The Case Against Sugar

Why has diabetes—and a host of other chronic disorders—exploded in prevalence in just over a century? Gary Taubes argues that sugar is not merely a source of calories but a biochemical trigger of the metabolic disturbance that underlies obesity, type 2 diabetes, heart disease, gout, and several other Western diseases. In this sweeping narrative, he combines the history of sugar’s rise, the biochemistry of fructose and insulin, epidemiological patterns across cultures, and the political and industrial forces that protected sugar’s reputation.

Taubes begins with an unsettling question: “Why diabetes?” Around 1885, Elliott Joslin and other physicians began recording an exponential rise in diabetes cases in Boston hospitals—a pattern mirrored from Copenhagen to China. Few could explain the trend by improved diagnostics alone. The timing coincided with the fall in sugar prices and the invention of industrial candy, soft drinks, and sweetened cereals. Wherever refined sugar entered diets, diabetes followed within decades.

A recurring global pattern

Across continents—from the Pima Indians to Maoris and Pacific Islanders—Taubes notes that the modern epidemic appears when populations adopt Western diets. Epidemiologists once documented that diabetes mortality fell during sugar rationing in wartime and then surged when sugar returned to markets. This pattern repeats too consistently to ignore. You see the same curve: modernization brings sugar, then metabolic disease.

From historical luxury to daily staple

Taubes reconstructs sugar’s transformation from exotic spice to everyday necessity. Born from millennia-old cane cultivation, sugar financed slavery, conquered empires, and served as “white gold.” By the 20th century, beet and cane refining made sugar cheap enough to saturate global diets. The rise of chocolate, soda, and processed foods turned sweetness from celebration into habit. Once sugar became ubiquitous, chronic disease rates shifted worldwide.

The biochemical culprit

Taubes’s core argument is metabolic: sucrose and high-fructose corn syrup deliver both glucose and fructose, but it’s fructose that transforms the story. Fructose is processed primarily by the liver, where it drives lipogenesis—the creation of fat. Over time this creates fatty liver, elevates triglycerides, and induces insulin resistance. The result is what Gerald Reaven termed metabolic syndrome: high triglycerides, central obesity, hypertension, and impaired glucose tolerance, a constellation that predisposes to nearly every major Western disease.

Biochemists such as Luc Tappy and Eleazar Shafrir show why: large fructose loads bypass the hormonal controls that regulate glucose, flooding the liver with substrate for fat synthesis. In human trials, subjects fed the equivalent of multiple sodas per day developed liver insulin resistance within days. In animals and primates, chronic fructose exposure generates fatty liver and diabetes. This biochemical path aligns perfectly with epidemiologic data—making sugar not just correlated with disease but mechanistically plausible as its driver.

Institutional narratives and scientific blind spots

Taubes also tracks how the sugar industry, from the Sugar Research Foundation onward, systematically shaped scientific agendas and public opinion. By sponsoring carbohydrate chemistry at MIT and funding prominent voices such as Ancel Keys and Fred Stare, the industry reframed dietary debates: blame fat and cholesterol, not sugar. Through PR campaigns and lobbying, it secured FDA affirmations that sugar was “generally recognized as safe.” When the 1977 U.S. Dietary Goals committee proposed cutting sugar intake, industry pressure helped redirect guidance toward low-fat recommendations instead.

These institutional choices created decades of confusion. Nutrition authorities focused on fat while sugar consumption soared. When massive, expensive trials (like the Women’s Health Initiative) failed to confirm benefits of low-fat diets, the paradigm was already entrenched. Taubes demonstrates how this interplay between science, politics, and industry delayed serious inquiry into sugar’s role.

Sugar’s psychoactive pull

Why does sugar resist reform even when evidence mounts? The answer may be neurological. Newborns instinctively prefer sweetness, and dopamine imaging reveals sugar activates the brain’s reward circuits similar to nicotine or cocaine. Serge Ahmed’s studies show rats choosing sugar water over cocaine, implying a profound drive. This psychoactive dimension explains why societies reward themselves with sweetness—it comforts, celebrates, and compensates. Cultural rituals entwine sugar with emotional reward, making both personal and policy-level change hard to sustain.

The simplest possible explanation

Applying Occam’s razor, Taubes asks whether one dietary factor—refined sugar—can account for the family of Western diseases. The Tokelau Island Migrant Study crystallizes the logic: when islanders move from low-sugar, high-fat diets to Western high-sugar diets, obesity, gout, hypertension, and diabetes rise together. A single shift in sucrose and HFCS intake fits the timeline and pathology better than multifactorial theories.

Taubes’s main claim

Rather than fat or simple excess calories, it is sugar—especially its fructose half—that initiates metabolic syndrome, drives insulin resistance, raises uric acid, and acts cumulatively across generations. Wherever sugar floods the diet, chronic disease follows.

In sum, Taubes builds a unified argument linking historical patterns, biochemical pathways, and institutional responses. He invites you to reconsider not just what you eat, but how scientific consensus forms—and to recognize sugar as the common denominator in the modern epidemic of chronic disease.

Sugar’s distinctive power lies in its chemistry, especially fructose. Where glucose fuels muscles and the brain under hormonal regulation, fructose is metabolized mainly by the liver. That difference, Taubes explains, makes fructose uniquely capable of creating metabolic havoc. High-fructose corn syrup and sucrose, though chemically similar, deliver fructose quickly and without fiber—the metabolic equivalent of an intravenous dose compared to fruit.

From sugar to fat

When you consume fructose, your liver converts it not into glycogen (as with glucose) but into fatty acids, notably palmitate. These fats accumulate in liver cells, producing fatty liver disease and raising circulating triglycerides. Researchers such as Luc Tappy show that high-fructose feeding elevates triglycerides within days, setting the stage for insulin resistance—the defining feature of metabolic syndrome. Gerald Reaven later demonstrated that insulin resistance triggers a cascade of related disorders, including hypertension and heart disease.

The insulin connection

Rosalyn Yalow and Solomon Berson’s radioimmunoassay revolutionized endocrinology by allowing scientists to measure circulating insulin. Their discoveries showed that obese and diabetic individuals often maintain chronically elevated insulin levels. Insulin’s function is lipogenic—it promotes fat storage. Taubes turns the causality assumption on its head: rather than obesity causing high insulin, perhaps sugar-induced hyperinsulinemia causes obesity.

Fructose, uric acid, and hypertension

Taubes connects fructose metabolism to two surprising disorders: gout and high blood pressure. Fructose metabolism breaks down ATP, releasing purines that convert to uric acid. Elevated uric acid, a condition called hyperuricemia, can damage the kidneys and raise blood pressure. Richard Johnson’s research suggests uric acid may directly cause vascular injury and salt-sensitive hypertension. This mechanism unites gout, obesity, and hypertension under the sugar umbrella.

Metabolic syndrome as the unifying pathway

What emerges is a unified model: fructose increases liver fat and triglycerides, stimulating insulin resistance; insulin resistance raises blood pressure and disrupts lipid metabolism; and uric acid links sugar to gout and kidney disease. Diseases we treated separately may stem from the same root. By reducing added sugar, you target the entire syndrome, not just isolated symptoms.

Metabolic logic

Taubes’s argument rests on metabolic simplicity: sugar’s fructose component alone can explain Western disease patterns because it uniquely drives hepatic fat synthesis, insulin resistance, and systemic inflammation.

Think of sugar not as mere fuel but as a hormonal signal—one that misguides the liver, alters insulin dynamics, and sets in motion the chronic disorders that define modern life.

Taubes encourages you to look beyond isolated diseases and see the shared mechanism behind them. Whether you discuss heart disease, diabetes, fatty liver, or dementia, the thread connecting them is insulin resistance and the cluster known as metabolic syndrome.

Defining the syndrome

Clinically, metabolic syndrome is characterized by abdominal obesity, high triglycerides, low HDL cholesterol, elevated blood pressure, and impaired glucose regulation. Gerald Reaven named it “Syndrome X” to emphasize its unified physiology. Rather than treating each condition separately, Taubes shows how focusing upstream—on insulin regulation and sugar intake—offers leverage over all.

How sugar initiates the process

Fructose consumption fattens the liver, reducing insulin sensitivity. The pancreas compensates by secreting more insulin, promoting fat storage throughout the body. Over time, tissues become insulin-resistant. The result is not just high glucose but a multifaceted disturbance: lipid abnormalities, increased blood pressure, and systemic inflammation.

Intergenerational effects

In the Pima Indians of Arizona, NIH studies show how sugar-driven insulin resistance spirals across generations. Mothers with gestational diabetes bear children predisposed to obesity and diabetes by adolescence—a phenomenon called perinatal metabolic imprinting. The vicious cycle accelerates: when those daughters grow up insulin-resistant, they perpetuate the pattern in their own offspring. This mechanism explains how communities can become locked into epidemic-level disease within decades.

The practical implication

Prevention must start upstream. Target insulin resistance—and the sugar intake that causes it—especially among young women of childbearing age, rather than focusing only on calorie restriction in adults.

By recognizing metabolic syndrome as the hub of Western disease, you shift from fragmented cures to systemic prevention. Sugar, not fat, is the common ignition point for the metabolic fire.

Taubes devotes significant attention to how the sugar industry engineered both research priorities and public perception. From the 1940s onward, the Sugar Research Foundation (later the Sugar Association and the World Sugar Research Organization) funded scientists, sponsored conferences, and produced literature all aimed at maintaining sugar’s innocence.

Funding scientific allies

Industrial strategy was remarkably sophisticated. Grants went to established institutions—MIT, Harvard—and influential nutritionists like Fred Stare and Ancel Keys. Their output focused public concern on dietary fat and cholesterol, helping deflect scrutiny from sugar. The American Heart Association and key NIH programs reinforced that fat narrative, leaving sugar effectively exonerated.

Public relations and regulatory maneuvers

Through firms like Leo Burnett and Carl Byoir, the sugar industry launched massive PR campaigns. Reports such as “Sugar in the Diet of Man” (edited by Fred Stare) and FDA reviews argued sugar was safe. When the McGovern committee proposed a 40% reduction in sugar intake (1977), lobbying swiftly diluted the recommendation.

Institutional capture

The 1986 FDA Sugars Task Force claimed sugar was ‘generally recognized as safe at current levels,’ a statement that froze policy for decades. British committees echoed similar findings, sometimes chaired by scientists who previously accepted industry funding. By commissioning research that framed sugar as equivalent to any other calorie source, the industry redirected the scientific questions themselves.

A deeper lesson

Industry influence rarely depends on outright fraud. It works by shaping which hypotheses are tested. For decades, scientists studied calories and fat instead of examining fructose metabolism—because funding steered them that way.

If you read nutrition science today, Taubes urges, ask who funded the research and why the agenda looks the way it does. The politics of sugar is as important as the chemistry.

Beyond biochemistry, sugar grips you psychologically and culturally. Taubes explores its role as a psychoactive pleasure—something that acts on the brain’s reward system much like drugs do. This helps explain why, despite growing evidence of harm, sugar remains powerfully woven into daily rituals.

Biological attraction

Newborn reactions observed by Jacob Steiner show infants instinctively smile and suck after tasting sweetness. That reflex reflects evolutionary adaptation—sweet signals energy density and safety. This innate preference becomes culturally amplified by modern abundance. Sidney Mintz’s anthropological work shows how sugar evolved from medicinal luxury into emotional reward.

Neurochemical reinforcement

Sugar activates the nucleus accumbens—the same neural circuitry stimulated by nicotine, cocaine, and opioids. In Serge Ahmed’s experiments, rats repeatedly choose sugar solutions over cocaine, underscoring sugar’s potent reinforcement capacity. Clinically, humans demonstrate parallel behavior: during Prohibition, sweets substituted for alcohol; Alcoholics Anonymous once recommended candy to resist cravings. These examples show sugar’s ability to modulate mood and behavior.

Cultural embedding

From birthday cakes to morning coffee, sugar signifies comfort, celebration, and love. Its emotional associations make regulation politically treacherous. You’re not just limiting a nutrient—you’re tampering with a symbol of happiness. Taubes argues this cultural reinforcement may be as significant as biochemical addiction in sustaining overconsumption.

A critical insight

Public-health reform requires recognizing that sugar consumption is not merely rational choice; it’s conditioned, neurochemical, and cultural—each making conscious moderation harder than slogans like “eat less” suggest.

Understanding sugar’s psychoactive hold explains why its reduction demands both biological and cultural strategies—rewiring habits, not just adjusting guidelines.

Taubes closes with reflections on how nutritional science operates under pressure. The ideal of Popperian falsifiability—the rigorous testing of hypotheses—is often impossible in diet research. Long-term trials to prove causality between sugar and disease would require tens of thousands of participants and billions of dollars, lasting decades.

The dilemma of urgency vs. certainty

Public-health officials must act while evidence remains incomplete. When NIH launched its anti-fat campaigns in the 1980s, it relied on modest, short-term evidence linking saturated fat to heart disease risk factors. Yet massive population-level guidance followed before definitive long-term trials were done. When such trials (like the Women’s Health Initiative) later found no benefit, institutional inertia prevented reversal.

The lesson for sugar policy

Sugar now stands where fat once did: highly suspected but officially tolerated. Taubes cautions against both extremes—paralysis by demand for perfect proof and reckless certainty based on weak data. The challenge is to act proportionally while staying open to revision.

Scientific humility

Nutrition science must balance skepticism with responsiveness. Waiting for perfect proof can cost lives, but ignoring accumulating evidence—as with sugar—can perpetuate epidemics. The task is to evaluate credibility, not absolutes.

In essence, Taubes calls for a better scientific posture: test bold hypotheses like the sugar-disease link with rigor, acknowledge confounding pressures, and act responsibly. Only by blending humility and vigilance can nutrition move beyond decades of ideological confusion.