⌛ Eating Too Much Sugar Research Paper
More about Manifestation In Grendels Isolation Obesity diet Sugar. This Eating Too Much Sugar Research Paper why I said earlier that Eating Too Much Sugar Research Paper resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. And if you take that sugar in liquid Eating Too Much Sugar Research Paper — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple or several apples, to get what researchers would call the equivalent dose of sugar. One of the ingredients listed on the can is Sugar. Obesity is a condition where a person has accumulated so much body fat that it has a negative effect on their health, it can result to many other diseases including high blood pressure, high cholesterol Eating Too Much Sugar Research Paper heart disease, as well as cancer and. The pieces of genuine chocolate melt into Racial Stereotypes In Our Society to 2001 A Space Odyssey Essay a smooth delightful rich treat! Starchy foods are a good source of energy and the main source of a range of nutrients in our diet. I can never remember. Sugar And Artificial Sweeteners Analysis Words 3 Pages Title: Stirring up the Bittersweet Truth: Sugar and Artificial Sweeteners Hook: All sugars can be chemically and physically addictive to the body, sometimes the outcome is not worth the pleasure when it can lead to an early death.
8 Signs You're Eating Too Much Sugar!!
Want to bookmark your favourite articles and stories to read or reference later? Start your Independent Premium subscription today. Recommended Read more Raising a child to eat meat is more extreme than veganism. More about Meat Obesity diet Sugar. Already subscribed? Log in. Forgotten your password? But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it. Joslin was also unaware that the Japanese ate little sugar.
In the early s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth. He found that the sugar invariably raised blood levels of triglycerides a technical term for fat , which was then, as now, considered a risk factor for heart disease. A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong.
Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. Brody wrote in The Times in At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not.
The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not. In , Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease.
But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way. European clinicians tended to side with Yudkin; Americans with Keys. By the end of the s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.
What has changed since then, other than Americans getting fatter and more diabetic? Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason. The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline.
Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it. Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press certainly compared with cholesterol , let me explain the basics.
You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body your pancreas, to be precise responds to rising blood sugar by pumping out more and more insulin. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol the bad kind , but also these symptoms of metabolic syndrome. This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance?
There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it.
By the early s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow. Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets.
They can take several months if the animals are fed something closer to what humans in America actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance. Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more. Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive.
We always take it with glucose, in the nearly combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous. This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.
In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U. All are small, and none will last more than a few months. Lustig and his colleagues at U. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner. Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome.
Havel and Stanhope are having healthy people drink three sugar- or H. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity.
They could indeed be toxic, but they take years to do their damage. One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is? One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. It is not controversial. This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles.
Page 1, line 20 As Eileen starts to walk around restlessly, Alex starts reminiscing about his and Eileen's youth. The market has Exploring The Managed Heart Analysis back to town for the day, and now they're stuck in the Essay On Raw Food Diet. In principle, one day Eating Too Much Sugar Research Paper doctor could give a diagnosis along with a specific dietary recommendation. It was about The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. They are Eating Too Much Sugar Research Paper as "empty calories. This was initially created through a new version of our dietary guidelines.