Pour Some Sugar on Me: Pt. I

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Ah, the age-old questions: Are carbohydrates the devil? And my personal favorite: Is eating sugar going to make me fat?

I will specifically explore the first question in this article (the latter question will be answered shortly afterwards).

I will be explicit with this: This is not medical advice to go out and eat a ton of sugar and carbs. It is very important that you consult your medical doctor before making any drastic dietary changes, especially if you have any underlying metabolic disorders. I will be outlining the following for a metabolically flexible individual (someone who is not insulin-resistant). So as per usual, I am not telling you what to eat or what not to eat. I am just simply bringing the heat with quality scientific research.

I am a firm believer that for a metabolically flexible individual, carbohydrates, and in fact sugar as well (more on that later), have a proper place in one’s diet, and I will explain why.

It seems like every other day; the fitness industry decides to flip and flop on what is good for us and what is bad for us. All three of the macronutrients (protein, carbs, and fat) have been demonized at some period…and with the recent popularity of Keto and Carnivore dietary approaches, carbohydrates have found themselves in the spotlight once again. And I am sure that as long as you haven’t been living under a rock over the last several years, you are probably very familiar with the myth that one cannot simply lose weight or improve their health by eating carbohydrates.

As a biochemist, I am fascinated with the various models proposed to explain our current obesity epidemic (Flegal et al., 2016). Since obesity is a multifactorial problem, there are accordingly an unbelievable number of models that postulate the root cause of obesity. In all honesty, I do not believe we will ever be able to narrow it down to one cohesive model due to the complexity of the situation. Nevertheless, over the last several decades, that is exactly what has been attempted. Two major models have been proposed: one pointing the finger at high energy density fats, and one pointing the finger at carbohydrates and insulin.

First, I will briefly touch on the “Passive Consumption” model of obesity. This model touts that due to the high energy density, weak ability to satiate, and increased palatability, it is in fact high fat foods that are driving this obesity epidemic (J. E. Blundell & Macdiarmid, 1997; John E. Blundell & MacDiarmid, 1997; Bray & Popkin, 1998; Hopkins et al., 2016; Stubbs, 1998).

This model has prevailed for a while, yet with the rise of Keto and Carnivore, a new model has seemed to take the spotlight.

The touted model by Keto and Carnivore zealots is that of the Carbohydrate-Insulin Model (CIM). I am going to keep the biochemistry and physiology brief and simple here so bear with me, as this is needed to orient you. Our journey begins in the 1970s when we began to see the spike in obesity. At this point, researchers deciphered that a change in dietary quality subsequently generates hormonal responses that favors the ushering of calories to be stored in our fat cells (Ludwig, 2002; Ludwig & Friedman, 2014; Taubes, 2013). Thus, there is less circulating energy for the rest of the body, thereby driving hunger and overeating. So, with this model we place fat cells in the center of the problem, and that is where our good friend insulin comes into play. Insulin is an anabolic hormone that has mechanisms ranging from decreasing circulating fuel availability via glucose uptake stimulation, suppressing the release of fatty acids from your fat cells, and promoting fat and glycogen deposition (Ludwig, D & Ebbeling, C, 2018).

And of course, if you have taken any sort of basic biochemistry class, you are probably familiar with the fact that carbohydrates have the most powerful impact on insulin secretion, and this varies depending on the type and amount of said carbohydrates (Ludwig, D & Ebbeling, C, 2018). The Glycemic Index (GI) will tell us how fast certain foods spike our blood sugar, thereby inducing insulin secretion (Ludwig, 2002). Refined carbohydrates tend to have a higher GI, whereas non-starchy veggies, whole fruits, legumes, etc… have a lower GI. To factor in for the amount of carbohydrates, we can look at something called the glycemic load (multiplies carbohydrate amount by GI) which according to Wolever & Bolognesi, (1996) is “the best single predictor of postprandial blood glucose levels, explaining up to 90% of the variance.” It should also be mentioned that depending on the amino acid composition of certain proteins, this macronutrient will also elicit insulin secretion (but it is much more complicated than that, so we can deal with that later). In sum, the higher the glycemic load, the larger and more rapid the insulin spike.

So, with all that out of the way, the CIM is pretty straightforward. This model proposes the following:

A high carb diet (that includes copious amounts of refined starchy foods and sugars) produces post-meal hyperinsulinemia (increased insulin secretion), thereby leading to increased storage of calories in fat cells, thus suppressing our ability to burn those calories. Hence, it is the carbohydrates and insulin that predisposes us to gain weight via hunger stimulation and/or reduction in metabolic rate (Ford & Dietz, 2013; Ludwig, 2002; Ludwig & Friedman, 2014; O’Neil et al., 2012; Taubes, 2013).

Long story short…if the name didn’t give it away, this model points to carbohydrates and subsequent insulin secretion as the drivers of obesity. So I guess at this point we have two options: 1)We can be good little boys and girls and believe this model as gospel and avoid carbs like the plague, or 2) We can consult the relevant literature on the topic and see what the data says.

I like #2…let’s do that one 😊

Since I am at NIH, I love to highlight some of the amazing research that goes on here. One of my favorite researchers is Dr. Hall. I have mentioned some of his work in other articles. And thanks to the amazing resources we have here at NIH, Dr. Hall and his research team recently put the CIM to the test. Let me briefly outline the study design (Kevin D Hall et al., 2021):

20 healthy adults (11 women and 9 men) without diabetes stayed for four continuous weeks in the NIH Clinical Center’s Metabolic Clinical Research Unit. Hall and his team compared the effects of a low-carb and low-fat diet on calorie intake, hormone levels, body weight, etc…

For the first two weeks, participants received either a plant-based, low-fat diet with a high amount of carbohydrates (14% PRO, 75% CHO, 10% FAT) or an animal-based, low-carb diet that was high in fat (14% PRO, 10% CHO, 75% FAT). They were then given the other diet the following two weeks. They received three meals a day, plus snacks, and could eat as much or as little as desired (gotta love those ad libitum studies)

Both diets were matched for total calories

Both diets were minimally processed

The low-fat diet had a high GI (85g/1000kcal) whereas the high-fat diet was low GI (6g/1000kcal)

The high-fat diet was very high in energy density (2 kcal/g) whereas the low-fat diet was very low in energy density (1 kcal/g)

Hence, the idea of this study was simple: To determine whether low-carb or low-fat diets result in greater calorie intake. CIM vs Passive Overconsumption. A rivalry that would give Packers vs Bears a run for its money. So, what does the data say?

The low-fat diet led to 689 ± 73 kcal/day less energy intake than the low-carb diet over 2 weeks and 544 ± 68 kcal/day less over the final week. [Both with P values <0.0001…color me impressed]

No differences in hunger, enjoyment of meals, or fullness between the two diets.

Body weight decreased in both diets (remember this was not a weight loss study)

Low- carb lost 1.77 ± 0.32 kg over 2 weeks

Low-fat lost 1.09 ± 0.32 kg over 2 weeks

No significant difference here between diets

Low fat diet resulted in significant changes in fat mass after both the first week (−0.27 ± 0.12 kg) and the second week (−0.67 ± 0.19 kg). Whereas, the low-carb diet saw no significant change in body fat over the 2 weeks

The low-fat diet resulted in higher blood glucose and insulin levels compared with the low-carb diet.

So, there is a lot to unpack here. The fact that the low-fat diet led to reductions in caloric intake by 550–700 calories a day plus a reduction in body fat when compared to the low-carb diet certainly throws some shade on the CIM. However, the low-carb diet certainly has its benefits as well, as it demonstrated much better glucose tolerance and insulin sensitivity. And as I will briefly outline at the end (and have in other articles) I believe both fat and carbs have their place in a healthy, balanced diet.

Now many Keto and Carnivore fans are probably yelling right now that this study was too short (2 weeks for each diet arm) to allow for proper adaptation to a high-fat diet. For starters, there are many factors that need to be considered when adapting to a ketogenic diet, such as the multiple organ systems involved and various different time scales that come into play (Sherrier & Li, 2019). Yet, Hall and his team saw several physiologic adaptations that would indicate that individuals were sufficiently adapted to the low-carb diet after 2 weeks:

Impaired glucose tolerance at the end of the second week of the low-carb diet, indicating physiologic adaptation

Daily respiratory quotient was ~0.75 during the low-carb diet,

Indicates preference for fat and ketone oxidation

Typically occurs during 1st week of ketogenic diet adaptation, and does not change over the subsequent weeks (K.D Hall et al., 2016)

Nutritional ketosis was established within several days of instituting the low-carb diet and capillary β-hydroxybutyrate (the primary ketone made by the body) was stable during the second week of the diet

Blood ketone levels have been seen to remain stable at 2, 3, and 4 weeks of an isocaloric ketogenic diet, so these levels most likely would not have changed with prolonged exposure to a ketogenic diet (K.D Hall et al., 2016)

~35% greater than baseline uric acid levels were observed after 2 weeks of inpatient low-carb feeding

Plasma uric acid approximately doubles at the onset of a ketogenic diet but returns to ~20–50% greater than baseline after 4–8 weeks of adaptation in an outpatient setting (Mohorko, 2019; S D Phinney et al., 1982; Stephen D Phinney et al., 1980)

Yes, that was a lot of biochemistry I just threw at you, but long story short, this data tends to favor the notion that 2 weeks was enough time to adapt to the low-carb diet. Although a longer study would be better, the logistics of metabolic ward studies make it almost impossible for longer duration studies.

My lab (Molecular and Clinical Nutrition Branch) is in the process of finalizing our new clinical trial. We plan on having people stay at NIH for four days (all meals prepared here). The study is going to cost us several millions of dollars to run when we take into account the food, the planning, and compensation. Now, I don’t know how much this study cost, but they had 20 people stay for four whole weeks with unlimited amounts of food. So, I would say 2 weeks per diet is good enough for me at this point.

Now there is one more concern: Remember this study was not designed to formulate the best weight loss approach. Hence, results may have been different if the study participants were actively trying to lose weight. Also, let us not forget that the study was conducted in the very well controlled setting of the metabolic wing at the NIH (trust me I’ve walked those halls and am currently learning how to use the equipment…it’s insane). Food costs, food availability, and meal preparation in the real-world setting may have all factored into the outcome outside the walls of the NIH.

So, what does this study teach us?

Well the Passive Overconsumption model predicts that consuming a diet with high energy density results in excess energy intake and weight gain. Whereas, the CIM predicts that consuming a diet with high glycemic carbs results in post meal insulin spikes that drives body fat accumulation leading to increased energy intake.

However, this study demonstrated that a low-fat diet (with a high glycemic load) did in fact lead to post meal glucose and insulin levels when compared to the low-carb diet, but also led to less energy intake thereby contradicting the CIM. On the other hand, the low-carb diet was high in energy density, but did not yield body fat gain, thus contesting the merit of the Passive Overconsumption model.

So, if it isn’t carbs, high energy density fats, or protein (you can read that article here) that are driving the obesity epidemic…then what is?

If you have been following along for a while, I think you see where I am heading with this one. In fact, I have written two articles on what I (and Dr. Hall) point to as one of the main causal factors in the obesity epidemic. To give you a hint, I am pretty sure it has come up in every one of my articles:

Yeah that’s right processed foods.

So, at the end of the day maybe there is a more insidious villain lurking in the shadows of almost all our food products. I see no problem in eating carbohydrates if you are a metabolically healthy individual

Plotkin’s takeaway: If your great-grandmother would not have recognized it as food, it may be best to avoid it.

Each bite of food either takes us one step closer or one step further from our goals. So, if you can follow this rule 80–90% of the time, you are moving in the right direction on this treacherous journey we have embarked on to take back control of our health.

Head on over to part II of this series so I can blow your mind about the SWEET truth behind sugar consumption. Certainly, one cannot lose weight and improve their health if they are consuming copious amounts of sugar? Right? You won’t want to miss that one.

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Blundell, John E., & MacDiarmid, J. I. (1997). Passive overconsumption: Fat intake and short-term energy balance. Annals of the New York Academy of Sciences, 827, 392–407. https://doi.org/10.1111/j.1749-6632.1997.tb51850.x

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Post-Baccalaureate research assistant in the Molecular and Clinical Nutrition Lab at the National Institutes of Health