Published in the foundational article “What Is Fitness?” in 2002, CrossFit’s nutrition prescription ended with two words: no sugar. In Part 1, we covered why the body has no requirement for added sugar, how modern processing lets us consume it faster and in larger doses than ever, and where it goes once it’s absorbed. Now, look at the long-term costs. Some are still under investigation, and others are already showing up in kids, blood tests, and tendons.
Sugar, Metabolic Health, and Cancer
The relationship between sugar consumption and cancer is a growing area of scientific concern. Researchers are paying closer attention to the connections between high sugar intake, chronically elevated insulin, metabolic dysfunction, and both cancer development and progression. This does not mean sugar has been established as a direct cause of cancer, but the convergence of rising metabolic disease, increasing rates of several cancers in younger people, and a growing understanding of the unusual way cancer cells use glucose has made this an important area of research.
The connection between sugar and cancer is more complicated than the connection between, say, sugar and cavities, but it deserves our utmost attention. The digestive tract is essentially one continuous tube running from the mouth to the exit at the other end, and the foods that repeatedly pass through it affect more than just the teeth. The dramatic rise in colorectal cancer among younger adults makes this especially difficult to ignore. Colorectal cancer was historically considered a disease of older adults, but incidence in Americans younger than 50 has been climbing for decades. Recent American Cancer Society data show early-onset colorectal cancer increasing by roughly 2% to 4% per year, depending on racial and ethnic group. Colorectal cancer is now the leading cause of cancer death among Americans younger than 50. Diet, obesity, insulin resistance, metabolic health, the gut microbiome, and exposures beginning early in life are all being investigated as potential causes of this worsening epidemic.
There are some particularly interesting clues. In the Nurses’ Health Study II, researchers followed more than 95,000 women and found that those consuming two or more sugar-sweetened beverages per day had more than twice the risk of developing colorectal cancer before age 50 compared with women consuming less than one per week. Each additional daily serving during adolescence was associated with a 32% higher risk of early-onset colorectal cancer. Because this was an observational study, it cannot prove that sugary drinks caused the cancers, but the size of the association and its link to adolescent exposure allow us to form a hypothesis.
Colorectal cancer is also not the only cancer appearing more frequently in younger people. A large National Cancer Institute analysis found that incidence increased in at least one younger age group for 14 of 33 cancer types examined between 2010 and 2019. These included colorectal, breast, uterine, kidney, pancreatic, and testicular cancers, as well as several lymphomas. The causes are unlikely to be identical from one cancer to another, but what is striking is that several cancers associated with obesity and metabolic dysfunction are among those with increasing incidence in younger populations.
The relationship between cancer and glucose becomes even more interesting once a tumor exists. Nearly a century ago, Nobel Prize-winning German physiologist Otto Warburg observed that many cancer cells consume enormous quantities of glucose and convert much of it to lactate through a pathway that doesn’t require oxygen, even when oxygen is plentiful. This unusual metabolic behavior became known as the Warburg effect. Although cancer biology is more complicated than this one effect, abnormally high glucose consumption remains a key characteristic of many cancers.
In fact, modern medicine takes advantage of that appetite for glucose to locate tumors. During an FDG-PET scan, a patient receives a radioactively labeled form of glucose. Tissues that take up large amounts of glucose accumulate more of the tracer and light up on the scan, highlighting tumors that are ferociously consuming glucose.
The evidence shows that glucose metabolism, insulin signaling, body fat, and metabolic health are deeply intertwined with cancer biology. We don’t need to claim with certainty that sugar causes cancer to recognize that chronically flooding the body with added sugar is unjustified and unnecessary. Added sugar provides no essential nutrition and has no minimum requirement for health, and reducing it improves many of the same metabolic conditions now being investigated for their role in cancer risk. While we seek to understand those relationships more completely, “no added sugar” remains a remarkably simple, sensible place to start.
What Happens When Kids Eat Too Much Sugar?
Children live in the same food environment as adults, but they encounter it in much smaller bodies. A 40- or 50-gram dose of sugar from a soft drink or juice represents a very different exposure for a 30-kilogram child than for a 90-kilogram adult.
High sugar intake in children is associated with several problems, including dental cavities, obesity, insulin resistance, abnormal blood lipids, and fatty liver disease. Sugary foods also create an opportunity-cost problem. Children have substantial requirements for protein, essential fats, vitamins, and minerals to support growth and development, but they can eat only a finite amount of food. Filling up on juice, cereal, granola bars, gummy snacks, pastries, and soft drinks displaces foods with considerably more nutritional value.
Intervention research suggests some metabolic consequences can improve surprisingly quickly when sugar exposure drops. In a randomized clinical trial involving adolescent boys with fatty liver disease, researchers reduced free sugar intake to less than 3% of total calories for eight weeks. Liver fat decreased substantially more in the low-sugar group than in the group that continued its usual diet, and a subsequent analysis found that new fat production in the liver fell by nearly a third. All of that happened in just eight weeks.
That finding is significant because fatty liver was once considered a disease of adults with severe alcoholism. The first published case of fatty liver disease in a child appeared in 1983. Today, fatty liver affects roughly 1 in 10 children, about 7 million in the U.S. alone. Sit with that statistic for a moment and consider what has happened to our children’s health in just a generation or two.
A1C: Looking at Glucose Exposure Over Time
If you want to know how well your body manages glucose, the hemoglobin A1C test provides objective, medium-term data.
Glucose circulating in the bloodstream can attach to proteins through a process called glycation. Hemoglobin, the oxygen-carrying protein inside red blood cells, is one of those proteins. Because red blood cells circulate for about 120 days, measuring the percentage of glycated hemoglobin (think “candy-coated”) reveals glucose exposure over the previous several months, with more recent weeks contributing more heavily to the result.
Current diagnostic criteria classify an A1C below 5.7% as normal, 5.7% to 6.4% as prediabetes, and 6.5% or higher as meeting the laboratory threshold for diabetes. In the absence of unequivocal hyperglycemia, a diabetes diagnosis generally requires confirmation with repeat or additional testing.
It should be noted that A1C has limitations, though. Conditions that change red blood cell lifespan can make the result misleading, and two people with identical A1C values can have very different daily glucose patterns. Still, it provides a useful window into chronic glucose exposure.
To appreciate how tightly the body regulates blood glucose, consider how much actually circulates in the bloodstream. An average adult with normal blood glucose carries only about 4 to 5 grams of glucose in the blood at any given moment, roughly one teaspoon. To a doctor assessing a patient, 9 grams persistently in circulation (180 milligrams per deciliter, or 10 millimoles per liter) would warrant medical intervention. Twelve grams persistently in circulation (240 mg/dL, or 13.3 mmol/L) would be a serious red flag that major, life-threatening diabetic complications could be developing.
Now compare that with a meal containing 75 or 100 grams of rapidly digestible carbohydrate.
The body has an enormous job to do after that meal. Tissues have to take up the glucose for energy production or storage, and insulin plays a central role in coordinating that process. A metabolically healthy, active person can perform that job remarkably well. As insulin sensitivity deteriorates, the same carbohydrate load becomes increasingly difficult to manage.
Glycation: When Sugar Sticks Around
High blood sugar creates another problem that has nothing to do with whether those molecules eventually get burned or stored. Glucose and other sugars are chemically reactive. When they remain in contact with proteins, fats, and other structures in the body, they can spontaneously attach to them through glycation, a process that becomes irreversible in its later stages.
As discussed above, hemoglobin A1C is glycated hemoglobin. The more glucose circulating in the blood over time, the more opportunities glucose has to attach to hemoglobin inside red blood cells. But glycation does not stop with hemoglobin. Sugars can react with proteins throughout the body, and some early glycation products undergo additional chemical reactions until they become advanced glycation end products, appropriately abbreviated AGEs. These compounds can accumulate in tissues and alter the structure and function of the proteins they attach to. AGEs can also bind to cellular receptors called RAGE, triggering signaling pathways that promote oxidative stress and inflammation. Over time, excessive AGE formation has been implicated in the blood vessel, kidney, nerve, eye, and connective tissue damage associated with chronically elevated blood glucose. Glycation and AGEs even contribute to premature skin aging, as the loss of collagen integrity leads to wrinkles, laxity, and sagging.
Collagen is particularly vulnerable because it lasts a long time. Unlike proteins that break down and are replaced quickly, collagen in tissues such as tendons can remain for years or even decades. That gives glycation products plenty of time to accumulate. AGEs can form abnormal cross-links between neighboring collagen molecules, changing the tissue’s mechanical properties. Instead of sliding and moving normally under load, glycated collagen fibers become stiff and less able to dissipate mechanical stress. Think brittle candy vs. supple rubber bands.
This has obvious implications for athletes. Tendons, ligaments, cartilage, bone, and other connective tissues depend heavily on collagen, and their ability to tolerate training depends not only on strength but also on how well they move, absorb force, remodel, and repair themselves. Experiments show that AGE cross-linking interferes with collagen-fibril sliding and some of the microscopic mechanisms that allow tendons to absorb load before failure.
In practical terms, an athlete can have strong muscles pulling on low-quality connective tissue degraded by a poor diet. Muscle adapts relatively quickly to training; collagen turns over much more slowly. Glycation that accumulates in long-lived connective tissue doesn’t disappear after a few good workouts or a week without dessert.
Caring about chronic glucose exposure is not just for people with obesity or chronic disease. Keeping blood sugar well regulated isn’t only about avoiding a poor A1C result decades from now. If you want to lift, run, jump, throw, and train hard for a long time without blowing a biceps tendon or rupturing an Achilles, you need to protect the collagen that holds the whole operation together.
Understanding the damage is only half the equation. In Part 3, learn how to spot the signs that you’re eating too much sugar, what happens when you stop, and what to eat instead.
Put It Into Practice
Knowing what sugar does to your body is the first step. Knowing what to eat instead, and how to make it stick, is the next. Join us for Applied Nutrition, a one-day, in-person course where you’ll learn how to build meals around meat and vegetables, nuts and seeds, some fruit, little starch, and no sugar, then leave with a personal nutrition plan you can start the next day. [Find an Applied Nutrition course near you.]
Prefer to learn on your own schedule? Take Nutrition I online and get the fundamentals of CrossFit’s nutrition prescription from anywhere. [Enroll in Nutrition I.]
About the Author
Jocelyn Rylee (CF-L4) and her husband David founded CrossFit BRIO in 2008, starting in a modest 1500 sq ft space and focusing on personal training. Her dedication to excellence has also earned her a position on CrossFit LLC’s Level 1 Seminar Staff, a role that allows her to share her passion and expertise with aspiring coaches. Jocelyn holds specialties in Endurance, Gymnastics, Competition, and Weightlifting and is also a certified Strength and Conditioning Specialist through the NSCA. As a Level 2 Olympic Weightlifting Coach and a Level 3 referee, she has been deeply involved in the sport, even serving as a board member of the Saskatchewan Weightlifting Association for five years. Her achievements include being Saskatchewan’s top-ranked female Olympic Weightlifter from 2012 to 2015, during which she held provincial records in the Snatch, Clean & Jerk, and Total in her weight class. With an MS in Human Nutrition, Jocelyn loves sharing her knowledge on nutrition and performance through her blog and Instagram as “The Keto Athlete,” where she delves into the science of nutrition and its impact on athletic performance.