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Chapter 9: Sugar: Frequency Over Quantity

In which we learn that the dose doesn't make the poison—the pattern does—and understand why five small candies throughout the day is worse than one large dessert

The Tooth Fairy, exhausted by the endless parade of sweets.

"Cut back on sugar."

You've heard this advice your entire life. Dentists say it. Parents say it. Public health campaigns say it. And it's not wrong, exactly. Sugar does contribute to tooth decay. Reducing sugar intake is generally good for oral health.

But the conventional framing misses something crucial: how and when you consume sugar matters far more than how much.

This chapter will reframe your understanding of sugar's role in dental disease. By the end, you'll think differently about that piece of cake—and you might actually enjoy it more, knowing that the way you're eating it determines whether it's a dental threat or a relatively harmless indulgence.

The Stephan Curve

In 1944, a dental researcher named Robert Stephan made a foundational discovery.1 He measured the pH in dental plaque after volunteers rinsed with glucose solutions, and he plotted the results over time.

What he found was consistent and reproducible:

  1. Immediate drop: Within minutes of sugar exposure, plaque pH fell sharply—often to 5.0 or below (well under the critical 5.5 threshold).

  2. Minimum reached: pH reached its lowest point approximately 5-20 minutes after exposure.

  3. Gradual recovery: Over the next 30-60 minutes, pH slowly rose back toward baseline as saliva buffered the acid and bacteria metabolized the remaining sugar.

This pattern became known as the Stephan Curve, and it remains foundational to understanding caries development.

The key insight: each sugar exposure triggers an acid attack lasting 20-60 minutes. During this window, demineralization is occurring. Between attacks, when pH is above critical threshold, remineralization can happen.

Your dental fate depends on the balance between these phases.

The Mathematics of Frequency

Let's do some simple math.

Single daily exposure: One dessert after dinner. One acid attack, lasting approximately 30-40 minutes. That's about 40 minutes of demineralization per day, and 23+ hours of potential remineralization.

Three daily exposures: Breakfast includes fruit juice, lunch includes soda, dinner includes dessert. Three acid attacks, totaling perhaps 100-120 minutes of demineralization, with substantial recovery time between.

Continuous exposure: A sweetened coffee sipped throughout the morning, a few candies in the afternoon, a soda with dinner, a snack before bed. Five or six separate exposures, or—worse—continuous exposure during sipping. pH rarely rises above critical threshold. Demineralization dominates the day.

The total amount of sugar might be similar across these scenarios. But the dental outcomes would be dramatically different.

The person with one large dessert might never get a cavity. The person with continuous small exposures will almost certainly develop them.

Historical Evidence: The Hopewood House Study

One of the most compelling demonstrations of this principle comes from the Hopewood House Study, conducted in Australia in the 1950s.

Hopewood House was a children's home where, due to philosophical beliefs of the founders, children were raised on a vegetarian diet extremely low in refined sugar.2 The diet wasn't designed for dental research—it was an ideological choice—but researchers took advantage of the natural experiment.

The children of Hopewood House had remarkably low rates of tooth decay compared to the general population. Their teeth weren't inherently different; their genetic backgrounds were typical for Australian children of the era. What was different was their sugar exposure pattern: nearly absent.

When some children left Hopewood House and adopted normal Australian diets, their cavity rates rose to match the general population within a few years.

The study suggested that sugar exposure below a certain threshold resulted in minimal caries, while exposure above that threshold caused disease. The relationship wasn't strictly linear—there seemed to be a threshold effect where the repair system could handle low levels of challenge but became overwhelmed above a certain frequency.

The Vipeholm Study: Ethics and Evidence

The most definitive—and ethically troubling—study on sugar consumption patterns was the Vipeholm Study, conducted in Sweden from 1945 to 1953.3

Researchers at the Vipeholm mental institution fed different groups of patients controlled diets with varying sugar amounts and patterns. Some received sugar with meals only. Others received sugar between meals. Others received sticky toffees that adhered to teeth for extended periods.

The findings were clear:

  1. Sugar consumed with meals caused minimal additional caries beyond baseline.
  2. Sugar consumed between meals substantially increased caries.
  3. Sticky sugars consumed between meals caused the most caries of any pattern tested.

The study would never be approved today—conducting dietary experiments on institutionalized psychiatric patients is indefensible by modern ethical standards. But the data, however uncomfortably obtained, transformed understanding of sugar's role in caries.

It's not the sugar in your food. It's the sugar between your food.

Why Frequency Matters: The Biological Logic

The Stephan Curve explains why frequency matters so much. Each sugar exposure triggers an independent acid attack. More frequent exposures mean more attacks, less recovery time, and net demineralization.

But there's more to the story.

Biofilm Metabolism

The bacteria in dental plaque don't metabolize sugar instantly. When you eat sugar, you're feeding a microbial community that takes time to absorb, process, and excrete acidic byproducts. A single large sugar dose saturates this metabolic capacity relatively quickly—the bacteria can only work so fast.

Frequent small doses, however, keep the bacteria in constant production mode. Each new sugar arrival restarts the metabolic clock. The total acid produced may actually be greater from many small exposures than from one large one.

Bacterial Selection

Remember the ecological plaque hypothesis? Frequent acid stress selects for acid-tolerant species like S. mutans. If you eat sugar once a day, the acid environment is transient—there's a lot of time at neutral pH, favoring a diverse community.

If you consume sugar continuously, the environment is persistently acidic. Acid-tolerant species gain competitive advantage. The community shifts toward organisms that produce more acid. A self-reinforcing cycle develops.

Frequency doesn't just cause more acid attacks—it reshapes the ecosystem toward one that causes even more acid attacks.

Salivary Exhaustion

Saliva provides buffering, remineralization minerals, and antimicrobial factors. But these resources aren't unlimited. Continuous acid challenges may partially exhaust buffering capacity. The minerals deposited during remineralization take time to accumulate in saliva.

Spacing out sugar exposures allows salivary resources to replenish between challenges.

The "Free Sugars" Distinction

Nutritional guidelines increasingly distinguish between free sugars and intrinsic sugars:

Free sugars are monosaccharides and disaccharides added to foods by manufacturers, cooks, or consumers, plus sugars naturally present in honey, syrups, and fruit juices.

Intrinsic sugars are sugars that are naturally present within the structure of whole fruits and vegetables.

This distinction matters for dental health because:

  1. Free sugars are more readily available to bacteria. They dissolve quickly in saliva and reach plaque rapidly.

  2. Intrinsic sugars are released more slowly as the food matrix is chewed and digested. The sugar release is spread over time rather than arriving as a bolus.

  3. Whole fruits contain fiber that stimulates saliva and provides mechanical cleaning. The chewing required extends exposure time but also activates defenses.

This doesn't mean whole fruit is decay-proof—someone who constantly snacks on grapes will still experience acid challenges. But whole fruit consumed in normal meal patterns is far less cariogenic than equivalent sugar from juice or candy.

Practical Applications

Good Patterns

Sugar with meals: Consuming sweets as part of a meal rather than separately. The other foods provide buffering, stimulate saliva, and dilute the sugar. You're already having an acid challenge from the meal; the dessert extends it slightly rather than creating a new one.

Consolidated treats: If you're going to have candy, eat a reasonable amount at one time rather than grazing throughout the day. One 30-minute acid attack from a candy bar is better than six 30-minute attacks from six individually unwrapped candies.

Sweet beverages consumed quickly: If you drink soda (which I'd generally discourage), drink it over a short period rather than sipping throughout the day.

Bad Patterns

Continuous sipping of sweetened beverages: Coffee with sugar throughout the morning. Sports drinks during extended exercise. Soda nursed over an afternoon. Each sip restarts the acid clock.

Hard candies and lozenges: These dissolve slowly in the mouth, providing continuous sugar release. A single hard candy might deliver sugar for 15-20 minutes—an extended acid attack from a tiny amount of sugar.

Dried fruits as constant snacks: Raisins, dates, and other dried fruits are sticky, adherent, and sugar-concentrated. Snacking on them throughout the day is a dental disaster.

Nighttime sugar: Any sugar before bed gets extended access to your teeth during the low-saliva overnight period.

Sugar in beverages retained in the mouth: Adding sugar to tea or coffee that you hold in your mouth while working extends contact dramatically.

Xylitol: The Exception

Xylitol is a sugar alcohol that tastes sweet but cannot be effectively metabolized by S. mutans. When you consume xylitol, you get sweetness without the acid attack.

Even better, xylitol appears to actively disadvantage S. mutans. The bacteria take up xylitol, attempt to metabolize it, waste energy, and become less competitive. Regular xylitol exposure shifts the oral ecosystem away from cariogenic dominance.

Clinical trials have demonstrated that xylitol exposure of 5-10 grams daily, divided across multiple exposures (gum, mints, candy), significantly reduces caries incidence.4

Xylitol turns the frequency principle on its head: more frequent exposure to xylitol is beneficial rather than harmful. You're repeatedly reminding S. mutans that it's living in an inhospitable environment.

The Permission Structure

I want to be clear about what this chapter is and isn't saying.

I'm not saying sugar is fine in unlimited quantities. Total sugar intake does matter, and the metabolic health consequences of excessive sugar go far beyond dental disease.

I'm not saying you should eat dessert with every meal. Concentrated sugar is still a challenge; it's just a more manageable challenge when consolidated.

I am saying that the pattern matters more than you've been told. If you're going to consume sugar—and most people will—understanding the frequency effect lets you minimize harm without necessarily minimizing pleasure.

That birthday cake at a party? Eat it. Enjoy it. It's one acid attack, occurring with a meal, likely followed by hours without additional sugar.

That candy jar on your desk that you nibble from throughout the day? That's where the damage accumulates.

The most important change you can make isn't eliminating sugar—it's restructuring when you consume it. Same total sugar, dramatically different dental outcomes.

Now let's examine the structure that makes bacteria so difficult to dislodge: the biofilm, or plaque. Understanding this fortress is essential to understanding why mechanical disruption matters so much.

  1. Stephan, R. M. (1944). Intra-oral hydrogen-ion concentrations associated with dental caries activity. Journal of Dental Research, 23(4), 257-266. ↩

  2. Harris, R. (1963). Biology of the children of Hopewood House, Bowral, Australia. 4. Observations on dental-caries experience extending over five years (1957-61). Journal of Dental Research, 42(6), 1387-1399. ↩

  3. Gustafsson, B. E., et al. (1954). The Vipeholm dental caries study; the effect of different levels of carbohydrate intake on caries activity in 436 individuals observed for five years. Acta Odontologica Scandinavica, 11(3-4), 232-264. ↩

  4. Mäkinen, K. K. (2010). Sugar alcohols, caries incidence, and remineralization of caries lesions: a literature review. International Journal of Dentistry, 2010, 981072. ↩