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December 21, 2010

The Integrated Supplements Newsletter - A Diet For Long-Term Weight Control And Optimal Health Part 2 - The True Role of Sugar in Weight Gain, Diabetes, and Metabolic Syndrome

HeaderPicSep10 At first blush, it’s tempting to indict sugar as a major contributor to the rampant rate of obesity and related disorders that have befallen Western civilization in recent decades. In the U.S., per capita intake of sugar, after all, has increased more or less in step with rates of overweight and obesity. But, while our intake of sugar has increased during this time of increasing weight gain, the true role of sugar in obesity (and in related disorders such as diabetes) is probably quite different than most people imagine.

For decades, and with no small degree of zealotry, many health writers have warned against the dangers of refined sugar consumption. Continuing this trend recently, we find that fructose and fructose–containing commercial sweeteners such as high–fructose corn syrup are often aggressively demonized as unique contributors to the modern obesity epidemic. While it is true that refined sugars, which lack the nutrients needed for their metabolism, are sub–optimal sources of calories, many researchers and health writers have condemned sugars with such fervor, that the true nutritional roles of all sugars (especially sugars which are components of whole foods) have been hopelessly obfuscated. The faulty logic often employed by sugar’s detractors exposes some fundamental misunderstandings regarding sugar and carbohydrate metabolism. As these misunderstandings are perpetuated by repetition in the scientific and popular literature alike, it’s easy for the expert as well as the layperson to lose perspective on the amounts and types of sugars and carbohydrates which have a place in a healthy diet.

The existing data on food consumption in the U.S. seems to clearly indicate that starch (grains in particular) and polyunsaturated fats (i.e., seed oils) are far more likely to be contributors to obesity than sugar. The consumption of starches and polyunsaturated fats have both increased to a far greater extent than sugar consumption over the last four decades; and unlike sugar, the intake of both has increased not only in absolute quantities, but as a percentage of overall calories. In addition to such epidemiological data, decades–worth of laboratory research investigating the metabolic effects of sugar, starch, and polyunsaturated fats provide further evidence of what the food consumption data clearly shows. Ultimately, those who are too quick to indict sugar are doing a disservice by diverting attention away from these other, more significant, causes of obesity and weight gain.

Unlike the mixture of glucose, fructose, and sucrose found in fruit, for example, starches are all, ultimately, digested into glucose. In the previous edition of the Integrated Supplements Newsletter, we saw how the human brain is designed to respond positively to glucose – its valued fuel source. We saw as well that, in many respects, the brain’s response to glucose is so powerful as to mimic its response to addictive drugs.

The biological imperative to consume glucose likely served our ancestors well as a hedge against starvation – which may be a clue as to why the consumption of starch so greatly stimulates appetite. In modern times, however, where starvation is rarely a threat, an excessive appetite and excessive intakes of starch often appear to impart biological effects conducive to weight gain and metabolic syndrome.

From the anthropological and addiction research we can surmise that an important goal of any diet is to supply our body and brain with a consistent enough supply of fuel so as not to trigger biological defenses against starvation. In so doing, our appetite will naturally come under control, and will more likely represent the actual energy needs of the body. In practice, this leads to weight loss success without weighing or measuring portions, and without calorie counting.

Despite the negative attention it’s received in recent years, fructose may play a unique role in diets geared towards weight control and optimal health by countering the negative effects of glucose and starch upon appetite, weight gain, and numerous markers of metabolic syndrome.

Ultimately, our dietary goal is to foster optimal cellular energy production which equates to the sort of vigorous and efficient metabolism needed to burn fat and keep weight in check. To begin to construct such a diet – one that ensures long–term weight control and optimal health – it’s clear that a more nuanced understanding of sugar metabolism is desperately needed.

Sugar in the U.S. Diet

It’s common knowledge that consuming an excess of calories can lead to weight gain – and where Americans have been consuming an increasing amount of calories from sugar in recent decades, it’s logical to assume that this extra sugar could lead to increases in the rate of overweight and obesity. After all, the consumption of refined sugars has risen in step with the obesity epidemic during the past several decades.

But it’s important to realize that the average daily caloric intake has increased over the past several decades as well – and the majority of these extra calories aren’t coming from sugar. Fruit intake has remained constant, and the data shows that refined sugar intake, when expressed as a percentage of overall caloric intake, has actually declined during the time period from 1970 to 2008:

Study Link – Straight talk about high–fructose corn syrup: what it is and what it ain't.

Quote from the above study:

In fact, use of added sugars as a fraction of daily calorie intake actually decreased slightly, along with vegetables, dairy, and meat, eggs, and nuts

In other words, as the above graphs illustrate, foods besides sugar, such as oils and grains (the consumption of both of which has increased significantly in overall amounts, and as a percentage of overall calories) are likely to shoulder more of the blame for our modern obesity epidemic than sugar.

Additionally, a closer look at the animal research which we looked at in the last Integrated Supplements Newsletter shows that “sugar addicted” rats (rats which are fed in such a way as to develop a voracious appetite for sugar) maintain a normal body weight:

Study Link – Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake.

Quote from the above study:

Rats fed Daily Intermittent Sugar and Chow regulate their caloric intake by decreasing their chow intake to compensate for the extra calories obtained from sugar, which results in a normal body weight.

All told, the case for a causative role for added sugar alone in the increasing obesity rate isn’t quite as convincing as it would, at first, seem. The increase in grain (and, as we’ll see in future articles, PUFA) consumption during the same time period, however, is worth further investigation.

Grains are composed of starches which break down into glucose. For this reason, grains are likely to trigger some of the same addictive biology as glucose. There are even numerous reasons to believe, as we shall see, that some grains (such as wheat) may have an even greater addictive potential than refined sugars. To understand why, it will help to take a look at how various carbohydrates and sugars are metabolized, and their ultimate effect on appetite.

Insulin, Bood Sugar, and the Stress Response

When blood sugar becomes low (due to fasting, sleep, exercise, poor food choices, or too much time between meals, etc.), the body responds with a general stress response which includes the release of various stress hormones, including: adrenaline, cortisol, growth hormone, and prolactin.

As a defensive measure against low blood sugar, or hypoglycemia – which the body views as the threat of starvation – adrenaline serves to liberate glycogen from the liver to be utilized by the rest of the body. Similarly, one of the functions of cortisol is to break down proteins from muscle to be converted into glucose.

The release of these stress hormones in response to hypoglycemia can cause many negative physical and mood–related symptoms. Most people recognize hunger, fatigue, dizziness, irritability, nausea, headaches, anxiety, panic, etc. as common symptoms of low–blood sugar.

Somewhat ironically, however, the consumption of certain carbohydrates (especially in the context of unbalanced meals) can trigger hypoglycemia. Insulin, which is released in the greatest amounts in response to the ingestion of glucose, starch, and some proteins, serves to shuttle glucose from the blood into the body’s cells. Insulin triggers the conversion of glucose to glycogen (the storage form of sugar) and fat. After an initial blood sugar spike, foods which trigger the greatest insulin response can cause blood sugar to drop to particularly low levels soon after their ingestion.

Many starches, for example, are known to trigger particularly heightened insulin responses. Importantly, starches have been associated with lessened satiety (i.e., they fail to reduce appetite) in direct correlation with the degree to which they stimulate insulin release:

Study Link – Increased insulin responses to ingested foods are associated with lessened satiety.

Quote from the above study:

A significant negative association was found between the individual insulin and satiety AUC responses to the four foods. These results suggest that increased rate of starch digestion and higher insulin responses are associated with lessened satiety.

So, in addition to stimulating the insulin release which can cause fat storage and trigger the stress response, starches appear to impart a unique effect upon appetite which could lead to overeating. It’s interesting to note that the obesity epidemic has increased in parallel with the USDA’s recommendation for Americans to consume historically–unprecedented high levels of starch and “complex carbohydrates” over the past several decades.

The Effects of Fructose, Glucose, and Starch on Appetite and Metabolism

Scientists, doctors, and lay health writers alike have been quick to indict the sugar, fructose, as a unique contributor to the modern obesity epidemic. In a frenzy of nutritional reductionism, fructose and high–fructose corn syrup have become the nutritional whipping boys for people seeking an easy answer to the particularly complex problem of modern obesity. But, as is usually the case in biology, the full answer to the problem is quite a bit more complicated than it would at first seem.

A major role for fructose in human physiology is as a substrate for liver glycogen. As we’ve seen, during periods of low blood sugar (stress, starvation, etc.), this storage form of sugar can be released from the liver into the bloodstream as glucose to fuel the rest of the body (e.g., the brain, the muscles, etc.). On average, the liver of an adult human may be able to store approximately 100 grams of glycogen, while the musculature may store approximately 500 grams. People who are physically active, or who exercise will logically use up more glycogen than sedentary individuals. The ability to store glycogen in the liver represented a major asset to human survival during periods of history when food may have been scarce, and energy demands high.

One of the knocks against fructose – as it serves as a substrate for liver glycogen, and not muscle glycogen – is that it can be readily converted to fat if our intake overwhelms our liver’s limited capacity to store it. Along these lines, studies have shown that high intakes of fructose can lead to elevated triglycerides, insulin resistance, and related metabolic disorders:

Study Link – Consumption of fructose–sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein–B concentrations in overweight and obese women.

Quote from the above study:

The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose)… In summary, consumption of fructose–sweetened beverages increased postprandial [triglycerides] and fasting apoB concentrations, and the present results suggest that long–term consumption of diets high in fructose could lead to an increased risk of [cardiovascular disease].

But, in actuality, the studies like those above, which associate negative health effects with fructose, usually have little real–world significance. Universally, the animal and human studies which show negative metabolic effects from fructose consumption use doses of fructose significantly higher than those found in most diets. A fructose intake of 25% of calories (as used in the above study) equates to over 156 grams of fructose per day in a 2500 calorie diet. By contrast, data from the USDA Continuing Survey of Food Intake by Individuals estimated that greater than 95% of the adult population in the U.S. consumes less than 100 grams of fructose per day.

Fructose detractors usually fail to notice the research which shows that fructose intake at this level has been shown to actually enhance insulin sensitivity and reduce the marker of glycation, HbA1 (higher levels of which are associated with reduced blood sugar control and cardiovascular disease risk). For example, the following study examined the intake of a more realistic 45 to 60 grams of fructose per day (in type–2 diabetics, no less):

Study Link – Fructose and insulin sensitivity in patients with type 2 diabetes.

Quote from the above study:

The HbA1 concentration improved (P < 0.02) only during the fructose diet. Insulin sensitivity increased by 34% (P < 0.05) during the fructose diet, but remained unchanged during the control period. Serum insulin, triglyceride, apoprotein A–I and A–II concentrations, body weight, blood pressure and blood lactate remained unchanged during both diets. In conclusion, substitution of moderate amounts of fructose for complex carbohydrates can improve glycaemic control and insulin sensitivity in patients with type 2 diabetes.

Similarly, the following study found that 7.5 grams of fructose, taken three times daily after meals, significantly improved measures of blood sugar control:

Study Link – Catalytic amounts of fructose may improve glucose tolerance in subjects with uncontrolled non–insulin–dependent diabetes.

Quote from the above study:

No changes were observed in the difference between postprandial and pre–meal glucose, insulin or triglyceride levels in each group or between groups. No significant statistical differences were found in weight, total cholesterol, LDL –c and high–density lipoprotein cholesterol ( HDL –c) in each group or between groups along the study period. After 1 month fructosamin levels decreased in the fructose–supplemented group but not in the maltodextrin–supplemented group (P<0.052). Hgb(A1C) levels decreased with time in both groups but were significantly lower at 2 months in the fructose group as compared to the maltodextrin group (P<0.03).

(Note: The above studies used refined fructose added to the diet, and still, benefits were observed. As we’ll see, it’s likely that the overall health benefits would have been even greater if fructose were incorporated in its natural form – as in fruits, for example.)

These studies aren’t anomalies – reviews of the relevant literature on fructose have found that, in moderate, real–world doses, fructose may actually improve many of the conditions which it exacerbates at extremely high doses:

Study Link – Fructose Ingestion: Dose–Dependent Responses in Health Research.

Quote from the above study:

By focusing on the adverse effects of very high and excessive doses [of fructose], we risk not noticing the potential benefits of moderate to higher doses, which might moderate the advent and progress of type–2 diabetes, cardiovascular disease, and might even contribute to longevity. A salutary rather than hyperbolic examination of the evidence base needs to be undertaken.

Fructose Reduces Hunger, Glucose Stimulates Hunger

The human body is likely to have many mechanisms (both chemical and mechanical) by which it senses the fed state and therefore, reduces hunger. Alterations in blood sugar levels, the sensory and chemical effects of food, and even the physical distention of the digestive tract after a meal are likely to play overlapping roles in mediating hunger and satiety.

In a previous Integrated Supplements Newsletter, we saw that glutamate is able to trigger addiction–like brain chemistry, not just by triggering a pleasant taste on the tongue, but by stimulating glutamate receptors throughout the gastrointestinal tract.

Similarly, it’s not just the sweet taste of sugar which drives its “addictive” (i.e., appetite–accelerating) potential. Studies have found that, although fructose is sweeter than glucose, glucose conditions taste preferences more significantly than fructose via postingestive conditioning. In other words, glucose receptors lining the intestines send powerful reinforcing signals to the brain in response to glucose and starch ingestion:

Study Link – Glucose– and fructose–conditioned flavor preferences in rats: Taste versus postingestive conditioning.

Quote from the above study:

These findings, along with other recent data, indicate that fructose–conditioned preferences are based primarily on the sugar's palatable taste. Glucose, in contrast, can condition strong preferences based on its taste as well as its postingestive actions.

This may be one reason why glucose and starch appear to stimulate feeding and appetite significantly more than fructose. Even without being sweet, starches – because they are rapidly broken down into glucose – can trigger preferences for foods which contain them. Animal studies which used intra–gastric feeding (allowing food to bypass the taste buds), have shown that rats show preference for glucose–containing starches, even without tasting them:

Study Link – Flavor preferences conditioned by intragastric polycose infusions: a detailed analysis using an electronic esophagus preparation.

Quote from the above study:

…in the absence of unique flavor cues, the rats learned to prefer, apparently based on somatosensory cues, the sipper tube that was paired with [intragastric] Polycose infusions.

Similar studies in humans have shown that children show a preference for artificially–sweetened drinks containing digestible maltodextrin (glucose polymers which don’t impart sweetness) versus artificially–sweetened drinks without maltodextrin:

Study Link – Conditioned flavor preferences in young children

By contrast, not only does fructose not impart these sorts of postingestive effects, consuming fructose seems to reduce the amount of food consumed at subsequent meals:

Study Link – Effects of fructose and glucose preloads on subsequent food intake.

Quote from the above study:

Subjects consumed 50 g of glucose or fructose in 500 ml of water or water alone and were given a "buffet" containing a variety of foods two and a quarter hours later. Subjects in glucose conditions ate, on the average, 252 X 7 calories more than subjects in the water condition, who in turn ate, on the average, 225 X 9 calories more than subjects in the fructose condition.

Study Link – Metabolic effects of fructose and glucose: implications for food intake.

Quote from the above study:

Significant differences in caloric intake were observed between load conditions with the fructose group consuming fewer calories than the glucose group.

Even epidemiological attempts to link fructose and high–fructose corn syrup consumption with increased caloric intake have largely come up empty:

Study Link – Fructose and satiety.

Quote from the above study:

On balance, the case for fructose being less satiating than glucose or HFCS being less satiating than sucrose is not compelling.

One of the reasons that fructose may impart such an appetite–reducing effect is because of its preferential incorporation into liver glycogen. Evolutionarily, liver glycogen was a great asset to survival as it could be used to fuel the rest of the body in periods of stress or starvation. Many researchers believe that the human body uses indicators of liver glycogen status as major regulators of appetite. It’s likely that the body views a lack of liver glycogen as a profound threat to survival, and thus may stimulate appetite whenever liver glycogen stores are compromised:

Study Link – The role of the liver in the control of food intake?

Quote from the above study:

The liver is at the crossroads of metabolism, being in the unique position of receiving almost all of the absorbed nutrients some of which it takes up to replenish its glycogen stores. It is therefore ideally suited to be an important monitor of nutrient flow into the animal and evidence has been accumulating during the last decade that food intake in a variety of species responds to the energy status of the liver, which is relayed to the brain by hepatic branches of the vagus nerve.

Additionally, studies have found that optimal liver glycogen repletion is apt to be achieved via the simultaneous ingestion of glucose and fructose (a combination likely to be found in fruit, for example):

Study Link – Enhancement of glycogen concentrations in primary cultures of rat hepatocytes exposed to glucose and fructose.

Quote from the above study:

…the presence of fructose greatly stimulates the incorporation of carbon from glucose into glycogen, and the presence of glucose enhances the glycogenic utilization of fructose carbon, as compared with that seen in the presence of either glucose or fructose alone.

From this accumulated research, it seems reasonable to believe that excessive hunger, blood–sugar disorders, and weight gain could all be triggered, in part, by the consumption of grains and starches which have become an increasingly prevalent part of the American diet in recent decades. Small to moderate amounts of sugars (ideally, as fruits – mixtures of glucose, fructose, and sucrose along with other nutrients), are more likely to blunt appetite, regulate blood sugar, and foster a healthy weight.

Many of the low–carb and “paleo” diets which eschew the usage of grains “allow” the usage of fruits in moderation – usually with the caveat that low–sugar fruits be chosen. The implication is often that fruits will compromise the maximal effectiveness of the diet, but can be eaten as somewhat of a “guilty pleasure.” Very few, if any, of these diets, however, emphasize the fact that moderate amounts of fruit/sugar are likely to be better for weight loss (especially, avoiding “plateaus”) and overall health than none at all. In actual practice, moderate consumption of fruit seems to optimize the results people achieve with such diets.

These research and empirical findings make sense from an evolutionary perspective as well. Many plants – and, in particular, seeds (i.e., the offspring of plants) have evolved mechanisms to protect them from being eaten. Most seeds (in their unaltered form) are unsuitable nutritionally because the human digestive system can’t break down the fibrous outer shell of the seed. With the advent of cooking, agriculture, milling, and refining, however, the starches and other components in grain seeds (i.e., wheat, barley, rye, etc.) have become increasingly prevalent in the human diet in the form of flours, breads, baked goods, and pasta. Unfortunately, as we’ve seen in previous Integrated Supplements Newsletters, Nature has also concentrated mild, yet cumulatively harmful, toxins in the seeds of such plants. These toxins (e.g., pytates, trypsin inhibitors, unsaturated oils, goitrogens, phytoestrogens, cyanogenic glycosides, et al.) serve to harm potential predators, thus enhancing the seeds chances of flourishing into a full–grown plant.

Fruits, on the other hand, have cleverly evolved to enclose their seeds within the sweet edible pulp which is so tempting to numerous members of the animal kingdom. An animal eating the fruit will, eventually, and often at a great distance away, excrete the ingested seed unaltered (along with natural fertilizer, to boot). This greatly enhances the chances that a seed from fruit will flourish into a full–grown plant. In other words, fruits (including the fructose and other nutrients they contain) seem to be evolutionarily designed to be food for omnivorous humans. Though the consumption of fruit is pleasurable, unlike refined sugars and grains, fruits don’t quite seem to trigger the addictive biology, or addictive patterns of consumption in the same fashion (from a survival perspective, a fruit–bearing plant wouldn’t “want” one animal to gorge on its entire “offspring”).

With a thumbnail sketch of how different carbohydrates are utilized, and their effects upon metabolism and appetite, in the next Integrated Supplements Newsletter we’re poised to look at some of the accessory nutrients needed for optimal carbohydrate metabolism. We’ll see how micronutrient deficiencies and imbalances – and not sugars per se – may be responsible for many of the health effects commonly blamed on sugar.

About Us: At Integrated Supplements, our goal is to bring you the wellness information and products you need to live your life to the fullest. We are dedicated to producing the highest–quality, all–natural nutritional supplements; and to educating the world on the health promoting power of proper nutrition. You can find out more by visiting: www.IntegratedSupplements.com

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These statements have not been evaluated by the FDA. No Integrated Supplements product is intended to diagnose, treat, cure or prevent any disease.

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