Ketosis v.s. Ketoacidosis: Insulin makes the Difference

Ketosis is a word which you may have seen recently in print and online media, usually in material about a very low carbohydrate diet in which most calories come from fat and protein. One recent headline alluded to a plan by the Pentagon to increase military fitness by imposing the “keto diet” on some of its soldiers. But you might also have the impression that there is some controversy around the diet, and that ketosis, whatever it is, might not be good for you. After all, it is very similar to that word ketoacidosis which is associated with poorly controlled diabetes, the problem that put your friend’s daughter in the hospital ICU for a week. In fact, both ketosis and ketoacidosis refer to physiologic body states that occur when come chemicals called ketones are produced from normal metabolic processes that produce energy from the body’s own fat. The circumstances surrounding ketone production determine whether ketones cause ketoacidosis (bad) or ketosis (not so bad but maybe not so good over a long period of time).

How your body produces energy

Most of the time you are utilizing at least some fat to create energy and producing ketones in small amounts as the fats are metabolized. At the same time, the bulk of your energy is derived from the carbohydrates you eat, all of which, even the “healthy” grains, vegetables and fruits, become a simple sugar called glucose in the process of digestion. That is correct – for the most part, you burn sugar to produce energy. Under normal circumstances, with sufficient food and regular eating schedules, some glucose is burned immediately by all parts of the body for energy production. Any remaining glucose gets shuttled off to the liver and muscles to be clumped into long chains called glycogen and stored for use between meals. These reserves last for about 24 hours at which point your metabolism switches over to fat burning, and to breaking down a little protein, mainly from muscle, to supply the liver with building blocks for making more glucose.

The brain has special needs

At this point, you must eat again or rely on free fatty acids from the triglycerides stored in your body fat. The brain, however cannot burn free fatty acids. But it can burn some of the ketones, called ketone bodies, that come from the breakdown of triglycerides. By about three days of starvation, the brain is a ketone burning organ, supplemented by a little glucose constructed in the liver from amino acids given up by proteins. The body is in a state of ketosis, with excess ketones exhaled, giving the breath a fruity odor, and released in the urine, turning a dipstick stick test positive.

Acidity makes the difference

Ketosis is not ketoacidosis. Ketoacidosis appears when the acidity rises in all the body’s tissues while it is in a state of ketosis. Acidity is measured as pH, and a fall in the body’s pH signals rising acidity. Outside a narrow range of pH, the body’s metabolic workings begin to fail. Rising acidity produces symptoms like rapid breathing, nausea, vomiting, abdominal pain, low blood pressure, mental impairment, lethargy, heart arrhythmias and ultimately, if uncorrected, death. In otherwise healthy people, diets that promote ketosis by restricting carbohydrates do not appreciably change the body’s pH, despite the acid nature of ketones and other breakdown products of triglycerides. What keeps severe acidity and its dire consequences at bay? In short, insulin, the central hormone of metabolism.

Insulin keeps the brakes on fat burning

Insulin is secreted by the pancreas in response to eating carbohydrates. In fact insulin is such a reponsive hormone that a burst appears from the pancreas in response to anything sweet in the mouth (the so called cephalic insulin response that prepares the gut to receive expected incoming carbohydrate, even when the sweetness is artificial and no carbs arrive in the stomach). In addition to its role escorting glucose into cells for energy production, insulin keeps the brakes on fat burning. When insulin circulates at normal or high levels in response to carbohydrate ingestion, triglycerides remain locked in fat cells, unavailable for energy production. As night falls and eating ceases, the liver and muscles break down their glycogen to glucose to keep the supply up. When this supply dwindles, insulin levels fall, unleashing fat burning. Free fatty acids and ketones appear in the blood, but in a controlled manner, unless insulin disappears altogether. Then the brakes come off fat burning, fatty acids and ketones flood the system, and their acidity begins to drop the body’s pH.

Ketoacidosis comes from insulin’s diappearance in type 1 diabetes

Type 1 diabetics are the most at risk for ketoacidosis because immune attacks against the insulin producing cells in their pancreases severely diminish or obliterate insulin production. Their blood sugar levels rise because sugar cannot get into cells. Fat burning comes to the rescue for energy production, and, with little or no interference from insulin, free fatty acids and ketones pour out into the blood. In new Type 1 diabetics, before treatment with insulin, major weight loss is very common – as is presentation to an emergency room in a state of profound ketoacidosis, requiring intensive medical care. Once patients are stabilized, urinary ketones are a useful guide for adjusting insulin dose– their appearance means more insulin is needed.

Type 2 diabetes is a different problem

Type 2 diabetics have a different problem, called insulin resistance. Their cells do not allow insulin to bring glucose in from the blood. In an attempt to compensate, their pancreases make more insulin. Blood glucose levels rise, but at the same time high levels of insulin block fat breakdown, preventing the release of large amounts of potentially acidifying fuels, and diminishing the risk of ketoacidosis. But if a crisis such as trauma, infection, or surgery occurs, sugar levels can rise to extraordinary levels in Type 2 diabetics, causing huge amounts of water to be lost in urination as the body passes the sugar out through the kidneys. Severe dehydration and electrolyte abnormalities make this condition, called hyperosmolar hyperglycemia, a crisis requiring intensive care, even without acidosis. When insulin production begins to fail in Type 2 diabetics, ketoacidosis does occur and type 2 diabetics account for 20-30% of ketoacidosis cases in hospitals. One class of Type 2 diabetes drugs, the SGLT2 inhibitors known as gliflozins, has been reported to trigger ketoacidosis.

The caveat about ketosis as a dietary strategy

There is some concern, from epidemiological research, that when a very low carbohydrate diet is continued over the long term, chronic ketosis may trigger insulin resistance, the underlying problem in type 2 diabetes. Insulin resistance is not well understood, but it is associated with a cascade of health problems associated with metabolic problems. If chronic ketosis does somehow trigger insulin resistance, the enthusiasm for deliberately inducing ketosis to lose weight and improve fitness will wane. The word ketosis will fade back into the scientific world.

Posted by medical plaintalk

Physician turned medical writer.

Alzheimer’s Disease: A Power Failure?

Like Willy Sutton, the bank robber famed for his explanation of why he robbed banks (because that’s where the money is), Alzheimer’s disease researchers have aimed most of their efforts at the well-known, visible pathology of the disease, the collections of debris scattered among the dying cells in the brains of patients suffering from the dementing illness. Made of a protein known called beta-amyloid, these plaques are the cause of the progressive death of brain cells and consequent loss of mental function – or so it has been thought. Research focus on amyloid plaques has been disappointing, though, yielding neither effective treatments nor preventive strategies. Moreover, the dramatic rise in the incidence of Alzheimer’s disease (AD), from 2% of people over age 85 in 1960 to 50% in 2000 indicates that something else is in play, something other than bad genetic luck that supposedly causes beta-amyloid to accumulate and nerve cells to die.

Energy production in the brain

As attention has turned to other potential causes of AD, older research findings seemingly unrelated to AD have assumed new importance, particularly discoveries related to brain energy metabolism. The preferred fuel for the brain is glucose. Until the 1980s, researchers thought that the brain, unlike other organs, did not need use the hormone insulin to allow glucose to enter its cells. But in the 1970s insulin receptors were discovered in brain cells and insulin was found in the spinal fluid, implying that the brain did indeed use the hormone. Because progressive resistance to insulin and difficulty getting glucose into cells to provide energy are the hallmarks of type 2 diabetes, and because the rise in AD incidence paralleled rising rates of type 2 diabetes in the last few decades, researchers began to wonder if AD might be rooted in insulin resistance and impaired energy production in brain cells. Insulin resistance in the brain might also explain the results of glucose metabolism studies in the brains of people at high genetic risk for AD, showing as much as 25% decrease in the use of glucose in areas concerned with memory and learning – long before any symptoms suggestive of AD have appeared.

Insulin resistance

By 2005, the idea that insulin resistance in the brain plays a significant role in the development of AD gained traction. Since not all type 2 diabetics get AD and not all AD patients have type 2 diabetes, insulin resistance cannot be the sole cause of AD. But a high blood insulin level is one of the two biggest risk factors for the disease. The other is a genetic factor – the gene for the E4 version of a protein called apolipoprotein B (apoB). Like insulin, apoB’s function is moving the building blocks for energy production into place in the various cells of the body. ApoB is like a delivery vehicle, packed with fats and cholesterol which are necessary for building the cellular machinery in the brain and providing fatty fuel for use when glucose is unavailable.

The tie between glucose, insulin and amyloid

Does impairment of glucose metabolism in the brain have any relationship to the classic pathological components of the disease – the amyloid plaques littering the brain, the destruction of nerve cell architecture, and the non-specific inflammatory changes? There are tantalizing clues. In the brain amyloid protein is a normal waste product. What is not normal is its accumulation in clumps around nerve cells. Beta-amyloid is usually broken down by an enzyme called IDE, insulin destroying enzyme. IDE breaks down insulin much more readily than it does amyloid proteins and when insulin is present in high amounts, the amyloid waits longer to be cleaned up and precipitates out of solution, forming clumps. Uncleared amyloid also prevents insulin from attaching to nerve cells to let more glucose in, depriving them of fuel.

Competition for IDE may not explain beta-amyloid accumulation completely, but it is a link between insulin, glucose metabolism and AD. In addition, high levels of glucose in all parts of the body prompt the development of abnormal collections of proteins/glucose combinations called advanced glycation products which trigger inflammatory damage to tissues in all organs. The brain is no exception.

A link between poor sleep and AD?

Sleep is another subject beginning to gain attention in the prevention and treatment of AD. Lack of good sleep contributes to the development of the metabolic syndrome, including type 2 diabetes, though disruption of normal hormonal rhythms. In normal people and in people with sleep apnea, sleep deprivation produces measurable impairments in working memory, thinking speed, attention, vigilance, and higher cognitive functions – the same functions affected by dementing illnesses such as AD.

Reasons for optimism

Do changing theories about AD have any practical consequences? Indeed. First, there is more reason for optimism about the future. If AD rates have risen because of changing dietary habits and lifestyles, we can change them again. The factors known to produce the metabolic syndrome are weight gain, lack of exercise and poor diet. Regular exercise is recognized as a deterrent to the development of AD. Some people are beginning to feel that the low fat dietary recommendations must also be changed since they have resulted in diets high in processed foods and carbohydrates, and low in foods with high amounts of antioxidants which counter inflammation. Fat metabolism, abnormal in the metabolic syndrome, is also important in the brain, which contains 25% of the body’s cholesterol. It needs sufficient healthy fats in the diet for normal function.

The second practical implication of the changing view of AD is the application of known drug treatments for type 2 diabetes, both for attempted prevention and for treatment of AD. Clinical studies in AD patients are already under way, using medications that improve insulin resistance. Intranasal insulin has also been tried. It is delivered directly into the brain, without fear of lowering body glucose levels and has shown some promise in improving AD symptoms. These approaches are entirely new and evidence of shifting focus in research. If Willy Sutton were an AD researcher he would be changing his targets.

Terminal Lucidity and Lucid Intervals

Caregivers of Alzheimer’s patients have long reported episodes of the patient returning briefly to “themselves,” for periods of hours to days. Some dramatic cases of such returns have been reported in the terminal phases of life. All of these cases have fallen into the “we don’t know why that happens” category of clinical observations. The concept of brain cells failing to function because of lack of energy is one that fits the appearance of lucid intervals better than a theory of the disease that implicates cellular destruction alone as the underlying cause of symptoms.

Arch Gerontol Geriatr. 2012 Jul-Aug;55(1):138-42. doi: 10.1016/j.archger.2011.06.031. Epub 2011 Jul 20. Terminal lucidity: a review and a case collection.

Nahm M¹, Greyson B, Kelly EW, Haraldsson E.

Posted by medical plaintalk

Physician turned medical writer.

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.

Epidemic

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:

Avoid weight gain
Lose any extra weight
Exercise 30 minutes per day.
Eat regular, small, balanced meals, and 25-30gm/day of fiber
Avoid the “white stuff:” Flour, sugar, white rice
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.

Posted by medical plaintalk

Physician turned medical writer.

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

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

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.

Splenda

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

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.”

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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