Thursday, April 29, 2010

Doctor's Rebuttal/Other Comments




Even though this looks like a rebuttal to the article about antidepressants I posted, it says there is a lot to be done yet in this field. Too many patients with depression do not see a real mental health professional, just their primary care doctors, who have little training in menatl health. Then there is the stigma...a lot of people won't talk about it..then there is the problem with insurance companies..too many do not cover visits to mental health therapists.

He says, too, antidepressants CAN work for some people who have had depression for 2 years or more...but milder cases that are shorter?

What is nteresting about this uy is that he had a major trauma (his sister died in 9/1 attack on World Trade Center...and he was depressed...so turned to Rx.} Well..you are supposed to be depressed!!!!!!!!! It is such a cultural thing that you have to bounce back quick from trauma. It used to be...back in the 19th century...everyone was given 30 days to grieve...no one cared if you spent that 30 days bawling in your bedroom...you did what you had to do to work out the grief. People excted you to be non funtioning for 30 days at least.
To me, this is all very fascinating...how people are willing to mess with drugs.




A Doctor Disagrees
Antidepressants have helped not only my patients, but myself.

By Robert Klitzman NEWSWEEK


Published Jan 29, 2010

From the magazine issue dated Feb 8, 2010
The TV screen stayed black. Except for the occasional car whishing by outside, the room was silent. I stared at the white ceiling, unable to get out of bed. Two weeks earlier, on 9/11, my sister had died at the World Trade Center, where she worked. I had helped plan a memorial service for her and empty her apartment. Then my body gave out.
For the first time in my life, I didn't feel like doing anything—reading, writing, or even listening to music. I went to psychotherapy, and visited a synagogue, a church, and a Buddhist sanctuary, where we walked in circles and rang bells.

I didn't think an antidepressant would help me, but I decided to try one. Perhaps I should have experienced my grief longer, as a "growing experience." But I soon felt better, and was glad. I also changed how I thought about disease and treatment.

Last month, The Journal of the American Medical Association published an article that argued that for patients with mild or moderate depression, antidepressants work no better than placebos. Countless patients wondered if they should stop their medication. Others have insisted that Americans are overmedicating themselves.

What should we make of all this? First, some facts: antidepressants have clearly been shown to work for serious major depression. Most evidence shows that they are effective for dysthymia: milder but chronic depression that continues for two years or longer. The question is whether they work for milder depression that may be shorter or less intense.

That's important, since major depression affects almost one out of five people at some point in their lives. And most people with depression do not have severe forms of it.
My own sense, based in part on my own personal experience, as well as that of patients I have treated, is that antidepressants can definitely work for milder depression—not for everyone, but for many. Why, then, the debate and apparently contradictory findings?

In part, the answer hinges on what we mean by "milder" depression. Experiences of depression vary enormously in intensity, length, and impact: from momentarily feeling blue to more major symptoms. Medications, which take several weeks to work, will neither help nor be appropriate for a few days of depression that result from passing disappointments.

Just as Tolstoy wrote that "every unhappy family is unhappy in its own way," I would argue that every unhappy individual is unhappy in his or her own way. Depression, even if moderate, can last from minutes to years, and can change your ability to function in life radically—or not at all.

The JAMA article included minor depression but did not examine degrees of impairment in daily functioning or quality of life, or durations of symptoms before treatment was begun—all of which might influence these drugs' effectiveness.

Alas, this debate is polarized, with strong advocates—each with their own biases—on both sides. Drug companies want to market drugs as widely as possible. Many psychologists and social workers, who don't prescribe drugs, fear that increased antidepressant use will rob them of clients.

The debate about these medications obscures larger social issues as well. In general, most patients with major depression receive no treatment. Many patients have difficulty telling a doctor that they feel depressed because of fears of stigma and shame. Of those who get treatment, most obtain it from primary-care doctors, not mental-health professionals. Yet general practitioners receive little training in psychiatry. Many insurance plans cover little, if any, psychotherapy.

We need to educate physicians better about psychiatric symptoms and treatment, improve public attitudes, increase insurance coverage for appropriate mental-health treatment, and conduct research to understand more fully who exactly may benefit from various treatments.
Patients with milder depression may benefit from antidepressants, but won't know until they try them. Studies examine large group averages—not individuals. Still, caution makes sense. These drugs are not panaceas.


The meds I took worked for me. Eventually, I turned on the TV, and read, and wrote. But I still wonder how, and who else, these drugs may help.

Klitzman is a psychiatrist, the author of When Doctors Become Patients , and director of the Master's of Bioethics program at Columbia University.

Find this article at http://www.newsweek.com/id/232782
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Here are leters to the editor on the subject:
(NOTE: I, Joan, am coming to believe that the world needs really good psycho-therapists!!!!!!!!)


The dangers of not treating depression are so great that any responsible physician will err on the side of caution and prescribe antidepressants.
Elizabeth Hinds,
Morris, Minn.

As a psychopharmacologist who treats patients, I feel Sharon Begley does a disservice to those who live with depression. She bases her argument largely on two meta-analyses by Irving Kirsch and Guy Sapirstein. The psychiatric community understands that meta-analyses, which combine different medications and methodologies (as in Kirsch and Sapirstein's research), or which handpick studies and exclude others (as did, in my view, the recent JAMApaper published by Jay C. Fournier of the University of Pennsylvania and his colleagues), are susceptible to biased interpretations. The research that practitioners use to determine how to treat their patients is based on analyses that require statistically proven effectiveness. Those of us who treat patients on a daily basis understand that medications are not magic pills, and that treatment combining antidepressant medication with psychotherapy offers patients the best chance of recovery.
Julie Hatterer, M.D.,
American Psychiatric Association Council on Communications, New York, N.Y.

Antidepressants do work when administered to patients who really suffer from depression. The problem is that many people who are not clinically depressed are being administered medication. That's because Big Pharma dominates medical education and aggressively targets the public through advertisements, as if medication were candy.
Stergios Kaprinis, M.D.,
Thessaloniki, Greece

As a psychiatrist who has spent more of the last 35 years taking patients off antidepressants than putting patients on them, I was gratified by your article. Nonetheless, placebo-driven or not, these drugs can still be a valuable tool in our therapeutic armory. The key is to precisely determine which individuals are the right fit. In the struggle with emotional duress, it is always better to have more arrows in the quiver than fewer.
Isaac Steven Herschkopf, M.D.,
NYU School of Medicine, New York, N.Y.
I have suffered from severe depression for years. The combination of antidepressants and therapy has saved my life.
Jessica Knowles, Bethesda, Md.

'A Doctor Disagrees'
As a clinical social worker, I'm generally supportive of Robert Klitzman's disagreement with your article about SSRIs. However, his comment that psychologists and social workers fear having patients medicated because it will "rob them of clients" is libelous. My colleagues and I all have collaborative relationships with M.D.s to arrange medications for patients. Our goal is to help people improve their lives, not to unethically collect fees without a proper treatment plan.
Stephen Rosenbaum, Highland Park, Ill.
http://www.newsweek.com/id/233406

Wednesday, April 28, 2010

Antidepressants



Here is an article from a Feb. 2010 Newsweek. Hmmmm.

The Depressing News About Antidepressants
http://www.newsweek.com/id/232781/page/3

Tom Schierlitz for Newsweek; Illustration by Serfcan Ozcan

By Sharon Begley | NEWSWEEK
Published Jan 29, 2010
From the magazine issue dated Feb 8, 2010

Although the year is young, it has already brought my first moral dilemma. In early January a friend mentioned that his New Year's resolution was to beat his chronic depression once and for all. Over the years he had tried a medicine chest's worth of antidepressants, but none had really helped in any enduring way, and when the side effects became so unpleasant that he stopped taking them, the withdrawal symptoms (cramps, dizziness, headaches) were torture. Did I know of any research that might help him decide whether a new antidepressant his doctor recommended might finally lift his chronic darkness at noon?

The moral dilemma was this: oh, yes, I knew of 20-plus years of research on antidepressants, from the old tricyclics to the newer selective serotonin reuptake inhibitors (SSRIs) that target serotonin (Zoloft, Paxil, and the granddaddy of them all, Prozac, as well as their generic descendants) to even newer ones that also target norepinephrine (Effexor, Wellbutrin). The research had shown that antidepressants help about three quarters of people with depression who take them, a consistent finding that serves as the basis for the oft-repeated mantra "There is no question that the safety and efficacy of antidepressants rest on solid scientific evidence," as psychiatry professor Richard Friedman of Weill Cornell Medical College recently wrote in The New York Times. But ever since a seminal study in 1998, whose findings were reinforced by landmark research in The Journal of the American Medical Association last month, that evidence has come with a big asterisk. Yes, the drugs are effective, in that they lift depression in most patients. But that benefit is hardly more than what patients get when they, unknowingly and as part of a study, take a dummy pill—a placebo. As more and more scientists who study depression and the drugs that treat it are concluding, that suggests that antidepressants are basically expensive Tic Tacs.

Hence the moral dilemma. The placebo effect—that is, a medical benefit you get from an inert pill or other sham treatment—rests on the holy trinity of belief, expectation, and hope. But telling someone with depression who is being helped by antidepressants, or who (like my friend) hopes to be helped, threatens to topple the whole house of cards. Explain that it's all in their heads, that the reason they're benefiting is the same reason why Disney's Dumbo could initially fly only with a feather clutched in his trunk—believing makes it so—and the magic dissipates like fairy dust in a windstorm. So rather than tell my friend all this, I chickened out. Sure, I said, there's lots of research showing that a new kind of antidepressant might help you. Come, let me show you the studies on PubMed.

It seems I am not alone in having moral qualms about blowing the whistle on antidepressants. That first analysis, in 1998, examined 38 manufacturer-sponsored studies involving just over 3,000 depressed patients. The authors, psychology researchers Irving Kirsch and Guy Sapirstein of the University of Connecticut, saw—as everyone else had—that patients did improve, often substantially, on SSRIs, tricyclics, and even MAO inhibitors, a class of antidepressants that dates from the 1950s. This improvement, demonstrated in scores of clinical trials, is the basis for the ubiquitous claim that antidepressants work. But when Kirsch compared the improvement in patients taking the drugs with the improvement in those taking dummy pills—clinical trials typically compare an experimental drug with a placebo—he saw that the difference was minuscule. Patients on a placebo improved about 75 percent as much as those on drugs. Put another way, three quarters of the benefit from antidepressants seems to be a placebo effect. "We wondered, what's going on?" recalls Kirsch, who is now at the University of Hull in England. "These are supposed to be wonder drugs and have huge effects."

The study's impact? The number of Americans taking antidepressants doubled in a decade, from 13.3 million in 1996 to 27 million in 2005.
To be sure, the drugs have helped tens of millions of people, and Kirsch certainly does not advocate that patients suffering from depression stop taking the drugs. On the contrary. But they are not necessarily the best first choice. Psychotherapy, for instance, works for moderate, severe, and even very severe depression. And although for some patients, psychotherapy in combination with an initial course of prescription antidepressants works even better, the question is, how do the drugs work? Kirsch's study and, now, others conclude that the lion's share of the drugs' effect comes from the fact that patients expect to be helped by them, and not from any direct chemical action on the brain, especially for anything short of very severe depression.

As the inexorable rise in the use of antidepressants suggests, that conclusion can't hold a candle to the simplistic "antidepressants work!" (unstated corollary: "but don't ask how") message. Part of the resistance to Kirsch's findings has been due to his less-than-retiring nature. He didn't win many friends with the cheeky title of the paper, "Listening to Prozac but Hearing Placebo." Nor did it inspire confidence that the editors of the journal Prevention & Treatment ran a warning with his paper, saying it used meta-analysis "controversially." Al-though some of the six invited commentaries agreed with Kirsch, others were scathing, accusing him of bias and saying the studies he analyzed were flawed (an odd charge for defenders of antidepressants, since the studies were the basis for the Food and Drug Administration's approval of the drugs). One criticism, however, could not be refuted: Kirsch had analyzed only some studies of antidepressants. Maybe if he included them all, the drugs would emerge head and shoulders superior to placebos.
Kirsch agreed. Out of the blue, he received a letter from Thomas Moore, who was then a health-policy analyst at George Washington University. You could expand your data set, Moore wrote, by including everything drug companies sent to the FDA—published studies, like those analyzed in "Hearing Placebo," but also unpublished studies. In 1998 Moore used the Freedom of Information Act to pry such data from the FDA. The total came to 47 company-sponsored studies—on Prozac, Paxil, Zoloft, Effexor, Serzone, and Celexa—that Kirsch and colleagues then pored over. (As an aside, it turned out that about 40 percent of the clinical trials had never been published.

That is significantly higher than for other classes of drugs, says Lisa Bero of the University of California, San Francisco; overall, 22 percent of clinical trials of drugs are not published. "By and large," says Kirsch, "the unpublished studies were those that had failed to show a significant benefit from taking the actual drug.") In just over half of the published and unpublished studies, he and colleagues reported in 2002, the drug alleviated depression no better than a placebo. "And the extra benefit of antidepressants was even less than we saw when we analyzed only published studies," Kirsch recalls. About 82 percent of the response to antidepressants—not the 75 percent he had calculated from examining only published studies—had also been achieved by a dummy pill.

The extra effect of real drugs wasn't much to celebrate, either. It amounted to 1.8 points on the 54-point scale doctors use to gauge the severity of depression, through questions about mood, sleep habits, and the like. Sleeping better counts as six points. Being less fidgety during the assessment is worth two points. In other words, the clinical significance of the 1.8 extra points from real drugs was underwhelming. Now Kirsch was certain. "The belief that antidepressants can cure depression chemically is simply wrong," he told me in January on the eve of the publication of his book The Emperor's New Drugs: Exploding the Anti-depressant Myth.
The 2002 study ignited a furious debate, but more and more scientists were becoming convinced that Kirsch—who had won respect for research on the placebo response and who had published scores of scientific papers—was on to something. One team of researchers wondered if antidepressants were "a triumph of marketing over science." Even defenders of antidepressants agreed that the drugs have "relatively small" effects. "Many have long been unimpressed by the magnitude of the differences observed between treatments and controls," psychology researcher Steven Hollon of Vanderbilt University and colleagues wrote—"what some of our colleagues refer to as 'the dirty little secret.' " In Britain, the agency that assesses which treatments are effective enough for the government to pay for stopped recommending antidepressants as a first-line treatment, especially for mild or moderate depression.

But if experts know that antidepressants are hardly better than placebos, few patients or doctors do. Some doctors have changed their prescribing habits, says Kirsch, but more "reacted with anger and incredulity." Understandably. For one thing, depression is a devastating, underdiagnosed, and undertreated disease. Of course doctors recoiled at the idea that such drugs might be mirages. If that were true, how were physicians supposed to help their patients?

Two other factors are at work in the widespread rejection of Kirsch's (and, now, other scientists') findings about antidepressants. First, defenders of the drugs scoff at the idea that the FDA would have approved ineffective drugs. (Simple explanation: the FDA requires two well-designed clinical trials showing a drug is more effective than a placebo. That's two, period—even if many more studies show no such effectiveness. And the size of the "more effective" doesn't much matter, as long as it is statistically significant.) Second, doctors see with their own eyes, and feel with their hearts, that the drugs lift the black cloud from many of their depressed patients. But since doctors are not exactly in the habit of prescribing dummy pills, they have no experience comparing how their patients do on them, and therefore never see that a placebo would be almost as effective as a $4 pill. "When they prescribe a treatment and it works," says Kirsch, "their natural tendency is to attribute the cure to the treatment." Hence the widespread "antidepressants work" refrain that persists to this day.

Drug companies do not dispute Kirsch's aggregate statistics. But they point out that the average is made up of some patients in whom there is a true drug effect of antidepressants and some in whom there is not. As a spokesperson for Lilly (maker of Prozac) said, "Depression is a highly individualized illness," and "not all patients respond the same way to a particular treatment." In addition, notes a spokesperson for Glaxo-Smith-Kline (maker of Paxil), the studies analyzed in the JAMA paper differ from studies GSK submitted to the FDA when it won approval for Paxil, "so it is difficult to make direct comparisons between the results. This study contributes to the extensive research that has helped to characterize the role of antidepressants," which "are an important option, in addition to counseling and lifestyle changes, for treatment of depression." A spokesperson for Pfizer, which makes Zoloft, also cited the "wealth of scientific evidence documenting [antidepressants'] effects," adding that the fact that antidepressants "commonly fail to separate from placebo" is "a fact well known by the FDA, academia, and industry." Other manufacturers pointed out that Kirsch and the JAMA authors had not studied their particular brands.

Even Kirsch's analysis, however, found that antidepressants are a little more effective than dummy pills—those 1.8 points on the depression scale. Maybe Prozac, Zoloft, Paxil, Celexa, and their cousins do have some non-placebo, chemical benefit. But the small edge of real drugs compared with placebos might not mean what it seems, Kirsch explained to me one evening from his home in Hull. Consider how research on drugs works. Patient volunteers are told they will receive either the drug or a placebo, and that neither they nor the scientists will know who is getting what. Most volunteers hope they get the drug, not the dummy pill. After taking the unknown meds for a while, some volunteers experience side effects. Bingo: a clue they're on the real drug. About 80 percent guess right, and studies show that the worse side effects a patient experiences, the more effective the drug. Patients apparently think, this drug is so strong it's making me vomit and hate sex, so it must be strong enough to lift my depression. In clinical-trial patients who figure out they're receiving the drug and not the inert pill, expectations soar.

That matters because belief in the power of a medical treatment can be self-fulfilling (that's the basis of the placebo effect). The patients who correctly guess that they're getting the real drug therefore experience a stronger placebo effect than those who get the dummy pill, experience no side effects, and are therefore disappointed. That might account for antidepressants' slight edge in effectiveness compared with a placebo, an edge that derives not from the drugs' molecules but from the hopes and expectations that patients in studies feel when they figure out they're receiving the real drug.


The boy who said the emperor had no clothes didn't endear himself to his fellow subjects, and Kirsch has fared little better. A nascent collaboration with a scientist at a medical school ended in 2002 when the scientist was warned not to submit a grant proposal with Kirsch if he ever wanted to be funded again. Four years later, another scientist wrote a paper questioning the effectiveness of antidepressants, citing Kirsch's work. It was published in a prestigious journal. That ordinarily brings accolades. Instead, his department chair dressed him down and warned him not to become too involved with Kirsch.

But the question of whether antidepressants—which in 2008 had sales of $9.6 billion in the U.S., reported the consulting firm IMS Health—have any effect other than through patients' belief in them was too important to scare researchers off.

Proponents of the drugs have found themselves making weaker and weaker claims. Their last stand is that antidepressants are more effective than a placebo in patients suffering the most severe depression.

So concluded the JAMA study in January. In an analysis of six large experiments in which, as usual, depressed patients received either a placebo or an active drug, the true drug effect—that is, in addition to the placebo effect—was "nonexistent to negligible" in patients with mild, moderate, and even severe depression. Only in patients with very severe symptoms (scoring 23 or above on the standard scale) was there a statistically significant drug benefit. Such patients account for about 13 percent of people with depression. "Most people don't need an active drug," says Vanderbilt's Hollon, a coauthor of the study. "For a lot of folks, you're going to do as well on a sugar pill or on conversations with your physicians as you will on medication. It doesn't matter what you do; it's just the fact that you're doing something." But people with very severe depression are different, he believes. "My personal view is the placebo effect gets you pretty far, but for those with very severe, more chronic conditions, it's harder to knock down and placebos are less adequate," says Hollon. Why that should be remains a mystery, admits coauthor Robert DeRubeis of the University of Pennsylvania.

Like every scientist who has stepped into the treacherous waters of antidepressant research, Hollon, DeRubeis, and their colleagues are keenly aware of the disconnect between evidence and public impression. "Prescribers, policy-makers, and consumers may not be aware that the efficacy of [antidepressants] largely has been established on the basis of studies that have included only those individuals with more severe forms of depression," something drug ads don't mention, they write. People with anything less than very severe depression "derive little specific pharmacological benefit from taking medications. Pending findings contrary to those reported here … efforts should be made to clarify to clinicians and prospective patients that … there is little evidence to suggest that [antidepressants] produce specific pharmacological benefit for the majority of patients."

Right about here, people scowl and ask how anti-depressants—especially those that raise the brain's levels of serotonin—can possibly have no direct chemical effect on the brain. Surely raising serotonin levels should right the synapses' "chemical imbalance" and lift depression. Unfortunately, the serotonin-deficit theory of depression is built on a foundation of tissue paper. How that came to be is a story in itself, but the basics are that in the 1950s scientists discovered, serendipitously, that a drug called iproniazid seemed to help some people with depression. Iproniazid increases brain levels of serotonin and norepinephrine. Ergo, low levels of those neurotransmitters must cause depression. More than 50 years on, the presumed effectiveness of antidepressants that act this way remains the chief support for the chemical-imbalance theory of depression. Absent that effectiveness, the theory hasn't a leg to stand on. Direct evidence doesn't exist. Lowering people's serotonin levels does not change their mood. And a new drug, tianeptine, which is sold in France and some other countries (but not the U.S.), turns out to be as effective as Prozac-like antidepressants that keep the synapses well supplied with serotonin. The mechanism of the new drug? It lowers brain levels of serotonin. "If depression can be equally affected by drugs that increase serotonin and by drugs that decrease it," says Kirsch, "it's hard to imagine how the benefits can be due to their chemical activity."

Perhaps antidepressants would be more effective at higher doses? Unfortunately, in 2002 Kirsch and colleagues found that high doses are hardly more effective than low ones, improving patients' depression-scale rating an average of 9.97 points vs. 9.57 points—a difference that is not statistically significant. Yet many doctors increase doses for patients who do not respond to a lower one, and many patients report improving as a result. There's a study of that, too. When researchers gave such nonresponders a higher dose, 72 percent got much better, their symptoms dropping by 50 percent or more. The catch? Only half the patients really got a higher dose. The rest, unknowingly, got the original, "ineffective" dose. It is hard to see the 72 percent who got much better on ersatz higher doses as the result of anything but the power of expectation: the doctor upped my dose, so I believe I'll get better.
Something similar may explain why some patients who aren't helped by one antidepressant do better on a second, or a third. This is often explained as "matching" patient to drug, and seemed to be confirmed by a 2006 federal study called STAR*D. Patients still suffering from depression after taking one drug were switched to a second; those who were still not better were switched to a third drug, and even a fourth. No placebos were used. At first blush, the results offered a ray of hope: 37 percent of the patients got better on the first drug, 19 percent more on their second, 6 percent more improved on their third try, and 5 percent more on their fourth. (Half of those who recovered relapsed within a year, however.)

Crepes

OOPs...this should go in my food blog...but anyway..it was a great discovery many years ago when John and I and Kelsy and Kim went to the biggest mall in America..The Great Mall Of America inMinneapolis and had a Banana Fosters Crepe at the Magic Pan. Since then, John
has always wanted to open up a crepe stand.

And when I was in Colorado last year I got to go to this great crepe stand that had hundreds of varietes of fillings, sweet or savory. I was smitten again!

Well...there is this place now...Harajuku Crepe..(Japanese on the Go)that is popluar in some places now..wait...Crepes are French..what is with the Japanese theme here?????



There is one such place in Beverly Hills and here is a review of it from yelp.

http://www.yelp.com/biz/harajuku-crepe-beverly-hills

Century City, CA

4/22/2010
Are you getting tired and hungry after spending your entire monthly check on shoes and bags from Rodeo Drive?

Worried that you won't be able to fit in that dress if you eat those calorie filled sprinkles cupcakes from next door?

Just sick and tired of waiting in the line at the Pinkberry?

Then try visiting "Harajuku Crepe"!

Trust me,
I love Japanese folks, culture and especially their food!
What I love best about them is that they take other's specialty stuff, spice things up and make it into theirs. They modify them so good that people think that some of these stuff actually came from Japan!

For example:

Croquette - came from the French croquer, "to crunch". It was a French invention that gained worldwide popularity, both as a delicacy and as a fast food. Croquette is a small fried food roll containing usually as main ingredients mashed potatoes, and/or minced meat.

Koroke - A japanese food consisting of potato and usually bits of vegetables inside all mashed up together. After mashing, it is deep fried in breaded balls. This is usually served with "bulldog sauce" a popular sauce used in Japanese cooking.

Curry -is a generic description used throughout European and American culture to describe a general variety of spiced dishes, best known in South Asian cuisines, especially Indian cuisine.

Kare ( Japanese curry) is one of the most popular dishes in Japan. It is commonly served in three main forms: curry rice Curry rice is most commonly referred to simply as 'curry' (kare).

I am a huge fan of Crepes.

A crêpe is a type of very thin pancake (usually made from wheat flour). the word is of French origin, deriving from the Latin crispa, meaning "curled."

Now...
Japanese "Street Crepes" are spanking awesome. Mainly they are " sweet crepes" where you can easily carry them like ice cream cones and eat them while you walk down the street.

Harajuku Creperie is owned by a fluent English speaking crepe man. ( Tried my rusty Japanese..and he gave me props with extra toppings! )

The creperie is located right next to pinkberry... and I mean.. who needs pinkberry if you can walk down rodeo drive with "oh so cool Japanese Harajuku Crepe?!?!"

Chic décor, fast and clean service, very kind and attentive, fresh ingredients!
They have 3 different selections of batters to choose from... and of course one of them is green tea batter.

Pretty awesome.



My hubby wanted me to make copies of this article....
I thought I would put it here on the blog to refer to later, if need be.

Note: Chia seeds are said to have more omega 3 oils than flax seeds! latimes.com/features/health/la-he-omega-3s-20100426,0,4578236.story
latimes.com
Omega-3 fatty acids are key to a healthier life

Research shows they promote heart health and reduce pain in people with rheumatoid arthritis. They also may help treat autism, bipolar disorder, depression, Alzheimer’s disease, ADHD and prostate cancer.
By Emily Sohn

Special to the Los Angeles Times

April 26, 2010

Pregnant women need them for their babies' brains. Kids need them to learn. Adults get healthier hearts from them. The do-it-all nutrients known as omega-3 fatty acids appear to reduce pain in people with rheumatoid arthritis — and may help treat autism, bipolar disorder, depression, Alzheimer's disease, ADHD and prostate cancer.

Even dogs and cats need omega-3s to stay healthy.

So eat more fish. Take fish oil pills (or their vegetarian counterparts). Start buying fortified foods. However you do it, you — like most Americans — could likely benefit from getting more omega-3 fatty acids, specifically DHA and EPA.

"There's very strong, medical-nutrition, literature-based evidence in humans suggesting that the average American would probably have a healthier life, a lower risk of dying from heart disease and improved brain function by consuming more fish, more supplements or more functional foods with DHA and EPA," says nutritional scientist Bruce Holub, of the University of Guelph in Ontario and executive director of the DHA/EPA Omega-3 Institute there.

But keep in mind, omega-3 fatty acids are not just a single nutrient. The term refers to a family of compounds that are naturally abundant in fish, seafood and algae, and it's their surprising chemical variety that may hold the key to improving our health.

Increasing evidence suggests that each type of omega-3 plays a different role. The benefits depend on the amount, one's life stage and specific medical conditions. Such complexity is something that guidelines, at least in the United States, don't yet reflect.

Researchers are still trying to clarify the details, but some health experts already are pushing for clearer recommendations that will help people reap the benefits of omega-3s without wasting money on useless varieties.

"There are strong indications that requirements for many groups should be higher and that there should be specific requirements for different types of omega-3s," says Bruce A. Watkins, professor of food science at Purdue University in West Lafayette, Ind., and director of the International Omega-3 Learning and Education Consortium for Health and Medicine, an educational resource.

The various types

Omega-3 fatty acids are long chains of carbon atoms that bond to each other in different ways to produce molecules with various functions. Out of the five forms that we consume, the three that matter most to human health are alpha-linolenic acid (ALA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).

Of those three, ALA is the only form that is specified in the United States' official guidelines with a dietary reference intake. According to the Institute of Medicine, men should consume 1.6 grams of the fatty acid a day. Women should get 1.1 grams.

Most Americans easily consume that much. Sources include flax, canola oil, soybean oil, olive oil, walnuts and other plant-based fats, many of which people eat every day. There are 1.3 grams of ALA in a tablespoon of canola oil and 7.6 grams in a tablespoon of flaxseed oil.

The problem is that, on its own, ALA has no known function in the body. The only reason it's required, Holub says, is because the human body can convert a small amount of ALA to DHA and EPA, which are far more essential for healthy brains, hearts and other bodily functions. The amount that gets converted, however, is not nearly enough.

Accumulating evidence now suggests that it is far more important to consume DHA and EPA directly — in amounts ranging from 200 milligrams to 4 grams a day, depending on the person. Salmon, herring, sardines and other oily varieties of fish have large amounts. Seafood, algae and meat have lesser amounts.

Although flaxseed doesn't appear to convey the benefits of fish oil, some algae contain omega-3s that are just as potent as those in fish. Further, fortified products contain omega-3s derived from the aquatic plants.

The health effects

Interest in fish-based omega-3s spiked in the 1970s, when scientists observed that Inuit people of Greenland ate tons of fatty fish but had extremely low rates of heart disease.

Decades later, in a landmark study published in 1999, Italian scientists studied more than 11,000 men who had suffered heart attacks. After 3-1/2 years, a group that took about a gram a day of EPA and DHA were 20% less likely to die than a group that didn't take omega-3 supplements.

In an even larger trial in 2007, Japanese researchers followed more than 18,000 people with high cholesterol for nearly five years and found that those who took 1.8 grams of EPA a day — in addition to cholesterol-lowering medications known as statins — were almost 20% less likely to suffer a major coronary event than people who took statins alone.

Those trials build on hundreds of smaller, more focused studies that clearly link EPA and DHA with heart health. (EPA and DHA are usually measured, and taken, together.)

For example, Holub says, studies show that for every extra gram of EPA and DHA a person takes per day, triglyceride levels drop by 8%, with benefits showing up in just two weeks. High triglyceride levels are a major risk factor for heart disease in Americans older than 35. Taking 2 to 4 grams of EPA and DHA a day for a couple of weeks could reduce levels in the blood by up to 32% in people with high triglyceride levels.

While EPA and DHA are both essential for heart health — they seem to lower blood pressure, reduce fat levels in the blood, slow the development of clots and avert abnormal heart rhythms, among other things — DHA is the star player in the developing brain and eyes.

Studies show that women who eat at least four servings of fish a week or take supplements of up to 1.1 grams of DHA daily while pregnant have kids with higher IQ scores through age 4. Their babies have lower rates of allergies, better sleep patterns and better vision. DHA-fortified moms also have lower rates of postpartum depression.

How they work

Scientists have yet to work out many of the details about how omega-3s work their magic, but inflammation is probably one clue, at least for some conditions. That would explain why high doses of DHA and EPA on top of more traditional medicines can reduce morning stiffness and joint pain in arthritis patients and can help reduce the amount of pain medication people need to take.

Brain-based disorders are another area of interest. Some studies have found lower blood levels of omega-3s in adults with Alzheimer's and kids with ADHD than in comparable groups without those problems.

"All of these pathologies are about things that have to do with cells misbehaving," says Philip Calder, a nutritionist and omega-3 researcher at the University of Southampton in England. "You can make cells behave more optimally by having enough omega-3 fatty acids. Then tissues behave properly, and you don't have these manifestations of disease."

To some extent, consumers are catching on. In a recent survey of more than 6,000 people who already take supplements, 74% took fish oil or other types of omega-3 supplements last year, making them more popular than multivitamins, found ConsumerLab.com, an independent health-products testing company.

And in 2009, sales of products enriched with omega-3s, omega-6s and omega-9s jumped by 42% compared with 2008, according to market research firm Nielsen.

Looking ahead

To date, however, most Americans don't appear to be getting nearly enough omega-3s.

Americans consume fish an average of only once every 10 days, Holub says, and 50% don't consume fish over a seven-day period. Supplements, meanwhile, are not a universal dietary staple. As a result, he points out, the average intake of DHA and EPA in the U.S. is an eighth of what people normally get in Japan and a quarter of what many experts now think we need.

Food labels aren't especially helpful. The packaging on a box of granola bars or loaf of bread might tout omega-3s even though they contain a form that doesn't do much in the body or their concentrations of nutrients might be too small to make a difference.

And even when detailed information is available, it's not always clear how much a given individual should get.

Regardless, consumption needs to rise, nutrition experts say.

"Why have societies consumed fish for so many centuries?" Watkins says. "I think we're just beginning to understand the benefits."

Health@latimes.com
Copyright © 2010, The Los Angeles Times

Friday, April 23, 2010

Rush's Op Ed


This microphone represents Rush Limbaugh, who I listen to once in a while. This article today in the Wall Street Journal by him is worth reading.

Liberals and the Violence Card

Conservative protest is motivated by a love of what America stands for.
By RUSH LIMBAUGH


The latest liberal meme is to equate skepticism of the Obama administration with a tendency toward violence. That takes me back 15 years ago to the time President Bill Clinton accused "loud and angry voices" on the airwaves (i.e., radio talk-show hosts like me) of having incited Oklahoma City bomber Timothy McVeigh. What self-serving nonsense. Liberals are perfectly comfortable with antigovernment protest when they're not in power.

From the halls of the Ivy League to the halls of Congress, from the antiwar protests during the Vietnam War and the war in Iraq to the anticapitalist protests during International Monetary Fund and World Bank meetings, we're used to seeing leftist malcontents take to the streets. Sometimes they're violent, breaking shop windows with bricks and throwing rocks at police. Sometimes there are arrests. Not all leftists are violent, of course. But most are angry. It's in their DNA. They view the culture as corrupt and capitalism as unjust.

Former President Bill Clinton smiles as he receives a medallion from Cathy Keating, wife of former Oklahoma Governor Frank Keating, as a part of the Reflections of Hope Award ceremony in Oklahoma City. (photo)

Now the liberals run the government and they're using their power to implement their radical agenda. Mr. Obama and his party believe that the election of November 2008 entitled them to make permanent, "transformational" changes to our society. In just 16 months they've added more than $2 trillion to the national debt, essentially nationalized the health-care system, the student-loan industry, and have their sights set on draconian cap-and-trade regulations on carbon emissions and amnesty for illegal aliens.

Had President Obama campaigned on this agenda, he wouldn't have garnered 30% of the popular vote.

Like the millions of citizens who've peacefully risen up and attended thousands of rallies in protest, I seek nothing more than the preservation of the social contract that undergirds our society. I do not hate the government, as the left does when it is not running it. I love this country. And because I do, I insist that the temporary inhabitants of high political office comply with the Constitution, honor our God-given unalienable rights, and respect our hard-earned private property. For this I am called seditious, among other things, by some of the very people who've condemned this society?

Former President Bill Clinton broadened his warning that Tea Party protesters could fuel violence reminiscent of the Oklahoma City bombing. Video courtesy of Fox News.

I reject the notion that America is in a well-deserved decline, that she and her citizens are unexceptional. I do not believe America is the problem in the world. I believe America is the solution to the world's problems. I reject a foreign policy that treats our allies like our enemies and our enemies like our allies. I condemn the president traveling the world apologizing for America's great contributions to mankind. And I condemn his soft-pedaling the dangers we face from terrorism. For this I am inciting violence?

Few presidents have sunk so low as Mr. Clinton did with his accusations about Oklahoma City. Last week—on the very day I was contributing to and raising more than $3 million to fight leukemia and lymphoma on my radio program—Mr. Clinton used the 15th anniversary of that horrific day to regurgitate his claims about talk radio.
At a speech delivered last Friday at the Center for American Progress in Washington, D.C., the former president said: [T]here were a lot of people who were in the business back then of saying that the biggest threat to our liberty and the cause of our domestic economic problem was the federal government itself. And we have to realize that there were others who fueled this both because they agreed with it and because it was in their advantage to do so. . . . We didn't have blog sites back then so the instrument of carrying this forward was basically the right-wing radio talk show hosts and they understand clearly that emotion was more powerful than reason most of the time."

Timothy McVeigh was incensed by the Clinton administration's 1993 siege on the Branch Davidian compound in Waco, Texas. It's no coincidence that the bombing took place two years to the day of the Waco siege. McVeigh was not inspired by anything I said or believe and to say otherwise is outright slander. In the aftermath of the bombing, I raised millions of dollars for the children of federal employees killed in that cowardly attack through my association with the Marine Corp Law Enforcement Foundation.

Let me just say it. The Obama/Clinton/media left are comfortable with the unrest in our society today. It allows them to blame and demonize their opponents (doctors, insurance companies, Wall Street, talk radio, Fox News) in order to portray their regime as the great healer of all our ills, thus expanding their power and control over our society.

A clear majority of the American people want no part of this. They instinctively know that the Obama way is not how things get done in this country. They are motivated by love. Not hate, not sedition. They love their country and want to save it from those who do not.

Mr. Limbaugh is a nationally syndicated radio talk-show host.
http://online.wsj.com/article/SB10001424052748703876404575199743566950622.html?mod=WSJ_hp_mostpop_read

Some Italian History

When I read articles like this, I feel like I understand Europe a little better. Someday I will go to Europe.



The book is....
Ravenna in Late Antiquity
By Deborah Mauskopf Deliyannis
Cambridge, 444 pages,$95

The other picture is...
A groin-vault mosaic in the sixth-century Capella Arcivescovile (the chapel of St. Andrew) in Ravenna, Italy. Picture courtesy of
Dr. Urs Peschlow/Cambridge University Press

Where Kings and Emperors Once Lived

By STUART FERGUSON
Ravenna, along Italy's northeast coast, is in many ways a typically modern city, with tourist-welcoming hotels, outdoor cafés, Vespas zipping by and, a few miles away, populous beaches that ease their way down into the Adriatic Sea. But it is also a place with a fabled imperial history and a host of literary resonances: Boccaccio lived in Ravenna in the mid-14th century; Dante wrote the "Divine Comedy" there and is buried alongside one of the city's churches; and Byron spent a memorable several months in Ravenna in 1820-21 (with a mistress, naturally) while he composed parts of "Don Juan," his mock-epic about daring deeds and lost loves. Oscar Wilde later paid tribute to the city: "Mighty thy name when Rome's lean eagles flew . . . [but now] in ruined loveliness thou liest dead."

Dr. Urs Peschlow/Cambridge University Press A groin-vault mosaic in the sixth-century Capella Arcivescovile (the chapel of St. Andrew) in Ravenna, Italy.
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In fact, Ravenna's heyday— roughly the fifth century to the eighth—is anything but dead. It is alive in an array of churches, basilicas, baptisteries and tombs, many with evocative images on their surfaces and interiors. Other periods make themselves present in Ravenna, too. There are Roman ruins that reach back to the days of the republic and city gates from the late Middle Ages and Renaissance—and a 15th-century castle from the era of Venetian rule.

Ravenna was once the home of emperors, kings and viceroys, many of whom tried to leave behind a material legacy as grand as their aspirations to political glory. Poised between West and East, the city served as a major outpost for two empires: those of Rome and Byzantium. "Ravenna in Late Antiquity," by Deborah Mauskopf Deliyannis, is both a narrative history of the city's ruling elites and a survey of its architectural and artistic treasures.

These treasures are worth pausing over. Staring down from the walls of the Basilica of San Vitale, for instance, are portraits in stone and glass tesserae of several figures. The Byzantine ruler Justinian (483-535) is shown wearing a halo and, well below, startling red and purple shoes; his archbishop Maximimian is wrapped in a white tunic and gold vestment, with the pallium draped over his shoulders, his "blazing blue eyes" staring from a "lean, intense face," as Ms. Deliyannis puts it; the Empress Theodora, for her part, stands among eunuchs and female attendants holding a gem-encrusted chalice. No visitor to the basilica in the early sixth century, peering up at such august notables, would have any doubts about who was in charge, in the earthly realm at least.

In fact, Justinian and Theodora never lived in Ravenna—and apparently never visited. But many other rulers made the city their home. For example: the Western Roman Emperor Honorius, who moved the seat of government there in 402; the Visigoth kings, who swooped down from the north in the fifth century and controlled, for a time, most of the Italian peninsula; and the so-called exarchs—the viceroys who governed Italy from Ravenna on behalf of the Byzantine emperor well into the eighth century, before the Franks and Lombards arrived from Gaul and the Danube Valley and the city became more a repository of architectural fragments than a thriving capital.

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It was in Ravenna that Honorius's half-sister—the devout, powerful empress and regent Galla Placidia (c. 388-450)—would sometimes spend her nights prostrate on the marble floor of Santa Croce (the Church of the Holy Cross) praying. Her purported tomb, the so-called "mausoleum of Galla Placidia," is still a chapel within the church. Its dark-blue domed ceiling is decorated with 567 eight-pointed gold stars that make the entire space seem like a magnificent jewel box.

Another striking space from Ravenna's years of imperial glory, the Capella Arcivescovile (the chapel of St. Andrew), was built by Bishop Peter II during the sixth century. At the apex of its groin vault are mosaics depicting a gold chrismon (a Christian symbol) against a blue background. Four angels hold the chrismon aloft, while at their feet lurk beasts of the Apocalypse. It is enough to make even the most blasé visitor pause and consider where he will spend eternity."

Ms. Deliyannis's narrative is at its most fascinating and dense when she enters the sixth century, when Ravenna served as the capital for the Visigoth king Theodoric. He had come to power memorably. After years of war with his rival Odoacer, he proposed a "reconciliation" banquet in Ravenna in 493. To quote from John Julius Norwich's "The Middle Sea" (2006): "As his guest took his place in the seat of honor, Theodoric stepped forward and, with one tremendous stroke of his sword, clove through the body of Odoacer from collarbone to thigh."

DetailsRavenna in Late Antiquity
By Deborah Mauskopf Deliyannis
Cambridge, 444 pages, $95
.
Theodoric reigned for the next three decades, and Ravenna became, Ms. Deliyannis writes, "a center of Arian Christianity." The city churned with rival Christian sects. The Arians believed Jesus to be a fully human, unequal member of the Trinity, an idea that put them at odds with other contending movements, including the Nestorians (who said Christ had two separate persons, one human and one divine) and the Eutychians (for whom Christ's divine nature subsumed his human one).

In the sixth century, rivalrous believers argued and worshiped in Ravenna, though only the Arians and the members of the official Rome-led church had their own places of worship. The Arians, it should be said, eventually lost out in the struggle for doctrinal supremacy. Arian figures originally portrayed on the south wall of the great church of Sant'Apolllinare Nuovo in Ravenna were "disappeared" a century later, tessera by tessera, like disgraced leaders in Stalinist-era photographs. Only images of their hands were left intact—most likely to remind viewers that dissenters had challenged Orthodox views and lost.

For all its future pre-eminence, Ravenna was considered great even in the first century, as Ms. Deliyannis reminds us. It was then that the geographer Strabo first described the city: "Situated in the marshes is the great Ravenna, built entirely on piles, and traversed by canals, which you cross by bridges or ferry-boats. At the full tides it is washed by a considerable quantity of sea-water, as well as by the river, and thus the sewage is carried off. And the air purified; in fact, the district is considered so salubrious that the governors have selected it a spot to bring up and exercise the gladiators in."

Ravenna was a major base for the Roman navy, and Julius Caesar spent the night in the city before he crossed the Rubicon in 49 B.C. The epigram-writer Martial complained that potable water was so rare that when he ordered wine mixed with it, he got his drink neat and thus was cheated.

After the Gallo-Roman aristocrat Sidonius Apollinaris visited Ravenna in 467, he too groused about the soggy conditions but remarked on the decline in morals brought about by the city's new status as a capital: "Ravenna is a mere marsh where all the conditions of life are reversed, where walls fall and waters stand . . . the clergy lend money while the Syrian merchants sing psalms, the elderly apply themselves to ball games, the youths to dice, the eunuchs to weapons and the federate troops to letters."

The city's natural defenses and access to the sea helped it to achieve prominence: As the western Roman Empire began to crumble in the late fourth century, its emperors sought a strategic refuge that could be easily re-supplied by sea and easily reached by their imperial counterparts in Constantinople. Ravenna, in short, was not as vulnerable as Rome, and its population of only 10,000 was easier to overawe than the Roman mob.

From the research of historians and from imperial decrees we know that Ravenna housed a vast bureaucracy (with accountants, registrars, secretaries, clerks and notaries) and that its rulers left behind "marvelous" palaces, theaters, aqueducts and a mint, but none of these structures is in evidence today. Still, the "surviving works of art and architecture," Ms. Deliyannis says, allow us still to "experience Ravenna, if only in fragments, as did its inhabitants."

The illustrations and diagrams in "Ravenna in Late Antiquity" add to our understanding of the city's history and iconography—and can even serve as a kind of guidebook to an ambitious tourist. Because of the marshy setting and the passage of time, the original ground floors of some of Ravenna's existing monuments are below the modern-day street level, giving some a more squat appearance than they originally had. But step inside and time has seemingly stood still.

— Mr. Ferguson is a Rossetter House Foundation Scholar of the Florida Historical Society.

http://online.wsj.com/article/SB10001424052748703630404575053701579423056.html?KEYWORDS=Kings+and+Emperors

Wednesday, April 21, 2010

Be Careful How You Vote in 2010


Picture courtesy of http://drianostudios.com/assigned_illustrations.htm
Narrative courtesy of http://zh-cn.facebook.com/topic.php?uid=471458670367&topic=11864
The ant works hard in the withering heat all summer long, building his house and laying up supplies for the winter.

The grasshopper thinks the ant is a fool and laughs and dances and plays the summer away..

Come winter, the ant is warm and well fed.

The grasshopper has no food or shelter, so he dies out in the cold.

MORAL OF THE STORY: Be responsible for yourself!



--------------------------------------------------------------------------------



MODERN VERSION

The ant works hard in the withering heat and the rain all summer long, building his house and laying up supplies for the winter.

The grasshopper thinks the ant is a fool and laughs and dances and plays the summer away.

Come winter, the shivering grasshopper calls a press conference and demands to know why the ant should be allowed to be warm and well fed while he is cold and starving.

CBS, NBC, PBS, CNN, and ABC show up to provide pictures of the shivering grasshopper next to a video of the ant in his comfortable home with a table filled with food.

America is stunned by the sharp contrast..

How can this be, that in a country of such wealth, this poor grasshopper is allowed to suffer so?

Kermit the Frog appears on Oprah with the grasshopper and everybody cries when they sing, 'It's Not Easy Being Green.'

Acorn stages a demonstration in front of the ant's house where the news stations film the group singing, 'We shall overcome.' Rev. Jeremiah Wright then has the group kneel down to pray to God for the grasshopper's sake.

President Obama condemns the ant and blames President Bush, President Reagan, Christopher Columbus, and the Pope for the grasshopper's plight.

Nancy Pelosi & Harry Reid exclaim in an interview with Larry King that the ant has gotten rich off the back of the grasshopper, and both call for an immediate tax hike on the ant to make him pay his fair share.

Finally, the EEOC drafts the Economic Equity & Anti-Grasshopper Act retroactive to the beginning of the summer.

The ant is fined for failing to hire a proportionate number of green bugs and, having nothing left to pay his retroactive taxes, his home is confiscated by the Government Green Czar and given to the grasshopper.

The story ends as we see the grasshopper and his freeloading friends finishing up the last bits of the ant's food while the government house he is in, which, as you recall, just happens to be the ant's old house, crumbles around them because the grasshopper doesn't maintain it.

The ant has disappeared into the snow, never to be seen again.

The grasshopper is found dead in a drug related incident, and the house, now abandoned, is taken over by a gang of spiders who terrorize the ramshackle, once prosperous and once peaceful, neighborhood.

The entire Nation collapses bringing the rest of the free world with it.

MORAL OF THE STORY: Be careful how you vote in 2010

http://zh-cn.facebook.com/topic.php?uid=471458670367&topic=11864

Dr. Mercola

Dr. Mercola has recently published this article. I get all his articles in his newsletters direct to my email account. I thought this was important to save on my blog.

It seems that sugar consumption may be the reason cancer is on the rise.

It is so much fun to eat candy, cookies, brownies, ice cream sundaes, etc! I love all these things. Now I must re-evaluate! And chose wisely accordingly.



This Addictive Commonly Used Food Feeds Cancer Cells, Triggers Weight Gain, and Promotes Premature Aging
Posted by Dr. Mercola | April 20 2010 | 250,185 views
Is sugar a sweet old friend that is secretly plotting your demise?
There is a vast sea of research suggesting that it is. Science has now shown us, beyond any shadow of a doubt, that sugar in your food, in all its myriad of forms, is taking a devastating toll on your health.
The single largest source of calories for Americans comes from sugar—specifically high fructose corn syrup. Just take a look at the sugar consumption trends of the past 300 years:[1]
In 1700, the average person consumed about 4 pounds of sugar per year.
In 1800, the average person consumed about 18 pounds of sugar per year.
In 1900, individual consumption had risen to 90 pounds of sugar per year.
In 2009, more than 50 percent of all Americans consume one-half pound of sugar PER DAY—translating to a whopping 180 pounds of sugar per year!
Sugar is loaded into your soft drinks, fruit juices, sports drinks, and hidden in almost all processed foods—from bologna to pretzels to Worcestershire sauce to cheese spread. And now most infant formula has the sugar equivalent of one can of Coca-Cola, so babies are being metabolically poisoned from day one if taking formula.
No wonder there is an obesity epidemic in this country.
Today, 32 percent of Americans are obese and an additional one-third are overweight. Compare that to 1890, when a survey of white males in their fifties revealed an obesity rate of just 3.4 percent. In 1975, the obesity rate in America had reached 15 percent, and since then it has doubled.
Carrying excess weight increases your risk for deadly conditions such as heart disease, kidney disease and diabetes.
In 1893, there were fewer than three cases of diabetes per 100,000 people in the United States. Today, diabetes strikes almost 8,000 out of every 100,000 people.[1]
You don’t have to be a physician or a scientist to notice America’s expanding waistline. All you have to do is stroll through a shopping mall or a schoolyard, or perhaps glance in the mirror.
Sugars 101 -- Basics of How to Avoid Confusion on this Important Topic
It is easy to become confused by the various sugars and sweeteners. So here is a basic overview:
Dextrose, fructose and glucose are all monosaccharides, known as simple sugars. The primary difference between them is how your body metabolizes them. Glucose and dextrose are essentially the same sugar. However, food manufacturers usually use the term “dextrose” in their ingredient list.
The simple sugars can combine to form more complex sugars, like the disaccharide sucrose (table sugar), which is half glucose and half fructose.
High fructose corn syrup (HFCS) is 55 percent fructose and 45 percent glucose.
Ethanol (drinking alcohol) is not a sugar, although beer and wine contain residual sugars and starches, in addition to alcohol.
Sugar alcohols like xylitol, glycerol, sorbitol, maltitol, mannitol, and erythritol are neither sugars nor alcohols but are becoming increasingly popular as sweeteners. They are incompletely absorbed from your small intestine, for the most part, so they provide fewer calories than sugar but often cause problems with bloating, diarrhea and flatulence.
Sucralose (Splenda) is NOT a sugar, despite its sugar-like name and deceptive marketing slogan, “made from sugar.” It’s a chlorinated artificial sweetener in line with aspartame and saccharin, with detrimental health effects to match.
Agave syrup, falsely advertised as “natural,” is typically HIGHLY processed and is usually 80 percent fructose. The end product does not even remotely resemble the original agave plant.
Honey is about 53 percent fructose[2], but is completely natural in its raw form and has many health benefits when used in moderation, including as many antioxidants as spinach.
Stevia is a highly sweet herb derived from the leaf of the South American stevia plant, which is completely safe (in its natural form). Lo han (or luohanguo) is another natural sweetener, but derived from a fruit.
All Sugars are Not Equal
Glucose is the form of energy you were designed to run on. Every cell in your body, every bacterium—and in fact, every living thing on the Earth—uses glucose for energy.
But as a country, sucrose is no longer the sugar of choice. It’s now fructose.
If your diet was like that of people a century ago, you’d consume about 15 grams per day—a far cry from the 73 grams per day the typical person gets from sweetened drinks. In vegetables and fruits, it’s mixed in with vitamins, minerals, enzymes, and beneficial phytonutrients, all which moderate the negative metabolic effects. Amazingly, 25 percent of people actually consume more than 130 grams of fructose per day.
Making matters worse, all of the fiber has been removed from processed foods, so there is essentially no nutritive value at all. And the very products most people rely on to lose weight—the low-fat diet foods—are often the ones highest in fructose.
It isn’t that fructose itself is bad—it is the MASSIVE DOSES you’re exposed to that make it dangerous.
There are two overall reasons fructose is so damaging:
Your body metabolizes fructose in a much different way than glucose. The entire burden of metabolizing fructose falls on your liver.
People are consuming fructose in enormous quantities, which has made the negative effects much more profound.
The explosion of soda consumption is the major cause of this.
Today, 55 percent of sweeteners used in food and beverage manufacturing are made from corn, and the number one source of calories in America is soda, in the form of high fructose corn syrup.
Food and beverage manufacturers began switching their sweeteners from sucrose to corn syrup in the 1970s when they discovered that HFCS was not only far cheaper to make, it’s about 20 percent sweeter than conventional table sugar that has sucrose.
HFCS contains the same two sugars as sucrose but is more metabolically risky to you, due to its chemical form.
The fructose and the glucose are not bound together in HFCS, as they are in table sugar, so your body doesn’t have to break it down. Therefore, the fructose is absorbed immediately, going straight to your liver.
Too Much Fructose Creates a Metabolic Disaster in Your Body
Dr. Robert Lustig, Professor of Pediatrics in the Division of Endocrinology at the University of California, San Francisco, has been a pioneer in decoding sugar metabolism. His work has highlighted some major differences in how different sugars are broken down and used by the human body.
I highly recommend watching Lustig’s lecture in its entirety if you want to learn how fructose is ruining your health biochemically.
As I mentioned earlier, after eating fructose, most of the metabolic burden rests on your liver. This is NOT the case with glucose, of which your liver breaks down only 20 percent. Nearly every cell in your body utilizes glucose, so it’s normally “burned up” immediately after consumption.
So where does all of this fructose go, once you consume it?
Onto your thighs. It is turned into FAT (VLDL and triglycerides), which means more fat deposits throughout your body.
Eating Fructose is Far Worse than Eating Fat
However, the physiological problems of fructose metabolism extend well beyond a couple of pant sizes:
Fructose elevates uric acid, which decreases nitric oxide, raises angiotensin, and causes your smooth muscle cells to contract, thereby raising your blood pressure and potentially damaging your kidneys.[1]

Increased uric acid also leads to chronic, low-level inflammation, which has far-reaching consequences for your health. For example, chronically inflamed blood vessels lead to heart attacks and strokes; also, a good deal of evidence exists that some cancers are caused by chronic inflammation. (See the next section for more about uric acid.)
Fructose tricks your body into gaining weight by fooling your metabolism—it turns off your body’s appetite-control system. Fructose does not appropriately stimulate insulin, which in turn does not suppress ghrelin (the “hunger hormone”) and doesn’t stimulate leptin (the “satiety hormone”), which together result in your eating more and developing insulin resistance.[3] [4]
Fructose rapidly leads to weight gain and abdominal obesity (“beer belly”), decreased HDL, increased LDL, elevated triglycerides, elevated blood sugar, and high blood pressure—i.e., classic metabolic syndrome.
Fructose metabolism is very similar to ethanol metabolism, which has a multitude of toxic effects, including NAFLD (non-alcoholic fatty liver disease). It’s alcohol without the buzz.
These changes are not seen when humans or animals eat starch (or glucose), suggesting that fructose is a “bad carbohydrate” when consumed in excess of 25 grams per day. It is probably the one factor responsible for the partial success of many “low-carb” diets.
One of the more recent findings that surprised researchers is that glucose actually accelerates fructose absorption, making the potential health risks from HFCS even more profound.[1]
You can now see why fructose is the number one contributing factor to the current obesity epidemic.
Is Uric Acid the New Cholesterol?
By now you are probably aware of the childhood obesity epidemic in America—but did you know about childhood hypertension?
Until recently, children were rarely diagnosed with high blood pressure, and when they were, it was usually due to a tumor or a vascular kidney disease.
In 2004, a study showed hypertension among children is four times higher than predicted: 4.5 percent of American children have high blood pressure. Among overweight children, the rate is 10 percent. It is thought that obesity is to blame for about 50 percent of hypertension cases in adolescents today.[1]
Even more startling is that 90 percent of adolescents who have high blood pressure have elevated uric acid levels.
This has led researchers to ask, what does uric acid have to do with obesity and high blood pressure?
In his groundbreaking book, The Sugar Fix: The High-Fructose Fallout That is Making You Fat and Sick, Dr. Robert J. Johnson makes a compelling argument for a previously unrecognized connection between excess sugar consumption and high uric acid levels.
There are more than 3,500 articles to date showing a strong relationship between uric acid and obesity, heart disease, hypertension, stroke, kidney disease, and other conditions. In fact, a number of studies have confirmed that people with elevated serum uric acid are at risk for high blood pressure, even if they otherwise appear to be perfectly healthy.
Uric acid levels among Americans have risen significantly since the early half of the 20th Century. In the 1920s, average uric acid levels were about 3.5 ml/dl. By 1980, average uric acid levels had climbed into the range of 6.0 to 6.5 ml/dl and are probably much higher now.
How Does Your Body Produce Uric Acid?
It’s a byproduct of cellular breakdown. As cells die off, DNA and RNA degrade into chemicals called purines. Purines are further broken down into uric acid.
Fructose increases uric acid through a complex process that causes cells to burn up their ATP rapidly, leading to “cell shock” and increased cell death. After eating excessive amounts of fructose, cells become starved of energy and enter a state of shock, just as if they have lost their blood supply. Massive cellular die-off leads to increased uric acid levels.
And cells that are depleted of energy become inflamed and more susceptible to damage from oxidative stress. Fat cells actually become “sickly,” bloating up with excessive amounts of fat.
There is a simple, inexpensive blood test for determining your uric acid level, which I recommend you have done as part of your routine health checkups. Your level should be between 3.0 and 5.5 mg/dl, optimally.
There is little doubt in my mind that your uric acid level is a more potent predictor of cardiovascular and overall health than your total cholesterol level is. Yet virtually no one is screening for this.
Now that you know the truth you don’t have to be left out in the cold, as this is a simple and relatively inexpensive test that you can get at any doctor’s office. Odds are very good your doctor is clueless about the significance of elevated uric acid levels, so it will not likely be productive to engage in a discussion with him unless he is truly an open-minded truth seeker.
Merely get your uric acid level, and if it is over 5 then eliminate as much fructose as you can (also eliminate all beer), and retest your level in a few weeks.
Sugar Sensitization Makes the Problem Even WORSE!
There is yet another problem with sugar—a self-perpetuating one.
According to Dr. Johnson1, sugar activates its own pathways in your body—those metabolic pathways become “upregulated.” In other words, the more sugar you eat, the more effective your body is in absorbing it; and the more you absorb, the more damage you’ll do.
You become “sensitized” to sugar as time goes by, and more sensitive to its toxic effects as well.
The flip side is, when people are given even a brief sugar holiday, sugar sensitization rapidly decreases and those metabolic pathways become “downregulated.” Research tells us that even two weeks without consuming sugar will cause your body to be less reactive to it.
Try it for yourself! Take a two-week sugar sabbatical and see how different you feel.
Are Fruits Good or Bad for You?
Keep in mind that fruits also contain fructose, although an ameliorating factor is that whole fruits also contain vitamins and other antioxidants that reduce the hazardous effects of fructose.
Juices, on the other hand, are nearly as detrimental as soda, because a glass of juice is loaded with fructose, and a lot of the antioxidants are lost.
It is important to remember that fructose alone isn’t evil as fruits are certainly beneficial. But when you consume high levels of fructose it will absolutely devastate your biochemistry and physiology. Remember the AVERAGE fructose dose is 70 grams per day which exceeds the recommend limit by 300 percent.
So please BE CAREFUL with your fruit consumption. You simply MUST understand that because HFCS is so darn cheap, it is added to virtually every processed food. Even if you consumed no soda or fruit, it is very easy to exceed 25 grams of hidden fructose in your diet.
If you are a raw food advocate, have a pristine diet, and exercise very well, then you could be the exception that could exceed this limit and stay healthy.

Dr. Johnson has a handy chart, included below, which you can use to estimate how much fructose you’re getting in your diet. Remember, you are also likely getting additional fructose if you consume any packaged foods at all, since it is hidden in nearly all of them.
```````````
Fruit Serving Size Grams of Fructose

Limes 1 medium 0 Lemons 1 medium 0.6 Cranberries 1 cup 0.7 Passion fruit 1 medium 0.9 Prune 1 medium 1.2 Apricot 1 medium 1.3 Guava 2 medium 2.2 Date (Deglet Noor style) 1 medium 2.6 Cantaloupe 1/8 of med. melon 2.8 Raspberries 1 cup 3.0 Clementine 1 medium 3.4 Kiwifruit 1 medium 3.4 Blackberries 1 cup 3.5 Star fruit 1 medium 3.6 Cherries, sweet 10 3.8 Strawberries 1 cup 3.8 Cherries, sour 1 cup 4.0 Pineapple 1 slice
(3.5" x .75") 4.0 Grapefruit, pink or red 1/2 medium 4.3

Boysenberries 1 cup 4.6 Tangerine/mandarin orange 1 medium 4.8 Nectarine 1 medium 5.4 Peach 1 medium 5.9 Orange (navel) 1 medium 6.1 Papaya 1/2 medium 6.3 Honeydew 1/8 of med melon 6.7 Banana 1 medium 7.1 Blueberries 1 cup 7.4 Date (Medjool) 1 medium 7.7 Apple (composite) 1 medium 9.5 Persimmon 1 medium 10.6 Watermelon 1/16 med. melon 11.3 Pear 1 medium 11.8 Raisins 1/4 cup 12.3 Grapes, seedless (green or red) 1 cup 12.4 Mango 1/2 medium 16.2 Apricots, dried 1 cup 16.4 Figs, dried 1 cup 23.0

```````````
In addition to limiting your intake of fructose, you should eliminate all sweetened beverages and fruit juices (including all artificial sweeteners) and drink only pure water and raw milk.
You can buy pure glucose (dextrose) as a sweetener for about $1 a pound. It is only 70% as sweet as sucrose, so you’ll end up using a bit more of it for the same amount of sweetness, making it slightly more expensive than sucrose—but still well worth it for your health as it has ZERO grams of fructose.
Remember that glucose can be used directly by every cell in your body and as such is far safer than the metabolic poison fructose.
Beer is also a good beverage to AVOID since it increases uric acid levels, just like fructose does, resulting in many of the same toxic effects.
All alcoholic beverages cause you to produce excess uric acid (and block your kidneys from excreting it), but beer seems to have a more pronounced effect on uric acid levels because it’s a rich source of guanosine, the type of purine that is most readily absorbed by the body.1
76 Additional Ways Sugar Can Ruin Your Health
In addition to throwing off your body's homeostasis and wreaking havoc on your metabolic processes, excess sugar has a number of other significant consequences.
Nancy Appleton, PhD, author of the book Lick the Sugar Habit[5], contributed an extensive list of the many ways sugar can ruin your health from a vast number of medical journals and other scientific publications.
Sugar can suppress your immune system and impair your defenses against infectious disease.[6] [7]
Sugar upsets the mineral relationships in your body: causes chromium and copper deficiencies and interferes with absorption of calcium and magnesium.[8] [9] [10] [11]
Sugar can cause a rapid rise of adrenaline, hyperactivity, anxiety, difficulty concentrating, and crankiness in children.[12] [13]
Sugar can produce a significant rise in total cholesterol, triglycerides and bad cholesterol and a decrease in good cholesterol.[14] [15] [16] [17]
Sugar causes a loss of tissue elasticity and function.[18]
Sugar feeds cancer cells and has been connected with the development of cancer of the breast, ovaries, prostate, rectum, pancreas, biliary tract, lung, gallbladder and stomach.[19] [20] [21] [22] [23] [24] [25]
Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia.[26] [27]
Sugar can weaken eyesight.[28] 1
Sugar can cause many problems with the gastrointestinal tract including: an acidic digestive tract, indigestion, malabsorption in patients with functional bowel disease, increased risk of Crohn's disease, and ulcerative colitis.[29] [30] [31] [32] [33]
Sugar can cause premature aging.[34] In fact, the single most important factor that accelerates aging is insulin, which is triggered by sugar. 1
Sugar can lead to alcoholism.[35]
Sugar can cause your saliva to become acidic, tooth decay, and periodontal disease.[36] [37] [38]
Sugar contributes to obesity. [39] 1
Sugar can cause autoimmune diseases such as: arthritis, asthma, and multiple sclerosis.[40] [41] [42]
Sugar greatly assists the uncontrolled growth of Candida Albicans (yeast infections) [43]
Sugar can cause gallstones.[44]
Sugar can cause appendicitis.[45]
Sugar can cause hemorrhoids.[46]
Sugar can cause varicose veins.[47]
Sugar can elevate glucose and insulin responses in oral contraceptive users.[48]
Sugar can contribute to osteoporosis.[49]
Sugar can cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes.[50] [51] [52]
Sugar can lower your Vitamin E levels.[53]
Sugar can increase your systolic blood pressure.[54]
Sugar can cause drowsiness and decreased activity in children.[55]
High sugar intake increases advanced glycation end products (AGEs),which are sugar molecules that attach to and damage proteins in your body. AGEs speed up the aging of cells, which may contribute to a variety of chronic and fatal diseases. [56] 1
Sugar can interfere with your absorption of protein.[57]
Sugar causes food allergies.[58]
Sugar can cause toxemia during pregnancy.[59]
Sugar can contribute to eczema in children.[60]
Sugar can cause atherosclerosis and cardiovascular disease.[61] [62]
Sugar can impair the structure of your DNA.[63]
Sugar can change the structure of protein and cause a permanent alteration of the way the proteins act in your body.[64] [65]
Sugar can make your skin age by changing the structure of collagen.[66]
Sugar can cause cataracts and nearsightedness.[67] [68]
Sugar can cause emphysema.[69]
High sugar intake can impair the physiological homeostasis of many systems in your body.[70]
Sugar lowers the ability of enzymes to function.[71]
Sugar intake is higher in people with Parkinson's disease.[72]
Sugar can increase the size of your liver by making your liver cells divide, and it can increase the amount of fat in your liver, leading to fatty liver disease.[73] [74]
Sugar can increase kidney size and produce pathological changes in the kidney such as the formation of kidney stones.[75] [76] Fructose is helping to drive up rates of kidney disease. 1
Sugar can damage your pancreas.[77]
Sugar can increase your body's fluid retention.[78]
Sugar is enemy #1 of your bowel movement.[79]
Sugar can compromise the lining of your capillaries.[80]
Sugar can make your tendons more brittle.[81]
Sugar can cause headaches, including migraines.[82]
Sugar can reduce the learning capacity, adversely affect your children's grades and cause learning disorders.[83] [84]
Sugar can cause an increase in delta, alpha, and theta brain waves, which can alter your ability to think clearly.[85]
Sugar can cause depression.[86]
Sugar can increase your risk of gout.[87]
Sugar can increase your risk of Alzheimer's disease.[88] MRI studies show that adults 60 and older who have high uric acid are four to five times more likely to have vascular dementia, the second most common form of dementia after Alzheimer’s.1
Sugar can cause hormonal imbalances such as: increasing estrogen in men, exacerbating PMS, and decreasing growth hormone.[89] [90] [91] [92]
Sugar can lead to dizziness.[93]
Diets high in sugar will increase free radicals and oxidative stress.[94]
A high sucrose diet of subjects with peripheral vascular disease significantly increases platelet adhesion.[95]
High sugar consumption by pregnant adolescents can lead to a substantial decrease in gestation duration and is associated with a twofold-increased risk for delivering a small-for-gestational-age (SGA) infant.[96] [97]
Sugar is an addictive substance.[98]
Sugar can be intoxicating, similar to alcohol.[99]
Sugar given to premature babies can affect the amount of carbon dioxide they produce.[100]
Decrease in sugar intake can increase emotional stability.[101]
Your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch.[102]
The rapid absorption of sugar promotes excessive food intake in obese subjects.[103]
Sugar can worsen the symptoms of children with attention deficit hyperactivity disorder (ADHD).[104]
Sugar adversely affects urinary electrolyte composition.[105]
Sugar can impair the function of your adrenal glands.[106]
Sugar has the potential of inducing abnormal metabolic processes in normal, healthy individuals, thereby promoting chronic degenerative diseases.[107]
Intravenous feedings (IVs) of sugar water can cut off oxygen to your brain.[108]
Sugar increases your risk of polio.[109]
High sugar intake can cause epileptic seizures.[110]
Sugar causes high blood pressure in obese people.[111]
In intensive care units, limiting sugar saves lives.[112]
Sugar may induce cell death.[113]
In juvenile rehabilitation centers, when children were put on low sugar diets, there was a 44 percent drop in antisocial behavior.[114]
Sugar dehydrates newborns.[115]
Sugar can cause gum disease.[116]
It should now be crystal clear just how damaging sugar is. You simply cannot achieve your highest degree of health and vitality if you are consuming a significant amount of it.
Fortunately, your body has an amazing ability to heal itself when given the basic nutrition it needs, and your liver has an incredible ability to regenerate. If you start making changes today, your health WILL begin to improve, returning you to the state of vitality that nature intended.

References:
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[2] “What sweetener should you choose? Sugar? Honey? Agave nectar?” Fitnessspotlight
[3] Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L and Havel PJ. “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans,” J Clin Invest. 2009; 119(5):1322-1334
[4] Park A. “All sugars aren’t the same: Glucose is better, study says,” Time Magazine, April 21, 2009
[5] Appleton N. Lick the Sugar Habit (1996) Avery, 2nd Ed. 272 pp.
[6] Sanchez, A., et al. Role of Sugars in Human Neutrophilic Phagocytosis, American Journal of Clinical Nutrition. Nov 1973;261:1180_1184. Bernstein, J., al. Depression of Lymphocyte Transformation Following Oral Glucose Ingestion. American Journal of Clinical Nutrition.1997;30:613
[7] Ringsdorf, W., Cheraskin, E. and Ramsay R. Sucrose, Neutrophilic Phagocytosis and Resistance to Disease, Dental Survey. 1976;52(12):46_48
[8] Couzy, F., et al. "Nutritional Implications of the Interaction Minerals," Progressive Food and Nutrition Science 17;1933:65-87
[9] Kozlovsky, A., et al. Effects of Diets High in Simple Sugars on Urinary Chromium Losses. Metabolism. June 1986;35:515_518
[10] Fields, M.., et al. Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets, Journal of Clinical Nutrition. 1983;113:1335_1345
[11] Lemann, J. Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium. Journal of Clinical Nutrition. 1976 ;70:236_245
[12] Goldman, J., et al. Behavioral Effects of Sucrose on Preschool Children. Journal of Abnormal Child Psychology.1986;14(4):565_577
[13] Jones, T. W., et al. Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children. Journal of Pediatrics. Feb 1995;126:171-7
[14] Scanto, S. and Yudkin, J. The Effect of Dietary Sucrose on Blood Lipids, Serum Insulin, Platelet Adhesiveness and Body Weight in Human Volunteers, Postgraduate Medicine Journal. 1969;45:602_607
[15] Albrink, M. and Ullrich I. H. Interaction of Dietary Sucrose and Fiber on Serum Lipids in Healthy Young Men Fed High Carbohydrate Diets. American Journal of Clinical Nutrition. 1986;43:419­
[16] Reiser, S. Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease. Nutritional Health. 1985;203_216
[17] Lewis, G. F. and Steiner, G. Acute Effects of Insulin in the Control of Vldl Production in Humans. Implications for The insulin-resistant State. Diabetes Care. 1996 Apr;19(4):390-3 R. Pamplona, M. .J., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses. 1990;40:174-181
[18] Cerami, A., Vlassara, H., and Brownlee, M. "Glucose and Aging." Scientific American. May 1987:90. Lee, A. T. and Cerami, A. The Role of Glycation in Aging. Annals of the New York Academy of Science; 663:63-67
[19] Takahashi, E., Tohoku University School of Medicine, Wholistic Health Digest. October 1982:41:00
[20] Quillin, Patrick, Cancer's Sweet Tooth, Nutrition Science News. Ap 2000 Rothkopf, M.. Nutrition. July/Aug 1990;6(4)
[21] Michaud, D. Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study. J Natl Cancer Inst. Sep 4, 2002 ;94(17):1293-300
[22] Moerman, C. J., et al. Dietary Sugar Intake in the Etiology of Biliary Tract Cancer. International Journal of Epidemiology. Ap 1993.2(2):207-214.
[23] The Edell Health Letter. Sept 1991;7:1
[24] De Stefani, E."Dietary Sugar and Lung Cancer: a Case control Study in Uruguay." Nutrition and Cancer. 1998;31(2):132_7
[25] Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France. European Journal of Epidemiology 11 (1995):55-65
[26] Kelsay, J., et al. Diets High in Glucose or Sucrose and Young Women. American Journal of Clinical Nutrition. 1974;27:926_936. Thomas, B. J., et al. Relation of Habitual Diet to Fasting Plasma Insulin Concentration and the Insulin Response to Oral Glucose, Human Nutrition Clinical Nutrition. 1983; 36C(1):49_51
[27] Dufty, William. Sugar Blues. (New York:Warner Books, 1975)
[28] Acta Ophthalmologica Scandinavica. Mar 2002;48;25. Taub, H. Ed. Sugar Weakens Eyesight, VM NEWSLETTER;May 1986:06:00
[29] Dufty.
[30] Yudkin, J. Sweet and Dangerous.(New York:Bantam Books,1974) 129
[31] Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France, European Journal of Epidemiology. 1995;11
[32] Persson P. G., Ahlbom, A., and Hellers, G. Epidemiology. 1992;3:47-52
[33] Jones, T. W., et al. Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children. Journal of Pediatrics. Feb 1995;126:171-7
[34] Lee, A. T.and Cerami A. The Role of Glycation in Aging. Annals of the New York Academy of Science.1992;663:63-70
[35] Abrahamson, E. and Peget, A. Body, Mind and Sugar. (New York: Avon, 1977)
[36] Glinsmann, W., Irausquin, H., and Youngmee, K. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force. 1986:39:00 Makinen K.K.,et al. A Descriptive Report of the Effects of a 16_month Xylitol Chewing_gum Programme Subsequent to a 40_month Sucrose Gum Programme. Caries Research. 1998; 32(2)107_12
[37] Glinsmann, W., Irausquin, H., and K. Youngmee. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force.1986;39:36_38
[38] Appleton, N. New York: Healthy Bones. Avery Penguin Putnam:1989
[39] Keen, H., et al. Nutrient Intake, Adiposity, and Diabetes. British Medical Journal. 1989; 1:00 655_658
[40] Darlington, L., Ramsey, N. W. and Mansfield, J. R. Placebo Controlled, Blind Study of Dietary Manipulation Therapy in Rheumatoid Arthritis, Lancet. Feb 1986;8475(1):236_238
[41] Powers, L. Sensitivity: You React to What You Eat. Los Angeles Times. (Feb. 12, 1985). Cheng, J., et al. Preliminary Clinical Study on the Correlation Between Allergic Rhinitis and Food Factors. Lin Chuang Er Bi Yan Hou Ke Za Zhi Aug 2002;16(8):393-396
[42] Erlander, S. The Cause and Cure of Multiple Sclerosis, The Disease to End Disease." Mar 3, 1979;1(3):59_63
[43] Crook, W. J. The Yeast Connection. (TN:Professional Books, 1984)
[44] Heaton, K. The Sweet Road to Gallstones. British Medical Journal. Apr 14, 1984; 288:00:00 1103_1104. Misciagna, G., et al. American Journal of Clinical Nutrition. 1999;69:120-126
[45] Cleave, T. The Saccharine Disease. (New Canaan, CT: Keats Publishing, 1974)
[46] Ibid
[47] Cleave, T. and Campbell, G. (Bristol, England:Diabetes, Coronary Thrombosis and the Saccharine Disease: John Wright and Sons, 1960)
[48] Behall, K. Influ ence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters. Disease Abstracts International. 1982;431437
[49] Tjäderhane, L. and Larmas, M. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. Journal of Nutrition. 1998:128:1807_1810
[50] Beck, Nielsen H., Pedersen O., and Schwartz S. Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects. Diabetes. 1978;15:289_296
[51] Sucrose Induces Diabetes in Cat. Federal Protocol. 1974;6(97). diabetes
[52] Reiser, S., et al. Effects of Sugars on Indices on Glucose Tolerance in Humans. American Journal of Clinical Nutrition. 1986;43:151-159
[53] Journal of Clinical Endocrinology and Metabolism. Aug 2000
[54] Hodges, R., and Rebello, T. Carbohydrates and Blood Pressure. Annals of Internal Medicine. 1983:98:838_841
[55] Behar, D., et al. Sugar Challenge Testing with Children Considered Behaviorally Sugar Reactive. Nutritional Behavior. 1984;1:277_288
[56] Furth, A. and Harding, J. Why Sugar Is Bad For You. New Scientist. Sep 23, 1989;44
[57] Simmons, J. Is The Sand of Time Sugar? LONGEVITY. June 1990:00:00 49_53
[58] Appleton, N. New York: LICK THE SUGAR HABIT. Avery Penguin Putnam:1988. allergies
[59] Cleave, T. The Saccharine Disease: (New Canaan Ct: Keats Publishing, Inc., 1974).131
[60] Ibid. 132
[61] Pamplona, R., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses . 1990:00:00 174_181
[62] Vaccaro O., Ruth, K. J. and Stamler J. Relationship of Postload Plasma Glucose to Mortality with 19 yr Follow up. Diabetes Care. Oct 15,1992;10:328_334. Tominaga, M., et al, Impaired Glucose Tolerance Is a Risk Factor for Cardiovascular Disease, but Not Fasting Glucose. Diabetes Care. 1999:2(6):920-924
[63] Lee, A. T. and Cerami, A. Modifications of Proteins and Nucleic Acids by Reducing Sugars: Possible Role in Aging. Handbook of the Biology of Aging. (New York: Academic Press, 1990)
[64] Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology 1990:45(4):105_110
[65] Cerami, A., Vlassara, H., and Brownlee, M. Glucose and Aging. Scientific American. May 1987:00:00 90
[66] Dyer, D. G., et al. Accumulation of Maillard Reaction Products in Skin Collagen in Diabetes and Aging. Journal of Clinical Investigation. 1993:93(6):421_22
[67] Veromann, S.et al."Dietary Sugar and Salt Represent Real Risk Factors for Cataract Development." Ophthalmologica. 2003 Jul-Aug;217(4):302-307
[68] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI
[69] Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990:45(4):105_110
[70] Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):27­29
[71] Appleton, Nancy. New York; Lick the Sugar Habit. Avery Penguin Putnam, 1988 enzymes
[72] Hellenbrand, W. Diet and Parkinson's Disease. A Possible Role for the Past Intake of Specific Nutrients. Results from a Self-administered Food-frequency Questionnaire in a Case-control Study. Neurology. Sep 1996;47(3):644-650
[73] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38
[74] Ibid.
[75] Yudkin, J., Kang, S. and Bruckdorfer, K. Effects of High Dietary Sugar. British Journal of Medicine. Nov 22, 1980;1396
[76] Blacklock, N. J., Sucrose and Idiopathic Renal Stone. Nutrition and Health. 1987;5(1-2):9­Curhan, G., et al. Beverage Use and Risk for Kidney Stones in Women. Annals of Internal Medicine. 1998:28:534-340
[77] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI
[78] Ibid. fluid retention
[79] Ibid. bowel movement
[80] Ibid. compromise the lining of the capillaries
[81] Nash, J. Health Contenders. Essence. Jan 1992; 23:00 79_81
[82] Grand, E. Food Allergies and Migraine.Lancet. 1979:1:955_959
[83] Schauss, A. Diet, Crime and Delinquency. (Berkley Ca; Parker House, 1981)
[84] Molteni, R, et al. A High-fat, Refined Sugar Diet Reduces Hippocampal Brain-derived Neurotrophic Factor, Neuronal Plasticity, and Learning. NeuroScience. 2002;112(4):803-814
[85] Christensen, L. The Role of Caffeine and Sugar in Depression. Nutrition Report. Mar 1991;9(3):17-24
[86] Ibid,44
[87] Yudkin, J. Sweet and Dangerous.(New York:Bantam Books,1974) 129
[88] Frey, J. Is There Sugar in the Alzheimer's Disease? Annales De Biologie Clinique. 2001; 59 (3):253-257
[89] Yudkin, J. Metabolic Changes Induced by Sugar in Relation to Coronary Heart Disease and Diabetes. Nutrition and Health. 1987;5(1-2):5-8
[90] Yudkin, J and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988:32(2):53-55
[91] The Edell Health Letter. Sept 1991;7:1
[92] Gardner, L. and Reiser, S. Effects of Dietary Carbohydrate on Fasting Levels of Human Growth Hormone and Cortisol. Proceedings of the Society for Experimental Biology and Medicine. 1982;169:36_40
[93] Journal of Advanced Medicine. 1994;7(1):51-58
[94] Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):27­29
[95] Postgraduate Medicine.Sept 1969:45:602-07
[96] Lenders, C. M. Gestational Age and Infant Size at Birth Are Associated with Dietary Intake among Pregnant Adolescents. Journal of Nutrition. Jun 1997;1113-1117
[97] Ibid.
[98] Sugar, White Flour Withdrawal Produces Chemical Response. The Addiction Letter. Jul 1992:04:00 Colantuoni, C., et al. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obes Res. Jun 2002 ;10(6):478-488. Annual Meeting of the American Psychological Society, Toronto, June 17, 2001 www.mercola.com/2001/jun/30/sugar.htm
[99] Ibid.
[100] Sunehag, A. L., et al. Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition Diabetes. 1999 ;48 7991_800
[101] Christensen L., et al. Impact of A Dietary Change on Emotional Distress. Journal of Abnormal Psychology.1985;94(4):565_79
[102] Nutrition Health Review. Fall 85 changes sugar into fat faster than fat
[103] Ludwig, D. S., et al. High Glycemic Index Foods, Overeating and Obesity. Pediatrics. March 1999;103(3):26-32
[104] Pediatrics Research. 1995;38(4):539-542. Berdonces, J. L. Attention Deficit and Infantile Hyperactivity. Rev Enferm. Jan 2001;4(1)11-4
[105] Blacklock, N. J. Sucrose and Idiopathic Renal Stone. Nutrition Health. 1987;5(1 & 2):9­
[106] Lechin, F., et al. Effects of an Oral Glucose Load on Plasma Neurotransmitters in Humans. Neurophychobiology. 1992;26(1-2):4-11
[107] Fields, M. Journal of the American College of Nutrition. Aug 1998;17(4):317_321
[108] Arieff, A. I. Veterans Administration Medical Center in San Francisco. San Jose Mercury; June 12/86. IVs of sugar water can cut off oxygen to the brain
[109] Sandler, Benjamin P. Diet Prevents Polio. Milwakuee, WI,:The Lee Foundation for for Nutritional Research, 1951
[110] Murphy, Patricia. The Role of Sugar in Epileptic Seizures. Townsend Letter for Doctors and Patients. May, 2001 Murphy Is Editor of Epilepsy Wellness Newsletter, 1462 West 5th Ave., Eugene, Oregon 97402
[111] Stern, N. & Tuck, M. Pathogenesis of Hypertension in Diabetes Mellitus. Diabetes Mellitus, a Fundamental and Clinical Test. 2nd Edition, (PhiladelphiA; A:Lippincott Williams & Wilkins, 2000)943-957
[112] Christansen, D. Critical Care: Sugar Limit Saves Lives. Science News. June 30, 2001; 159:404
[113] Donnini, D. et al. Glucose May Induce Cell Death through a Free Radical-mediated Mechanism.Biochem Biohhys Res Commun. Feb 15, 1996:219(2):412-417
[114] Schoenthaler, S. The Los Angeles Probation Department Diet-Behavior Program: Am Empirical Analysis of Six Institutional Settings. Int J Biosocial Res 5(2):88-89
[115] Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition. Diabetes. 1999 Apr;48(4):791-800
[116] Glinsmann, W., et al. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners." FDA Report of Sugars Task Force -1986 39 123

Yudkin, J. and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988;32(2):53-5

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