Amino Acids:
	Alanine	1190 mg		Lysine *	1890 mg
	Arginine	730 mg		Methionine *	410 mg
	Aspartic Acid	2170 mg		Phenylalanine *	820 mg
	Cystine	480 mg		Proline	980 mg
	Carnitine	70 mg		Serine	910 mg
	Covalent Bonded Glutamine	2000 mg		Taurine	30 mg
	Glutamic Acid	3290 mg		Threonine *	1010 mg
	Glysine	570 mg		Trytophan *	370 mg
	Histadine	440 mg		Tyrosine	760 mg
	Isoleucine + + *	910 mg		Valine + + *	960 mg
	Leucine + + *	2.36 grams
* Essential Amino Acid + + Branched Chain Amino Acid

- Back to top -

Contains no Fructose

The Dangers Of Using Fructose Sweetener Article on the dangers of using high fructose corn sweetener in your diet. dangers of fructose, fructose

How bad is fructose? 1,2

George A Bray

1 From the Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA

2 Reprints not available. Address correspondence to GA Bray, Boyd Professor, Pennington Biomedical Research Center, LSU System, 6400 Perkins Road, Baton Rouge, LA 70808. E-mail: brayga@pbrc.edu.

See corresponding article on page 1174.

This issue of the Journal contains another disturbing article on the biology of fructose (1). Why is fructose of concern? First, it is sweeter than either glucose or sucrose. In fruit, it serves as a marker for foods that are nutritionally rich. However, in soft drinks and other "sweets," fructose serves to reward sweet taste that provides "calories," often without much else in the way of nutrition. Second, the intake of soft drinks containing high-fructose corn syrup (HFCS) or sucrose has risen in parallel with the epidemic of obesity, which suggests a relation (2). Third, the article in this issue of the Journal (1) and another article published elsewhere last year (3) implicate dietary fructose as a potential risk factor for cardiovascular disease.

The intake of dietary fructose has increased significantly from 1970 to 2000. There has been a 25% increase in available "added sugars" during this period (4). The Continuing Survey of Food Intake by Individuals from 1994 to 1996 showed that the average person had a daily added sugars intake of 79 g (equivalent to 316 kcal/d or 15% of energy intake), approximately half of which was fructose. More important, persons who are ranked in the top one-third of fructose consumers ingest 137 g added sugars/d, and those in the top 10% consume 178 g/d, with half of that amount being fructose. If there are health concerns with fructose, then this increased intake could aggravate those problems.

Before the European encounter with the New World 500 years ago and the development of the worldwide sugar industry, fructose in the human diet was limited to a few items. For example, honey, dates, raisins, molasses, and figs have a content of >10% of this sugar, whereas a fructose content of 5–10% by weight is found in grapes, raw apples, apple juice, persimmons, and blueberries. Milk, the main nourishment for infants, has essentially no fructose, and neither do most vegetables and meats, which indicates that human beings had little dietary exposure to fructose before the mass production of sugar.

Most fructose in the American diet comes not from fresh fruit, but from HFCS or sucrose (sugar) that is found in soft drinks and sweets, which typically have few other nutrients (2). Soft drink consumption, which provides most of this fructose, has increased dramatically in the past 6 decades, rising from a per-person consumption of 90 servings/y ({approx}2 servings/wk) in 1942 to that of 600 servings/y ({approx}2 servings/d) in 2000 (5). More than 50% of preschool children consume some calorie-sweetened beverages (6). Children of this age would not normally be exposed to fructose, let alone in these high amounts. Because both HFCS and sucrose are "delivery vehicles for fructose," the load of fructose has increased in parallel with the use of sugar.

Fructose is an intermediary in the metabolism of glucose, but there is no biological need for dietary fructose. When ingested by itself, fructose is poorly absorbed from the gastrointestinal tract, and it is almost entirely cleared by the liver—the circulating concentration is {approx}0.01 mmol/L in peripheral blood, compared with 5.5 mmol/L for glucose.

Fructose differs in several ways from glucose, the other half of the sucrose (sugar) molecule (4). Fructose is absorbed from the gastrointestinal tract by a different mechanism than that for glucose. Glucose stimulates insulin release from the isolated pancreas, but fructose does not. Most cells have only low amounts of the glut-5 transporter, which transports fructose into cells. Fructose cannot enter most cells, because they lack glut-5, whereas glucose is transported into cells by glut-4, an insulin-dependent transport system. Finally, once inside the liver cell, fructose can enter the pathways that provide glycerol, the backbone for triacylglycerol. The growing dietary amount of fructose that is derived from sucrose or HFCS has raised questions about how children and adults respond to fructose alone or when it is accompanied by glucose. In one study, the consumption of high-fructose meals reduced 24-h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerols in women, but it did not suppress circulating ghrelin, a major appetite-stimulating hormone (4).

Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step (4). Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets (4). In the study conducted by Aeberli et al (1), dietary factors, especially fructose, were examined in relation to body mass index, waist-to-hip ratio, plasma lipid profile, and LDL particle size in 74 Swiss schoolchildren who were 6–14 y old. In that study, plasma triacylglycerols were higher, HDL-cholesterol concentrations were lower, and lipoprotein (LDL) particle size was smaller in the overweight children than in the normal-weight children. Fatter children had smaller LDL particle size, and, even after control for adiposity, dietary fructose intake was the only dietary factor related to LDL particle size. In this study, it was the free fructose, and not sucrose, that was related to the effect of LDL particle size. Studies in rodents, dogs, and nonhuman primates eating diets high in fructose or sucrose consistently show hyperlipidemia (4). The current report by Aeberli et al suggests that the higher intake of fructose by school-age children may have detrimental effects on their future risk of cardiovascular disease by reducing LDL particle size. It is interesting that this study did not find a relation of dietary fructose with triacylglycerols but did find a relation with the more concerning lipid particle, LDL cholesterol. Another recent report has proposed a hypothesis relating fructose intake to the long-known relation between uric acid and heart disease (3). The ADP formed from ATP after phosphorylation of fructose on the 1-position can be further metabolized to uric acid. The metabolism of fructose in the liver drives the production of uric acid, which utilizes nitric oxide, a key modulator of vascular function (3). The studies by Aeberli et al and Nakagawa et al suggest that the relation of fructose to health needs reevaluation.

ACKNOWLEDGMENTS

This article, courtesy of medaus.com

The author had no personal or financial conflict of interest.

REFERENCES

1. Aeberli I, Zimmermann MB, Molinari L, et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr 2007;86:1174–8.[Abstract/Free Full Text]
2. Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004;79:537–43.[Abstract/Free Full Text]
3. Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol (Renal Physiol) 2006;290:F625–31.[Abstract/Free Full Text]
4. Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005;63:133–57.
5. Vartanian LR, Schwartz MB, Brownell KD. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health 2007;97:667–75.[Abstract/Free Full Text]
6. Harnack L, Stang J, Story M. Soft drink consumption among US children and adolescents: nutritional consequences. J Am Diet Assoc 1999;99:436–41.

Related articles in AJCN:

- Back to top -

The Origins Of Spizerinctum

My friend, the late Dr. Bob Breedlove, sent me an article published in the Des Moines Sunday Register in early May about 6 weeks before his untimely death in the 2005 Race Across America. His comment alongside the article was, “I thought you made Spizerinctum up!” Here is the complete article illustrating the word Spizerinctum has been around for quite some time and actually has had many meanings. The author works for the Merriam-Webster’s Collegiate Dictionary, 10th edition Wordwatch program.

Question: My nephew claims that there is a word, “Spizzerinctum” that means something like “zest for life.” I looked in several dictionaries and did not find this word. It sounds to me like something he made up and I wonder if he is pulling my leg.

Answer: Over the years, we’ve answered a number of inquiries like yours about “spizzerinctum” (a word that has many spelling variants.) Here’s one from a letter written in 1917: “I have just had a discussion about some such word as “spizzerinctum.” Last winter I heard a speaker use the word and say it then was the newest word in the English vocabulary and meant “vim and vigor.” My friends maintain there is no such word. Could you kindly advise me?

“Spizzerinctum” is one of those words that people love to discover. It is indeed a real word – real enough to be entered in our unabridged Webster’s Third New International Dictionary, where it is defined as “the will to succeed; vim, energy, ambition.”

Spelled “Spizarinctum,” this peculiar word was used in the mid – 1800’s for “specie,” that is, for money in the form of coins. In fact, the word “spizarinctum” is thought to be simply a fanciful coinage” from “Specie.” Here’s the word used with a slightly different spelling in 1869, by someone writing about “greenbacks,” or paper money: “They (greenbacks) had gotten no further west than Marshall (Texas), and everywhere west of that, when a man named a price, he meant “Spizerinctums.”

A 1913 streetcar sign in Washington, D.C. announcing the publication of a new dictionary featured “Spizzerinktum”; “See if you can find the word in any other dictionary, “the sign boasted. As “pizzeringtom” the word was noted circa 1922 as meaning “the quintessence of pep”. “Spizerinkum” was defined in a 1944 book of US Marine Corps slang as “intestinal fortitude.”

A mayor in Columbus, Ohio is said to have been fond of the word in the 1950’s and 60’s, but in general the word seems to have floated in and out of popularity.

Now it may be experiencing something of a revival. Not long ago, a catalog featuring chickens for breeding even described one particular breed as noted for being especially endowed with “spizzerinktum.”

The true story behind how I came across the word Spizerinctum goes back to 1993 when I was doing home health physical therapy. A Louisiana woman announced when I entered her home and asked how she was, “I don’t have any spizerinctum today!” I said, “What is that?” She explained it was a Southern term for pep or energy! I loved that word and when the opportunity to use it came along after the demise of my 1986 Pete Penseyres concocted complete liquid food drink known as “Ultra Energy,” I jumped at it! Spizerinctum (my spelling) made perfect sense for a nutritionally complete energy drink, especially now in light of so many other appropriate meanings for what I have tried to create with this product. To my friend Bob Breedlove I wish you God’s speed and thank you for your long friendship and camaraderie. You will be greatly missed!

Randy Ice P.T., C.C.S.

Longevity Plus

- Back to top -