robert-lustig-offers-insights-into-connection-between-food-choices-and-chronic-disease/
  2. Understanding insulin resistance. American Diabetes Association. Accessed June 21, 2024. https://diabetes.org/health-wellness/insulin-resistance
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