Gout and Girth: A Sweet Relationship?

At Hampton Court, one of King Henry VIII’s sixteenth century palaces outside London, tour guides regale visitors with tales of Henry’s obesity and the miseries he suffered during flare-ups of gout – exquisitely painful episodes of arthritis that come from the buildup of uric acid crystals in joints.  Gout was known as “the king’s disease,” because it afflicted wealthy people who could afford the meats and sea foods that trigger uric acid crystal formation.   The guides also point out the “confectionary,” a corner room near the kitchen wing, and describe the sugar-rotted royal teeth produced by the then scarce sweetener.  The guides do not link Henry’s gout to the royal sweets, but perhaps they should.  Sugar is composed of equal parts glucose and fructose, and scientists are now beginning to link increased fructose intake not only to obesity and type II diabetes, but also to increased uric acid in the blood – a risk factor for gout.

What is uric acid

Some uric acid in the blood is normal, because every cell in the body makes uric acid out of purines, chemical compounds that come from the regular breakdown of DNA and RNA as cells recycle themselves.   Purines also come from many foods, but are particularly concentrated in red meat, organ meats like liver, many fish and shellfish, and yeasty beverages like beer and red wine.  Uric acid in the blood is not bad – it serves as a powerful antioxidant.  However, in some genetically susceptible people, uric acid levels become too high because they make too much, or  because their kidneys don’t excrete enough into the urine.

When uric acid crystallizes

Abnormally high uric acid levels in the blood, a condition called hyperuricemia, can be present for 10-20 years without any symptoms.  But just as minerals crystallize out of water in caves and form stalagmites and stalactites, uric acid can crystallize out of fluids in the body, forming microscopic deposits in tissues, especially kidneys, joints, tendon sheaths and skin.  The painful part comes with the inflammation that ensues when the body attempts to eliminate the crystals. The classic case of gout, also known as podagra, begins suddenly with exquisitely painful, bright red swelling in the joint space between the foot and the big toe. Symptoms last from days to weeks.

The swelling comes from inflammatory fluid in the joint space. Diagnosis of gout depends on withdrawing some of this fluid through a needle and examining it under a microscope, where the uric acid crystals show up as pointy spicules which bend light waves in an identifiable way. Fluid withdrawal can also relieve some of the pain, but the mainstays of treatment during acute attacks are anti-inflammatory drugs such as Indocin, ice and or heat, and plenty of water.  Prevention of attacks depends on efforts to lower uric acid levels, by diet, weight loss and use of medications that block uric acid production or increase its elimination in the urine.

Fructose is a building block for uric acid

For centuries, dietary advice about gout has revolved around foods high in protein.  But as numbers of gout cases climbed steadily over the last forty years and average uric acid levels in people without gout also increased, a correlation with increased sugar consumption began to emerge.  Scientists are now studying the relationship of sugar intake to uric acid and gout and also attempting to tie uric acid to hypertension, obesity and heart disease.

Sugar consumption was once rare to non-existent.  Table sugar, a mixture of the two simple sugars sucrose and fructose, came only from sugar cane, which originally grew only tropical regions.  Sugar’s spread around the world followed trade routes, and accelerated markedly after the discovery of the beet as a sugar source in the 18th C.  But the most dramatic rise in sugar consumption followed the invention of high fructose corn syrup (HFCS) in the 1970s. From work done so far, it appears that sugar’s fructose is a bigger culprit than its glucose in aggravating the metabolic syndrome (obesity, high blood pressure, heart disease and diabetes). And the metabolism of fructose actually produces uric acid.  

When the glucose/fructose mix of sugar enters the body, glucose is transported directly into cells for use, but fructose requires processing.  This requires energy, provided by ATP (adenosine triphosphate), and ATP breakdown produces uric acid. Eating fructose regularly also makes fructose easier to metabolize because it “induces,” or makes the body produce specific enzymes required to break it down.   For someone prone to overproducing uric acid, or someone whose kidneys excrete it inefficiently, a diet chronically high in fructose may not only provide the building blocks for uric acid, but also speed its production.

Cutting fructose may help – and will do no harm

Cutting purine-rich foods down in a diet helps many susceptible people remain gout free. There is no data yet on the effectiveness of limiting fructose intake on gout or hyperuricemia, but such a diet can do no harm. Limiting fructose sources to whole fruits would dramatically lower total fructose intake for most people. Fructose is the major sugar in fruits, but it is combined with fiber and vital nutrients and present in much lesser quantities than in sugar-sweetened beverages, soft drinks, baked goods and many processed foods. Even ketchup contains HFCS.

When dietary modification is not enough to keep people gout free, drugs that block uric acid production or increase its elimination help. Ideally, uric acid levels should be in the range of 3-6 mg/dl. Diet is important not only for those who have suffered acute gout attacks, but also for those who have high uric acid levels without any symptoms. Hyperuricemia warrants a good look at the amount of dietary fructose.

Henry VIII’s confectionary was a clue to the relationship of girth to gout.  As  uric acid research progresses,  blood tests for uric acid will probably become routine,  because high levels  often precede  the development of high blood pressure and Type II diabetes, even in people not susceptible to gout.


 Other Gout Facts

Many diuretics in common use raise uric acid levels and can trigger gout, especially the thiazide group.

Gout attacks commonly follow trauma or surgery because tissue breakdown produces purines.

Cancer treatments may also raise uric acid levels as tumor cells break down.

Uric acid levels increase in women after menopause and women rarely suffer from gout before then.

Uric acid levels in men rise at the time of puberty.

The Problem with Sugar: Insulin

This article is about insulin, not diabetes. Diabetic or not, you need to know about insulin. My epiphany about the importance of this hormone occurred when one of my children brought Micah, a friend with Type 1 diabetes, home for dinner. We had a healthy “Mediterranean” dinner – pasta tossed with olive oil, chicken, fresh tomatoes, and cilantro, with accompanying salad and French bread. And birthday cake.  Fresh from life in a college dorm, the young friend ate with gusto – at least two helpings of everything. We all did.  Later, I found him groggy and in need of two to three times his normal insulin dose. The epiphany was this: all the non-diabetics at the table that night required a lot of insulin to cover hefty carbohydrate intakes, but we were blissfully unaware of the consequences of over-indulgence. We did not have to fill syringes with extra insulin. Our pancreases did the work behind the scenes.

Awash in Insulin

Why was this realization an epiphany? Because we live in an age of excess, consuming large amounts of refined carbohydrates and frequently eating more than our energy requirements demand.  We are awash in insulin of our own making and need to understand this hormone’s central role in metabolism. More and more research links insulin to the chronic diseases of civilization: high blood pressure, heart disease, obesity, and Type II diabetes (the variety in which insulin is too plentiful and doesn’t work properly, as opposed to Type I, in which the pancreas fails to produce insulin).

How insulin works

Insulin is the hormone that moves sugar from the blood into all the body’s cells. Blood sugar comes from carbohydrates in food and from glycogen made by liver and muscles as a way to store a twelve-hour supply of sugar. When glycogen stores run out and little food is coming in, as in starvation or very low calorie diets, we make sugar, first from our muscle proteins and then from our fat.  The main goal of all metabolism is to keep blood sugar in a tight range – just right for the brain’s needs, because sugar is the only fuel the brain uses under normal circumstances. (It will resort to using ketone bodies, formed from fat in the liver during prolonged fasting or total carbohydrate restriction, but if sugar is available it is the preferred fuel).

Incoming dietary sugar elicits a burst of insulin from the pancreas. Insulin’s job is ferry the needed sugar to cells and to squirrel away extra sugar as glycogen and fat. Insulin is a lipogenic, or fat-producing hormone. Every time we overindulge, insulin goes into high gear to produce fat. It also raises triglyceride levels and lowers high density lipoproteins, exactly the changes in blood lipids that are associated with heart disease.

When insulin fails to work

Insulin is also mysterious. For unknown reasons, many people –   one in every three of us – have a tendency to become “resistant” to insulin’s effects. Their pancreases put out more and more insulin to handle routine blood sugar levels. No one knows what makes the insulin inefficient, though fat accumulation in muscle cells may be part of the problem.  This stage of “insulin resistance” goes unnoticed for years because there are no symptoms. Blood insulin levels are expensive to measure and difficult to standardize, so they are not part of any kind of routine, preventive screening.

Insulin promotes fat storage

High levels of insulin make fat storage and weight gain easier. Weight gain, particularly around the middle, promotes insulin resistance, and the pancreas responds with yet more insulin. A vicious cycle is underway.  Insulin resistance can become so pronounced that blood sugar escapes control and spills into the urine. Insulin resistance is now Type II diabetes, treated with medicines that help insulin work, and ultimately, with shots of yet more insulin.   Before this happens, and even afterwards, weight loss and exercise can reverse insulin resistance, leading medical researchers to believe that insulin resistance has something to do with abnormal energy processing in muscle cells. They’ve found that the muscles of some lean, healthy relatives of Type II diabetics show insulin resistance long before there is any fat in muscle, or abnormality in blood insulin levels.


In our sedentary age of super-sized, sugar-laced, low fiber meals, we produce far more insulin than our ancestors did. In addition, the genetic make-up of many people, particularly Hispanics, Native Americans and some African-Americans makes their insulin less effective.  We don’t measure insulin levels routinely. Instead, we concentrate on easily-measured cholesterol and fret about fat in the diet. At the same time we are in the middle of an epidemic of insulin resistance and on the verge of an epidemic of Type II diabetes, which is no longer just a disease of middle and older age. For the first time in history, type II diabetes is appearing regularly in children, teens and twenty year olds.

The average American fast food diet sets people on the road to obesity, insulin resistance and type II diabetes.  Lack of exercise keeps them there.In a world of easily available food that requires little or no work, the only defense against overeating is mental.  Education and self- discipline are the weapons. Insulin-requiring, Type I diabetics like Micah know how much insulin has to be paid out for a big meal. The rest of us have to visualize that syringe full of extra insulin and imagine tucking away excess calories as fat. We have to see ourselves requiring more and more insulin as time goes on and becoming unable to produce enough to meet the needs of an insulin resistant body. It’s enough to make that second helping seem less desirable and regular exercise more attractive.

Keeping insulin levels under control:

  1. Avoid weight gain
  2. Lose any extra weight
  3. Exercise 30 minutes per day.
  4. Eat regular, small, balanced meals, and 25-30gm/day of fiber
  5. Avoid the “white stuff:” Flour, sugar, white rice
  6.  If you are overweight and/or have relatives who have diabetes do all the above, and see if your doctor thinks a glucose tolerance test is warranted.







A Sweet Decision: Artificial Sweetener or Sugar?

“I would feel more optimistic about a bright future for man

if he spent less time proving that he can outwit Nature

and more time tasting her sweetness and respecting her seniority.E. B. White

         Little packets of faux sugar sit beside all convenience store coffee pots. Grocery store shelves are lined with lo-cal, no-cal, and no-sugar foods.  Authorities assure us that these staples of modern life are safe. Nevertheless, unease persists.  Should millions of people, including children, be engaged in an attempt to “outwit Nature?”  In deciding whether or not to participate in this vast modern experiment, there are two questions to answer:

1. Are artificial sweeteners necessary for me?

The first question has an easy answer. Artificial sweeteners are not necessary for anyone at any time. But for someone struggling with weight problems or diabetes, artificial sweeteners can add some “better living through chemistry.”  Bear in mind, though, that the only studies showing any positive effects on weight loss by the addition of artificial sweeteners are those involving serious attempts at long term dieting – the kind that involves lifestyle change. Casual, habitual users of sweeteners typically weigh more and gain more than non-users.  In addition, frequent consumption of sweetened foods and beverages aggravates the sugar addiction that drives so many poor food choices. Artificial sweeteners also contribute to elevated insulin levels.  As soon as the tongue perceives sweetness, a quick burst of insulin begins the body’s preparation for an influx of sugar (the “cephalic insulin repsonse”). When no real sugar appears, insulin falls back quickly, stimulating hunger. Or if food  accompanies the diet drink, the insulin helps make any excess calories into fat.

2. What is the likely harm if I choose to use them?

The question of potential harm is difficult to answer. Wading through the contradictory literature on safety studies of non-nutritive sweeteners is a confusing trek that exposes the influences of politics, power, money and fear on science. FDA approval of food additives, or designation of them as “GRAS”  – generally recognized as safe – does not make safety questions disappear. Saccharin (Sweet’N Low) for instance, is known to produce bladder cancer in rats, but human population studies show only “a trend” toward more bladder cancer if more than 6 packs a day are used.

Widespread use of any substance is very hard to tie to small changes in physiology or upticks in disease processes for which there are no clear, single causes. For instance, one of the worries about aspartame (NutraSweet, Equal) was its ability to cause brain tumors in rats. There was a  rise in human brain tumor rate that coincided with the introduction of aspartame in the early 1980s. But the increase may well have reflected better diagnosis due to the introduction of the CAT scan.  A more recent increase in brain tumors of high malignancy prompted some scientists in 1996 to call for a reevaluation of aspartame’s role, but other opinions prevailed.

Safety testing

Safety testing of individual sweeteners in bacteria and laboratory animals involves huge doses over months to years.  But only when the products reach the market does the most important test begin – long term consumption under varying circumstances by large numbers of people who have not been prescreened for other problems.  To make sweeteners more palatable, manufacturers often combine them in foods, exposing the consumer to chemical mixes never tested in the lab.  Anyone using artificial sweeteners regularly is a volunteer in long term safety experimentation, so wisdom dictates having at least a rudimentary understanding of the most common ones.


Saccharin, a petroleum derivative, is one of the oldest sweeteners. Time on the market has given it an aura of safety, but it has been used sparingly in soft drinks, making it less used than aspartame. A persistent group of scientists still rings the warning bell about saccharin’s carcinogenic potential and about its unstudied effects on fetuses and children. Even a weak carcinogen, they say is of concern over a lifetime of use.


Aspartame is dogged by the most complaints, including legitimate ones like headache and mood disorders and skin rashes, and unproven ones like links to Alzheimer’s disease and brain tumors.  Rare people with an inherited condition called phenylketonuria cannot tolerate one of the amino acids from which it is made. In 2002, a new version of aspartame without that that amino acid (Neotame) was approved but is not yet widely used.


Sucralose (Splenda) has the shortest track record. Better taste, heat stability that enables it to be used in cooking, and masterful marketing as “made from sugar” and “not absorbed”  gave Splenda 60% of the sweetener market by 2006. Eleven per cent of prepared foods on the grocery shelves are now sucralose sweetened. The additive does start out as sugar.  Chemical alteration replaces three parts of the sugar molecule with chlorine atoms, making a “chlorocarbon” that is structurally most similar to insecticides – but still called “natural.” On average, about 15% of Splenda is absorbed into the body. (The legal definition of “unabsorbed” applies if at least 80% of the product passes through the intestine unchanged.)  Test rats wound up with enlarged kidneys and livers, but so far, the large pool of human subjects seems to be tolerating the sweetener. Splenda is also not quite free of calories. While the chlorocarbon compound at the heart the sweetness has no calories, the added bulk needed to stabilize it is a mixture of carbohydrates – which contain about 12 cal/ teaspoon or 96 calories per cup.


Acesulfame-K(Sunette) is bitter tasting sugar substitute seldom used alone. It has undergone safety evaluation multiple times since the 1980s and is considered by some to have a poor test record

    Before you make your decision, consider one more thing. Eating real, whole fresh food rather than artificially flavored processed versions revives dormant taste buds. Smaller amounts are more satisfying,  allowing room for a few extra calories from naturally sweetsources.

Addendum: What about the “natural” sugar substitutes?

      Stevia, a no-calorie sweetener chemically extracted from plant leaves was in exile in health food stores since an anonymous complaint to the FDA in the early 1990s. Some say this was political exile since Stevia requires no patent. The beverage industry subsequently developed Stevia flavored products and the FDA changed its stance in Dec. 2008. There is already a long history of Stevia use in Japan and China, but expect to see it combined with other sweeteners to improve its vaguely licorice-like flavor.

Nectresse is the Splenda manufacturer’s entry into the natural market. It is derived from the monk plant and is 300 times sweeter than sugar, but must be combined with molasses and a sugar alcohol to make it work. It interferes with sugar absorption and the alcohol can ferment in the gut causing gas production. And yes, these plant derived substances have some calories – the FDA allows up to 5 cal/.5 tsp. in its definition of “no-cal.”

The Sweet Tooth: Pathway to a Broken Heart?

For the last half a century or more we have believed the dietary cholesterol theory about heart disease, a hypothesis (idea to be tested by experiment) that found favor with researchers, grant makers, doctors and drug makers. What if this theory is wrong? What if cholesterol in artery walls has less to do with dietary fat than with the way the body processes carbohydrates? What if refined sugars and grains are the dietary culprits? Could insulin, the master hormone at the center of all energy processing, be a better marker than cholesterol for heart disease?

What is blood sugar?

The first thing to understand about sugar is that the blood sugar is not the same thing as the sugar in your pantry. Or the sugar in soft drinks or the sugar in fresh fruit. Blood sugar is a simple molecule called glucose – a product of plants’ ability to convert the energy of the sun into starches, long chains of glucose linked together. When you eat a starch, the digestion process breaks down the chains into simple glucose molecules which circulate in your blood. Glucose is used by every cell in the body for energy, and is also made into glycogen for storage in liver and muscle.The sugar in your pantry is sucrose extracted from plants, specifically cane grasses and beets, by a refining process that concentrates and crystallizes it. Each sucrose molecule is a combination of one glucose molecule with another of fructose, a chemically different plant sugar molecule.

The taste for sweetness is innate and possibly addictive. Before the advent of refined sugar, indulging the sweet tooth was difficult. The only edible sources were berries and fruits and small amounts of honey guarded by nasty bees – all confined by climate and geography. Sugar made its way into the human diet slowly, spreading from the East to the West as the secret of this “liquid gold” made its way along routes of commerce.

Sugar and the diseases of civilization

With time and commerce, consumption of sugar and refined grains skyrocketed. The diseases of civilization – diabetes, heart disease and obesity – followed refined sugar, flour and rice around the world, appearing wherever old dietary staples were replaced by these “white” foods. By the 1920s, the Americans averaged 110-120 pounds of sugar per person per year. We inched up to 124 pounds by the late 1970s. Then came the Japanese chemical innovation that made high-fructose corn syrup (HFCS) a dietary staple. By 2000, HFCS bumped sugar consumption up to 150 lbs. per year, largely in the form of sweetened drinks.

High fructose corn syrup 

HFCS differs from sucrose because the ratio of fructose to glucose in corn syrup is 10% higher than in table sugar – 55:45 instead of 50:50. Some scientists believe that it is the remarkable increase in fructose consumption in modern times that correlates with the appearance of the metabolic syndrome – abdominal obesity, high fasting blood sugar, high triglycerides, abnormal lipoprotein levels and high blood pressure. If so, a 10% increase in fructose combined with a recent, large jump in overall sugar consumption may spell real trouble.
How can fructose cause trouble? Isn’t it the primary sugar of fruits? Yes, but eating an apple with a small amount of fructose combined with absorption-slowing fiber hardly nudges blood sugar up – a far cry from the blood sugar spike after 20 ounces of an HFCS sweetened beverage. Drink a coke, and about 60% of the glucose in the HFCS goes directly into the blood for immediate use, and 40 % into the liver for storage as glycogen. The fructose all goes to the liver for conversion into fat – released into the blood as triglycerides. The higher the fructose in the diet, the higher the triglycerides in the blood. Fructose is a “lipogenic” or fat-producing sugar, and long term consumption also raises LDL or bad cholesterol.

The problems with too much sugar

Once sugar consumption exceeds the small amounts nature provides without refining techniques, trouble begins. The different ways the body processes fructose and glucose combine to produce very efficient fat production. A rise in blood glucose prompts the pancreas to put out insulin to help ferry glucose into cells for energy use or storage. Insulin, like fructose, is “lipogenic” because it helps move fats into storage depots in three areas – the liver, fat tissue, and the walls of arteries. And as triglycerides are formed from fructose, insulin busies itself shuttling them around the liver and out into the blood. The pancreas then produces even more insulin to take care of the glucose – this is the phenomenon known as insulin resistance, part of the metabolic syndrome associated with heart disease.

Is it the cholesterol or the sugar?

The theory that cholesterol in dietary fat is the direct cause of cholesterol deposits in arteries requires a leap over the metabolic pathways that process simple sugars and are intimately involved in fat formation and storage – and over the fact that many people with low cholesterol levels have heart disease. Over the last half century, many researchers and doctors made the leap because they believed the theory. Just as important to widespread acceptance, though, were less scientific influences like the cheap availability of a test for blood cholesterol, the difficulty and expense of measuring insulin, and the dominance of researchers devoted to the dietary cholesterol theory over those who questioned it.

Medical history books contain an embarrassing array of once-unassailable theories and practices that have fallen by the wayside. Despite a modern sense of scientific invincibility, current medical ideas are not immune from error. Sugar and refined carbohydrates are not yet the poster children for the scourge of heart disease, but they may be a far better target than cholesterol. If the dietary fat theory gives way to the sugar theory, the massive push to lower cholesterol by diet and drugs may go into the books as one of those once-unassailable ideas that eventually fell.

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