Sugar Restriction: The Evidence for a Drug-Free Intervention to Reduce Cardiovascular Disease Risk

ByCrossFitMarch 3, 2020

Question
Are recommendations to selectively restrict sugar intake more justified than those to restrict fat or salt intake?
Takeaway
Multiple lines of evidence indicate sugar can be more directly linked to increased risk of cardiovascular disease and other metabolic disorders than saturated fat or salt. The shift in Western dietary patterns away from fat consumption and toward increased consumption of sugars is a likely contributor to the concurrent increase in rates of metabolic disease.

This 2012 review argues the focus public health authorities place on fat and salt restriction is misguided and may be counterproductive if it leads to increased sugar consumption.

Research has linked increased sugar intake to increased disease risk since at least the 1960s, and such research was heavily promoted by T. L. Cleave in the mid-1970s (1). During this same period, however, public health authorities in the United States and other English-speaking Western nations began to recommend population-wide decreases in fat intake, believing fat played a causal role in the development of heart disease (2).

In the 1980s, David Jenkins developed the concept of the glycemic index, a measure of the extent to which a food raises blood glucose levels (3). Sugar was found to have a lower glycemic index than refined starches such as white bread, which led some to recommend that diabetics consume sugar as a healthy carbohydrate to help manage blood sugar levels (4). As a result of these and other forces, sugar intake increased more than 30% between 1970 and 2000 (5). By 2002, the American Heart Association (AHA) had explicitly concluded there was “no definitive evidence” to support the limitation of sugar intake (6).

It is difficult to assess exactly how much sugar the average American consumes, as it is known that surveys relying on self-report underestimate intake by at least 20% (7). With this caveat in mind, economic and survey-based estimates indicate the average American adult consumes between 25 and 45 teaspoons of sugar each day (100 – 180 grams), with one-third of this intake coming from soft drinks; one-third from cakes, cookies, and candies; and the remaining one-third from a variety of other sources (8).

Mechanistically, sugar directly contributes to fatty buildup in organs including the liver and thus contributes to insulin resistance and poor glycemic control as well. Through the effects of insulin, 80% of circulating glucose is cleared out of the blood into skeletal and smooth muscle; only 5% of starch is directed toward liver fat. Fructose, conversely, is taken up directly by the liver after absorption in the intestines, where 50% is converted into glucose and the other 50% is converted into fat. This fatty fraction is either exported by the liver as triglycerides/VLDL or retained in the liver as hepatic fat. This same metabolic process leads to liver cell energy depletion and uric acid production. Higher circulating fat levels lead to fat accumulation in the liver, pancreas, and other organs (9).

At the time of this review (2012), relatively little clinical trial data was available directly linking increased sugar intake to disease progression, or a reduction in sugar intake to disease reversal. A variety of observational data, however, has linked increased intake of sugar or sugar-containing foods to weight gain, diabetes, heart disease, and dental caries. The handful of studies that have failed to show a link between sugar and disease have generally been industry-funded, while independently funded studies have consistently associated increased sugar intake with increased disease risk (10).

As reviewed extensively on CrossFit.com, the evidence linking either saturated fat or salt to increased disease risk is relatively weaker. The Cochrane Collaboration and other groups have found reducing saturated fat intake does not improve cardiovascular mortality and has only an inconsistent effect on the rate of cardiovascular events (11). Recent research has more narrowly argued replacing saturated fats specifically with monounsaturated or polyunsaturated fats is beneficial, but this may be more due to the protective effects of these other fats than any deleterious effects of saturated fat itself (12). Recent reviews of the evidence surrounding salt intake suggest no effect or a limited effect of increased salt intake on heart disease risk, with reduced salt intake potentially increasing overall mortality (13). Low-glycemic-index diets have been consistently linked to reduced mortality, but given a reduction in dietary glycemic index generally involves a variety of dietary changes — i.e., a shift from highly refined foods to vegetables, nuts, and other whole foods — it is impossible to isolate the impact of a change related to glycemic index alone (14).

The authors briefly note anecdotal evidence and previous reviews arguing sugar may have addictive properties and specifically that high-consuming individuals may experience withdrawal symptoms (15). Given the ubiquity of sugar in the Western diet, the effects of abstaining from sugar for extended periods are difficult to study, but these cognitive effects may have contributed to the rapid rise in consumption levels (16).

Since 2009, the AHA has recommended restricting sugar intake to nine teaspoons per day for men, six for women (17). At the intake levels listed above, this represents a two-thirds reduction in sugar intake.

Read the review

Notes