Matt Lentzner, Janine Jagger and I have designed a survey for participants of Gluten-free January, using the online application StatCrunch. Janine is an epidemiologist who studies healthcare worker safety at the University of Virginia; she has experience designing surveys for data collection so we're glad to have her on board. The survey will allow us to systematically gather and analyze data on the results of Gluten-free January. It will be 100 percent anonymous-- none of your answers will be connected to your identity in any way.
This survey has the potential to be really informative, but it will only work if you respond! The more people who take the survey, the more informative it will be, even if you didn't avoid gluten for a single day. If not very many people respond, it will be highly susceptible to "selection bias", where perhaps the only people who responded are people who improved the most, skewing the results.
Matt will be sending the survey out to everyone on his mailing list. Please complete it, even if you didn't end up avoiding gluten at all! There's no shame in it. The survey has responses built in for people who didn't avoid gluten. Your survey will still be useful!
We have potential data from over 500 people. After we crunch the numbers, I'll share them on the blog.
Senin, 31 Januari 2011
OVARIAN AND PRIMARY PERITONEAL CANCER STAGING
- Stage I - limited to one or both ovaries
- IA - involves one ovary; capsule intact; no tumor on ovarian surface; no malignant cells in ascites or peritoneal washings
- IB - involves both ovaries; capsule intact; no tumor on ovarian surface; negative washings
- IC - tumor limited to ovaries with any of the following: capsule ruptured, tumor on ovarian surface, positive washings
- Stage II - pelvic extension or implants
- IIA - extension or implants onto uterus or fallopian tube; negative washings
- IIB - extension or implants onto other pelvic structures; negative washings
- IIC - pelvic extension or implants with positive peritoneal washings
- Stage III - microscopic peritoneal implants outside of the pelvis; or limited to the pelvis with extension to the small bowel or omentum
- IIIA - microscopic peritoneal metastases beyond pelvis
- IIIB - macroscopic peritoneal metastases beyond pelvis less than 2 cm in size
- IIIC - peritoneal metastases beyond pelvis > 2 cm or lymph node metastases (retroperitoneal or inguinal)
- Stage IV - distant metastases to the liver or outside the peritoneal cavity
- Note: Liver capsule metastasis T3/Stage III; liver parenchymal metastasis M1/Stage IV.
Pleural effusion must have positive cytology for M1/Stage IV.
How much sodium? Decoding nutrition labels
Guidelines for Americans, designed to give Americans a sense of what their diets need based on the newest food research.But interpreting this information as a consumer can be tricky. After all, the numbers companies must print on packaged foods are only useful if you have a point of reference.When you're deciding what to make for dinner, experts say that having a bit of background information
Minggu, 30 Januari 2011
TESTICULAR CANCER THERAPY INCREASES RISK FOR CARDIOVASULAR DISEASE
Testicular cancer survivors who were treated with chemotherapy, radiotherapy or both have increased long-term risks for cardiovascular disease, a new study found.
Because such cancers are usually diagnosed before age 40, survivors can live several decades after treatment and doctors should watch for complications, the researchers note in their paper published online September 20th in the Journal of Clinical Oncology.
The lifelong follow-up for these men should focus on their cardiovascular risk profile and lifestyle interventions to prevent cardiovascular disease, lead author Dr. Hege Haugnes, of the University of Tromso, Norway, told Reuters Health in an email.
Dr. Haugnes' team studied 990 men treated for unilateral testicular cancer, following them for a median of 19 years. They stratified the men into four groups according to their treatment: 206 who had surgery only, 386 who had radiotherapy, 364 who had chemotherapy, and 34 who had both radiation and chemotherapy.
Compared to the surgery group, there was a higher risk for diabetes in men treated with radiotherapy alone (odds ratio: 2.3) or the combination of radiotherapy and chemotherapy (OR: 3.9).
The authors also found that 74 men (8%) developed atherosclerotic disease during follow up. Cox regression analysis showed increased hazard ratios for atherosclerosis after all cytotoxic treatments compared with surgery only (radiotherapy, HR 2.3; chemotherapy, HR: 2.6; both, HR 4.8).
Most chemotherapy was cisplatin-based, combined with bleomycin and either etoposide or vinblastine. When the researchers analyzed the men according to their treatments, etoposide was linked with a 5.7-fold higher risk for coronary artery disease and a 4.7-fold higher risk for atherosclerotic disease compared to surgery.
Compared to a separate group of matched controls, patients who received etoposide had a significantly higher risk of myocardial infarction (HR, 3.1) as did those in the combination therapy group (HR, 4.8).
Except for the etoposide results, previous studies had shown similar patterns, Dr. Haugnes said. She called the etoposide findings the most surprising in the study.
"A possible bias here is the inclusion of living men only, and thus only cardiovascular disease morbidity and not mortality has been reported," she said.
Because such cancers are usually diagnosed before age 40, survivors can live several decades after treatment and doctors should watch for complications, the researchers note in their paper published online September 20th in the Journal of Clinical Oncology.
The lifelong follow-up for these men should focus on their cardiovascular risk profile and lifestyle interventions to prevent cardiovascular disease, lead author Dr. Hege Haugnes, of the University of Tromso, Norway, told Reuters Health in an email.
Dr. Haugnes' team studied 990 men treated for unilateral testicular cancer, following them for a median of 19 years. They stratified the men into four groups according to their treatment: 206 who had surgery only, 386 who had radiotherapy, 364 who had chemotherapy, and 34 who had both radiation and chemotherapy.
Compared to the surgery group, there was a higher risk for diabetes in men treated with radiotherapy alone (odds ratio: 2.3) or the combination of radiotherapy and chemotherapy (OR: 3.9).
The authors also found that 74 men (8%) developed atherosclerotic disease during follow up. Cox regression analysis showed increased hazard ratios for atherosclerosis after all cytotoxic treatments compared with surgery only (radiotherapy, HR 2.3; chemotherapy, HR: 2.6; both, HR 4.8).
Most chemotherapy was cisplatin-based, combined with bleomycin and either etoposide or vinblastine. When the researchers analyzed the men according to their treatments, etoposide was linked with a 5.7-fold higher risk for coronary artery disease and a 4.7-fold higher risk for atherosclerotic disease compared to surgery.
Compared to a separate group of matched controls, patients who received etoposide had a significantly higher risk of myocardial infarction (HR, 3.1) as did those in the combination therapy group (HR, 4.8).
Except for the etoposide results, previous studies had shown similar patterns, Dr. Haugnes said. She called the etoposide findings the most surprising in the study.
"A possible bias here is the inclusion of living men only, and thus only cardiovascular disease morbidity and not mortality has been reported," she said.
BREAST IMPLANTS INCREASE RISK OF A RARE LYMPHOMA FORM
Patients with either saline- or silicone gel–filled breast implants may have a very small but significant risk for a rare cancer called anaplastic large-cell lymphoma (ALCL) adjacent to the implant, the US Food and Drug Administration (FDA) announced today.
While the agency continues to investigate the possible association between ALCL and breast implants, it is advising clinicians to consider the possibility of the cancer in patients with breast implants with late onset of fluid build-up called persistent peri-implant seroma. Clinicians also should report any confirmed cases of ALCL in women with breast implants to the FDA.
The agency is advising women with breast implants not to change their routine medical care and follow-up. Because the risk for ALCL appears to be very small, the agency believes the weight of evidence "supports a reasonable assurance that FDA-approved breast implants are safe and effective when used as labeled."
A rare cancer of the immune system that can occur anywhere in the body, ALCL is diagnosed in 1 of every 500,000 women per year in the United States. ALCL in the breast is rarer still, diagnosed annually in roughly 3 of every 100 million women without implants. In women with breast implants, it is usually inside the fibrous scar tissue — called a capsule — surrounding the implant. It is not a cancer of the breast per se.
Treatment options for ALCL are chemotherapy, radiation, and surgery, said William Maisel, MD, MPH, chief scientist and deputy director for science in the FDA's Center for Devices and Radiological Health, at a press conference today. The evidence suggests that the kind of ALCL found in conjunction with breast implants is less aggressive and is sometimes treatable by simply removing the implant, the capsule, and collected fluid, according to Dr. Maisel.
An FDA review of scientific literature published from January 1997 through May 2010 uncovered 34 unique cases of ALCL in women with breast implants throughout the world. The agency is aware of 60 cases in all, some of them identified through other channels. The FDA does not know how many of the 60 may be duplicates of cases found in the literature. An estimated 5 million to 10 million women worldwide have received breast implants, according to the FDA.
Of the 31 published cases of ALCL, 24 involved silicone implants, and 7 saline implants. The median time from implant to ALCL diagnosis was 8 years. For most of the women, the cancer was diagnosed when they sought treatment for implant-related symptoms, such as pain, lumps, swelling, or asymmetry, after their surgical sites had healed. These symptoms result from persistent peri-implant seroma, hardening of the breast area around the implant, or masses surrounding the implant.
Plastic Surgeons and FDA Will Develop Patient Registry
The vast majority of data suggesting a link between ALCL and breast implants emerged only after the FDA approved silicone gel breast implants made by Allergan and Mentor in 2006, said Dr. Maisel. From 1992 to 2006, such silicone gel implants were available only on an investigational basis.
Dr. Maisel noted that silicone from ruptured and even intact implants has been found in nearby breast tissue. According to one theory about the origins of ALCL, this silicone chronically stimulates immune system T cells and induces lymphoma.
"Please understand that is speculative, and a hypothesis," said Dr. Maisel.
To get to firmer scientific ground, the FDA will collaborate with the American Society of Plastic Surgeons and other groups to develop a registry to collect more information that would better characterize ALCL in women with breast implants. The agency also is asking implant manufacturers to report ALCL cases. And for the sake of patient and clinician education, the FDA will work with these manufacturers to update product labeling materials.
More information about today's announcement is available on the FDA Web site. The FDA's preliminary findings and analyses are available here.
While the agency continues to investigate the possible association between ALCL and breast implants, it is advising clinicians to consider the possibility of the cancer in patients with breast implants with late onset of fluid build-up called persistent peri-implant seroma. Clinicians also should report any confirmed cases of ALCL in women with breast implants to the FDA.
The agency is advising women with breast implants not to change their routine medical care and follow-up. Because the risk for ALCL appears to be very small, the agency believes the weight of evidence "supports a reasonable assurance that FDA-approved breast implants are safe and effective when used as labeled."
A rare cancer of the immune system that can occur anywhere in the body, ALCL is diagnosed in 1 of every 500,000 women per year in the United States. ALCL in the breast is rarer still, diagnosed annually in roughly 3 of every 100 million women without implants. In women with breast implants, it is usually inside the fibrous scar tissue — called a capsule — surrounding the implant. It is not a cancer of the breast per se.
Treatment options for ALCL are chemotherapy, radiation, and surgery, said William Maisel, MD, MPH, chief scientist and deputy director for science in the FDA's Center for Devices and Radiological Health, at a press conference today. The evidence suggests that the kind of ALCL found in conjunction with breast implants is less aggressive and is sometimes treatable by simply removing the implant, the capsule, and collected fluid, according to Dr. Maisel.
An FDA review of scientific literature published from January 1997 through May 2010 uncovered 34 unique cases of ALCL in women with breast implants throughout the world. The agency is aware of 60 cases in all, some of them identified through other channels. The FDA does not know how many of the 60 may be duplicates of cases found in the literature. An estimated 5 million to 10 million women worldwide have received breast implants, according to the FDA.
Of the 31 published cases of ALCL, 24 involved silicone implants, and 7 saline implants. The median time from implant to ALCL diagnosis was 8 years. For most of the women, the cancer was diagnosed when they sought treatment for implant-related symptoms, such as pain, lumps, swelling, or asymmetry, after their surgical sites had healed. These symptoms result from persistent peri-implant seroma, hardening of the breast area around the implant, or masses surrounding the implant.
Plastic Surgeons and FDA Will Develop Patient Registry
The vast majority of data suggesting a link between ALCL and breast implants emerged only after the FDA approved silicone gel breast implants made by Allergan and Mentor in 2006, said Dr. Maisel. From 1992 to 2006, such silicone gel implants were available only on an investigational basis.
Dr. Maisel noted that silicone from ruptured and even intact implants has been found in nearby breast tissue. According to one theory about the origins of ALCL, this silicone chronically stimulates immune system T cells and induces lymphoma.
"Please understand that is speculative, and a hypothesis," said Dr. Maisel.
To get to firmer scientific ground, the FDA will collaborate with the American Society of Plastic Surgeons and other groups to develop a registry to collect more information that would better characterize ALCL in women with breast implants. The agency also is asking implant manufacturers to report ALCL cases. And for the sake of patient and clinician education, the FDA will work with these manufacturers to update product labeling materials.
More information about today's announcement is available on the FDA Web site. The FDA's preliminary findings and analyses are available here.
Jumat, 28 Januari 2011
Health Buzz Diabetes Rising Among Americans
Approximately 26 million American adults over age 20 have diabetes,compared to 23.6 million in 2008—a 9 percent jump, according to estimates released Wednesday by the U.S. Centers for Disease Control and Prevention. In total, more than 100 million Americans now have diabetes or prediabetes, Diabetes arises when the body has trouble producing or using the hormone insulin, which leads to the
Kamis, 27 Januari 2011
The Diabetes Epidemic
The CDC just released its latest estimate of diabetes prevalence in the US (1):
These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.
The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.
Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.
* In other words, it's the best predictor of future diabetes risk.
** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).
Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):
These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.
The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.
Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.
* In other words, it's the best predictor of future diabetes risk.
** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).
Two Wheat Challenge Ideas from Commenters
Some people have remarked that the blinded challenge method I posted is cumbersome.
Reader "Me" suggested:
Reader "Me" suggested:
You can buy wheat gluten in a grocery store. Why not simply have your friend add some wheat gluten to your normal protein shake.Reader David suggested:
They sell empty gelatin capsules with carob content to opacify them. Why not fill a few capsules with whole wheat flour, and then a whole bunch with rice starch or other placebo. For two weeks take a set of, say, three capsules every day, with the set of wheat capsules in line to be taken on a random day selected by your friend. This would further reduce the chances that you would see through the blind, and it prevent the risk of not being able to choke the "smoothie" down. It would also keep it to wheat and nothing but wheat (except for the placebo starch).The reason I chose the method in the last post is that it directly tests wheat in a form that a person would be likely to eat: bread. The limitation of the gluten shake method is that it would miss a sensitivity to components in wheat other than gluten. The limitation of the pill method is that raw flour is difficult to digest, so it would be difficult to extrapolate a sensitivity to cooked flour foods. You might be able to get around that by filling the pills with powdered bread crumbs. Those are two alternative ideas to consider if the one I posted seems too involved.
Rabu, 26 Januari 2011
Being plump is good for health
The researchers said the idea that weight is harmful has been "exaggerated" and people who are little heavier may actually live longer.The California University (CU) study that looked at about 350,000 people in the US also suggested that the obese put their health in greater danger when they obsessively try to slim down.It recommended that people should eat a varied and balanced diet, and take "
Selasa, 25 Januari 2011
The Many Benefits of Acupuncture
Growing up with a family that was dedicated to health and wellness prepared me for a life-long commitment to nutrition and fitness, but I never knew it would lead to a career. I always had a passion for natural medicine and healing, but wasn’t sure if I wanted to actually pursue a career in the field. I thought about being a nurse or exercise instructor, but decided it wasn’t for me. As I began
Use of EMR in the Ophthalmic Field
Electronic Medical Records (EMRs) are computerized medical records that allow hospitals and other medical practices to organize patient data in digital files instead of paper files. EMR systems can allow for easier storage, retrieval and modification of patients’ medical records, integrating data generated by diagnostics instruments, imaging devices and administrative records. Though most
PROSTATE CANCER STAGING
TX: The primary tumor cannot be evaluated.
T0: There is no evidence of a tumor in the prostate.
T1: The tumor cannot be felt during the DRE and is not seen during imaging (any test that produces pictures of the inside of the body, such as a CT scan). It may be found when surgery is done for another reason, usually for BPH, or abnormal growth of benign prostate cells.
T1a: The tumor is in 5% or less of the prostate tissue removed through surgery.
T1b: The tumor is in more than 5% of the prostate tissue removed through surgery.
T1c: The tumor is found during a needle biopsy, usually because the patient has an elevated PSA level.
T2: The tumor is found only within the prostate, not other areas of the body. It is large enough to be felt during the DRE.
T2a: The tumor has invaded one-half of one lobe (part or side) of the prostate.
T2b: The tumor has spread to more than one-half of one lobe of the prostate, but not to both lobes.
T2c: The tumor has invaded both lobes of the prostate.
T3: The tumor has grown through the prostate capsule (into the tissue just outside the prostate on one side).
T3a: The tumor has grown through the prostate capsule either on one side or on both sides of the prostate or has spread to the neck of the bladder.
T3b: The tumor has invaded the seminal vesicle(s), the tube(s) that carry semen.
T4: The tumor is fixed, or it is invading nearby structures besides the seminal vesicles, such as the external sphincter (part of the muscle layer that helps to control urination), the rectum, levator muscles, and/or the pelvic wall.
NODES
NX: The regional lymph nodes cannot be evaluated.
N0: The cancer has not spread to the regional lymph nodes.
N1: The cancer has spread to the regional lymph node(s).
DISTANT METASTASIS
MX: Distant metastasis cannot be evaluated.
M0: The disease has not metastasized.
M1: There is distant metastasis.
M1a: The cancer has invaded nonregional, or distant, lymph node(s).
M1b: The cancer has invaded bone(s) in the body.
M1c: The cancer has spread to another part of the body, with or without spread to the bone.
PROGNOSTIC FACTORS
PSA-GLEASON SCORE-STAGE
GLEASON SCORE
Gleason X: The Gleason score cannot be determined.
Gleason 6 or lower: The cells are well-differentiated.
Gleason 7: The cells are moderately differentiated.
Gleason 8, 9, or 10: The cells are poorly differentiated or undifferentiated .
STAGE GROUPING
Stage | T | N | M |
I | T1a, T1b, or T1c | N0 | M0 |
T2a | N0 | M0 | |
Any T1 or T2a | N0 | M0 | |
IIA | T1a, T1b, or T1c | N0 | M0 |
T1a, T1b, or T1c | N0 | M0 | |
T2a | N0 | M0 | |
T2b | N0 | M0 | |
T2b | N0 | M0 | |
IIB | T2c | N0 | M0 |
Any T1 or T2 | N0 | M0 | |
Any T1 or T2 | N0 | M0 | |
III | T3a or T3b | N0 | M0 |
IV | T4 | N0 | M0 |
Any T | N1 | M0 | |
Any T | Any N | M1 |
Senin, 24 Januari 2011
Blinded Wheat Challenge
Self-experimentation can be an effective way to improve one's health*. One of the problems with diet self-experimentation is that it's difficult to know which changes are the direct result of eating a food, and which are the result of preconceived ideas about a food. For example, are you more likely to notice the fact that you're grumpy after drinking milk if you think milk makes people grumpy? Maybe you're grumpy every other day regardless of diet? Placebo effects and conscious/unconscious bias can lead us to erroneous conclusions.
The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.
Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.
Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?
Procedure for a Blinded Wheat Challenge
1. Find a friend who can help you.
2. Buy a loaf of wheat bread and a loaf of gluten-free bread.
3. Have your friend choose one of the loaves without telling you which he/she chose.
4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.
5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.
6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.
7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.
If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.
* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.
** More subjective forms of inquiry have their own advantages.
The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.
Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.
Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?
Procedure for a Blinded Wheat Challenge
1. Find a friend who can help you.
2. Buy a loaf of wheat bread and a loaf of gluten-free bread.
3. Have your friend choose one of the loaves without telling you which he/she chose.
4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.
5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.
6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.
7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.
If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.
* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.
** More subjective forms of inquiry have their own advantages.
Plan would charge state retirees more for health care
State lawmakers, fresh off of passing a major income tax increase, are turning toward a trio of other ideas as they try to capitalize on a newfound mood at the Capitol of dealing with long-festering budget problems.The new push is a crackdown on the rising cost of health care for retired state workers. The program costs the state nearly $500 million a year, and more than 90 percent of the
Jumat, 21 Januari 2011
Kidney transplants could save health-care system millions
The number of Canadians living with kidney failure has tripled in 20 years and thousands of patients are waiting for kidney transplants, researchers say in a report that suggests if transplants were available, $150 million spent on expensive treatments would be saved.There were nearly 38,000 Canadians living with kidney failure in 2009 -more than triple the number recorded in 1990 -with 3,000
Kamis, 20 Januari 2011
Eating Wheat Gluten Causes Symptoms in Some People Who Don't Have Celiac Disease
Irritable bowel syndrome (IBS) is a condition characterized by the frequent occurrence of abdominal pain, diarrhea, constipation, bloating and/or gas. If that sounds like an extremely broad description, that's because it is. The word "syndrome" is medicalese for "we don't know what causes it." IBS seems to be a catch-all for various persistent digestive problems that aren't defined as separate disorders, and it has a very high prevalence: as high as 14 percent of people in the US, although the estimates depend on what diagnostic criteria are used (1). It can be brought on or exacerbated by several different types of stressors, including emotional stress and infection.
Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.
During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.
Here's what I take away from this study:
I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?
* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.
** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.
*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.
Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.
During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.
Here's what I take away from this study:
- Wheat gluten can cause symptoms in susceptible people who do not have celiac disease.
- A lack of circulating antibodies against gluten does not necessarily indicate a lack of gluten sensitivity.
- People with mysterious digestive problems may want to try avoiding gluten for a while to see if it improves their symptoms**.
- People with mysterious fatigue may want to try avoiding gluten.
I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?
* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.
** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.
*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.
Medicare Is for Your Health Again
Sometimes I wonder if Medicare is even meant for our health concerns, or if it’s all just another way to lose money. Ask yourself this question: are you over sixty-five and feel like you’re not getting enough coverage from Medicare? Do you feel stressed and burned by health costs that seem to never go away? If answered yes, Medicare insurance is the option for you to take. Don’t feel that your
Health Bill: facts and fiction, by Carol Propper
I have to admit to being stunned by the level of misinformation that is currently accompanying the Health and Social Care Bill as it is introduced into Parliament.Yesterday, the shadow health secretary John Healey stated that ‘the changes would make the health service profit centred rather than patient centred, health secretary Andrew Lansley said ‘competition would be on quality and not cost’
Rabu, 19 Januari 2011
Spice And Dye Point Toward Better Treatment For Traumatic Brain Injuries
An old Indian spice and a dye whose cousin makes sports drinks blue are pointing scientists toward better treatment of traumatic brain injuries.TBIs, the signature wound of the Iraq and Afghanistan wars, occur on football fields and roadways as well when an injured brain swells inside the closed confines of the skull, causing cell damage and symptoms ranging from headaches and confusion to
Selasa, 18 Januari 2011
GOP lacks clear health-care plan
With the House preparing to vote this week on whether to repeal the health-care law, the chamber's new Republican majority is confronting a far more delicate task: forging its own path to expand medical coverage and curb costs. The House's GOP leaders have made clear that they regard the repeal vote, scheduled to begin Tuesday, as the prelude to a two-prong strategy that is likely to
Senin, 17 Januari 2011
Weight-Loss Tricks Around the World: USA Today’s Hellmich Maneuvers and China’s Weird New Roundworm Diet
Weight-Loss Tricks Around the World: USA Today’s Hellmich Maneuvers and China’s Weird New Roundworm DietGiven Lab Notes’ almost Twitter-like space limitations, however, only a few of Hellmich’s tips could be cited, which is sufficiently unfortunate to serve as justification for a more elaborate summary of her various suggestions. A lot of them are staple weight-loss tips that are familiar entries
Sabtu, 15 Januari 2011
BEVACIZUMAB INCREASES HEART FAILURE RISK
Less than a month after the US Food and Drug Administration announced it was revoking bevacizumab's indication for metastatic breast cancer, citing myriad serious toxicities, more bad news for the embattled drug has emerged.
A study led by Toni K. Choueiri, MD, from the Dana-Farber Cancer Institute in Boston, Massachusetts, reports that advanced breast cancer patients treated with bevacizumab are at increased risk for congestive heart failure (CHF).
The study was published online January 4 in the Journal of Clinical Oncology. Dr. Choueiri and colleagues report a nearly 5-fold increase in the risk for CHF in bevacizumab-treated patients, compared with control subjects.
However, an accompanying editorial is critical of the paper, and urges "extreme caution" in interpreting these results.
Meta-Analysis of 5 Trials
To collect their data, Dr. Choueiri and colleagues conducted a PubMed search of articles published from 1966 to March 2010, and abstracts presented at the American Society of Clinical Oncology and San Antonio Breast Cancer Symposium annual meetings. They eventually selected 5 trials, comprising 3784 patients with metastatic breast cancer, for their final analysis.
The trials were E2100, AVADO, RIBBON-1, RIBBON-2, and a randomized phase 3 trial comparing capecitabine with bevacizumab plus capecitabine in patients with previously treated metastatic breast cancer (J Clin Oncol. 2005;23:792-799).
All these trials excluded patients with uncontrolled hypertension, clinically significant CHF, cerebrovascular disease or peripheral vascular disease, and unstable angina or a recent history of myocardial infarction. They included patients previously treated with anthracycline, and 1 trial in which patients were treated with concomitant anthracycline.
In 2 of the trials, patients had HER2-positive disease and had received previous treatment with trastuzumab.
The analysis showed close to a 5-fold increase in the risk for CHF in bevacizumab-treated patients, compared with control subjects.
Of the 2366 patients who received bevacizumab, 36 had high-grade CHF, for an overall incidence rate of 1.6% (95% confidence interval [CI], 1.0% to 2.6%). Among the 1418 control or placebo patients, 4 had CHF events, for an incidence rate of 0.4% (95% CI, 0.2% to 1.0%).
"To our knowledge, this is the first large report to show a significant increase in the risk of CHF in bevacizumab-treated patients with metastatic breast cancer," the authors write. "Patients with metastatic breast cancer may be at an especially increased risk of CHF because of prior concomitant exposure to other cardiotoxic medications in the adjuvant or metastatic settings."
Editorial Critical of Study
However, an accompanying editorial is somewhat critical of the paper, saying it has several limitations, and urging "extreme caution" in interpreting its results.
One of the editorialists, Sandra M. Swain, MD, medical director of the Washington Cancer Institute at Washington Hospital Center in DC, explained to Medscape Medical News in an interview that the editorial is critical "because the paper is just an analysis of 5 trials. It's not unique research; they're just getting data from papers that have been either published or only presented. Performing a meta-analysis with retrospectively collected heart failure data adds little to our current body of evidence."
A big limitation is previous anthracycline use among the patients. In the meta-analysis, the rate of anthracycline exposure among patients in the trials ranged from 30% to 100%.
Patients with previous anthracyclines already have a damaged heart, so it is possible that the bevacizumab could add to that. Or, it could just be related to the anthracyclines, period, and not at all related to the bevacizumab," Dr. Swain said.
Moreover, large randomized trials of bevacizumab in metastatic colorectal cancer, lung cancer, and renal cell cancer have not reported any cases of heart failure, Dr. Swain pointed out.
The lack of information about individual patients is another important limitation, she said.
"I personally don't agree with writing these kinds of papers, because — as even [the authors point] out — you're not looking at the individual patient. There was no information about the underlying risk factors that predispose to heart failure in individual patients. They didn't put in anything about cumulative [doxorubicin] dose for each patient, radiation, heart disease history, diabetes, or any of the other things that could contribute to heart failure. None of those things were evaluated, or if they were evaluated, they weren't presented."
Although the study has flaws, there are still ways that bevacizumab could be cardiotoxic, Dr. Swain said.
"Vascular endothelial growth factor is important for blood vessels, so you decrease your perfusion and decrease your ability to repair any kind of injury. If, for example, you have gotten a drug like doxorubicin that affects the heart, and then get bevacizumab afterward, you may have a limited ability to repair any kind of injury and you could develop heart failure. So there certainly are a lot of preclinical and physiologic reasons why you could have heart failure," she said.
The other adverse effect with bevacizumab that has been very clearly demonstrated and that could lead to heart failure is its effect on blood pressure. "Bevacizumab does confer a significant risk of hypertension, and there is no controversy about that. That is very clear, and the hypertension could contribute to heart failure," Dr. Swain said.
Awaiting Adjuvant Trial Results
The final word on bevacizumab's role in heart failure in advanced breast cancer will come when data from adjuvant trials are analyzed, Dr. Swain suggested.
The adjuvant trials include E5103, which was actually stopped briefly in 2009 because of fears of heart failure, but was started again, she said. They also include BEST, and BEATRICE. Together, these 3 trials should provide answers to this question, she reported.
"These trials will really give us the data because those patients are evaluated prospectively with different heart imaging. We should really wait for those trials before we pass sentence on bevacizumab with regard to heart failure. There are certainly reasons why it can occur, and it obviously did occur in some patients. The question is: Is it related to the bevacizumab or is it the anthracycline, or is it the combination of both these things, or is it because the patients had left-sided radiation? There are a lot of questions."
Dr. Choueiri reports financial relationships with Bayer/Onyx Pharmaceuticals, Novartis, GlaxoSmithKline, Genentech, Eisai, and Aveo. Dr. Swain reports that she was on an advisory board for Genentech and Roche and is the principal investigator of a National Surgical Adjuvant Breast and Bowel Project trial sponsored by Roche, but was not compensated in either instance.
A study led by Toni K. Choueiri, MD, from the Dana-Farber Cancer Institute in Boston, Massachusetts, reports that advanced breast cancer patients treated with bevacizumab are at increased risk for congestive heart failure (CHF).
The study was published online January 4 in the Journal of Clinical Oncology. Dr. Choueiri and colleagues report a nearly 5-fold increase in the risk for CHF in bevacizumab-treated patients, compared with control subjects.
However, an accompanying editorial is critical of the paper, and urges "extreme caution" in interpreting these results.
Meta-Analysis of 5 Trials
To collect their data, Dr. Choueiri and colleagues conducted a PubMed search of articles published from 1966 to March 2010, and abstracts presented at the American Society of Clinical Oncology and San Antonio Breast Cancer Symposium annual meetings. They eventually selected 5 trials, comprising 3784 patients with metastatic breast cancer, for their final analysis.
The trials were E2100, AVADO, RIBBON-1, RIBBON-2, and a randomized phase 3 trial comparing capecitabine with bevacizumab plus capecitabine in patients with previously treated metastatic breast cancer (J Clin Oncol. 2005;23:792-799).
All these trials excluded patients with uncontrolled hypertension, clinically significant CHF, cerebrovascular disease or peripheral vascular disease, and unstable angina or a recent history of myocardial infarction. They included patients previously treated with anthracycline, and 1 trial in which patients were treated with concomitant anthracycline.
In 2 of the trials, patients had HER2-positive disease and had received previous treatment with trastuzumab.
The analysis showed close to a 5-fold increase in the risk for CHF in bevacizumab-treated patients, compared with control subjects.
Of the 2366 patients who received bevacizumab, 36 had high-grade CHF, for an overall incidence rate of 1.6% (95% confidence interval [CI], 1.0% to 2.6%). Among the 1418 control or placebo patients, 4 had CHF events, for an incidence rate of 0.4% (95% CI, 0.2% to 1.0%).
"To our knowledge, this is the first large report to show a significant increase in the risk of CHF in bevacizumab-treated patients with metastatic breast cancer," the authors write. "Patients with metastatic breast cancer may be at an especially increased risk of CHF because of prior concomitant exposure to other cardiotoxic medications in the adjuvant or metastatic settings."
Editorial Critical of Study
However, an accompanying editorial is somewhat critical of the paper, saying it has several limitations, and urging "extreme caution" in interpreting its results.
One of the editorialists, Sandra M. Swain, MD, medical director of the Washington Cancer Institute at Washington Hospital Center in DC, explained to Medscape Medical News in an interview that the editorial is critical "because the paper is just an analysis of 5 trials. It's not unique research; they're just getting data from papers that have been either published or only presented. Performing a meta-analysis with retrospectively collected heart failure data adds little to our current body of evidence."
A big limitation is previous anthracycline use among the patients. In the meta-analysis, the rate of anthracycline exposure among patients in the trials ranged from 30% to 100%.
Patients with previous anthracyclines already have a damaged heart, so it is possible that the bevacizumab could add to that. Or, it could just be related to the anthracyclines, period, and not at all related to the bevacizumab," Dr. Swain said.
Moreover, large randomized trials of bevacizumab in metastatic colorectal cancer, lung cancer, and renal cell cancer have not reported any cases of heart failure, Dr. Swain pointed out.
The lack of information about individual patients is another important limitation, she said.
"I personally don't agree with writing these kinds of papers, because — as even [the authors point] out — you're not looking at the individual patient. There was no information about the underlying risk factors that predispose to heart failure in individual patients. They didn't put in anything about cumulative [doxorubicin] dose for each patient, radiation, heart disease history, diabetes, or any of the other things that could contribute to heart failure. None of those things were evaluated, or if they were evaluated, they weren't presented."
Although the study has flaws, there are still ways that bevacizumab could be cardiotoxic, Dr. Swain said.
"Vascular endothelial growth factor is important for blood vessels, so you decrease your perfusion and decrease your ability to repair any kind of injury. If, for example, you have gotten a drug like doxorubicin that affects the heart, and then get bevacizumab afterward, you may have a limited ability to repair any kind of injury and you could develop heart failure. So there certainly are a lot of preclinical and physiologic reasons why you could have heart failure," she said.
The other adverse effect with bevacizumab that has been very clearly demonstrated and that could lead to heart failure is its effect on blood pressure. "Bevacizumab does confer a significant risk of hypertension, and there is no controversy about that. That is very clear, and the hypertension could contribute to heart failure," Dr. Swain said.
Awaiting Adjuvant Trial Results
The final word on bevacizumab's role in heart failure in advanced breast cancer will come when data from adjuvant trials are analyzed, Dr. Swain suggested.
The adjuvant trials include E5103, which was actually stopped briefly in 2009 because of fears of heart failure, but was started again, she said. They also include BEST, and BEATRICE. Together, these 3 trials should provide answers to this question, she reported.
"These trials will really give us the data because those patients are evaluated prospectively with different heart imaging. We should really wait for those trials before we pass sentence on bevacizumab with regard to heart failure. There are certainly reasons why it can occur, and it obviously did occur in some patients. The question is: Is it related to the bevacizumab or is it the anthracycline, or is it the combination of both these things, or is it because the patients had left-sided radiation? There are a lot of questions."
Dr. Choueiri reports financial relationships with Bayer/Onyx Pharmaceuticals, Novartis, GlaxoSmithKline, Genentech, Eisai, and Aveo. Dr. Swain reports that she was on an advisory board for Genentech and Roche and is the principal investigator of a National Surgical Adjuvant Breast and Bowel Project trial sponsored by Roche, but was not compensated in either instance.
COLONOSCOPY SCREENING IS EFFECTIVE
A new community-based study from Germany confirms that colonoscopy is an effective tool for preventing colorectal cancer (CRC), according to an editorial accompanying the study published in the January 4 issue of the Annals of Internal Medicine.
In Germany, colonoscopy has been the primary screening method offered to people 55 years and older since 2002, explain the authors, headed by Hermann Brenner, MD, MPH, from the German Cancer Research Center in Heidelberg. The introduction of colonoscopy was accompanied by "major efforts" in training and quality assurance measures, they note.
In this setting of high-quality colonoscopy, they conducted a population-based case–control study comparing 1688 patients and 1932 control subjects.
They found that for individuals who had undergone colonoscopy in the previous 10 years, the overall risk for any colorectal cancer was reduced by 77%.
As has been seen in previous studies, there was a larger reduction in the risk for left-sided colorectal cancer (84%) than in right-sided colorectal cancer (56%). Both of these reductions were "significant," they note.
These results show a greater risk reduction than has been reported recently in other studies, Dr. Brenner and colleagues note. Although the original trial that led to the adoption of colonoscopy — the National Polyp Study, published in 1993 — reported up to a 90% reduction in the risk for CRC, more recent population studies from Germany and Canada have reported reductions of only 30% to 50%.
In addition, this latest study shows a substantial reduction in the risk for right-sided CRC, Dr. Brenner and colleagues point out. This is in contrast to the lack of effect seen in a recent study from Canada (based on administrative claims), which found no protection from deaths from right-sided cancer (JAMA. 2008;299:1027-1035). However, the reduction in right-sided CRC seen in the German study showed an age gradient; in patients aged younger than 60 years, the reduction was modest (26%) and statistically nonsignificant, the authors point out.
The new results "vindicate colonoscopy as an effective prevention tool," writes David Weinberg, MD, MSc, from the Fox Chase Cancer Center in Philadelphia, Pennsylvania, in an accompanying editorial.
They also offer reassurance that colonoscopy can provide substantial protection against both right- and left-sided CRC, he adds. Although it does appear that colonoscopy is "less effective" in the right colon, this is not the same as "ineffective," he points out.
Colonoscopy Most Popular Method in the United States
Colonoscopy has become a standard — and for some the preferred — method of screening for CRC, Dr. Weinberg explains. It is certainly the most popular method in the United States, he adds, where more than 14 million colonoscopies are performed annually.
In contrast, other screening methods, such as flexible sigmoidoscopy and fecal occult blood testing, are performed with decreasing frequency in the United States, despite their lower costs and a stronger evidence base demonstrating their effectiveness, he notes.
Against this backdrop, there has been "recent and unwelcome news that colonoscopy may not protect against CRC as effectively as we would like to think," Dr. Weinberg notes.
These latest results from Germany provide reassurance that colonoscopy is effective, he writes. The study was methodologically rigorous, and the protective effect against CRC was "impressive." The protective effect was seen in both sexes and all ages, and even in patients with a family history of CRC, who are presumably at higher risk.
Nonetheless, there are several questions and issues that remain. Colonoscopy is operator dependent, and there is consistent evidence that gastroenterologists, as opposed to practitioners from other backgrounds, miss fewer lesions, Dr. Weinberg notes. There is also research showing that the ability to detect polyps and other lesions depends on the quality of the laxative preparation, he explains. Preparations that work best should become the standard, although any regimen remains a challenge for older sicker patients, he acknowledges.
Colonoscopy is more expensive and carries a higher risk than other CRC screening methods, so there are appropriate concerns about its "value," he writes.
"It is unrealistic to expect that colonoscopy to prevent all cases of CRC," Dr. Weinberg writes. "Physicians need to inform patients that colonoscopy offers very good, but not perfect, protection," he concludes.
The study was funded by the German Research Council and German Federal Ministry of Education and Research. Dr. Weinberg has disclosed no relevant financial relationships.
In Germany, colonoscopy has been the primary screening method offered to people 55 years and older since 2002, explain the authors, headed by Hermann Brenner, MD, MPH, from the German Cancer Research Center in Heidelberg. The introduction of colonoscopy was accompanied by "major efforts" in training and quality assurance measures, they note.
In this setting of high-quality colonoscopy, they conducted a population-based case–control study comparing 1688 patients and 1932 control subjects.
They found that for individuals who had undergone colonoscopy in the previous 10 years, the overall risk for any colorectal cancer was reduced by 77%.
As has been seen in previous studies, there was a larger reduction in the risk for left-sided colorectal cancer (84%) than in right-sided colorectal cancer (56%). Both of these reductions were "significant," they note.
These results show a greater risk reduction than has been reported recently in other studies, Dr. Brenner and colleagues note. Although the original trial that led to the adoption of colonoscopy — the National Polyp Study, published in 1993 — reported up to a 90% reduction in the risk for CRC, more recent population studies from Germany and Canada have reported reductions of only 30% to 50%.
In addition, this latest study shows a substantial reduction in the risk for right-sided CRC, Dr. Brenner and colleagues point out. This is in contrast to the lack of effect seen in a recent study from Canada (based on administrative claims), which found no protection from deaths from right-sided cancer (JAMA. 2008;299:1027-1035). However, the reduction in right-sided CRC seen in the German study showed an age gradient; in patients aged younger than 60 years, the reduction was modest (26%) and statistically nonsignificant, the authors point out.
The new results "vindicate colonoscopy as an effective prevention tool," writes David Weinberg, MD, MSc, from the Fox Chase Cancer Center in Philadelphia, Pennsylvania, in an accompanying editorial.
They also offer reassurance that colonoscopy can provide substantial protection against both right- and left-sided CRC, he adds. Although it does appear that colonoscopy is "less effective" in the right colon, this is not the same as "ineffective," he points out.
Colonoscopy Most Popular Method in the United States
Colonoscopy has become a standard — and for some the preferred — method of screening for CRC, Dr. Weinberg explains. It is certainly the most popular method in the United States, he adds, where more than 14 million colonoscopies are performed annually.
In contrast, other screening methods, such as flexible sigmoidoscopy and fecal occult blood testing, are performed with decreasing frequency in the United States, despite their lower costs and a stronger evidence base demonstrating their effectiveness, he notes.
Against this backdrop, there has been "recent and unwelcome news that colonoscopy may not protect against CRC as effectively as we would like to think," Dr. Weinberg notes.
These latest results from Germany provide reassurance that colonoscopy is effective, he writes. The study was methodologically rigorous, and the protective effect against CRC was "impressive." The protective effect was seen in both sexes and all ages, and even in patients with a family history of CRC, who are presumably at higher risk.
Nonetheless, there are several questions and issues that remain. Colonoscopy is operator dependent, and there is consistent evidence that gastroenterologists, as opposed to practitioners from other backgrounds, miss fewer lesions, Dr. Weinberg notes. There is also research showing that the ability to detect polyps and other lesions depends on the quality of the laxative preparation, he explains. Preparations that work best should become the standard, although any regimen remains a challenge for older sicker patients, he acknowledges.
Colonoscopy is more expensive and carries a higher risk than other CRC screening methods, so there are appropriate concerns about its "value," he writes.
"It is unrealistic to expect that colonoscopy to prevent all cases of CRC," Dr. Weinberg writes. "Physicians need to inform patients that colonoscopy offers very good, but not perfect, protection," he concludes.
The study was funded by the German Research Council and German Federal Ministry of Education and Research. Dr. Weinberg has disclosed no relevant financial relationships.
ESTROGEN ACCELERATES PROGRESSION OF HEAD-NECK CANCER
Estrogen might increase the movement of precancerous cells in the oral cavity, thereby promoting the progression of head and neck cancer, according to new research published in the January issue of Cancer Prevention Research.
"The finding is still from cultured cells in a dish, so we're far from the clinic, but the hope is that our research will lead to the development of new compounds that will block this progression," senior author Margie L. Clapper, PhD, from the Fox Chase Cancer Center in Philadelphia, Pennsylvania, told Medscape Medical News.
Exposure to tobacco smoke and use of alcohol are major risk factors for the development of head and neck cancer. More recently, infection with human papillomavirus has been linked to squamous cell cancer of the oropharynx.
However, a recent report indicates that 75% of individuals who develop primarily oral tongue squamous cell cancer are female, suggesting that estrogen contributes to the development of head and neck cancer.
In previous work, Dr. Clapper and her team from the Cancer Prevention and Control Program at Fox Chase reported that estrogen metabolism changes after tobacco smoke exposure in the lungs, suggesting that estrogen metabolism plays a role in the formation of lung and other cancers in the aerodigestive tract.
In the current study, the researchers, led by Ekaterina Shatalova, PhD, a postdoctoral fellow at the Fox Chase Cancer Center, examined the contribution of estrogen to the development of head and neck cancers.
They found that estrogen induces the expression of the cytochrome P450 1B1 (CYP 1B1) enzyme, which is responsible for breaking down toxins and metabolizing estrogen, but only in leukoplakia cells. In a surprise finding, the researchers discovered that estrogen did not induce the enzyme in cancer cells.
Specifically, exposure to estrogen increased levels of CYP 1B1 transcripts 2.3- to 3.6-fold, compared with control cells (P = .0004), in leukoplakia cells but not in head and neck squamous cell cancer cells.
When the CYP 1B1 enzyme was deleted, migration and proliferation of the precancerous leukoplakia cells were reduced by 57% and 45%, respectively.
The study also found that exposure of the precancerous cells to estrogen inhibited apoptosis by 26%, but supplementation with the antiestrogen fulvestrant restored estrogen-dependent apoptosis.
"In the future, we would like to find a natural or dietary agent to deplete the CYP 1B1 enzyme to see if we can prevent oral cancer at the precancerous stage," Dr. Shatalova said in a statement.
Dr. Clapper added that "our previous studies showed that the CYP 1B1 enzyme sits at the hub of changes that occur in the lungs after smoke exposure. CYP 1B1 could be a wonderful target in precancerous lesions of the head and neck because by attacking it, we might stop those lesions from progressing or from moving to a more advanced stage," she said. "In the lab, we reduced this protein genetically. But if we could find drugs or natural compounds that could reduce it, you can imagine that it might be a good treatment for cancerous lesions."
The results from this study might help researchers "understand factors that cause head and neck cancer, in addition to the traditional risk factors of tobacco and alcohol exposure," said Jennifer R. Grandis, MD, professor and director of the Head and Neck Cancer Program at the University of Pittsburgh School of Medicine in Pennsylvania, in a statement.
She added that because these results are limited to a single premalignant cell line, "further studies are needed to validate these findings in head and neck cancer in a human population."
Dr. Clapper and Dr. Shatalova have disclosed no relevant financial relationships. Dr. Grandis is an editorial board member for Cancer Prevention Research.
"The finding is still from cultured cells in a dish, so we're far from the clinic, but the hope is that our research will lead to the development of new compounds that will block this progression," senior author Margie L. Clapper, PhD, from the Fox Chase Cancer Center in Philadelphia, Pennsylvania, told Medscape Medical News.
Exposure to tobacco smoke and use of alcohol are major risk factors for the development of head and neck cancer. More recently, infection with human papillomavirus has been linked to squamous cell cancer of the oropharynx.
However, a recent report indicates that 75% of individuals who develop primarily oral tongue squamous cell cancer are female, suggesting that estrogen contributes to the development of head and neck cancer.
In previous work, Dr. Clapper and her team from the Cancer Prevention and Control Program at Fox Chase reported that estrogen metabolism changes after tobacco smoke exposure in the lungs, suggesting that estrogen metabolism plays a role in the formation of lung and other cancers in the aerodigestive tract.
In the current study, the researchers, led by Ekaterina Shatalova, PhD, a postdoctoral fellow at the Fox Chase Cancer Center, examined the contribution of estrogen to the development of head and neck cancers.
They found that estrogen induces the expression of the cytochrome P450 1B1 (CYP 1B1) enzyme, which is responsible for breaking down toxins and metabolizing estrogen, but only in leukoplakia cells. In a surprise finding, the researchers discovered that estrogen did not induce the enzyme in cancer cells.
Specifically, exposure to estrogen increased levels of CYP 1B1 transcripts 2.3- to 3.6-fold, compared with control cells (P = .0004), in leukoplakia cells but not in head and neck squamous cell cancer cells.
When the CYP 1B1 enzyme was deleted, migration and proliferation of the precancerous leukoplakia cells were reduced by 57% and 45%, respectively.
The study also found that exposure of the precancerous cells to estrogen inhibited apoptosis by 26%, but supplementation with the antiestrogen fulvestrant restored estrogen-dependent apoptosis.
"In the future, we would like to find a natural or dietary agent to deplete the CYP 1B1 enzyme to see if we can prevent oral cancer at the precancerous stage," Dr. Shatalova said in a statement.
Dr. Clapper added that "our previous studies showed that the CYP 1B1 enzyme sits at the hub of changes that occur in the lungs after smoke exposure. CYP 1B1 could be a wonderful target in precancerous lesions of the head and neck because by attacking it, we might stop those lesions from progressing or from moving to a more advanced stage," she said. "In the lab, we reduced this protein genetically. But if we could find drugs or natural compounds that could reduce it, you can imagine that it might be a good treatment for cancerous lesions."
The results from this study might help researchers "understand factors that cause head and neck cancer, in addition to the traditional risk factors of tobacco and alcohol exposure," said Jennifer R. Grandis, MD, professor and director of the Head and Neck Cancer Program at the University of Pittsburgh School of Medicine in Pennsylvania, in a statement.
She added that because these results are limited to a single premalignant cell line, "further studies are needed to validate these findings in head and neck cancer in a human population."
Dr. Clapper and Dr. Shatalova have disclosed no relevant financial relationships. Dr. Grandis is an editorial board member for Cancer Prevention Research.
Kamis, 13 Januari 2011
Anthem Blue Cross CA Finally Gets Approvals!
Just received a voicemail from Anthem Blue Cross California that the plan portfolios held up by the California Dept of Insurance have finally been approved.These plans have been pending approval since September 22, 2010.According to the voicemail the new plans (all PPACA-compliant) will be available for sale tomorrow (1/14/11) to the public. I will update this post with the particulars of the
Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational Studies
The diet-heart hypothesis states three things:
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between saturated fat intake and blood cholesterol, they haven't found one. Those findings have essentially been ignored, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They twisted the data every which way, but were never able to squeeze even a hint of an association out of it:
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends little or no support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was mostly white rice in some areas. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and perhaps bordering on malnourishment.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold change in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's being trumped by other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat an impoverished diet that differs in many ways from the diets at the upper end of the range.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no hint of a relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol. If it's a factor at all, it must be rather weak, which is consistent with what has been observed in multiple non-human species (13). I think it's likely that the diet-heart hypothesis rests in part on an over-interpretation of short-term controlled feeding studies. I'd like to see a more open discussion of this in the scientific literature. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a small long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators made no effort to adjust for confounding variables.
- Dietary saturated fat increases blood cholesterol
- Elevated blood cholesterol increases the risk of having a heart attack
- Therefore, dietary saturated fat increases the risk of having a heart attack
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between saturated fat intake and blood cholesterol, they haven't found one. Those findings have essentially been ignored, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They twisted the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk***.
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends little or no support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was mostly white rice in some areas. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and perhaps bordering on malnourishment.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold change in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's being trumped by other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat an impoverished diet that differs in many ways from the diets at the upper end of the range.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no hint of a relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol. If it's a factor at all, it must be rather weak, which is consistent with what has been observed in multiple non-human species (13). I think it's likely that the diet-heart hypothesis rests in part on an over-interpretation of short-term controlled feeding studies. I'd like to see a more open discussion of this in the scientific literature. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a small long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators made no effort to adjust for confounding variables.
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Dr. Fat
A blog reader recently made me a Wordle from Whole Health Source. A Wordle is a graphical representation of a text, where the size of each word represents how often it appears. Click on the image for a larger version.
Apparently, the two most common words on this blog are "Dr" and "fat." It occurred to me that Dr. Fat would be a great nom de plume.
Apparently, the two most common words on this blog are "Dr" and "fat." It occurred to me that Dr. Fat would be a great nom de plume.