We love it. As a people Americans eat 66 pounds of added sugar a year per person. Each one of us eat that much added sugar. Yes, that much table sugar, sucrose, the bad stuff.

It may be bad but I love it, passionately, and with the fondness only time can add to a relationship. Frankly, only the writing of this site put me on to the dangers of excess added sugar. A physician all of my adult years yet blithe enough about added sugar I knew its main drawback as mere obesity. Now I know better and plan to leave it be and live my life without its company.

The pretty graph at the right comes from the US government’s five year report on the diet of the American people. Men and women eat far more sugar than ideal, especially during childhood and early midlife. Although you might think otherwise, women are no better or worse than men in this one special behavior.

Still life with sweetmeats by Georg Flegel, German, Olomouc (Olmütz) 1566–1638 hangs in the Städelsches Kunstinstitut und Städtische Galerie. The image is available for public educational useNeed I say why it fits this article?

What is Added Sugar?

Added has a special meaning. It means not natural to the food. Manufacturers have to add it into the food. You will know they did it when you see sugar on the ingredient list. They name sugar so many ways you may miss it altogether.

Let’s start with the proper common names. Glucose and dextrose are two names for one sugar. It is the main sugar in our blood and the main sugar in starch. Fructose comes in fruits and is altogether different in chemistry and in the way our bodies metabolize it. Sugar, what we buy in sacks, is the two molecules, glucose and fructose, linked together to make one bigger molecule containing both. So when you eat table sugar you are eating glucose and fructose. The proper name for table sugar is sucrose.

Invert sugar is simply sucrose broken into its two components – glucose and fructose. It tastes sweeter and does not crystallize as much as sucrose so bakers may prefer to use it. Same calories, same molecules.

Here, I use the common name ‘sugar’ to cover all of the sweet things, and the special names – glucose vs. fructose – only when we need them.

Why Do Stone Formers Care?

When you eat sugar, your urine calcium will rise. And, as an added insult, your urine volume will go down.

Urine Calcium Goes Up

Normal People

This figure is from 1969, New England Journal of Medicine. The scientist, Jack Lemann, gave normal people 100 gm of glucose or sucrose in water where the arrow points. Before the sugar, the four 20 minute ‘control’ measurements, urine calcium loss – vertical axis was stable. After the sugar, urine calcium was up a bit even at the first experimental period – 20 minutes after the sugar, and kept going up to peak at about 60 – 120 minutes. That peak waned appreciably by 120 minutes.

CaOx Stone Formers

Even during the control periods their urine calcium was higher than the normals. We know why. Because they had idiopathic hypercalciuria, the genetic problem that is so common in calcium stone forming people.

After the sugar load their urine calcium rose far above the normals and stayed up about as long – two hours. It is not so much that they raised their urine calcium by a greater increment as that they started higher so their peak was a lot higher than normal.

Relatives of Calcium Stone Formers

Their control urine calcium losses were perhaps even higher than the patients who formed stones. We now know that idiopathic hypercalciuria is hereditary, and presume these relatives carried the trait but had thus far escaped the stones. The sugar load raised their urine calcium just as for the other two groups.

Urine Volume Goes Down

All of the subjects drank a lot of water during this study so urine could be reliably obtained at 20 minute intervals. The patients and relatives had flows of about 15 ml/minute, the normals about 12 ml/min. With the sugar loads, urine volume fell by 4 ml/minute in the patients and relatives but only by 1 ml/minute in the normals. As a result, urine volumes fell as urine calcium rose – a perfect storm for stone formation. This would be a recipe for high urine calcium concentration.

Urine Calcium Concentration Goes Way Up

Just as predicted, urine calcium concentrations rose remarkably in the patients and relatives. And fast, too. In even 20 minutes urine calcium concentration peaked in some of them. By contrast, the normals showed almost no rise in calcium concentration.

This site teems with articles about supersaturation as the final pathway connecting excretion rates to crystal formation. Here is the perfect reagent, the ideal foodstuff for raising calcium supersaturations. What better than to raise urine calcium and at the same time lower urine volume?

The Calcium Comes From Bone

The glucose or sucrose drinks had no calcium in them. None. So the extra calcium losses into the urine could not come from food. The only storage cabinet for calcium in our bodies is our bones. So sugar loads can deplete bones of their mineral. Perhaps it would take a long time to matter. But our lives have a lot of sugar in them.

Worse, stone formers have a higher than average risk of bone disease with fractures. At least part of that increased risk arises from idiopathic hypercalciuria. The urine calcium loss in IH arises from reduced renal calcium conservation. In these two graphs, the sugar effect was as large in those with IH as in normals. But because the effect began from a higher baseline of calcium loss, the total loss from sugar was larger.

The Sugar Acts On the Kidneys

If from this you expect that the sugar loads reduce kidney calcium conservation, your expectation is correct. The authors measured glomerular filtration rates during all of the periods shown on the figures. Sugar did not change it. The filterable blood calcium – for those of you into this kind of thing – actually fell slightly with sugar (-0.04 mmol/l) in each group, so the increase of urine calcium had to come from a reduction of kidney cell calcium reabsorption.  In other experiments, Lemann lowered calcium filtration and proved that the increased urine calcium arose from reduced tubule reabsorption. This mechanism is exactly parallel to that of idiopathic hypercalciuria, as we have shown in our own work here. But we do not know exactly where along the nephron sugar acts, nor precisely where the defects are in IH itself.

Why Everyone Should Care

Masses of experimental data going back into the 1950’s indicate that fructose – one half of the sucrose molecule and therefore of table sugar – causes diabetes and lipid disorders. It does this not simply because of obesity, but because fructose metabolism differs from that of glucose. But most of the evidence comes from animal experiments that might not fully mimic human behavior.

Perhaps for this reason, Kimber Stanhope and her colleagues performed what seems to me a well designed human experiment asking if fructose consumption can indeed cause these undesired consequences. Her paper reviews the main prior evidence, so I present here mainly her results. I believe the article is free access.

Let me say here, she had powerful and supportive colleagues essential to the final research. Alone, she nor anyone else could possibly accomplish what this paper reports. But she was given the pride of first authorship by those she worked with, and so, for brevity, I refer to what she did, and what she found. Though all the while it was they, even so, without her would they have come together to construct this mighty work?

Who She Studied

Men and women of average age 50 – 55, and BMI ranging from 28 to 30. Essentially chubby and middle age. They were well as far as they knew and had normal blood glucose and insulin levels.

What She Did

During a two week inpatient (meaning the subjects had to live at the research center and consume identical, specifically formulated meals) baseline period she performed a set of complex measurements that included measuring insulin responsiveness, visceral and subcutaneous fat, and hepatic lipid production. This was followed by a 10-week intervention, during which subjects received 25% of their energy requirement as beverages sweetened with either glucose or fructose.

During the first 8 weeks of intervention, subjects lived at home and consumed the beverages along with their usual diets. During the last 2 weeks, they again lived at the research center and consumed the beverages with specifically formulated meals that were as identical as possible to the baseline meals, except that bread, pasta, and rice calories were replaced with the glucose or fructose calories provided by the beverages.

In other words, as best she could, during the first 2 weeks and final 2 weeks of the study, she kept their diets similar with the exception of the kind of sugar – glucose vs. fructose. Precautions were taken so no one knew which. During this final 2 weeks of the study,  she repeated all of her measurements so she could compare how each person changed in response to the glucose or fructose consumption.


What She Found

Fructose Increased Visceral Fat

During the eight weeks of the study when the subjects lived at home and consumed the glucose- or fructose-sweetened beverages with their usual diets, the groups gained comparable amount of body weight (about 1.4 kg) body fat (measured by DEXA).

However, with the help of John McGahan, one of the leading radiologist researchers in the country, she specifically investigated fat gain in the abdominal area using the belly button as a landmark. Eight weeks of fructose but not glucose raised total abdominal fat content significantly (VAT). Although the increase of total fat from glucose was not significant, the increase of subcutaneous fat (SAT) was.

By now everyone who reads health magazines or newspapers knows that it is visceral fat that can cause insulin resistance and blood lipid disorders. Subcutaneous fat concerns us for mainly cosmetic reasons. That is not to say visceral fat has no cosmetic effects. It enlarges bellies and waistlines.

Fructose Increased Blood Triglycerides

What are Triglycerides?

Decades of health advice have trained us to watch blood cholesterol but recent evidence implicates triglycerides as perhaps as dangerous or worse for blood vessels. Even more, high triglycerides appear related to all cause mortality including cancer. The main evidence comes from recent meta analyses such as this one, and all such are suspect as being mere observations. These suspicions may be confirmed or allayed by a current trial that tests effects of icosapent ethyl a drug that selectively lowers triglyceride levels, asking if it reduces mortality. In the meantime, suspicion is enough one might want to avoid foods that increase triglycerides.

What Fructose Did to Blood Triglycerides

Unfortunately that is precisely what fructose does. It raises blood triglycerides.

On the left of this large figure, those treated with glucose showed no change in their blood triglyceride levels. Each curve traces out multiple blood measurements

of triglycerides throughout 24 hour days at time 0 and after 2, 8, and 10 weeks of glucose thereafter. The message is easy. All four curves melt together. You cannot tell them apart. This means that glucose had no effect.

But fructose raised triglycerides, a lot. At baseline, the black 0 week curve in the right panel, those who would get glucose and those who would get fructose had similar curves. After weeks of eating fructose, triglyceride levels rose much more with meals and the total triglyceride exposure to blood vessels, the region under the curves, rose a lot.

Why Does This Matter?

Does this mean that fructose causes early mortality from vascular disease? Perhaps. Trials of selective lowering of triglycerides will help decide. But other kinds of data have linked added sugar to disease for decades, and triglycerides may well be only one part of the harm sugar can do. I am not an expert on lipids or on mortality from added sugar. My core skills concern kidney stones and associated bone diseases. But other writers have expertise about the broader damage from sugar. A recent book by one such presents a lot of the main information. The Case Against Sugar’ by Gary Taubes seems the best source, to me and this NYT reviewer.

Elsewhere on this site I have written about earlier public statements about sugar and health, and about the scandals concerning the sugar industry’s efforts to suborn scientists into outright dishonesty. 

Fructose Increased Hepatic Lipid Production.

Where do the extra triglycerides come from?

The liver, of course, so you might think the graph above sufficient.

To think so ignores the character and behavior of experimental scientists. Yes, it must be the liver, but we need to prove that. Why? Because it might be otherwise and knowledge fail of its purpose to disclose the workings of nature. So, with considerably more effort than it took to measure the triglycerides in blood, she found and executed ways to measure hepatic lipid production.

This graph shows change from baseline (week 0) to after weeks of fructose or glucose. The units for the change in hepatic liver production are percent of the baseline.The change in percent from baseline is plotted vs. time of day. The points are the averages of all of the people who ate the extra glucose or fructose.  ‘DNL’ refers to de novo lipid production. This means producing lipids not from other lipids but from their constituent precursor molecules.

One need not be scientifically trained or even that observant to understand the results this rather bold and spare graph presents. The fructose averages tower over glucose. Whereas glucose raised lipid production by about 2 percent, sugar raised it by 8 percent. Keep in mind that both groups gained the same amount of weight, and both groups had eaten the same modest excess of calories from carbohydrate. Moreover, both groups had consumed identical diets for 7 days prior to both the baseline and intervention measurements.The only difference is in the fructose.

Fructose Caused Insulin Resistance

Resistance to the action of insulin powers adult onset diabetes. But insulin resistance itself may well arise from the effects of the visceral fat cells whose numbers fructose increases. The linked review is not the most recent I can find but among the most frequently cited and by outstanding scientists writing in a premier journal. Given the increased visceral fat stores and abnormal lipid metabolism from fructose one might well expect insulin resistance.

What is Insulin Resistance?

But what exactly is insulin resistance and how will we know it?

It is precisely what its name says. A sugar or food load will evoke insulin release from the pancreatic beta cells. That insulin normally causes prompt disposal of serum glucose into cells – mainly muscle. If cells resist the action of insulin, blood glucose will remain elevated over an abnormal time. LIkewise the beta cells will produce more insulin because they sense the high glucose. So you will know insulin resistance from a prolonged disposal of a glucose load despite a higher than normal amount of insulin in the blood.

Blood Glucose After a Glucose Load

Weeks of extra glucose enough to raise body weight also raised blood glucose after an oral glucose load. Take a look at the upper left panel. The baseline, or week 0 curve lies lower than that from 9 weeks. None of the individual means differed from each other, and the total area under the 9 week curve did not surpass the 0 week curve. But even so, glucose weight gain did something. Maybe gaining weight itself has some drawbacks.

Fructose feeding did a lot more. The 9 week curve rises a lot higher above the 0 week curve; take a look at the upper right panel. The stars mean the points differ more than by chance – so called statistical significance.

Now, compare the 0 week curves from the glucose and fructose groups. They would overlap if you could place one on top of the other. If anything, the week 0 curve of those who eventually got fructose seems a bit lower.

Blood Insulin After a Glucose Load

Here, fructose differs even more dramatically from glucose. The people who ate the extra calories as glucose showed no change at all in blood insulin after a glucose load. The left lower panel shows how the week 0 and week 9 curves overlap completely.

But those who ate their extra calories as fructose had a remarkable increase in insulin output. If you combine their higher blood glucose and blood insulin levels you have the very make and mark of insulin resistance: Glucose stays too high and all the while the beta cells provide more insulin than normal. Why did the extra high insulin not lower the blood glucose? Insulin resistance.

Should One Research Paper Matter That Much?

It would not except that decades of research have all pointed in this same direction but using mainly animal models or studies of people who had already developed insulin resistance. By contrast, this was a trial, a trial of fructose as against glucose. And the result disfavors fructose as a chemical that can and does produce lipid abnormalities and insulin resistance – in humans otherwise normal.

It is as if a long suspected toxin were tried directly in humans to see if what we thought it could do by way of harm might be caused by the giving of it. Were fructose some unnatural chemical, who would permit such a trial unless that chemical had some special value that made toxic effects acceptable – think about chemotherapy drugs. But fructose is a food, a nutrient we all eat. So its toxicity could be tried as if it were a drug.

The answer: It causes lipid disorders and insulin resistance. We should eat as little as possible.

Did I Review Her Work Correctly?

You could say with some justice that I am not an expert on sugar or lipids and perhaps swimming in deep and unaccustomed waters here. You would be right to say so. Being prudent I asked the author for the courtesy of her review, which she gracefully provided. The text contains her edits, and I have her permission to say that with those edits in place I have presented her work properly.

How Much Added Sugar Can I Eat?

The Center for Disease Control echoing the 2015 – 2020 US recommendations has clarified that the goal is less than 10% of calories as added sugar. So, if you eat 2000 calories this would be 200 calories. Sugar has 4 calories per gram which makes 50 gm of added sugar a day. This example fits for a good sized adult man in midlife. A woman would usually eat less – 1200 calories, making added sugar 120 calories or 30 gm/day. By law labels presently show sugar in grams but will soon change to percentage of total calories.

So, all my loves have to go. Way too much sugar.

It is Time to Say Goodbye

Ice Cream

Ben and Jerry’s ice cream contains 26 gm in 1/2 cup, and I have never eaten less than 1.5 – 2 cups for dessert. You know sugar has been added by looking at the ingredient list. For example, sugar is the third item, meaning more important, and also the fifth and later as cane sugar. So of the 20 gm much is added.

I picked this ice cream not because it is worse than others but because I love it, and eat it. However, as in the title, I am breaking up with Ben and Jerry’s, filled with regrets and loving memories.


In general honey contains about 25 gm of glucose/100 gm of honey and between 40 and 50 gm of fructose. So it offers no advantage over table sugar; in fact it has more fructose and is therefore a poorer choice. Too bad.

Maple Syrup

A typical pure Maple syrup contains about 67% by weight of sucrose – table sugar. It is not added. It is made by the maple trees. But as we removed almost all of the water to make the delicious concentrate we put on pancakes, and waffles, and who knows what else, we essentially made liquid sucrose. The maple flavoring is sheer delight, but another love must end.

This one is serious. Pancakes and waffles are nothing more than sponges to soak in maple syrup. The syrup tastes best when warmed. And poured over buttered cakes, they absorb the syrup that blends with the butter into paradise. To give this up seems almost beyond the possible.

Cookies, and Cakes, and Pies, and Candy

All those cookies, filled with chocolate bits – dark and white chocolate, walnuts, butter. And cakes – my favorites; chocolate cake, yellow cake with chocolate icing. Pie, even, though it is a trailing third.

Did I say candy yet? A universe here, the very essence of luxury and happiness. Did you know I can read the little squiggles on the tops of chocolates that say what is inside? And the shapes, they also let you know what you will bite into.

What About Fruit?

All that saves me is volume. Fruit has fructose, of course. Look at the name. But dilute. You need a lot of apples or pears to make up what you get from all the wonderful stuff I just wrote about. But there is a way. You can throw 8 apples and 4 pears into a blender and make a smoothie. Throw away the pulp and drink the pure stuff. That can do it, if you get the pure juice away from all that fiber. No. Not for me.

What Will I Do When I’m Alone?

There is always fruit. Up here in Michigan the blueberries and peaches have divine qualities. But only in Summer. Fruit otherwise seems plain and foreign to one who has known the love of sugar. I could poach an apple, or a pear. Some have cheese for dessert, or nuts. Some have nothing – so spare, so austere.

And smoothies – I just said no. I mean no.

Have just a little – did someone suggest that to me? A nibble of candy? A cookie with walnuts and white chocolate bits?

That nibble would tempt me back to where I am, a hopeless addict.


So, it is goodbye.

What Will You Do?

Will you say goodbye? Join me in misery for sake of better health? Let me know.

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