An interesting article about living a gluten free life. It uses a bit of highly processed foods but there is lots of good information as well.
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Sunday, February 28, 2010
Gluten-free flour weight-volume measures : Real Food Made Easy
One of my pet peeves when I started baking gluten-free was that all the recipes used volume measures rather than weights %u2014 one person%u2019s %u201Cfull%u201D cup, is another%u2019s %u201Clevel%u201D cup. Knowing that this could create problems with rise with wheat-based recipes, I knew instinctively that this would create even more problems with gluten-free flours, where differences as small as 1-2 T can make huge differences,
I did a lot of poking around to try and find weight-conversions for many of the gluten-free flours. I am often baking with blends of GF flours that I have pre-mixed ahead of time, so it has also meant working out the weights of those mixes, but I feel it is worth it in the end!
I have put these volume-weight conversions into a print-ready table. Please feel free to download it and use it. I now have it taped on the inside of a cupboard door, and have a copy in a spreadsheet so I can quickly calculate weights of new flour mixes.
Found this on Facebook and just had to share. What a lovely way to know how much a cup of each type of flour weighs.
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Food - Field Report - Plow Shares
via nytimes.com
Who wants to help our local farmers? I would love to participate in a Crop Mob. Any local farmer want some help?
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Thursday, February 25, 2010
Meeting
Bellingham Gluten Intolerance Group...
March 2, 6:30-9 PM - Ferndale H.S. 5830 Golden Eagle Drive, Ferndale WA Home Economics Room
Member Cooking Demo
"Fun with Millet" join us for a delicious evening of ideas and cooking! We will be introducing uses for the tasy alternative GF grain, millet.
We will also feature Hempler's GF products. BGIG will have GF cookbooks for sale and "Toast-It" toaster bags.
Park in large parking lot off Vista Dr., walk between cafeteria building and gym and look for balloons/signage . . . .
Dr. Jean M. Layton
1329 King Street
Bellingham WA 98229
360-734-1659
twitter: GFDoctor
Facebook: GFDoctor
Posted via email from GF Doctor-a slightly biased view of gluten free life.
Ooops. I managed to confuse two different emails in posting yesterday. Bio Card Testing is at Manitoba Celiac
Register for the conference prior to March 1st to take advantage of the reduced rate!
Suport our chapter, so it can support you.
Dr, Joseph Murray talks about Celiac Disease Study Findings.
What you need to know about Celiac Disease and the gluten free diet.
Dr, Joseph Murray talks about Celiac Disease .
Celiac Disease is more common.
via celiac.mb.ca
Sometimes I just know that I am rushing a bit. Like when I cut and paste two different events from two different Celiac/Gluten Intolerant groups together and make it seem like something is happening.
Like yesterday when I put out the Bellingham Gluten Intolerance group meeting announcement and managed to include the Bio-Card testing kits that are going to be here in Winnipeg.
I feel a bit foolish.
I will slow down and make sure that my links are very accurate in the future, sorry for any confusion
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Clarification on Gluten-free status of King Arthur's new products
Dear Dr. Layton,
Thank you for posting King Arthur Flour’s new gluten-free items on your blog.
You can assure your readers that in addition to all seven of King Arthur Flour’s gluten-free baking mixes as well as the gluten-free multi-purpose flour; the four gluten-free ingredients:
Brown rice flour and
are all processed in the same dedicated gluten-free facility. Ours is the only major brand to be third-party certified by the Gluten Free Certification Organization, with standards twice as stringent as those set by the Food and Drug Administration. In addition, they are produced in a dedicated allergen-free facility, guaranteed to be free of the top eight most common food allergens. They are also certified Kosher by the Chicago Rabbinical Council.
Please let me know if you have any questions. Thanks for your interest.
Best regards,
Suzanne
Dr. Jean M. Layton
1329 King Street
Bellingham WA 98229
360-734-1659
twitter: GFDoctor
Facebook: GFDoctor
Posted via email from GF Doctor-a slightly biased view of gluten free life.
Wednesday, February 24, 2010
Gluten-Free Cookie Mix from King Arthur's Flours
This one says it is from a dedicated facility and is approved from the GIG group.
I like the idea that it creates a basic cookie to which you add whatever nuts, chips or fruits you desire. Nice that it is wheat, soy and nut free.
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Ancient Grains Flour Blend - 2 lb. from King Arthur's
I wonder about cross contamination though. Would love to know it was out of a dedicated facility.
Posted via web from GF Doctor-a slightly biased view of gluten free life.
King Arthur has Gluten-Free Multi-Purpose Flour !
Shop > Cake > Ingredients > Gluten-Free Multi-Purpose Flour
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Gluten-Free Multi-Purpose Flour
item# 4699 $7.95
New!
Be the first to rate this item
King Arthur Flour is proud to introduce the very best gluten-free flour blend you%u2019ll ever bake with.
�View packaging and nutritional information [453KB PDF]
- Certified Gluten-Free%u2122 by the non-profit Gluten-Free Certification Organization (GFCO), a program of the Gluten Intolerance Group (GIG�).
- Carefully tested blend of white rice and whole-grain (brown) rice flours, tapioca starch, and potato starch is perfect for all of your gluten-free recipes.
- No need to mix together the many different flours most gluten-free recipes call for; simply substitute our blend instead.
- Check kingarthurflour.com/recipes for delicious gluten-free recipes for cake, brownies, cookies, scones, pancakes, and more.
- Wheat-free, soy-free, nut-free blend is packed in a dedicated gluten-free facility.
- No additives, preservatives, or artificial flavors.
- Kosher.
- 24-ounce bag.
Reviews
Posted via web from GF Doctor-a slightly biased view of gluten free life.
iGive : Raise money for Healthy Gluten-Free Kids, every time you search the web.
via igive.com
Please help us reach every child who needs to be a Healthy Kid Eating Gluten-Free.
We want to create an interactive web page to educate each child about thriving gluten-free.
If you join iGive, we will get a small donation.
Thanks for your support
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Friday, February 19, 2010
Massachusetts Regulations Make Food Allergies a Restaurant Responsibility, Too - ABC News
Eating out is often a scary experience for someone with food allergies. Instead of relaxing all evening, he needs to convince a strange waiter and a cook he'll never see to follow strict instructions.
But on Thursday, Massachusetts became the first state to officially put some of the responsibility on restaurants.
Under new regulations, some 24,000 restaurants statewide will have to educate their staffs on food allergies and require managers to get a certified through a food allergy training course.
Suzanne Condon, director environmental health assessment for the Department of Public Health, said she hopes walking into a restaurant and seeing the food allergy certification on the wall will put some customers at ease.
"The certification is the most significant, I think, in terms of food safety training," said Condon.
Restaurants also will have to post information and instructions about food allergies in a staff area, and are required to print the warning: "Before placing your order, please inform your server if a person in your party has a food allergy" on menus.
Dr. Clifford Bassett, an allergist with the New York University School of Medicine, applauded the effort.
"The responsibility is shared -- on the patron, on the restaurant, on the food allergist -- to make sure they have a food allergy action plan," said Bassett. "Most restaurants don't do it, because what if the chef changes the recipe, or what if the chef changes where he gets the ingredients."
Bassett encourages his patients to bring a laminated card with instructions about their food allergies when they go out. This way they can hand the card to the waiter and the message will not be lost or forgotten by the time it reaches the kitchen.
Tarlan Ellis, 29, sees Bassett regularly for her allergies, including an allergy to seaweed.
"I'm quite lucky," said Ellis. "I just have to make sure I don't eat it. I can eat stuff that's been in contact with it, but I can't seaweed itself."
Others with allergies can have an anaphylactic reaction merely by eating something that's touched a peanut, shellfish or milk.
What to Do When Dealing With Food Allergies
Ellis carries an EpiPen with her, just in case she goes into anaphylactic shock, and she also orders carefully. But she still believes some responsibility lies with the restaurant staff to protect patrons.
"I think both are responsible," she said.
However, even doctors who treat food allergies don't necessarily agree.
"I'm a person who believes that you teach patients how to take care of yourself, and not rely on other people to take care of you," said Dr. Richard Lockey, director of allergy and immunology at University of South Florida College of Medicine.
"I believe the responsibility should be the customer's," he said.
Lockey questioned the cost effectiveness of educating tens of thousands of employees, many of whom are only in the profession for a few years.
Food allergies occur in 6 to 8 percent of children under age 4 and in 3.7 percent of adults, according to the National Institute of Allergy and Infectious Diseases.
"To me, a patient information program would be much more cost effective than having people in restaurants trained," said Lockey, who also recommended a program to provide EpiPens for people with food allergies.
Who Pays for It, Should They Pay?
Condon said the state found food safety training programs that volunteered to run the food allergy education free of charge for the state.
"They may charge some nominal fee for the certificate and training process, but we don't ask," said Condon.
Once a restaurant's managers are certified, Condon expected that the certification and food allergy education will be checked several times a year by local health inspections.
Dr. Scott H. Sicherer, of the Jaffe Food Allergy Institute at Mount Sinai School of Medicine in New York City, said studies have shown both patients and restaurant workers have a long way to go in learning how to deal with a food allergy.
Misconceptions About Food Allergy Safety
Sicherer completed a study of 100 employees in 100 New York restaurants in 2007 and found that most people had no food allergy training.
"Although over 70 percent expressed comfort in providing a safe meal, numerous misconceptions were found when we posed specific question about food allergy," said Sicherer.
For example, 24 percent of the restaurant employees thought a person could eat a small amount of the food to which they are allergic, 35 percent thought a fryer would destroy allergens, and a quarter of people thought it would be acceptable "to simply pick nuts from a finished meal to make it safe."
"None of these practices would be safe," said Sicherer. "Having training, raising awareness and increasing communication between the restaurant personnel and the person with food allergies will go a long way in making restaurant meals safer."
But Sicherer did a complementary study of restaurant patrons with food allergies, and found that often their communication of an allergy could be unclear.
"The problem we know is that sometimes the food allergy isn't communicated properly," said Sicherer. "If you say, 'I'm allergic to peanuts; even a small amount will make me sick,' that's different than saying, 'Hey, does that cake have peanuts in it?'"
Sicherer's research also has found that eating out is one of the major "quality of life" issues for people suffering from food allergies.
Chris Weiss, vice president of advocacy and government relations at the Food Allergy and Anaphylaxis Network (FAAN), said the legislation was a long ways coming.
"We track food allergy fatalities over the years," Weiss told MedPage Today. "We have looked at 63 deaths (in a 10 year period) and found almost half were caused by restaurants."
Weiss hoped that Massachusetts' regulation would catch on.
"We hope that other states will follow the lead," he said.
MedPage Today's Emily Walker contributed to this report
via abcnews.go.com
Posted via web from GF Doctor-a slightly biased view of gluten free life.
From a Colorado colleague: Soda increases Pancreatic Cancer Risk
Pancreatic cancer and soda consumption:
Jacob Schor ND FABNO
February 13, 2010
An odd coincidence in timing:
Perhaps it is because soda and candy have been a big story in Colorado legislative news over the last few months, that an article in an obscure epidemiology journal caught my attention this past week. Back in November 2009 Colorado’s currently democratic leadership announced plans to add a 2.9% tax to carbonated beverages and candy as part of a comprehensive plan to balance the state budget. The bill to turn Governor Ritter’s soda tax proposal into law was passed by the Colorado Senate just a few days ago. The lead up debate to this vote brought forth vocal opponents that made it apparent that many people believe unfettered access to soft drinks is a fundamental right guaranteed in the Constitution. Coincident with these Colorado legislative debates, but unmentioned, is a fascinating paper by Noel Mueller et al. that appeared in the February issue of Cancer Epidemiology, Biomarkers & Prevention. According to their analysis, drinking two or more sodas a week almost doubles a person’s risk of getting pancreatic cancer.
Their data was collected from a prospective cohort made up of 60,524 people who are taking part in the Singapore Chinese Health Study. Information on consumption of soft drinks, juice, and other dietary items, as well as lifestyle and environmental exposures, was collected through in-person interviews at recruitment. Following these people for 14 years yielded 648,387 person-years of data and 140 cases of pancreatic cancer (PC). Individuals who consumed two or more soft drinks a week experienced a statistically significant increase in risk of pancreatic cancer (hazard ratio, 1.87; 95% confidence interval, 1.10-3.15) compared with individuals who did not consume soft drinks. There was no association seen between drinking fruit juice and risk of PC.
A hazard ratio of 2.0 would mean soda drinkers were twice as likely to get pancreatic cancer. This ratio of 1.87 is just a little less than 2.0.Background is essential to understand the results of this study. This is just the latest in a series of studies on the subject that have yielded sometimes conflicting and confusing results. Yet the bottom line consensus appears to be that soda or other concentrated forms of sugar, such as candy bars, do increase risk of pancreatic cancer. The first thing we have to understand with PC is that it’s one of the bad cancers; five-year survival even with modern treatment is less than 5%. Treatment does little good; a better approach is to focus on prevention. Cigarette smoking is the one accepted risk factor consistently associated with increased risk of pancreatic cancer. Type 2 diabetes also increases risk. This led to a theory that producing high levels of insulin might somehow lead to malignant transformation of pancreatic cells.
In most cancers, the cells that become cancerous have been somehow overworked, irritated, or in some way abused prior to becoming cancer cells. They have been pushed by something to grow faster, work harder, secrete more or in some manner live harder lives. Estrogen pushes both breast and uterine cells to become cancerous. Testosterone pushes prostate cells to become prostate cancer. Infections push lymph cells to become lymphoma. Chronic inflammation pushes colon cancer cells, etc. This theory about pancreatic cancer suggests that high sugar intake pushes the pancreas. Granted, this is a vast oversimplification of both a complex process and a complicated hypothesis, but it works for my simple mind.
Diabetes has been associated with pancreatic cancer for decades. A study on Seventh Day Adventists published in 1988 reported that, “A prior history of diabetes was associated with increased risk of subsequent fatal pancreas cancer….” Overwork cells or abuse them and they aren’t happy.
A Kaiser Permanente study published that same year, found that while cigarette smoking increased risk of pancreatic cancer by a factor of 2.5, people who had been treated for diabetes had 4.5 times the risk. (Smoking: relative risk, 2.5; 95% confidence interval, 1.3-4.7. Diabetes: relative risk, 4.5; 95% confidence interval, 1.2-16.7).)
A Dutch paper published two years later in 1990, that analyzed data on 164 patients with pancreatic cancer, found, “…a significant, positive association between pancreatic cancer and past habitual intake of simple sugars…. (OR 1.95; 95% confidence interval 1.24-3.07).” This led the study authors to, “… suggest that the development of exocrine pancreatic carcinoma is positively related to past habitual intake of total energy, total carbohydrates and simple sugars, …” A 1991 Australian paper that analyzed the habits of 104 people who developed PC also found a link to sugar consumption. “For the top quartile of refined sugar intake, the estimated relative risk was 2.21 (95% confidence interval 1.07-4.55).”
[Of course sugars aren’t the only dietary culprit in the pancreatic cancer story. High fat diets have also been identified as a factor. A November 1993 study reported that high fat foods tripled risk. ]
A December 1995 study that looked at 179 cases of PC in French speaking Canadians found a similar effect of sugar consumption. Again, high sugar consumption nearly tripled risk. Of interest in this paper was the pronounced effect of cooking with firewood, a habit that increased relative risk by a factor of almost 5, while cooking in a pressure cooker lowered risk to 1/3 the average.
Sweetened carbonated drinks, what we call soft drinks, or soda, are a major source of simple sugars in western diets and as such, soda consumption provides a measure of overall sugar consumption. [16] Soda consumption is associated with hyperglycemia and hyperinsulinemia, obesity and type 2 diabetes.
Let us return to the current study by Mueller and colleagues. Rates of developing pancreatic cancer have plateaued and are stable in the United States but they are rising among Chinese men and women in Singapore. From 1968 to 1998 they have almost doubled going from 3.7 to 5.4 per 100,000 for men and 1.5 to 3.4 per 100,000 for women. One explanation for this increase is the shift toward a more western diet and increased consumption of sugar and sugar sweetened sodas. It may be that during this transition period between traditional diets and western diets that the effect of soda consumption is more pronounced. Soda may be adopted into the diet while traditional foods and recipes still comprise the basic diet. On the other hand as soda consumption increases so do other behaviors linked to higher risk of pancreatic cancer. For example in the Mueller study, people who drank more soda also consumed more red meat, total fat, sugar, candy, and alcohol. They smoked more, exercised less and were more likely to become diabetic. Is soda the cause of the increased risk or is it just a marker of overall poor lifestyle? The intricate dissection of this data using statistical tools is a delicate task. Simply gathering data on so rare a cancer is itself a challenge. In the last five years four other prospective cohort studies have been published that looked at this same equation of soda or sugar consumption and whether it is tied to pancreatic cancer risk. (Schernhammer, Larsson, Nothlings, Bao) Results from the current Mueller paper are consistent with three out of four of these earlier studies. One other study included fruit juice and found a positive association between juice intake and PC risk; this current study did not find an association. Eva Schernhammer and researchers from Harvard used data from two large cohorts, the Nurses' Health Study and the Health Professionals Follow-up Study, comprising 88,794 women and 49,364 men for their 2005 paper. These cohorts over the course of 20 years follow-up yielded data on 379 cases of pancreatic cancer. Schernhammer’s analysis found that the women who consumed more than 3 sodas a week had a 57% greater risk of pancreatic cancer than women who drank one or less sodas a month. (RR, 1.57; 95% CI, 1.02-2.41; P for trend = 0.05). No association was found in the 174 men who developed pancreatic cancer. In November 2006, the American Journal of Clinical nutrition published a paper by Susanna Larsson et al, analyzing Swedish dietary data from a cohort of 77,797 people who were followed for 7 years, 131 of whom developed pancreatic cancer. Those who drank 2 or more soft drinks a day had a 93% increased risk of pancreatic cancer. (OR1.93 (1.18, 3.14; P for trend = 0.02) A November 2007 study conducted by Nothlings and fellow researchers from the University of Hawaii analyzed data for 162,150 participants in the Hawaii-Los Angeles Multiethnic Cohort Study to investigate associations between glycemic load, dietary carbohydrates, sucrose, fructose, total sugars, and added sugars and the risk of pancreatic cancer. During 8 years of follow-up, 434 pancreatic cancer cases occurred within the group. Again the results though suggestive contradict, at least in part, other studies. The risk of PC increased with higher intakes of total sugars, fructose, and sucrose. The association with fructose was significant when the highest and lowest quartiles were compared (relative risk: 1.35; 95% CI: 1.02, 1.80; P for trend = 0.046). An almost identical association was found with high fruit and juice intake (1.37; 1.02, 1.84; P for trend = 0.04). But no association was seen with soda intake. The researchers concluded that, “High fructose and sucrose intakes may
play a role in pancreatic cancer etiology. Conditions such as overweight or obesity in which a degree of insulin resistance may be present may also be important.” The Bao study published in 2008 is the one report that did not find an association between sugar and PC. This is despite the fact that it was the largest of the studies. Rather than soda they calculated the total consumption of added sugar and sugar-sweetened foods and beverages, examining data from 487,922 men and women calculating total added dietary sugar intake. During 7.2 years of follow-up, 1,258 pancreatic cancer cases were found within the group. The lowest sugar consumers averaged about 3 tsp/day while the high consumers averaged almost 23 tsp/day. No difference in risk was seen between these two groups. We should clarify; no statistically significant difference was seen. The low sugar consumers had a relative risk of 0.85 compared to the high sugar eaters but this did not reach statistical significance. Thus these results did not support the sugar hypothesis. Just a year later in August 2009, another study reported different results, a positive but still confusing, association. June Chan and colleagues from the University of California in San Francisco reported in the journal Cancer Causes and Control on a comparison of the dietary habits of 532 people who developed PC with people who didn’t. “Among men, greater intakes of total and specific sweets were associated with pancreatic cancer risk…” that ranged from an overall risk of 1.9 for total sweets to 3.3 for candy bars but in this study, “…Sweets were not consistently associated with risk among women.” In contrast to other soda studies they also reported that, “Sweetened beverages were not associated with increased pancreatic cancer risk.” But to confuse things further, “… low-calorie soft drinks were associated with increased risk among men…” In November 2009 an Italian study was published that once again supported a link between sugar consumption and pancreatic cancer. Polesel et al. worked with data from 326 patients with pancreatic cancer comparing them to 652 control patients. Comparing the diets of the two groups they found that, “Frequent meat consumption was associated to a twofold increased risk of pancreatic cancer (95% CI: 1.18-3.36). Added table sugar (OR = 2.23; 95% CI: 1.34-3.71) and potatoes (OR = 1.79; 95% CI: 1.12-2.86) were related to pancreatic cancer.” Leading them to conclude that, “The increased risk for table sugar suggests that insulin resistance may play a role in pancreatic carcinogenesis.” Thus the results of the Mueller study do not stand-alone but are one of a series of studies that have parsed out this relationship between sugar and pancreatic cancer. If we are to accept these findings though we need an explanation to explain this relationship.There are two types of pancreatic cancer, endocrine or exocrine; endocrine tumors develop in the hormone producing tissues for secretion into the blood while exocrine cancers develop from the tissues that make digestive enzymes for secretion into the intestine. “Of pancreatic tumors, 95% develop from the exocrine portion of the pancreas, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.” These exocrine derived are the focus of this discussion. “It is tacitly assumed that the endocrine and exocrine parts of the pancreas are
Independent of each other, almost as though they were anatomically related by some sort of celestial coincidence.” But this is not the case. Instead, “…the two components are functionally related, and that the endocrine gland exerts a profound effect upon the digestive activities of the organ.” Blood and with it, insulin, are carried from insulin producing cells to exocrine cells in what has been named the Insulin-Pancreatic Acinar Axis. Insulin regulates the exocrine function of the pancreas. Exocrine cells are exposed to insulin concentrations that are 20-fold higher than in general circulation. Insulin has an effect on these cells increasing cell division and stimulating production of amylase. These high insulin levels may increase free insulin-like growth factor (IGF) by lowering levels of IGF-binding proteins. Low levels of IGF-binding proteins are suggested in some research to be risk factor for pancreatic cancer. [It should be noted that not all studies support this idea; an August 2009 paper found no link between IGF-1 or IGF-binding proteins and PC. ]The Mueller paper found no association between fasting plasma insulin levels and pancreatic cancer risk. “This suggests that postprandial insulin may be a better measure for the association with cancer risk than fasting insulin levels and is consistent with the independent role of soft drink consumption in the development of pancreatic cancer….” In other words it may be the surge of insulin produced after eating concentrated sugars that is the problem.
Abandoning these soda studies for a moment, this idea that elevated insulin levels increase cancer risk is supported by a paper published in September 2009 in Diabetologia. Currie and colleagues at Cardiff University looked for confirmation of this insulin theory by looking at the effects of different blood sugar lowering treatments on type 2 diabetics.They analyzed a retrospective cohort of 62,809 people who developed diabetes after age 40 and who were treated with either oral agents or insulin. These patients were divided into four groups according to whether they received monotherapy with metformin or sulfonylurea, combined therapy (metformin plus sulfonylurea), or insulin. The outcome measures were progression to any solid tumor, or cancer of the breast, colon, pancreas or prostate. “Metformin monotherapy carried the lowest risk of cancer. In comparison, the adjusted HR was 1.08 (95% CI 0.96-1.21) for metformin plus sulfonylurea, 1.36 (95% CI 1.19-1.54) for sulfonylurea monotherapy, and 1.42 (95% CI 1.27-1.60) for insulin-based regimens. Adding metformin to insulin reduced progression to cancer (HR 0.54, 95% CI 0.43-0.66). …. Compared with metformin, insulin therapy increased the risk of colorectal (HR 1.69, 95% CI 1.23-2.33) or pancreatic cancer (HR 4.63, 95% CI 2.64-8.10),….. Sulfonylureas were associated with a
similar pattern of risk as insulin.” It appears anything that increases insulin levels whether it is oral hypoglycemic drugs or actual insulin increased risk of some cancers, especially pancreatic cancer risk. Back to Colorado’s ‘Soda Tax’ for a moment. One of the arguments against taxing soda was that the price increase would dissuade consumers from purchasing it and therefore harm Colorado businesses and beverage dealers leading to job losses. Ignorant as I am about the economics of junk food marketing, I find it difficult to believe that a 2.9% price increase would influence anyone’s purchase decision to such an extent. Given the concerns raised by these studies regarding the health impact soda has, the tax sounds far too low as it will do little to shift consumption patterns. Perhaps my views are swayed by the task of sitting with people every day who ask me why they have cancer. A better argument against the soda and candy tax might be that they will effectively lower consumption and eventually cut pancreatic cancer incidence by half leading to unemployment among oncologists. We should be so lucky!A version of this newsletter is posted on our website with abstracts of all or almost all of the studies mentioned.http://denvernaturopathic.com/sodaandPC.htm
Jacob Schor ND FABNO
February 13, 2010
An odd coincidence in timing:
Perhaps it is because soda and candy have been a big story in Colorado legislative news over the last few months, that an article in an obscure epidemiology journal caught my attention this past week. Back in November 2009 Colorado’s currently democratic leadership announced plans to add a 2.9% tax to carbonated beverages and candy as part of a comprehensive plan to balance the state budget. The bill to turn Governor Ritter’s soda tax proposal into law was passed by the Colorado Senate just a few days ago. The lead up debate to this vote brought forth vocal opponents that made it apparent that many people believe unfettered access to soft drinks is a fundamental right guaranteed in the Constitution. Coincident with these Colorado legislative debates, but unmentioned, is a fascinating paper by Noel Mueller et al. that appeared in the February issue of Cancer Epidemiology, Biomarkers & Prevention. According to their analysis, drinking two or more sodas a week almost doubles a person’s risk of getting pancreatic cancer.
Their data was collected from a prospective cohort made up of 60,524 people who are taking part in the Singapore Chinese Health Study. Information on consumption of soft drinks, juice, and other dietary items, as well as lifestyle and environmental exposures, was collected through in-person interviews at recruitment. Following these people for 14 years yielded 648,387 person-years of data and 140 cases of pancreatic cancer (PC). Individuals who consumed two or more soft drinks a week experienced a statistically significant increase in risk of pancreatic cancer (hazard ratio, 1.87; 95% confidence interval, 1.10-3.15) compared with individuals who did not consume soft drinks. There was no association seen between drinking fruit juice and risk of PC.
A hazard ratio of 2.0 would mean soda drinkers were twice as likely to get pancreatic cancer. This ratio of 1.87 is just a little less than 2.0.Background is essential to understand the results of this study. This is just the latest in a series of studies on the subject that have yielded sometimes conflicting and confusing results. Yet the bottom line consensus appears to be that soda or other concentrated forms of sugar, such as candy bars, do increase risk of pancreatic cancer. The first thing we have to understand with PC is that it’s one of the bad cancers; five-year survival even with modern treatment is less than 5%. Treatment does little good; a better approach is to focus on prevention. Cigarette smoking is the one accepted risk factor consistently associated with increased risk of pancreatic cancer. Type 2 diabetes also increases risk. This led to a theory that producing high levels of insulin might somehow lead to malignant transformation of pancreatic cells.
In most cancers, the cells that become cancerous have been somehow overworked, irritated, or in some way abused prior to becoming cancer cells. They have been pushed by something to grow faster, work harder, secrete more or in some manner live harder lives. Estrogen pushes both breast and uterine cells to become cancerous. Testosterone pushes prostate cells to become prostate cancer. Infections push lymph cells to become lymphoma. Chronic inflammation pushes colon cancer cells, etc. This theory about pancreatic cancer suggests that high sugar intake pushes the pancreas. Granted, this is a vast oversimplification of both a complex process and a complicated hypothesis, but it works for my simple mind.
Diabetes has been associated with pancreatic cancer for decades. A study on Seventh Day Adventists published in 1988 reported that, “A prior history of diabetes was associated with increased risk of subsequent fatal pancreas cancer….” Overwork cells or abuse them and they aren’t happy.
A Kaiser Permanente study published that same year, found that while cigarette smoking increased risk of pancreatic cancer by a factor of 2.5, people who had been treated for diabetes had 4.5 times the risk. (Smoking: relative risk, 2.5; 95% confidence interval, 1.3-4.7. Diabetes: relative risk, 4.5; 95% confidence interval, 1.2-16.7).)
A Dutch paper published two years later in 1990, that analyzed data on 164 patients with pancreatic cancer, found, “…a significant, positive association between pancreatic cancer and past habitual intake of simple sugars…. (OR 1.95; 95% confidence interval 1.24-3.07).” This led the study authors to, “… suggest that the development of exocrine pancreatic carcinoma is positively related to past habitual intake of total energy, total carbohydrates and simple sugars, …” A 1991 Australian paper that analyzed the habits of 104 people who developed PC also found a link to sugar consumption. “For the top quartile of refined sugar intake, the estimated relative risk was 2.21 (95% confidence interval 1.07-4.55).”
[Of course sugars aren’t the only dietary culprit in the pancreatic cancer story. High fat diets have also been identified as a factor. A November 1993 study reported that high fat foods tripled risk. ]
A December 1995 study that looked at 179 cases of PC in French speaking Canadians found a similar effect of sugar consumption. Again, high sugar consumption nearly tripled risk. Of interest in this paper was the pronounced effect of cooking with firewood, a habit that increased relative risk by a factor of almost 5, while cooking in a pressure cooker lowered risk to 1/3 the average.
Sweetened carbonated drinks, what we call soft drinks, or soda, are a major source of simple sugars in western diets and as such, soda consumption provides a measure of overall sugar consumption. [16] Soda consumption is associated with hyperglycemia and hyperinsulinemia, obesity and type 2 diabetes.
Let us return to the current study by Mueller and colleagues. Rates of developing pancreatic cancer have plateaued and are stable in the United States but they are rising among Chinese men and women in Singapore. From 1968 to 1998 they have almost doubled going from 3.7 to 5.4 per 100,000 for men and 1.5 to 3.4 per 100,000 for women. One explanation for this increase is the shift toward a more western diet and increased consumption of sugar and sugar sweetened sodas. It may be that during this transition period between traditional diets and western diets that the effect of soda consumption is more pronounced. Soda may be adopted into the diet while traditional foods and recipes still comprise the basic diet. On the other hand as soda consumption increases so do other behaviors linked to higher risk of pancreatic cancer. For example in the Mueller study, people who drank more soda also consumed more red meat, total fat, sugar, candy, and alcohol. They smoked more, exercised less and were more likely to become diabetic. Is soda the cause of the increased risk or is it just a marker of overall poor lifestyle? The intricate dissection of this data using statistical tools is a delicate task. Simply gathering data on so rare a cancer is itself a challenge. In the last five years four other prospective cohort studies have been published that looked at this same equation of soda or sugar consumption and whether it is tied to pancreatic cancer risk. (Schernhammer, Larsson, Nothlings, Bao) Results from the current Mueller paper are consistent with three out of four of these earlier studies. One other study included fruit juice and found a positive association between juice intake and PC risk; this current study did not find an association. Eva Schernhammer and researchers from Harvard used data from two large cohorts, the Nurses' Health Study and the Health Professionals Follow-up Study, comprising 88,794 women and 49,364 men for their 2005 paper. These cohorts over the course of 20 years follow-up yielded data on 379 cases of pancreatic cancer. Schernhammer’s analysis found that the women who consumed more than 3 sodas a week had a 57% greater risk of pancreatic cancer than women who drank one or less sodas a month. (RR, 1.57; 95% CI, 1.02-2.41; P for trend = 0.05). No association was found in the 174 men who developed pancreatic cancer. In November 2006, the American Journal of Clinical nutrition published a paper by Susanna Larsson et al, analyzing Swedish dietary data from a cohort of 77,797 people who were followed for 7 years, 131 of whom developed pancreatic cancer. Those who drank 2 or more soft drinks a day had a 93% increased risk of pancreatic cancer. (OR1.93 (1.18, 3.14; P for trend = 0.02) A November 2007 study conducted by Nothlings and fellow researchers from the University of Hawaii analyzed data for 162,150 participants in the Hawaii-Los Angeles Multiethnic Cohort Study to investigate associations between glycemic load, dietary carbohydrates, sucrose, fructose, total sugars, and added sugars and the risk of pancreatic cancer. During 8 years of follow-up, 434 pancreatic cancer cases occurred within the group. Again the results though suggestive contradict, at least in part, other studies. The risk of PC increased with higher intakes of total sugars, fructose, and sucrose. The association with fructose was significant when the highest and lowest quartiles were compared (relative risk: 1.35; 95% CI: 1.02, 1.80; P for trend = 0.046). An almost identical association was found with high fruit and juice intake (1.37; 1.02, 1.84; P for trend = 0.04). But no association was seen with soda intake. The researchers concluded that, “High fructose and sucrose intakes may
play a role in pancreatic cancer etiology. Conditions such as overweight or obesity in which a degree of insulin resistance may be present may also be important.” The Bao study published in 2008 is the one report that did not find an association between sugar and PC. This is despite the fact that it was the largest of the studies. Rather than soda they calculated the total consumption of added sugar and sugar-sweetened foods and beverages, examining data from 487,922 men and women calculating total added dietary sugar intake. During 7.2 years of follow-up, 1,258 pancreatic cancer cases were found within the group. The lowest sugar consumers averaged about 3 tsp/day while the high consumers averaged almost 23 tsp/day. No difference in risk was seen between these two groups. We should clarify; no statistically significant difference was seen. The low sugar consumers had a relative risk of 0.85 compared to the high sugar eaters but this did not reach statistical significance. Thus these results did not support the sugar hypothesis. Just a year later in August 2009, another study reported different results, a positive but still confusing, association. June Chan and colleagues from the University of California in San Francisco reported in the journal Cancer Causes and Control on a comparison of the dietary habits of 532 people who developed PC with people who didn’t. “Among men, greater intakes of total and specific sweets were associated with pancreatic cancer risk…” that ranged from an overall risk of 1.9 for total sweets to 3.3 for candy bars but in this study, “…Sweets were not consistently associated with risk among women.” In contrast to other soda studies they also reported that, “Sweetened beverages were not associated with increased pancreatic cancer risk.” But to confuse things further, “… low-calorie soft drinks were associated with increased risk among men…” In November 2009 an Italian study was published that once again supported a link between sugar consumption and pancreatic cancer. Polesel et al. worked with data from 326 patients with pancreatic cancer comparing them to 652 control patients. Comparing the diets of the two groups they found that, “Frequent meat consumption was associated to a twofold increased risk of pancreatic cancer (95% CI: 1.18-3.36). Added table sugar (OR = 2.23; 95% CI: 1.34-3.71) and potatoes (OR = 1.79; 95% CI: 1.12-2.86) were related to pancreatic cancer.” Leading them to conclude that, “The increased risk for table sugar suggests that insulin resistance may play a role in pancreatic carcinogenesis.” Thus the results of the Mueller study do not stand-alone but are one of a series of studies that have parsed out this relationship between sugar and pancreatic cancer. If we are to accept these findings though we need an explanation to explain this relationship.There are two types of pancreatic cancer, endocrine or exocrine; endocrine tumors develop in the hormone producing tissues for secretion into the blood while exocrine cancers develop from the tissues that make digestive enzymes for secretion into the intestine. “Of pancreatic tumors, 95% develop from the exocrine portion of the pancreas, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.” These exocrine derived are the focus of this discussion. “It is tacitly assumed that the endocrine and exocrine parts of the pancreas are
Independent of each other, almost as though they were anatomically related by some sort of celestial coincidence.” But this is not the case. Instead, “…the two components are functionally related, and that the endocrine gland exerts a profound effect upon the digestive activities of the organ.” Blood and with it, insulin, are carried from insulin producing cells to exocrine cells in what has been named the Insulin-Pancreatic Acinar Axis. Insulin regulates the exocrine function of the pancreas. Exocrine cells are exposed to insulin concentrations that are 20-fold higher than in general circulation. Insulin has an effect on these cells increasing cell division and stimulating production of amylase. These high insulin levels may increase free insulin-like growth factor (IGF) by lowering levels of IGF-binding proteins. Low levels of IGF-binding proteins are suggested in some research to be risk factor for pancreatic cancer. [It should be noted that not all studies support this idea; an August 2009 paper found no link between IGF-1 or IGF-binding proteins and PC. ]The Mueller paper found no association between fasting plasma insulin levels and pancreatic cancer risk. “This suggests that postprandial insulin may be a better measure for the association with cancer risk than fasting insulin levels and is consistent with the independent role of soft drink consumption in the development of pancreatic cancer….” In other words it may be the surge of insulin produced after eating concentrated sugars that is the problem.
Abandoning these soda studies for a moment, this idea that elevated insulin levels increase cancer risk is supported by a paper published in September 2009 in Diabetologia. Currie and colleagues at Cardiff University looked for confirmation of this insulin theory by looking at the effects of different blood sugar lowering treatments on type 2 diabetics.They analyzed a retrospective cohort of 62,809 people who developed diabetes after age 40 and who were treated with either oral agents or insulin. These patients were divided into four groups according to whether they received monotherapy with metformin or sulfonylurea, combined therapy (metformin plus sulfonylurea), or insulin. The outcome measures were progression to any solid tumor, or cancer of the breast, colon, pancreas or prostate. “Metformin monotherapy carried the lowest risk of cancer. In comparison, the adjusted HR was 1.08 (95% CI 0.96-1.21) for metformin plus sulfonylurea, 1.36 (95% CI 1.19-1.54) for sulfonylurea monotherapy, and 1.42 (95% CI 1.27-1.60) for insulin-based regimens. Adding metformin to insulin reduced progression to cancer (HR 0.54, 95% CI 0.43-0.66). …. Compared with metformin, insulin therapy increased the risk of colorectal (HR 1.69, 95% CI 1.23-2.33) or pancreatic cancer (HR 4.63, 95% CI 2.64-8.10),….. Sulfonylureas were associated with a
similar pattern of risk as insulin.” It appears anything that increases insulin levels whether it is oral hypoglycemic drugs or actual insulin increased risk of some cancers, especially pancreatic cancer risk. Back to Colorado’s ‘Soda Tax’ for a moment. One of the arguments against taxing soda was that the price increase would dissuade consumers from purchasing it and therefore harm Colorado businesses and beverage dealers leading to job losses. Ignorant as I am about the economics of junk food marketing, I find it difficult to believe that a 2.9% price increase would influence anyone’s purchase decision to such an extent. Given the concerns raised by these studies regarding the health impact soda has, the tax sounds far too low as it will do little to shift consumption patterns. Perhaps my views are swayed by the task of sitting with people every day who ask me why they have cancer. A better argument against the soda and candy tax might be that they will effectively lower consumption and eventually cut pancreatic cancer incidence by half leading to unemployment among oncologists. We should be so lucky!A version of this newsletter is posted on our website with abstracts of all or almost all of the studies mentioned.http://denvernaturopathic.com/sodaandPC.htm
Dr. Jean M. Layton
1329 King Street
Bellingham WA 98229
360-734-1659
twitter: GFDoctor
Facebook: GFDoctor
Posted via email from GF Doctor-a slightly biased view of gluten free life.
Saturday, February 13, 2010
Friday, February 12, 2010
BPA Closer To Being Persona Non Grata in California — Washington Toxics Coalition ((BPA, California, Bisphenol a))
Bisphenol a (BPA) just can%u2019t catch a break these days. Already banned in children%u2019s food and beverage containers in Connecticut and Minnesota, and on its way out in Washington, Oregon, and several other states, the chemical has now come under new scrutiny by California regulators.
The California Environmental Protection Agency (CalEPA) announced today it plans to formally list the chemical as a reproductive toxicant on the state%u2019s Prop 65 list. A Prop. 65 listing means manufacturers may be required to disclose the presence of the chemical in products they sell. Often manufacturers choose to stop using a Prop 65 chemical rather than having to disclose that their product contains a harmful chemical.
CalEPA will hold a 60-day public comment period before a final decision is made on listing.
For more information on the proposed listing and what it means for California and the rest of the country, here's a press release from our California coalition partner, the Breast Cancer Fund.
BPA, it appears your days are numbered.
via watoxics.org
Posted via web from GF Doctor-a slightly biased view of gluten free life.
Monday, February 8, 2010
Fosamax needs a break
---------- Forwarded message ----------
From: denvernaturopathic
Date: Mon, Feb 8, 2010 at 1:00 PM
Subject: Fosamax needs a break
To: drjeannd@gmail.com Fosamax Needs a Break: Don’t use this drug for more than five years
Jacob Schor, ND, FABNO
February 2009
The drugs that have been used with apparent success to treat
osteoporosis may now be a problem. Alendronate may weaken bone and
lead to increased fracture risk. [a referenced version of this article is posted at:
http://denvernaturopathic.com/fosamaxBreak.htm] Alendronate is the drug we know as Fosamax. It belongs to a class of
drugs called Bisphosphonates. These chemicals were developed in the
19th century but were not investigated until the 1960s for use in
disorders of bone metabolism. Their non-medical use was to soften
water in irrigation systems used in orange groves. The rationale for
giving them to people is that they prevent the dissolution of
hydroxylapatite, the principal bone mineral, so stopping bone loss.
Only in the 1990s was their actual mechanism of action explained when
Merck brought Fosamax to the market place. There is little doubt that these drugs do what they are supposed to
over the short term: they increase bone density and decrease fracture
risk. The FOSIT study published in 1999 told us this quite clearly. This
study reported on 1,908 healthy, postmenopausal women with
osteoporosis, 950 of whom took either 10 mg of Fosamax for a year,
while the other 958 got a placebo. Both groups took 500 mg of calcium
per day. After a year, bone mineral density increased by almost 5% on
average in those taking the Fosamax compared to the placebo group.
Non-spinal fractures decreased. Of those taking the drug only 19
suffered fractures compared to 37 of those taking placebo. From the first use of these drugs, there was always a theoretical
worry. Recall that there are two main processes that occur constantly
in the bone: osteoclastic activity that breaks down old bone, and
osteoblastic activity that builds up new bone. This constant turnover
of bone maintains healthy and strong bone. These drugs stop the
osteoclastic activity so that the old bone is left untouched. This
increases bone density measurements. The worry was that because these
drugs halt normal bone turnover people using them would end up with
dense but more brittle bones. As the early studies consistently
showed a rapid reduction in fracture rates, this concern faded. These early worries unfortunately were not just a product of
naturopathic paranoia; the problems just took a few years to show up.
The May/June 2008 issue of The Journal of Orthopaedic Trauma published
a report on “Low-energy femoral shaft fractures associated with
alendronate use.” The authors reviewed records of 70 patients who had
sustained low energy femur fractures. That means their femurs broke
without any major stress. Rather they did little things such as
walking or stepped off a curb and thus triggered the breaks. These
weren’t young people, their average age was about 75. Of these 70
patients, 25 of them, a little over a third (36%), were taking
Fosamax. Nineteen (76%) of those 25 patients demonstrated a simple,
transverse fracture with a unicortical beak in an area of cortical
hypertrophy. This is a rare and peculiar type of fracture. Only 1
patient of those not taking Fossamax (2%) had this kind of bone break.
When the statistics were worked out, the numbers tell us that Fosamax
use significantly increased risk of these fractures: the odds ratio
was 139.33, 95% CI [19.0-939.4], P 0.0001). You can say those taking Fosamax were about 140 times more
likely to get one of these rare fractures. It took about 7 years for
this problem to occur. Those taking Fosamax less than 2.5 years were
not at greater risk. A 2009 paper in Geriatrics continued this story. It tells us that,
“The fractures are often preceded by pain in the affected thigh…” this
paper suggests that patients not take Fosamax for longer than five
years. Another 2009 article, this one in Clinical Calcium, echoed
this warning and suggested that, “… alendronate treatment might be
stopped for a while after 5 years to prevent [these kinds of]…
fractures.” Take a break to prevent a break might become a safety slogan. Researcher from Johns Hopkins repeated this same story in the journal
Orthopedics in August 2009. Then just last November, 2009, doctors
from New York University report on seven different patients who had
broken both legs. The average age of these patients was 61 years and
on average they had taken Fosmax for 8.6 years. One patient had
broken both legs simultaneously. The article suggests that we start
checking the ‘good leg’ when people who have been taking Fosamax
sustain a suspicious fracture. If a problem is seen, they suggest
prophylactic repair. Few doctors and fewer patients are paying attention to duration of
Fosamax use. Most patients will report they’ve taken Fosamax, “for
awhile.” We need to start spreading the message, “for awhile” should
be less than five years.
In our practice we are suggesting a break from use after a shorter
period of time, about three years. Discontinuing Fosamax use and
relying solely on naturopathic treatments even for an interval of
time, may, in the long run prove to be a safer course of action. Unfortunately over the years as Fosamax was used with apparent benefit
by so many people, many of us grew lax, thinking that our early
worries were unfounded. In hindsight this may have been a problem all
along. It’s only in the last few years that enough patients have
taken the drug long enough that we can actually see the results of
long term bone suppression.
................................................................
We hope you find the information in these newsletters useful,
informative and hopefully entertaining. If you want your name removed
simply leave a message at the office (303-337-4884) or go to the
website: denvernaturopathic.com and unsubscribe, or reply with the
message "REMOVE" in the subject line. If on the other hand you want
to be added to the mailing list follow the prior instructions but
subscribe.
We are posting most of these newsletters in our 'NEWS' section of the
website. The website versions contain more complete references and
often abstracts of the references quoted and links to the full text of
many of the journal articles mentioned. You don't have to be a patient
to sign up and we encourage you to get your friends on our mailing
list so you don't have to keep forwarding the newsletters that you
find interesting.
From: denvernaturopathic
Date: Mon, Feb 8, 2010 at 1:00 PM
Subject: Fosamax needs a break
To: drjeannd@gmail.com Fosamax Needs a Break: Don’t use this drug for more than five years
Jacob Schor, ND, FABNO
February 2009
The drugs that have been used with apparent success to treat
osteoporosis may now be a problem. Alendronate may weaken bone and
lead to increased fracture risk. [a referenced version of this article is posted at:
http://denvernaturopathic.com/fosamaxBreak.htm] Alendronate is the drug we know as Fosamax. It belongs to a class of
drugs called Bisphosphonates. These chemicals were developed in the
19th century but were not investigated until the 1960s for use in
disorders of bone metabolism. Their non-medical use was to soften
water in irrigation systems used in orange groves. The rationale for
giving them to people is that they prevent the dissolution of
hydroxylapatite, the principal bone mineral, so stopping bone loss.
Only in the 1990s was their actual mechanism of action explained when
Merck brought Fosamax to the market place. There is little doubt that these drugs do what they are supposed to
over the short term: they increase bone density and decrease fracture
risk. The FOSIT study published in 1999 told us this quite clearly. This
study reported on 1,908 healthy, postmenopausal women with
osteoporosis, 950 of whom took either 10 mg of Fosamax for a year,
while the other 958 got a placebo. Both groups took 500 mg of calcium
per day. After a year, bone mineral density increased by almost 5% on
average in those taking the Fosamax compared to the placebo group.
Non-spinal fractures decreased. Of those taking the drug only 19
suffered fractures compared to 37 of those taking placebo. From the first use of these drugs, there was always a theoretical
worry. Recall that there are two main processes that occur constantly
in the bone: osteoclastic activity that breaks down old bone, and
osteoblastic activity that builds up new bone. This constant turnover
of bone maintains healthy and strong bone. These drugs stop the
osteoclastic activity so that the old bone is left untouched. This
increases bone density measurements. The worry was that because these
drugs halt normal bone turnover people using them would end up with
dense but more brittle bones. As the early studies consistently
showed a rapid reduction in fracture rates, this concern faded. These early worries unfortunately were not just a product of
naturopathic paranoia; the problems just took a few years to show up.
The May/June 2008 issue of The Journal of Orthopaedic Trauma published
a report on “Low-energy femoral shaft fractures associated with
alendronate use.” The authors reviewed records of 70 patients who had
sustained low energy femur fractures. That means their femurs broke
without any major stress. Rather they did little things such as
walking or stepped off a curb and thus triggered the breaks. These
weren’t young people, their average age was about 75. Of these 70
patients, 25 of them, a little over a third (36%), were taking
Fosamax. Nineteen (76%) of those 25 patients demonstrated a simple,
transverse fracture with a unicortical beak in an area of cortical
hypertrophy. This is a rare and peculiar type of fracture. Only 1
patient of those not taking Fossamax (2%) had this kind of bone break.
When the statistics were worked out, the numbers tell us that Fosamax
use significantly increased risk of these fractures: the odds ratio
was 139.33, 95% CI [19.0-939.4], P 0.0001). You can say those taking Fosamax were about 140 times more
likely to get one of these rare fractures. It took about 7 years for
this problem to occur. Those taking Fosamax less than 2.5 years were
not at greater risk. A 2009 paper in Geriatrics continued this story. It tells us that,
“The fractures are often preceded by pain in the affected thigh…” this
paper suggests that patients not take Fosamax for longer than five
years. Another 2009 article, this one in Clinical Calcium, echoed
this warning and suggested that, “… alendronate treatment might be
stopped for a while after 5 years to prevent [these kinds of]…
fractures.” Take a break to prevent a break might become a safety slogan. Researcher from Johns Hopkins repeated this same story in the journal
Orthopedics in August 2009. Then just last November, 2009, doctors
from New York University report on seven different patients who had
broken both legs. The average age of these patients was 61 years and
on average they had taken Fosmax for 8.6 years. One patient had
broken both legs simultaneously. The article suggests that we start
checking the ‘good leg’ when people who have been taking Fosamax
sustain a suspicious fracture. If a problem is seen, they suggest
prophylactic repair. Few doctors and fewer patients are paying attention to duration of
Fosamax use. Most patients will report they’ve taken Fosamax, “for
awhile.” We need to start spreading the message, “for awhile” should
be less than five years.
In our practice we are suggesting a break from use after a shorter
period of time, about three years. Discontinuing Fosamax use and
relying solely on naturopathic treatments even for an interval of
time, may, in the long run prove to be a safer course of action. Unfortunately over the years as Fosamax was used with apparent benefit
by so many people, many of us grew lax, thinking that our early
worries were unfounded. In hindsight this may have been a problem all
along. It’s only in the last few years that enough patients have
taken the drug long enough that we can actually see the results of
long term bone suppression.
................................................................
We hope you find the information in these newsletters useful,
informative and hopefully entertaining. If you want your name removed
simply leave a message at the office (303-337-4884) or go to the
website: denvernaturopathic.com and unsubscribe, or reply with the
message "REMOVE" in the subject line. If on the other hand you want
to be added to the mailing list follow the prior instructions but
subscribe.
We are posting most of these newsletters in our 'NEWS' section of the
website. The website versions contain more complete references and
often abstracts of the references quoted and links to the full text of
many of the journal articles mentioned. You don't have to be a patient
to sign up and we encourage you to get your friends on our mailing
list so you don't have to keep forwarding the newsletters that you
find interesting.
Posted via email from GF Doctor-a slightly biased view of gluten free life.
Thursday, February 4, 2010
Fwd:HBD wins a Silver Medal!
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Posted via email from GF Doctor-a slightly biased view of gluten free life.
Monday, February 1, 2010
Health Risks Brochure - Institute for Responsible Technology
Print this document
GMO Health Risks Brochure
Genetically modified foods:
YES, you’re eating them.
NO, they’re not safe.Did you know... since 1996 Americans have been eating genetically modified (GM) ingredients in most processed foods.
Did you know... GM plants, such as soybean, corn, cottonseed, and canola, have had foreign genes forced into their DNA. The inserted genes come from species, such as bacteria and viruses, which have never been in the human food supply.
Did you know... The American Academy of Environmental Medicine states, “Several animal studies indicate serious health risks associated with GM food,” including infertility, immune problems, accelerated aging, faulty insulin regulation, and changes in major organs and the gastrointestinal system. They ask physicians to advise patients to avoid GM foods.1
Find out what the risks are and start protecting yourself and your family today!
Why isn’t the FDA protecting us?
In 1992, the Food and Drug Administration claimed they had no information showing that GM foods were substantially different from conventionally grown foods. Therefore they are safe to eat, and absolutely no safety studies were required. But internal memos made public by a lawsuit2 reveal that their position was staged by political appointees who were under orders from the White House to promote GMOs. In addition, the FDA official in charge of creating this policy was Michael Taylor, the former attorney for Monsanto, the largest biotech company, and later their vice president.
In reality, FDA scientists had repeatedly warned that GM foods can create unpredictable, hard-to-detect side effects, including allergies, toxins, new diseases, and nutritional problems. They urged long-term safety studies, but were ignored.
Today, the same biotech companies who have been found guilty of hiding toxic effects of their chemical products are in charge of determining whether their GM foods are safe. Industry-funded GMO safety studies are too superficial to find most of the potential dangers, and their voluntary consultations with the FDA are widely criticized as a meaningless façade.3
Genetic modification is radically different from natural breeding
Genetic engineering transfers genes across natural species barriers. It uses imprecise laboratory techniques that bear no resemblance to natural breeding, and is based on outdated concepts of how genes and cells work.4 Gene insertion is done either by shooting genes from a “gene gun” into a plate of cells or by using bacteria to invade the cell with foreign DNA. The altered cell is then cloned into a plant.
Widespread, unpredictable changes
The genetic engineering process creates massive collateral damage, causing mutations in hundreds or thousands of locations throughout the plant’s DNA.5 Natural genes can be deleted or permanently turned on or off, and hundreds may change their behavior.6 Even the inserted gene can be damaged or rearranged,7 and may create proteins that can trigger allergies or promote disease.
GM foods on the market
There are eight GM food crops. The five major varieties—soy, corn, canola, cotton, and sugar beets—have bacterial genes inserted, which allow the plants to survive an otherwise deadly dose of weed killer. Farmers use considerably more herbicides on these GM crops and so the food has higher herbicide residues. About 68% of GM crops are herbicide tolerant.
The second GM trait is a built-in pesticide, found in GM corn and cotton. A gene from the soil bacterium called Bt (for Bacillus thuringiensis) is inserted into the plant’s DNA, where it secretes the insect-killing Bt-toxin in every cell. About 19% of GM crops produce their own pesticide. Another 13% produce a pesticide and are herbicide tolerant.
There is also Hawaiian papaya and a small amount of zucchini and yellow crookneck squash, which are engineered to resist a plant virus.
Growing evidence of harm from GMOs
GM soy and allergic reactions
- Soy allergies skyrocketed by 50% in the UK, soon after GM soy was introduced.8
- A skin prick allergy test shows that some people react to GM soy, but not to natural soy.9
- Cooked GM soy contains as much as 7-times the amount of a known soy allergen.10
- GM soy also contains a new unexpected allergen, not found in natural soy.11
Bt corn and cotton linked to allergies
The biotech industry claims that Bt-toxin is harmless to humans and mammals because the natural bacteria version has been used as a spray by farmers for years. In reality, hundreds of people exposed to Bt spray had allergic-type symptoms,12 and mice fed Bt had powerful immune responses13 and damaged intestines.14 Moreover, the Bt in GM crops is designed to be more toxic than the natural spray and is thousands of times more concentrated.
Farm workers throughout India are getting the same allergic reactions from handling Bt cotton15 as those who reacted to Bt spray.16 Mice17 and rats18 fed Bt corn also showed immune responses.
GMOs fail allergy tests
No tests can guarantee that a GMO will not cause allergies. Although the World Health Organization recommends a screening protocol,19 the GM soy, corn, and papaya in our food supply fail those tests—because their GM proteins have properties of known allergens.20
GMOs may make you allergic to non-GM foods
- GM soy drastically reduces digestive enzymes in mice.21 If it also impairs your digestion, you may become sensitive and allergic to a variety of foods.
- Mice fed Bt-toxin started having immune reactions to formerly harmless foods.22
- Mice fed experimental GM peas also started reacting to a range of other foods.23 (The peas had already passed all the allergy tests normally done before a GMO gets on the market. Only this advanced test, which is never used on the GMOs we eat, revealed that the peas could actually be deadly.)
GMOs and liver problems
- Rats fed GM potatoes had smaller, partially atrophied livers.24
- The livers of rats fed GM canola were 12-16% heavier.25
- GM soy altered mouse liver cells in ways that suggest a toxic insult.26 The changes reversed after they switched to non-GM soy.27
GMOs, reproductive problems, and infant mortality
- More than half the babies of mother rats fed GM soy died within three weeks.28
- Male rats29 and mice30 fed GM soy had changed testicles, including altered young sperm cells in the mice.
- The DNA of mouse embryos functioned differently when their parents ate GM soy31
The longer mice were fed GM corn, the less babies they had, and the smaller their babies were.32
Babies of female rats fed GM soy were considerably smaller, and more than half died within three weeks (compared to 10% of the
non-GM soy controls).33Bt crops linked to sterility, disease, and death
- Thousands of sheep, buffalo, and goats in India died after grazing on Bt cotton plants after harvest. Others suffered poor health and reproductive problems.34
- Farmers in Europe and Asia say that cows, water buffaloes, chickens, and horses died from eating Bt corn varieties.35
- About two dozen US farmers report that Bt corn varieties caused widespread sterility in pigs or cows.36
- Filipinos in at least five villages fell sick when a nearby Bt corn variety was pollinating.37
The stomach lining of rats fed GM potatoes showed excessive cell growth, a condition that may lead to cancer. Rats also had damaged organs and immune systems.38
Functioning GM genes remain inside you
Unlike safety evaluations for drugs, there are no human clinical trials of GM foods. The only published human feeding experiment revealed that the genetic material inserted into GM soy transfers into bacteria living inside our intestines and continues to function.39 This means that long after we stop eating GM foods, we may still have their GM proteins produced continuously inside us.
- If the antibiotic gene inserted into most GM crops were to transfer, it could create super diseases, resistant to antibiotics.
- If the gene that creates Bt-toxin in GM corn were to transfer, it might turn our intestinal bacteria into living pesticide factories.
- Animal studies show that DNA in food can travel into organs throughout the body, even into the fetus.40
GM food supplement caused deadly epidemic
In the 1980s, a contaminated brand of a food supplement called L-tryptophan killed about 100 Americans and caused sickness and disability in another 5,000-10,000 people. The source of contaminants was almost certainly the genetic engineering process used in its production.41 The disease took years to find and was almost overlooked. It was only identified because the symptoms were unique, acute, and fast-acting. If all three characteristics were not in place, the deadly GM supplement might never have been identified or removed.
If GM foods on the market are causing common diseases or if their effects appear only after long-term exposure, we may not be able to identify the source of the problem for decades, if at all. There is no monitoring of GMO-related illnesses and no long-term animal studies. Heavily invested biotech corporations are gambling with the health of our nation for their profit.
Help end the genetic engineering of our food supply
When the tipping point of consumer concern about GMOs was achieved in Europe in 1999, within a single week virtually all major food manufacturers committed to remove GM ingredients. The Campaign for Healthier Eating in America is designed to reach a similar tipping point in the US soon.
Our growing network of manufacturers, retailers, healthcare practitioners, organizations, and the media, is informing consumers of the health risks of GMOs and helping them select healthier non-GMO alternatives with our Non-GMO Shopping Guides.
Go to www.responsibletechnology.org to get involved and learn how to avoid GMOs.
Start buying non-GMO today.
Help us stop the genetic engineering of our food supply.
Membership
Membership in our Campaign for Healthier Eating in America is free; Contributing members receive a free educational gift. Donations to the Institute For Responsible Technology are tax-deductible.
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The health information is from the book Genetic Roulette: The Documented Health Risk of Genetically Engineered Foods, by Jeffrey M. Smith.
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[2] See Part 2, Jeffrey M. Smith, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, Yes! Books, Fairfield, IA 2007
[3] See for example 233-236, chart of disproved assumptions, in Jeffrey M. Smith, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, Yes! Books, Fairfield, IA 2007
[4] J. R. Latham, et al., “The Mutational Consequences of Plant Transformation,” The Journal of Biomedicine and Biotechnology 2006, Article ID 25376: 1-7; see also Allison Wilson, et. al., “Transformation-induced mutations in transgenic plants: Analysis and biosafety implications,” Biotechnology and Genetic Engineering Reviews – Vol. 23, December 2006.
[5] Srivastava, et al, “Pharmacogenomics of the cystic fibrosis transmembrane conductance regulator (CFTR) and the cystic fibrosis drug CPX using genome microarray analysis,” Mol Med. 5, no. 11(Nov 1999):753–67.
[6] Latham et al, “The Mutational Consequences of Plant Transformation, Journal of Biomedicine and Biotechnology 2006:1-7, article ID 25376, http://www.hindawi.com/journals/JBB/index.html; Draft risk analysis report application A378, Food derived from glyphosate-tolerant sugarbeet line 77 (GTSB77),” ANZFA, March 7, 2001, www.agbios.com/docroot/decdocs/anzfa_gtsb77.pdf; E. Levine et al., “Molecular Characterization of Insect Protected Corn Line MON 810.” Unpublished study submitted to the EPA by Monsanto, EPA MRID No. 436655-01C (1995); Allison Wilson, PhD, Jonathan Latham, PhD, and Ricarda Steinbrecher, PhD, “Genome Scrambling—Myth or Reality? Transformation-Induced Mutations in Transgenic Crop Plants Technical Report—October 2004,” www.econexus.info; C. Collonier, G. Berthier, F. Boyer, M. N. Duplan, S. Fernandez, N. Kebdani, A. Kobilinsky, M. Romanuk, Y. Bertheau, “Characterization of commercial GMO inserts: a source of useful material to study genome fluidity,” Poster presented at ICPMB: International Congress for Plant Molecular Biology (n°VII), Barcelona, 23-28th June 2003. Poster courtesy of Dr. Gilles-Eric Seralini, Président du Conseil Scientifique du CRII-GEN, www.crii-gen.org; also “Transgenic lines proven unstable” by Mae-Wan Ho, ISIS Report, 23 October 2003, www.i-sis.org.uk
[7] Netherwood et al, “Assessing the survival of transgenic plant DNA in the human gastrointestinal tract,” Nature Biotechnology 22 (2004): 2; Chowdhury, et al, “Detection of genetically modified maize DNA fragments in the intestinal contents of pigs fed StarLink CBH351,” Vet Hum Toxicol. 45 , no. 2 (March 2003): 95–6; P. A. Chambers, et al, “The fate of antibiotic resistance marker genes in transgenic plant feed material fed to chickens,” J. Antimic. Chemother. 49 (2000): 161–164; and Paula S. Duggan, et al, “Fate of genetically modified maize DNA in the oral cavity and rumen of sheep,” Br J Nutr. 89, no 2 (Feb.2003): 159–66.
[8] Mark Townsend, “Why soya is a hidden destroyer,” Daily Express, March 12, 1999.
[9] Hye-Yung Yum, Soo-Young Lee, Kyung-Eun Lee, Myung-Hyun Sohn, Kyu-Earn Kim, “Genetically Modified and Wild Soybeans: An immunologic comparison,” Allergy and Asthma Proceedings 26, no. 3 (May–June 2005): 210-216(7).
[10] A. Pusztai and S. Bardocz, “GMO in animal nutrition: potential benefits and risks,” Chapter 17, Biology of Nutrition in Growing Animals, R. Mosenthin, J. Zentek and T. Zebrowska (Eds.) Elsevier, October 2005.
[11] Hye-Yung Yum, Soo-Young Lee, Kyung-Eun Lee, Myung-Hyun Sohn, Kyu-Earn Kim, “Genetically Modified and Wild Soybeans: An immunologic comparison,” Allergy and Asthma Proceedings 26, no. 3 (May–June 2005): 210-216(7).
[12] M. Green, et al., “Public health implications of the microbial pesticide Bacillus thuringiensis: An epidemiological study, Oregon, 1985-86,” Amer. J. Public Health 80, no. 7(1990): 848–852; and M.A. Noble, P.D. Riben, and G. J. Cook, Microbiological and epidemiological surveillance program to monitor the health effects of Foray 48B BTK spray (Vancouver, B.C.: Ministry of Forests, Province of British Columbi, Sep. 30, 1992)
[13] Vazquez et al, “Intragastric and intraperitoneal administration of Cry1Ac protoxin from Bacillus thuringiensis induces systemic and mucosal antibody responses in mice,” 1897–1912; Vazquez et al, “Characterization of the mucosal and systemic immune response induced by Cry1Ac protein from Bacillus thuringiensis HD 73 in mice,” Brazilian Journal of Medical and Biological Research 33 (2000): 147–155; and Vazquez et al, “Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal adjuvant,” Scandanavian Journal of Immunology 49 (1999): 578–584. See also Vazquez-Padron et al., 147 (2000b).
[14] Nagui H. Fares, Adel K. El-Sayed, “Fine Structural Changes in the Ileum of Mice Fed on Endotoxin Treated Potatoes and Transgenic Potatoes,” Natural Toxins 6, no. 6 (1998): 219–233.
[15] See for example “Bt cotton causing allergic reaction in MP; cattle dead,” Bhopal, Nov. 23, 2005, http://news.webindia123.com/news/showdetails.asp?id=170692&cat=Health;
[16] Ashish Gupta et. al., “Impact of Bt Cotton on Farmers’ Health (in Barwani and Dhar District of Madhya Pradesh),” Investigation Report, Oct–Dec 2005; and M. Green, et al., “Public health implications of the microbial pesticide Bacillus thuringiensis: An epidemiological study, Oregon, 1985-86,” Amer. J. Public Health 80, no. 7(1990): 848–852; and M.A. Noble, P.D. Riben, and G. J. Cook, Microbiological and epidemiological surveillance program to monitor the health effects of Foray 48B BTK spray (Vancouver, B.C.: Ministry of Forests, Province of British Columbi, Sep. 30, 1992)
[17] FAO-WHO, “Evaluation of Allergenicity of Genetically Modified Foods. Report of a Joint FAO/WHO Expert
Consultation on Allergenicity of Foods Derived from Biotechnology,” Jan. 22–25, 2001; http://www.fao.org/es/ESN/food/pdf/allergygm.pdf
[18] Gendel, “The use of amino acid sequence alignments to assess potential allergenicity of proteins used in genetically modified foods,” Advances in Food and Nutrition Research 42 (1998), 45–62; G. A. Kleter and A. A. C. M. Peijnenburg, “Screening of transgenic proteins expressed in transgenic food crops for the presence of short amino acid sequences indentical to potential, IgE-binding linear epitopes of allergens,” BMC Structural Biology 2 (2002): 8–19; H. P. J. M. Noteborn, “Assessment of the Stability to Digestion and Bioavailability of the LYS Mutant Cry9C Protein from Bacillus thuringiensis serovar tolworthi,” Unpublished study submitted to the EPA by AgrEvo, EPA MRID No. 447343-05 (1998); and H. P. J. M. Noteborn et al, “Safety Assessment of the Bacillus thuringiensis Insecticidal Crystal Protein CRYIA(b) Expressed in Transgenic Tomatoes,” in Genetically modified foods: safety issues, American Chemical Society Symposium Series 605, eds. K.H. Engel et al., (Washington, DC, 1995): 134–47.
[19] M. Malatesta, M. Biggiogera, E. Manuali, M. B. L. Rocchi, B. Baldelli, G. Gazzanelli, “Fine Structural Analyses of Pancreatic Acinar Cell Nuclei from Mice Fed on GM Soybean,” Eur J Histochem 47 (2003): 385–388.
[20] Vazquez et al, “Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal adjuvant,” Scandanavian Journal of Immunology 49 (1999): 578–584. See also Vazquez-Padron et al., 147 (2000b).
[21] V. E. Prescott, et al, “Transgenic Expression of Bean r-Amylase Inhibitor in Peas Results in Altered Structure and Immunogenicity,” Journal of Agricultural Food Chemistry (2005): 53.
[22] Arpad Pusztai, “Can science give us the tools for recognizing possible health risks of GM food,” Nutrition and Health, 2002, Vol 16 Pp 73-84
[23] Comments to ANZFA about Applications A346, A362 and A363 from the Food Legislation and Regulation Advisory Group (FLRAG) of the Public Health Association of Australia (PHAA) on behalf of the PHAA, “Food produced from glyphosate-tolerant canola line GT73,” http://www.iher.org.au/
[24] M. Malatesta, C. Caporaloni, S. Gavaudan, M. B. Rocchi, S. Serafini, C. Tiberi, G. Gazzanelli, “Ultrastructural Morphometrical and Immunocytochemical Analyses of Hepatocyte Nuclei from Mice Fed on Genetically Modified Soybean,” Cell Struct Funct. 27 (2002): 173–180.
[25] M. Malatesta, C. Tiberi, B. Baldelli, S. Battistelli, E. Manuali, M. Biggiogera, “Reversibility of Hepatocyte Nuclear Modifications in Mice Fed on Genetically Modified Soybean,” Eur J Histochem, 49 (2005): 237-242.
[26] I.V. Ermakova, “Diet with the Soya Modified by Gene EPSPS CP4 Leads to Anxiety and Aggression in Rats,” 14th European Congress of Psychiatry. Nice, France, March 4-8, 2006; “Genetically modified soy affects posterity: Results of Russian scientists’ studies,” REGNUM, October 12, 2005; http://www.regnum.ru/english/526651.html; Irina Ermakova, “Genetically modified soy leads to the decrease of weight and high mortality of rat pups of the first generation. Preliminary studies,” Ecosinform 1 (2006): 4–9.
[27] Irina Ermakova, “Experimental Evidence of GMO Hazards,” Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June 12, 2007
[28] L. Vecchio et al, “Ultrastructural Analysis of Testes from Mice Fed on Genetically Modified Soybean,” European Journal of Histochemistry 48, no. 4 (Oct–Dec 2004):449–454.
[29] Oliveri et al., “Temporary Depression of Transcription in Mouse Pre-implantion Embryos from Mice Fed on Genetically Modified Soybean,” 48th Symposium of the Society for Histochemistry, Lake Maggiore (Italy), September 7–10, 2006.
[30] I.V. Ermakova, “Diet with the Soya Modified by Gene EPSPS CP4 Leads to Anxiety and Aggression in Rats,” 14th
European Congress of Psychiatry. Nice, France, March 4-8, 2006; “Genetically modified soy affects posterity: Results of Russian scientists’ studies,” REGNUM, October 12, 2005; http://www.regnum.ru/english/526651.html; Irina Ermakova, “Genetically modified soy leads to the decrease of weight and high mortality of rat pups of the first generation. Preliminary studies,” Ecosinform 1 (2006): 4–9.
[31] “Mortality in Sheep Flocks after Grazing on Bt Cotton Fields—Warangal District, Andhra Pradesh” Report of the Preliminary Assessment, April 2006, http://www.gmwatch.org/archive2.asp?arcid=6494
[32] Mae-Wan Ho, “GM Ban Long Overdue, Dozens Ill & Five Deaths in the Philippines,” ISIS Press Release, June 2, 2006; and Mae-Wan Ho and Sam Burcher, “Cows Ate GM Maize & Died,” ISIS Press Release, January 13, 2004, http://www.isis.org.uk/CAGMMAD.php
[33] Personal communication with Jerry Rosman and other farmers, 2006; also reported widely in the farm press.
[34] See for example Mae-Wan Ho, “GM Ban Long Overdue, Dozens Ill & Five Deaths in the Philippines,” ISIS Press Release, June 2, 2006; “Study Result Not Final, Proof Bt Corn Harmful to Farmers,” BusinessWorld, 02 Mar 2004; and “Genetically Modified Crops and Illness Linked,” Manila Bulletin, 04 Mar 2004.
[35] Arpad Pusztai, “Can science give us the tools for recognizing possible health risks of GM food,” Nutrition and Health, 2002, Vol 16 Pp 73-84; Stanley W. B. Ewen and Arpad Pusztai, “Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine,” Lancet, 1999 Oct 16; 354 (9187): 1353-4; and Arpad Pusztai, “Facts Behind the GM Pea Controversy: Epigenetics, Transgenic Plants & Risk Assessment,” Proceedings of the Conference, December 1st 2005 (Frankfurtam Main, Germany: Literaturhaus, 2005)
[36] Netherwood et al, “Assessing the survival of transgenic plant DNA in the human gastrointestinal tract,” Nature Biotechnology 22 (2004): 2.
[37] Ricarda A. Steinbrecher and Jonathan R. Latham, “Horizontal gene transfer from GM crops to unrelated organisms,” GM Science Review Meeting of the Royal Society of Edinburgh on “GM Gene Flow: Scale and Consequences for Agriculture and the Environment,” January 27, 2003; Traavik and Heinemann, Genetic Engineering and Omitted Health Research; citing Schubbert, et al, “Ingested foreign (phage M13) DNA survives transiently in the gastrointestinal tract and enters the bloodstream of mice,” Mol Gen Genet. 242, no. 5 (1994): 495–504; Schubbert et al, “Foreign (M13) DNA ingested by mice reaches peripheral leukocytes, spleen, and liver via the intestinal wall mucosa and can be covalently linked to mouse DNA,” Proc Natl Acad Sci USA 94, no. 3 (1997): 961–6; Schubbert et al, “On the fate of orally ingested foreign DNA in mice: chromosomal association and placental transmission to the fetus,” Mol Gen Genet. 259, no. 6 (1998): 569–76; Hohlweg and Doerfler, “On the fate of plants or other foreign genes upon the uptake in food or after intramuscular injection in mice,” Mol Genet Genomics 265 (2001): 225–233; Palka-Santani, et al., “The gastrointestinal tract as the portal of entry for foreign macromolecules: fate of DNA and proteins,” Mol Gen Genomics 270 (2003): 201–215; Einspanier, et al, “The fate of forage plant DNA in farm animals; a collaborative case-study investigating cattle and chicken fed recombinant plant material,” Eur Food Res Technol 212 (2001): 129–134; Klotz, et al, “Degradation and possible carry over of feed DNA monitored in pigs and poultry,” Eur Food Res Technol 214 (2002): 271–275; Forsman, et al, “Uptake of amplifiable fragments of retrotransposon DNA from the human alimentary tract,” Mol Gen Genomics 270 (2003): 362–368; Chen, et al, “Transfection of mEpo gene to intestinal epithelium in vivo mediated by oral delivery of chitosan-DNA nanoparticles,” World Journal of Gastroenterology 10, no 1(2004): 112–116; Phipps, et al, “Detection of transgenic and endogenous plant DNA in rumen fluid, duodenal digesta, milk, blood, and feces of lactating dairy cows,” J Dairy Sci. 86, no. 12(2003): 4070–8.
[38] William E. Crist, Toxic L-tryptophan: Shedding Light on a Mysterious Epidemic, http://www.seedsofdeception.com/Public/L-tryptophan/index.cfm; and Jeffrey M. Smith, Seeds of Deception, Yes! Books, Fairfield, IA 2003, chapter 4, Deadly Epidemic
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