Simple questions tend to be the most profound.
The question above is one I have been revolving around for a few months.
Many people think that the answer to this question is a resounding yes!
But in reality sugar is relatively innocuous especially from an immunological perspective. The immune system is really only reactive to proteins that are greater than 15 amino acids in length and sugars are not proteins.
Nevertheless, something is going on. From cross-sectional and epi data we know that type II diabetes is related to a host of other inflammatory diseases and hyperglycemia has been found to induce the inflammatory cascade in those less resilient individuals. Yet, this is not surprising as bad things tend to happen to humans when we go beyond what our bodies can handle…especially long-term.
Now here is actually the real question that was posed so eloquently by Dr. Layne Norton
Would you be willing to provide me with research demonstrating that sugar makes a difference in inflammation & immune function when calories are equated?
The closest study I have been able to find is this one published in 2008 which investigated the acute NF kappa B response to sugar, pasta, and white bread in healthy adults.
It is evident from the body of research that this is was the next step. It was first elucidated that an oral glucose load of 75 grams induced an inflammatory response, thus the next logical transition was towards whole foods and then hopefully longer time points in the future with kcals and many other aspects of the diet matched. Clearly we are not even close to real world settings yet as these 17 subjects were eating 50 gram carbohydrate samples alone. But…
“The results of the present study show that a high-glycemic index source of carbohydrate in the form of white bread has the same capacity to acutely activate the redox-sensitive transcription factor NF-kappa B as does a 50-g oral glucose challenge. By contrast, a low-glycemic source of carbohydrate in the form of pasta had an almost negligible effect on NF kappa B activation. All 3 challenges contained the same amount of absorbable carbohydrate, and the pasta and bread meals were matched for protein, starch, fiber, and most micronutrients.”
These researchers published area under the curve data, which is fantastic. Yet, it makes it a bit more difficult to tell how high the insulin and blood glucose of these subjects rose in response to what they consumed. The change in insulin for white bread and glucose was somewhere between 15 and 20 µIU/mL. A modest insulin spike. The insulin spike for the pasta was much less. The change in venous blood glucose was about 22 mg/dL for the glucose sample and the venous blood glucose didn’t really rise for the white bread or pasta. Whereas, the change in capillary blood glucose was about 50 mg/dL for the white bread sample and about 35 mg/dL for the pasta.
“The findings suggest that high-normal physiologic increases in blood glucose after meals aggravate inflammatory processes in lean, young adults.”
This study is also even more pertinent because these subjects were young, disease free, and were on the lower end of the normal BMI range. They also had an average fasting glucose of 82.8 mg/dL and a fasting insulin of 2.0 µIU/m, nowhere near prediabetic and in the ideal range from a func med perspective.
Many would see this data and say, “Well, hell it was that damn postprandial rise in insulin!”
But, we would do well to just stop blaming the insulin fairy for everything that ails the world today.
“Although fasting insulin concentrations fell within the normal range, we found a significant positive relation between individual NF-kappa B concentrations and fasting insulin, a surrogate marker for insulin sensitivity, but not with postprandial insulin concentrations. The independent relation of NF- kappa B with fasting insulin suggests that insulin sensitivity may be a key determinant of the glycemia-induced inflammatory response.”
I want to put a giant exclamation point after that sentence.
“The findings suggest that NF-kappa B activation was not due to increased plasma insulin concentrations per se. Indeed, at physiologically relevant concentrations, insulin has been shown to inhibit NF- kappa B and other inflammatory mediators including ICAM-1, MCP-1, AP-1, and Egr-1 in both human aortic cells and in test subjects. Even at a concentration of 250 µIU/mL, insulin does not affect NF-kappa B activation.”
So what does this study tell us?
It lets us know that if we are randomly on the couch watching reruns of Friends we probably shouldn’t eat carbohydrates alone as this could result in inflammation. Is this going to kill you? No. Could decades of you housing bags of wonder bread and staring sedentarily at Jennifer Anniston kill you? Yea, probably.
This study does not tell us anything about the inflammatory response of a real food meal with a quality fat source, plenty of vegetables, a modest amount of protein, and maybe even a tuber or some rice. It also tells us nothing about the impact of quickly absorbable carbohydrates eaten post training that would be unlikely to result in a state of hyperglycemia.
Notably, inflammation in populations who exercise and replenish carbohydrates has generally been found to be very low. Also, anecdotally I have very very rarely seen elevations in high sensitivity C-reactive protein in training males who fuel accordingly.
Another hiccup would be fruits and vegetables are carbohydrate containing and anti-inflammatory. Thus, what happens in mixed meals with vegetables turnt up with a little sugar? AKA real life….and we are left with more questions than answers and that is ok.
All that said this research is exciting and I look forward to tracking the body of evidence on this subject as it mounts.
**It should be noted that running an RCT with different subjects with whole foods long term would be a relative study design nightmare, given that you would have to have some sort of immune reactivity testing for foods as an inclusion criteria and then you would have to match these diets for macronutrients and also fiber. These subjects would also have to live in a metabolic ward and keep physical activity, sleep, stress, etc equivalent between groups. Not impossible, but definitely not cheap or walk in the park.