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Jan. 25, 2010 - Freedomain Radio - Stefan Molyneux

18:59

1564 The Fructose Epidemic - An Article by Dr Robert H. Lustig - Freedomain Radio

'Fructose consumption has increased coincidentally with the worldwide epidemics of obesity...'

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	music The Fructose
	Epidemic by Robert H. Lustig, MD, read by Stefan Molyneux from Freedom Aid Radio.
	you.
	Abstract Fructose consumption, as both high fructose corn syrup and sucrose, has increased coincidentally with the worldwide epidemics of obesity and metabolic syndrome.
	Fructose is a primary contributor to human disease, as it is metabolized in the liver differently to glucose, and is more akin to that of ethanol.
	When consumed in large amounts, fructose promotes the same dose-dependent toxic effects as ethanol, promoting hypertension, hepatic and skeletal muscle insulin resistance, dyslipidemia and fatty liver disease.
	Also similar to ethanol, through direct stimulation of the central nervous system hedonic pathway and indirect stimulation of the starvation pathway, fructose induces alterations in central nervous system energy signaling that lead to a vicious cycle of excessive consumption with resultant morbidity and mortality.
	Fructose from any source should be regarded as alcohol without the buzz.
	Obesity prevention and treatment is ineffective in the face of the current fructose glut in our food supply.
	We must learn from our experiences with ethanol and nicotine that regulation of the food industry, along with individual and societal education, will be necessary to combat this fructose epidemic.
	Introduction As America's, and the world's, collective girth continues to increase, we ponder the answer to our dilemma.
	Who, or what, are to blame for the obesity epidemic?
	That depends upon who you ask.
	The Institute of Medicine says it is an interaction between genetics and environment.
	Well, our genetics have not changed in the past 30 years, but our environment sure has, and in particular, our diet.
	The distribution curve for Body Mass Index shows that all segments of the population are increasing in weight, so whatever is happening is clearly pervasive and insidious.
	Even developing countries that have adopted a Western diet for convenience and expense have paid for it by manifesting the same obesity prevalence, comorbidity profiles, and mortality.
	Secular trends in fructose consumption One of the striking features of the modern Western diet is its reliance on refined carbohydrate as the predominant energy source.
	Due to the low-fat admonition by the United States Department of Agriculture, American Medical Association and American Heart Association, in the early 1980s, the percentage of fat in the Western diet has reduced from 40% to 30% over the past 25 years, which has resulted in the percentage of carbohydrate rising from 40% to 55%, coinciding with the obesity epidemic.
	Of this, a sizeable and ever-increasing portion of the diet is attributable to monosaccharides and disaccharides used to sweeten foods and drinks.
	Furthermore, in response to the market for lower-fat fare, food companies have chosen to substitute disaccharides to maintain palatability of processed foods.
	Until recently, the most commonly used sugar in the US diet was disaccharide sucrose, e.g.
	cane or beet sugar, which is composed of 50% fructose and 50% glucose.
	However, in North America and many other countries, due to its abundance, sweetness, and low price, high-fructose corn syrup, HFCS, Which contains between 42% and 55% of the monosaccharide fructose, has overtaken sucrose as the most ubiquitous caloric sweetener.
	These factors have led to an inexorable rise in fructose consumption.
	Prior to 1900, Americans consumed approximately 15 grams per day of fructose, mainly through fruits and vegetables.
	Prior to World War II, this amount had increased to 24 grams per day.
	By 1977, fructose intake was 37 grams a day.
	By 1994, 55 grams per day.
	And currently, certain estimates are that adolescents average 72.8 grams per day.
	Thus, current fructose consumption has incrementally increased five-fold compared to a century ago.
	Disappearance data over the past 25 years from Economic Research Service, ERS, of the USDA also supports this secular trend.
	The ERS documents partial substitution for sucrose by high fructose corn syrup.
	However, annual per capita total caloric sweetener usage has increased from 73 to 95 pounds in that interval.
	Although soda has received most of the attention, high fruit juice intake, sucrose, is also associated with childhood obesity, especially by lower-income families, although it is not captured in the ERS. Thus, after adjustment for juice intake, per capita consumption of mono- and disaccharides is at approximately £113 a year, or a third of a pound a day, for all Americans.
	How we got here. Political, economic and medical drivers of fructose consumption.
	The reader is referred to the omnivore's dilemma for a complete discussion of the political and economic factors that led to the secular trend in fructose consumption.
	In brief, the 1966 industrialization of the discovery of the glucose oxidase process to convert glucose to fructose, combined with a directed policy by the USDA in the 1970s to reduce the price of food as a dietary staple, provided the political and economic impetus for this trend.
	In addition, during this decade, the medical establishment focused on dietary reduction of coronary heart disease.
	Two competing schools of thought dominated this discussion.
	John Yudkin, a British physiologist and nutritionist, championed the anti-sugar movement.
	His work, Pure, White and Deadly, exposed the primary role of sugar in human disease.
	Conversely, the anti-saturated fat movement was spearheaded by Minnesota epidemiologist Ancel Keys.
	His work, The Seven Countries Study, was one of the first multivariate linear regression analyses.
	A review of this document notes, quote, The fact that the incidence of coronary heart disease was significantly correlated with the average percentage of calories from sucrose in the diets is explained by the intercorrelation of sucrose with saturated fat.
	Partial correlation analysis demonstrates that with saturated fat constant, there was no significant correlation between dietary sucrose and the incidence of coronary heart disease.
	End quote. However, Keyes neglected to perform the converse analysis demonstrating that the effect of saturated fat on cardiovascular disease was independent of sucrose.
	In other words, sucrose and saturated fat co-migrated.
	It is impossible to tease out the relative contributions of sucrose versus saturated fat on cardiovascular disease from this study.
	Furthermore, the medical establishment based their low-fat recommendations on the goal of LDL reduction.
	However, several studies have since demonstrated little to no effect of low-fat diets on weight gain or cardiovascular disease events.
	However, we now know that there are two LDLs.
	The large, buoyant or type A LDL is driven by dietary fat, but is neutral from a cardiovascular standpoint.
	The small dense or type B LDL, which is driven by carbohydrate and fructose, is the species associated with cardiovascular disease.
	Conversely, we have ample evidence that triglyceride is a major factor for cardiovascular disease and that fructose consumption is a primary contributor to triglyceride accumulation.
	A recent analysis has led the AHA Nutrition Committee to publish a policy statement on the negative role of sugars in the pathogenesis of cardiovascular disease.
	High-fructose corn syrup versus sucrose.
	Although many consumer activist groups have specifically vilified high fructose corn syrup as the cause of obesity and cardiovascular disease, scientific studies of acute satiety versus energy intake support the notion that high fructose corn syrup is not metabolically different from sucrose.
	This has led to a vociferous campaign by the Corn Refiners Association to influence the debate on fructose consumption by equating high fructose corn syrup with sucrose, suggesting that it is no different, quote, natural, and it is safe, see sweetsurprise.com.
	Indeed, the distinction between high fructose corn syrup and sucrose is not metabolic, as they are essentially equivalent, but rather economic.
	The introduction of high fructose corn syrup to the Western diet in 1975 resulted in stability of the U.S. producer price index for sugar and sizable reductions in the U.S. and international price of sugar.
	High fructose corn syrup, on average, costs about one-third that of sucrose.
	This, along with changes in the Farm Bill and food policy, promoted the addition of fructose to our collective diets, not just in soft drinks and juice, but in salad dressing, condiments, baked goods, and virtually every processed food, which raised our total consumption five-fold in the last 100 years.
	In the chart below, which you can see in the PDF, it becomes clear that it is not the specific vehicle, sucrose versus high fructose corn syrup, that makes it unsafe, but rather the total dose of fructose.
	Correlation of fructose consumption with disease.
	Numerous reviews have indirectly implicated fructose consumption in the current epidemics of obesity and type 2 diabetes mellitus.
	Correlative studies in humans link soft drink consumption with energy overconsumption, body weight, poor nutrition, and T2DM. Similarly, juice consumption also correlates with risk for T2DM, suggesting that excessive fructose consumption is playing a role in the epidemics of insulin resistance, obesity, hypertension, dyslipidemia, and T2DM in humans.
	Collectively, this constellation of findings is referred to as the metabolic syndrome, METS. Conversely, early short-term prospective studies limiting soft drink ingestion in children have met with some success in stabilization of weight and CVD parameters.
	Mechanisms of Fructose Toxicity This highly technical section will be skipped.
	In this audio reading, the listener is urged to review the paper available at fdrurl.com forward slash sucrose.
	We move on to fructose effects on the central nervous system lead to excessive consumption.
	The limbic structure central to the hedonic pathway that motivates the reward of food intake are the ventral tegmental area and nucleus accumbens.
	The NA is also referred to as the pleasure center of the brain and is the seat of goal-oriented behavior.
	This is also the brain area responsive to nicotine, morphine, cannabinoids, amphetamine, nicotine and ethanol.
	Food intake is a result of activation of the reward pathway.
	For example, administration of morphine to the NA increases food intake in a dose-dependent fashion.
	Dopamine neurotransmission from the VTA to the NA mediate the reward properties of food.
	Leptin and insulin receptors are co-localized in VTA neurons, and both hormones have been implicated in modulating rewarding responses to food and other pleasurable stimuli.
	Leptin decreases VTA-NA activity and extinguishes reward for food.
	However, increasing the palatability of food by addition of fructose undermines normal satiety signals, and as a result, increases total caloric consumption, both in direct and indirect ways.
	Direct effects of fructose include motivation of food intake independent of energy needs.
	Indeed, in animal models, sugar consumption can lead to dependence.
	There are four indirect effects of fructose on excessive food consumption.
	First, fructose does not stimulate a leptin rise, thus contributing acutely to a diminished sense of satiety.
	Secondly, fructose induces hypertriglyceridemia which reduces leptin transport across the blood-brain barrier.
	The third is chronic hyperinsulinemia, which interferes with leptin signal transduction at the second messenger level.
	By reducing leptin's ability to extinguish hunger at the hypothalamus and likely leptin's ability to extinguish the dopamine reward signal at the NA, chronic hyperinsulinemia fosters a sense of starvation and need for reward, leading to increased caloric intake.
	Lastly, fructose has been shown to decrease the production in hypothalamic neurons of melanin COA, which may help promote a sense of energy inadequacy.
	Together with promoting hepatic and muscle insulin resistance, fructose ingestion may alter the hedonic response to food to drive excessive energy intake, setting up a positive feedback cycle of hepatic and central nervous system dysfunction, leading to persistent overconsumption.
	Whether this CNS vicious cycle is tantamount to true addiction or merely psychological dependence is not yet clear.
	What is clear is that obesity, depression, and sugar craving and consumption are linked epidemiologically and mechanistically.
	Summary The hepatic metabolic pathways outlined above demonstrate that fructose is a dose-dependent chronic hepatotoxin.
	Fructose is capable of promoting hepatic and skeletal muscle insulin resistance, hyperinsulinemia, dyslipidemia, hepatic lipid deposition, and inflammation, similar to the dose-dependent toxic effects of ethanol.
	Furthermore, these central pathways outlined above demonstrate that fructose is capable of promoting hypothalamic leptin resistance and activation of the reward pathway, resulting in an abnormal drive to continuous consumption, also similar to ethanol.
	Indeed, fructose may be described as alcohol without the buzz.
	The metabolic and central similarities between fructose and ethanol are striking.
	Other stimulators of the nucleus accumbens have led to disease and societal deterioration and thus have required education, regulation and, in some instances, intradiction.
	America attempted ethanol intradiction prohibition in the 1930s but was unsuccessful.
	It will be even harder to restrict fructose consumption.
	Furthermore, the Food and Drug Administration has given fructose GRAS, generally regarded as safe, status, thus declining to regulate its use.
	While many obesity programs cancel voluntary reductions in personal fructose consumption, recidivism is frequent, thus a major effort in public health education seems daunting.
	Nonetheless, we have made significant progress with ethanol reduction, mostly through regulation.
	Soda taxes have recently been proposed both in New York and California, and legislation for the removal of soft drinks from schools has been enacted in several states.
	However, until Jutkin's prophecies of 1972 are taken seriously and the public is made aware of the specific dangers of the fructose fraction of our current Western diet, our current vicious cycle of consumption and disease will continue.

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