Is Sugar Killing You?

Sugar seems to be the latest target for why we’re all fat, sick, and dying.

But, we also know (or you should all know by this point if you’ve been reading my articles for a while), the media tends to exaggerate and misconstrue what the evidence actually tells us. Sometimes, it’s outright wrong or out-of-date research that has since been refuted with newer and better-designed experiments.

Total Sugars: refers to glucose, fructose, galactose, lactose and sucrose and maltose

Fructose: monosaccharide, commonly known as “fruit sugar”

Sucrose: disaccharide consisting of 50% glucose + 50% fructose

High Fructose Corn Syrup (HFCS): 42-55% fructose + 42-53% glucose + 3-5% other sugars; HFCS 55 is typically found in soft drinks and HFCS 42 is typically found in desserts and canned fruit

Not all published research is good QUALITY research.

But, I digress. So…

What does the research say?


Added Sugar Consumption and Chronic Disease

Added sugars are among the most controversial and hotly debated topics in nutrition. Consumption of added sugars has been associated with increased risk of obesity as well as increased risk factors for cardiovascular disease (dyslipidemia, elevated blood pressure, diabetes, non-alcoholic fatty liver disease) as well as cognitive decline and cancer. Often this has been based on research trials which provide added sugars in dosages well above those typically found in human consumption.


Many of the controversies related to fructose are based on the difference in metabolism between fructose and glucose in the liver. Over 90% of fructose consumed is absorbed in the small intestine and metabolized in the liver. By contrast, glucose is metabolized by a number of organs and cells. However, these pathways are interactive. ~50% of fructose is converted to glucose within the liver, another 15-20% if converted to glycogen, 20-25% to lactate, and some to carbon dioxide gas. In studies, only 1-5% of consumed fructose may be converted into free fatty acids packaged as triglycerides and stored in the liver or released into the bloodstream – this in minimal.

While obesity rates have continued to rise, it should be noted that sugar consumption has actually declined. Therefore, it is more probable that an overall diet pattern, and not any individual component of it, that is associated with weight gain.


It has been argued that sugar may predispose individuals to gain fat and weight, ultimately leading to becoming overweight or obese. Several meta-analyses have shown that there is no significant effect of sugar or fructose on body weight if calories are controlled.

Many studies done on sugar and its effect on body weight have been associated with excess energy intake – therefore weight gain in these studies cannot be separated from overall calorie intake and cannot be attributed to any unique property of free sugar. It can only be argued that free sugar intake may predispose individuals to excess calorie intake.

A large body of literature associates both increase caloric consumption from all sources and decreased physical activity as major components of weight gain. Sugars may provide excess energy due to their hedonic (pleasurable) properties and increased sugar intake may be a marker for an overall less healthy and more energy dense diet.


In many studies, production data is used for consumption data. Because of international trade and sales, and due to food waste, production data cannot be assumed to be the equivalent of consumption data. Market availability of food is a highly unreliable indicator of consumption.

Little direct evidence exists that sugar consumption increases risk factors of diabetes. Since the relationship between diabetes and obesity is already well established, and due to the small amount of evidence available relating isocaloric substitution of sugars for other carbohydrates, it is important to focus on other risk factors for diabetes rather than singling out sugar.


The American Heart Association has recommended that male and female adults limit their added sugar consumption to 150 kcal/day and 100 kcal/day, respectively, implying that higher levels of added sugars may increase risk of heart disease.

Dietary sugars may have differential affects on blood lipids. Some studies have shown that diets high in simple sugars (>20% of total energy intake) may result in elevated fasting triglycerides. However, several reviews and analyses have shown that, when fructose (a simple sugar) is isocalorically substituted for other carbohydrates, it does not result in increased fasting triglycerides.

Effects of added sugars on LDL cholesterol have been variable. Taken together, the effects of added sugars on lipids in adults remains in dispute.

The major established risk factors for heart disease include smoking, being overweight or obese, having diabetes, and being physically inactive. Focus on controlling these risk factors would seem more important than focusing on sugar-sweetened beverage consumption.

Clearly, there are important links between nutrition and health. However, putting the focus on one single nutrient in the diet ignores the importance of other nutritional practices where significant evidence of linkages to health already exists. Overconsumption of calories (overall) represents the single greatest health threat to individuals.

Rippe JM and Angelopoulos TJ. “Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding”. Nutrients 2016, 8, 697; doi:10.3390/nu8110697


Sugar and Type 2 Diabetes Incidence

Sugar-sweetened beverages (SSBs), which represent the greatest source of fructose-containing sugars in the diet, form most of the basis for the link between sugar and incidence of type 2 diabetes.

Pooled analyses showed that intakes of total sugars and fructose were not associated with type 2 diabetes – intake of sucrose was actually associated with an 11% decrease in type 2 diabetes. Results from this study did not support a hypothesis that the positive association seen between SSBs and diabetes is mediated by the fructose-containing sugars they contain.

Although sugar-sweetened beverages are sources of most fructose-containing sugars in American diets, other sources contribute meaningfully to overall intake. These other food sources, which tend to be sweetened with sucrose, have shown no association (e.g. cakes, cookies) or a protective association (whole grain cereals, yogurt) with type 2 diabetes. Lack of an adverse association between intakes of total sugars, fructose, or sucrose and diabetes may reflect important contributions of these other food sources.

One possible explanation for the observed association between SSBs and diabetes is related to uncompensated energy. The adverse effect of sugars on cardiometabolic risk factors is mediated by excess energy with a signal for harm largely restricted to comparisons in which sugars supplement background diets with excess energy. Another possibility is that SSBs are a market of an unhealthy lifestyle. High consumers of SSBs consume more energy, engage in less physical activity, and smoke more.

Systematic review did not support an adverse association between intake of fructose-containing sugars independent of food form and risk of type 2 diabetes. Sugars alone do not appear to explain the relation between SSBs and type 2 diabetes.

Tsilas CS et al. “Relation of total sugars, fructose, and sucrose with incident type 2 diabetes: a systematic review and meta-analysis of prospective cohort studies”. CMAJ 2017 May 23;189:E711-20. doi:10.1503/cmaj.160706


Fructose vs. Glucose vs. HFCS

Consumption of sugar-sweetened beverages (SSBs) has been associated with increased risk of heart disease, type 2 diabetes, and metabolic syndrome. This may be due to increased body fat or possibly via a mechanism unrelated to body composition, such as chronic low-grade inflammation.

It has been theorized that the fructose component of high fructose corn syrup (HFCS) may be disproportionately responsible for the associations between SSB intake and risk factors for chronic inflammation, abnormal blood lipid values, and decreased insulin sensitivity. Metabolic comparisons to alcohol consumption have also been made to fructose (due to the role of the liver in both alcohol and fructose metabolism).

SSBs are associated with chronic inflammation, which can be related to increased risks for diabetes and heart disease.

In a study observing the effects of sweetened beverages on markers of systemic and adipose tissue inflammation as well as intestinal permeability, subjects drank 25% of their estimated calorie requirements as either fructose, glucose, or HFCS-sweetened beverages for three eight-day periods in which actual caloric intake was not controlled.

No substantial differences were seen in terms of markers of systemic inflammation, intestinal permeability, or adipose tissue inflammation.

However, this was a short-term study and the results cannot be used to determine what the effects of chronic consumption may be.

Animal research points to high consumption of fructose having deleterious effects on inflammation and intestinal permeability, but the small number of human studies do not support the same connections.

Patel K. “Fructose vs Glucose vs HFCS: Fight!” Published Sept 19, 2016. Updated Mar 28, 2017.

For comparison: 1 cup of most SSBs contains ~25-35g fructose

Fructose and Blood Lipids

With the rise in global obesity, diabetes, and cardiovascular disease, there is growing concern about the role of fructose-containing sugars (fructose, sucrose, and HFCS).

Currently, the American Heart Association recommends limiting fructose to <100g/day, 50-100g/day, and <50g/day for those with borderline, high, and very high triglyceride levels and the Canadian Diabetes Association recommends limiting added fructose to <10% of total energy intake (~60g/day) in those with diabetes. Most of the studies that these recommendations are based on are of poor quality.


Isocaloric exchange of fructose for other carbohydrate did not affect LDL cholesterol. No effect on apo B. No effect on non-HDL cholesterol. No effect on triglycerides. No effect on HDL cholesterol.


No effect on LDL cholesterol. Increased apo B. No effect on non-HDL cholesterol. Increased triglycerides. No effect on HDL cholesterol.


Study periods were fairly short-term so longstanding effects are unknown. Fructose dose administered was well beyond the highest 95% of the intake of an average person. Alone, most studies had a small subject size and the studies themselves were of poor design and study quality. Only published study data is available for use which could result in publication bias.


It appears unwarranted to set specific restrictions on the intake of fructose in the context of lipid effects. However, it does appear that fructose supplementing diets with excess calories at high doses does increase triglyceride and apo B levels – it should be noted that these effects would also be seen when overfeeding with any carbohydrate used, not just fructose.

Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories. When isocalorically exchanged for other carbohydrates, fructose had no adverse effects on blood lipids.

Chiavaroli L et al. “Effect of Fructose on Established Lipid Targets: A Systematic Review and Meta-Analysis of Controlled Feeding Trials”. JAHA 2015;4. doi:10.1161/jaha.114.001700



Is HFCS Worse Than Sugar?

High fructose corn syrup (HFCS) is a liquid blend of glucose and fructose commonly used in food products because it is cheap to produce and have a slightly sweeter perception than a similar dose of sugar. The fructose content varies from 42-55%.

Sucrose, what is most commonly thought of when referring to the term “sugar”, is essentially glucose connected to fructose in a 1:1 ratio, or 50% glucose and 50% fructose. Sucrose is broken into free glucose and fructose in the small intestine prior to absorption.

The difference between sucrose and HFCS is practically insignificant with moderate or moderately high consumption.


Both sugar and HFCS have been found to have the same effect on satiety and leptin, a major hormone involves in regulating feelings of fullness.

In at least one study, subjects in a caloric deficit (essential for weight loss) had equal rates of weight loss despite up to 10% and 20% of total calories coming from HFCS and sucrose – these levels mimic the 25th and 50th percentile of average American intakes. No gender differences were seen.

Currently, it has been concluded that HFCS and sucrose do not have different influences on body composition and obesity, independent of whether or not sugar in general influences obesity and weight gain.

HFCS is not blameless in the case of obesity. When overconsumed, it is constantly correlated with increases in obesity – although the degree of which is debated. However, in the issue of sucrose vs. HFCS, both seem to be about the same in terms of health effects. Additional calories tends to increase risk of obesity when not controlled for.

Patel K. “Is high fructose corn syrup (HFCS) worse than sugar?”

What You Need To Know

  • The apparent association between indexes of liver health and fructose or sucrose intake appear to be confounded by excessive energy intake. Fructose does not cause weight gain when substituted into diets providing similar calories.
  • Overeating fructose could possibly be worse in the long run, based on one study that showed fructose disproportionately makes extra fat go toward visceral rather than subcutaneous fat stores. However, fat accumulation is usually the result of a long-term energy surplus rather than consumption of a particular food.
  • The amount of fructose in fruits and whole foods is generally low compared to foods sweetened with HFCS, so it is unlikely that consumption of these foods would lead to weight gain. Whole foods and fruits also contain other beneficial substances like fiber, vitamins, and polyphenols.
  • Longer-term studies suggest that high intakes of fructose may be harmful if they are paired with excess calorie intake and visceral (abdominal) fat accumulation.

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