Tag Archive for: glucose

Another Theory of Obesity

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It’s been a while since someone has proposed a new theory of obesity. I’m still a believer in “a calorie is a calorie” but it’s always good to find out what may be driving us to overeat.

The latest addition is the Fructose Survival Hypothesis for Obesity. The diagram above was taken from an article published in the journal Obesity. The authors claim that their new theory explains and is consistent with the other theories that include the energy-balance hypothesis, the carbohydrate-insulin model, the protein-leverage hypothesis, and the seed-oil hypothesis. They’re depicted in the large red circles and also include genetics and the microbiome. It all seems complicated, to say the least.

Fructose Survival Theory Simplified

Let’s just focus on the fructose in the blue box and follow those arrows. The arrow that goes up simply suggests that people who eat more fructose-containing food and drinks increase their food intake and gain weight. Simple.

The arrow that angles down to mitochondrial stress leads to a whole host of metabolic changes, all of which result in the decrease or blockage of production of ATP and the increase in fat storage. The result is obesity, altered blood lipids, and a fatty liver.

This pathway is apparently related to getting ready for hibernation, but one gene with the ability to store fat to protect against starvation kicks in and we just gain weight. Of course, it’s more complicated with multiple enzymes involved, but in reality it just goes back to one thing: eating and drinking too much of, in this case, refined carbohydrates.

Questions about the Fructose Theory

We know how this potential theory of obesity involving fructose metabolism seems to work. There are at least three questions:

1. Does the source of fructose matter? In other words, is high-fructose corn syrup (HFCS) more likely to impact weight more than the fructose in grapes or watermelon? The research in animals and a human trial involved eating and drinking the calories in prepared mixtures, but what about real food?

2. They suggest a pathway where glucose can be made into fructose by being exposed to salt, umami, and dehydration. In the animal trial, I couldn’t find total body water ascertained nor what type of sodium might be more hazardous: table salt? MSG? Pink salt?

3. Would the theory apply to normal weight people eating just enough to maintain their weight as it is, regardless of diet composition? Or would people gain weight even while not overeating, regardless of diet? They tested for outcomes in animals and people who were overweight to begin with, but there’s no evidence that people couldn’t lose weight if they cut calories even while eating a high-fructose diet.

Chemical drivers of food behavior such as those proposed must be studied, if for no other reason than to see if there are negative effects for people who don’t follow the mainstream dietary recommendations and yet maintain a healthy body weight. All this research has led to the research group being awarded a patent on a pharmaceutical that would interfere with a specific enzyme called fructokinase. We’re interfering with what they claim to be a natural process against starvation. Is that safe?

The Bottom Line

The researchers and drug developers have spent over a decade researching the fructose theory of obesity and spent millions of research dollars. They have a patented pharmaceutical that may address the issue. But the one question that they must answer, besides discovering any harms in clinical trials, is this: would someone who ate a diet high in fructose and sodium be able maintain a normal body weight? Is a calorie a calorie? Until then, I’m not convinced.

What are you prepared to do today?

        Dr. Chet

References:
1. Obesity. 2023. https://doi.org/10.1002/oby.23920
2. Phil.Trans. R. Soc. B 378:20220230. https://doi.org/10.1098/rstb.2022.0230

Myths Busted: Eat Your Fruit

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If you’ve watched the video, you know Dr. Berry gave three myths of the sugars in fruit. We addressed Myth One and Myth Two in Tuesday’s Memo. Today let’s examine Myth Three, and then consider whether fruit will cause non-alcoholic fatty liver disease.

Myth Three: Fiber, Vitamins, Minerals, and Phytonutrients Aren’t Important

This myth is sort of grasping at straws to try to prove a point. He claims that the fiber, vitamins, minerals, and phytonutrients in fruit are meaningless because of all the sugar in the fruit. He makes the comparison of adding those nutrients to a 20-ounce cola and then asking if we would feed that to our child.

Let’s get the facts straight. A 3.3 ounce orange contains a total of 8.5 grams of sugars with all the associated nutrients that he’s saying aren’t important, and he’s comparing that to a 20-ounce cola with 65 grams of high-fructose corn syrup with some of those nutrients added. While the molecules may be identical (Myth Two), there are differences in metabolism between sucrose and high-fructose corn syrup he doesn’t seem to understand. A better way would have been to use equivalent serving sizes. Even better, don’t force an issue that’s marginal, at best, and uses observational science as the foundation.

Okay, I’ve used the term “observational science” several times—what does that mean? Dr. Berry appears to be a very good physician who has helped many people overcome type 2 diabetes and other metabolic disorders using a ketogenic diet. He deserves credit for that, but when you use what you observe as the basis for recommendations for everyone, that’s stretching it.

According to an observational rooster, his crowing makes the sun rise every morning. Observation alone isn’t enough basis for these kinds of recommendations. Unless you have documentation that someone eating 3.3 ounces of lemon containing a total of 2.3 grams of all sugars will spike her insulin and glucose levels, the argument is baseless. In fact, every example he gave should have actual examples to support it, not from the published science but from actual experience. (That would be easy enough to do just by feeding subjects the food in question and then checking their blood sugar at certain intervals.) And it should be published as a case study in a medical journal, because that metabolic response would be unusual to say the least. Until then, it’s observational science and is not meaningful applied to anyone else. Leave the observational science behind unless you have the data to support it.

The Bottom Line

In doing the background research, I found that eating fruit does not appear to be a cause of non-alcoholic fatty liver disease or even a fatty liver. Obesity always seems to precede metabolic disorders that lead to a fatty liver in the vast majority of people. The DASH Diet and the Mediterranean diet, which both recommend fruit, are often recommended to treat a fatty liver, and research shows they work—and that’s the complete opposite of what he recommends.

If you’re concerned about a fatty liver, don’t give that banana or bowl of berries a second thought; focus instead on weight reduction. As always, the key is the calories. Eat less. Eat better. Move more.

What are you prepared to do today?

        Dr. Chet

References:
1. Br J Nutr. 2020 Jul 14; 124(1): 1–13.
2. Iran J Public Health. 2017 Aug; 46(8): 1007–1017.

Fruit and Fatty Liver Disease

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Non-alcoholic fatty liver disease (NAFLD) is on the rise in the U.S. and around the world. Estimates are by 2030, NAFLD will be the primary cause of liver transplants in the world. NAFLD is caused by obesity; associated conditions such as type 2 diabetes and metabolic syndrome are contributing factors. But does fruit intake contribute to NAFLD? According to one physician it does; that inspired him to record a video titled “Secret Sugar in Fruit” or as he calls it, the Three Myths of Fruit. He’s an advocate of the ketogenic diet, as many people are today, but is he correct about fruit? I thought I’d check it out.

Myth One: Fruit Contains Only Fructose

His opening statement about fruit is that nutritionists and Internet gurus are suggesting that fructose is the only sugar in fruit. He gives examples of the breakdown of sugars in five fruits, based on the USDA Food Database. No problem with that. But to say that most nutritionists don’t know that fruit contains a variety of sugars means he’s never had a basic nutrition class on macronutrients, because it’s certainly taught in those classes. Anyone who’s ever looked up any type of fruit on the database would clearly see there’s more than one type of sugar.

He also claims that the sugar in some small servings of fruit with as little as two grams of glucose or sucrose will spike blood sugars and insulin levels and that five grams of fructose will cause a fatty liver. He offers no evidence to support those claims.

Myth One contains some accurate facts but is more observational science than fact. Myth One: busted.

Myth Two: The Chemical Structure of Sugars

According to Dr. Berry, nutritionists claim that the chemical structure of glucose, fructose, and sucrose are different in fruit than soda. Not exactly true; they’re chemically identical, but there’s more to it than that. Myth Two: mostly busted.

I’ll cover the third myth on Saturday and set the record straight on fruit and NAFLD. You can watch the short video at the link below. He’s a personable guy, committed to keto, but reliant on observational science. We’ll talk about why that’s a problem next time.

What are you prepared to do today?

        Dr. Chet

References:
1. Gastroenterology. 2020 May;158(7):1851-1864.
2. https://www.youtube.com/watch?v=URMLzoK95V4

Health Benefits of SCFA

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Let’s continue our look at short-chain fatty acids (SCFA) and what they do besides produce energy. Most of these are observational in nature; by that I mean when SCFA go up or down, effects are observed. What we don’t know at this point is why.

For example, when diabetic animals are given the SCFAs acetate and propionate, they maintain better glucose control. That means that adding SCFA to their diet can improve their ability to maintain blood sugar levels. Wait a second; is this the same acetate that’s found in vinegar? Yes. The problem is that the studies don’t provide consistent results.

The same is true for fat storage. When SCFA levels go up, fat storage appears to go down, but drinking vinegar doesn’t necessarily provide that benefit. Observational studies show that as SCFA levels made by the body go up, fat storage goes down. That can prevent weight gain, but we don’t know whether it causes weight loss. The same is true for cholesterol levels; SCFA are associated with lower cholesterol levels.

The problem is that we don’t know the precise mechanisms yet. In other words, what does making SCFA do to the metabolic systems in the body? To the genes? Or receptors for various functions? That’s what scientists are working on. Further, exactly what type of bacteria produce the right SCFA? There’s general agreement that Bifidobacteria produce acetate and propionate when fermenting fiber, but which Bifidobacterium? There are over 50 varieties. Maybe more than one—they may interact in sequence. We don’t know at this point.

What role do SCFA have in controlling blood pressure? Does sodium also have an impact on SCFA production? We’ll take a look at a recent study on Saturday.

What are you prepared to do today?

        Dr. Chet

References:
1. Benoit Chassaing, Andrew T. Gewirtz, in Physiology of the Gastrointestinal Tract (Sixth Edition), 2018.
2. Front Microbiol. 2016; 7: 925. doi: 10.3389/fmicb.2016.00925

A New Approach to HbA1c

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Type 2 diabetes is a significant problem in North America and it’s spreading throughout the entire world. The treatment standard has always focused on controlling blood sugar, especially HbA1c. Normal is less than 5.7%. For most individuals, reducing the HbA1c to under 6.5% has been the goal for pharmacologic treatment.

HbA1c is a protein found on red blood cells that indicates blood glucose levels over the past 90 days. It develops when hemoglobin, a protein within red blood cells that carries oxygen throughout your body, bonds with glucose in the blood. Think of it as the sugar you ate over the last three months getting stuck to your red blood cells; the higher your HbA1c, the worse your control of your blood sugar has been. For a prediabetic, that means your days of diabetes meds and finger pricks is getting closer. For a diabetic, that opens the door to many of the worst consequences of diabetes, such as heart and kidney disease, blindness, and nerve damage.

Recently, the American College of Physicians published new guidance statements for the use of medications for controlling HbA1c. A committee of physicians examined the data behind the current standards of treatment for four of the major physician organizations including the American Diabetes Association. In the simplest terms, they wanted to know what benefits or hazards occur when treating adults with type 2 diabetes with medications. Should the goal be to get the HbA1c as low as possible with drugs? Or should the individual be part of the treatment equation?

This is an important issue and the topic for this week. I’m going to review evidence-based medicine on Thursday. You can get the entire story by listening to the Straight Talk on Health on evidence-based medicine, normally available only to Members and Insiders; I cover the entire concept of how EBM began and what it was intended to be. For those of you who haven’t chosen a membership yet, get more info here.

What are you prepared to do today?

Dr. Chet

 

Reference: Ann Intern Med. doi:10.7326/M17-0939.

 

Keeping Track of Life’s Simple 7

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To complete American Heart Month, here’s an easy way to track your heart health called Life’s Simple 7 (LS7), developed by the American Heart Association. LS7 has been around since 2010 but it escaped my attention until recently. For those of you who like to track your progress to see how you’re doing, this is a great tool; you may remember I mentioned it last month, but I think you need the details to really understand how LS7 can work for you.

There are seven different categories of variables to track, hence the name Life’s Simple . . .

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