what you had for dinner last week or that you had a fight with your spouse or that you go to bed too late or that you don't like your job or that you don't drink enough water or that a parent said "X" runs in the family or that you exercise too much/not enough/inappropriately. or that you're worried about finances or that you have a dysfunctional breathing pattern.
It can only tell you one of the reasons you are in pain--and that's likely not even the main driver...
Artificial sweeteners have been widely used in the modern diet, and their observed effects on human health have been inconsistent, with both beneficial and adverse outcomes reported. Obesity and type 2 diabetes have dramatically increased in the U.S. and other countries over the last two decades. Numerous studies have indicated an important role of the gut microbiome in body weight control and glucose metabolism and regulation. Interestingly, the artificial sweetener saccharin could alter gut microbiota and induce glucose intolerance, raising questions about the contribution of artificial sweeteners to the global epidemic of obesity and diabetes.Acesulfame-potassium (Ace-K), a FDA-approved artificial sweetener, is commonly used, but its toxicity data reported to date are considered inadequate. In particular, the functional impact of Ace-K on the gut microbiome is largely unknown. In this study, we explored the effects of Ace-K on the gut microbiome and the changes in fecal metabolic profiles using 16S rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. We found that Ace-K consumption perturbed the gut microbiome of CD-1 mice after a 4-week treatment. The observed body weight gain, shifts in the gut bacterial community composition, enrichment of functional bacterial genes related to energy metabolism, and fecal metabolomic changes were highly gender-specific, with differential effects observed for males and females. In particular, ace-K increased body weight gain of male but not female mice. Collectively, our results may provide a novel understanding of the interaction between artificial sweeteners and the gut microbiome, as well as the potential role of this interaction in the development of obesity and the associated chronic inflammation.
Original Source found here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0178426
Flu Vaccine for All: A Critical Look at the Evidence
Eric A. Biondi, MD, MS; C. Andrew Aligne, MD, MPH
When Vaccination Became Routine
Vaccine proponents felt that the failure of the vaccine was explained by the immunization campaign being too little, too late. As a result, in 1960, national health experts recommended, for the first time, routine annual vaccination, with emphasis on high-risk groups, including those over the age of 65 years and individuals with chronic illness.By the early 1960s, routine influenza vaccination was generally adopted as a policy, with very little supporting evidence.
After several years of this policy, the CDC decided to evaluate its impact. In 1964, Alexander Langmuir, MD, MPH, then the chief epidemiologist at the CDC, published a paper that "reluctantly concluded that there is little progress to be reported. The severity of the epidemic of 1962-1963...demonstrates the failure to achieve effective control of excess mortality." The paper questioned whether widespread influenza immunization "should be continued without better evidence to justify the major costs to the general public."Despite this, annual vaccination campaigns were continued.
In 1968, the CDC finally performed a randomized, double-blind trial to examine the effect of vaccination on morbidity and mortality. The authors concluded that "Despite extensive use of influenza vaccines...attainment of [improved morbidity and mortality] has never been demonstrated."Nevertheless, flu immunization continued.
In 1976, H1N1 "swine flu" appeared, and a large-scale effort to immunize as many Americans as possible was launched.However, the anticipated levels of disease did not appear, and an epidemic of paralytic Guillain-Barré syndrome in recipients of vaccine led to the program's cancellation.An analysis in 1977 by the CDC concluded that influenza control had been "generally ineffective" and that statistically valid community trials were needed.
In 1995, a major review from the US Food and Drug Administration acknowledged the ongoing "paucity of randomized trials" and warned about serious methodological flaws in many existing flu vaccine studies.
In 2000, the CDC performed a placebo-controlled trial and found that "vaccination [when compared to placebo] may not provide overall economic benefit in most years."
Nonetheless, in 2004, the AAP recommended annual influenza immunization for young children, household contacts, and healthcare providers.
Vaccination coverage recommendations continued to expand, and now during every flu season, we watch commercials by retail pharmacies telling us about the importance of getting the flu shot. The fact that the AAP recommends "mandatory" flu vaccination for healthcare providers means that eventually clinicians could be fired for not getting vaccinated.
Summing Up the Data
A 2012 systematic review and meta-analysis examined the efficacy and effectiveness of licensed influenza vaccines in patients with confirmed influenza illness. The authors confirmed that the original "recommendation to vaccinate the elderly was made without data for vaccine efficacy or effectiveness." The main message was that we need a better vaccine and better studies to demonstrate its effectiveness.
Despite the lack of high-quality data supporting the value of the flu shot, widespread vaccination policy might still be reasonable if observational studies consistently showed a benefit. However, the observational studies cited by flu shot proponents are frequently flawed.[22,23,24,25,26,27,28]In many studies, relevant clinical outcomes are ignored in favor of immunogenicity (ie, the ability to elicit an antibody response)."Influenza-like illness" (ie, cold symptoms) is frequently measured instead of serious outcomes, such as pneumonia or death. When these more serious outcomes are examined, there is often a failure to control for healthy user bias—the propensity for healthier people to do such things as receive annual check-ups, eat healthier foods, and get the flu shot. So, although it's true that people who get flu shots live longer, it may have nothing to do with actually getting the flu shot.
A 2005 study of a 33-season, national data set attempted to reconcile the reduced all-cause morbidity and mortality found in some observational studies of influenza vaccination with the fact that "national influenza mortality rates among seniors increased in the 1980s and 1990s as the senior vaccination coverage quadrupled." In this study, the authors conclude that:
"[Our] estimates, which provide the best available national estimates of the fraction of all winter deaths that are specifically attributable to influenza, show that the observational studies must overstate the mortality benefits of the vaccine...[even during two pandemic seasons] the estimated influenza-related mortality was probably very close to what would have occurred had no vaccine been available."
The rationale for flu immunization as a national health priority is that influenza is a disease with serious complications, such as pneumonia, hospitalization, and death.[5,13,28] If the reason for influenza vaccination is that flu is such a serious disease, then the relevant outcomes are whether vaccination improves morbidity and mortality from flu. However, after decades of vaccine use, it is hard to detect any public health impact.This is in stark contrast to other routine vaccinations, such as polio and Haemophilus influenzae type b, where introduction of the vaccine led to obvious decline of the disease.
We are pediatricians, and we believe in childhood immunizations. Many vaccines have provided immense public health value. We simply question whether the policy of routine influenza vaccination has outpaced the data supporting its use.
Influenza vaccination now supersedes many other priorities of public health (such as obesity, illiteracy, and high school dropout), and we question whether so much time, effort, and money should be dedicated to flu vaccination while these other national healthcare priorities remain on the back burner.
Original source found here: https://www.medscape.com/viewarticle/855937_2
THE USE OF THERMOGRAPHY IN DETECTION OF METASTATIC BREAST CANCER
CORINNE FARRELL, M.D., JOHN D. WALLACE, A.B. and CARL M. MANSFIELD, M.D.
Our experience to date has shown that total body thermography can be an aid in the search for metastatic disease in patients with carcinoma of the breast. In our series of 126 patients, we found a true positive rate of 87 per cent, a false negative rate of 3 per cent, and the false positive rate was approximately 10 per cent. Of considerable interest were 7 false positive thermograms which were converted to true positives in 3 to 6 months after the original study.
We have found total body thermography useful in locating the site and extent of a primary lesion, a second carcinoma of the breast or recurrent anti metastatic lesions. It has also been an aid in differentiating associated benign disease. This examination is inexpensive, consumes little time, causes no patient discomfort and has the added advantage of no exposure to ionizing radiation. This technique is capable of detecting early manifestations of metastatic disease, but such manifestations of disease should be confirmed by conventional techniques at this time.
BREAST THERMOGRAPHY AFTER FOUR YEARS AND 10,000 STUDIES
HAROLD J. ISARD, M.D., WARREN BECKER, M.D., RUTH SHILO, M.D. and BERNARD J. OSTRUMM.D.
A total of approximately 10,000 breast thermograms was analyzed and further subdivided into symptomatic and asymptomatic groups of patients of 55 and 45 per cent, respectively.
Positive, or abnormal, mammatherms were recorded in 36 per cent of thesymptomatic and 23 per cent of the asymptomatic groups. Of the 306 histologically confirmed cancers, 270 were in the symptomatic group of patients and 36 were clinically occult.
Clinical accuracy was enhanced by the supplemental use of mammography and thermography. Sixty-one per cent of the occult cancers were suspect by thermography and if, in the asymptomatic group, thermography had been used as the initial screening procedure and mammography performed only on those with abnormal thermograms a yield of 21.4 cancers per 1,000 mammographic examinations would have been realized.
Thermography is an innocuous examination that can be utilized for preliminary screening of asymptomatic women to focus attention upon those who should be examined more intensively because of greater risk of breast cancer.
Efficacy of Computerized Infrared Imaging Analysis to Evaluate Mammographically Suspicious Lesions
R. Parisky1, A. Sardi2, R. Hamm3, K. Hughes4, L. Esserman5, S. Rust6 and K. Callahan7
OBJECTIVE. The purpose of this clinical trial was to determine the efficacy of a dynamic computerized infrared imaging system for distinguishing between benign and malignant lesions in patients undergoing biopsy on the basis of mammographic findings.
SUBJECTS AND METHODS. A 4-year clinical trial was conducted at five institutions using infrared imaging of patients for whom breast biopsy had been recommended. The data from a blinded subject set were obtained in 769 subjects with 875 biopsied lesions resulting in 187 malignant and 688 benign findings. The infrared technique records a series of sequential images that provides an assessment of the infrared information in a mammographically identified area. The suspicious area is localized on the infrared image by the radiologist using mammograms, and an index of suspicion is determined, yielding a negative or positive result.
RESULTS. In the 875 biopsied lesions, the index of suspicion resulted in a 97% sensitivity, a 14% specificity, a 95% negative predictive value, and a 24% positive predictive value. Lesions that were assessed as false-negative by infrared analysis were microcalcifications, so an additional analysis was performed in a subset excluding lesions described only as microcalcification. In this restricted subset of 448 subjects with 479 lesions and 110 malignancies, the index of suspicion resulted in a 99% sensitivity, an 18% specificity, a 99% negative predictive value, and a 27% positive predictive value. Analysis of infrared imaging performance in all 875 biopsied lesions revealed that specificity was statistically improved in dense breast tissue compared with fatty breast tissue.
CONCLUSION.Infrared imaging offers a safe noninvasive procedure that would be valuable as an adjunct to mammography in determining whether a lesion is benign or malignant.
Microwave thermography in the detection of breast cancer
AH Barrett, PC Myers and NL Sadowsky
Microwave thermography, a method of sensing subcutaneous temperatures, was used in a breast cancer detection study of about 5,000 female patients. The data were taken at wavelengths of 9.1 and 23 cm. Microwave thermography at 23 cm has true-positive and true-negative detection rates of 0.8 and 0.6, respectively, comparable to those of infrared thermography (0.7) and inferior to those of xeromammography (0.9). However, a potential advantage results if microwave and infrared thermography are used together for screening, and if mammography is used only for follow-up on those patients who were positive on either the microwave or the infrared thermograms. It is then possible to obtain true-positive and true-negative detection rates of 0.9 and 0.9, respectively, while only half the number of patients need be subjected to x-rays.
Effectiveness of a noninvasive digital infrared thermal imaging system in the detection of breast cancer.
Arora N, Martins D, Ruggerio D, Tousimis E, Swistel AJ, Osborne MP, Simmons RM.
BACKGROUND: Digital infrared thermal imaging (DITI) has resurfaced in this era of modernized computer technology. Its role in the detection of breast cancer is evaluated.
METHODS: In this prospective clinical trial, 92 patients for whom a breast biopsy was recommended based on prior mammogram or ultrasound underwent DITI. Three scores were generated: an overall risk score in the screening mode, a clinical score based on patient information and a third assessment by artificial neural network.
RESULTS: Sixty of 94 biopsies were malignant and 34 were benign. DITI identified 58 of 60 malignancies, with 97% sensitivity, 44% specificity, and 82% negative predictive value depending on the mode used. Compared to an overall risk score of 0, a score of 3 or greater was significantly more likely to be associated with malignancy (30% vs 90%, P < .03).
CONCLUSION: DITI is a valuable adjunct to mammography and ultrasound, especially in women with dense breast parenchyma.
Our study raises serious questions about the value of screening mammography. It clarifies that the benefit of mortality reduction is probably smaller, and the harm of overdiagnosis probably larger, than has been previously recognized. And although no one can say with certainty which women have cancers that are overdiagnosed, there is certainty about what happens to them: they undergo surgery, radiation therapy, hormonal therapy for 5 years or more, chemotherapy, or (usually) a combination of these treatments for abnormalities that otherwise would not have caused illness. Proponents of screening should provide women with data from a randomized screening trial that reflects improvements in current therapy and includes strategies to mitigate overdiagnosis in the intervention group. Women should recognize that our study does not answer the question “Should I be screened for breast cancer?” However, they can rest assured that the question has more than one right answer.
Screening with mammography uses X-ray imaging to find breast cancer before a lump can be felt. The goal is to treat cancer earlier, when a cure is more likely. The review includes seven trials that involved 600,000 women in the age range 39 to 74 years who were randomly assigned to receive screening mammograms or not. The studies which provided the most reliable information showed that screening did not reduce breast cancer mortality. Studies that were potentially more biased (less carefully done) found that screening reduced breast cancer mortality. However, screening will result in some women getting a cancer diagnosis even though their cancer would not have led to death or sickness. Currently, it is not possible to tell which women these are, and they are therefore likely to have breasts or lumps removed and to receive radiotherapy unnecessarily. If we assume that screening reduces breast cancer mortality by 15% after 13 years of follow-up and that overdiagnosis and overtreatment is at 30%, it means that for every 2000 women invited for screening throughout 10 years, one will avoid dying of breast cancer and 10 healthy women, who would not have been diagnosed if there had not been screening, will be treated unnecessarily. Furthermore, more than 200 women will experience important psychological distress including anxiety and uncertainty for years because of false positive findings.
Women invited to screening should be fully informed of both the benefits and harms. To help ensure that the requirements for informed choice for women contemplating whether or not to attend a screening programme can be met, we have written an evidence-based leaflet for lay people that is available in several languages on www.cochrane.dk. Because of substantial advances in treatment and greater breast cancer awareness since the trials were carried out, it is likely that the absolute effect of screening today is smaller than in the trials. Recent observational studies show more overdiagnosis than in the trials and very little or no reduction in the incidence of advanced cancers with screening.
THE USE OF THERMOGRAPHY IN DETECTION OF METASTATIC BREAST CANCER
CORINNE FARRELL, M.D., JOHN D. WALLACE, A.B. and CARL M. MANSFIELD, M.D.
Missed my morning FaceBook post due to a 90+ mile bike ride, but it served as motivation for what to write about today.
One of the amino acids which even the most nutritionally ignorant among us has heard of is tryptophan. After all, that's what makes you sleepy after that turkey dinner on Thanksgiving, right? Well, not exactly. But that's not my point.
Tryptophan is the precursor for the neurotransmitter 5-hydroxytryptamine (5-HT), which is involved in fatigue. It's also one of the primary amino acids released when muscle is catabolized during times when fuel is inadequate to meet the demands placed on an organism's physiology. In the case of my group ride this morning, there were many examples of people getting tired. Some of those cyclists could blame their training, of course. Others, however, need to consider how their fueling strategy--both on AND off the bike--might be contributing to their fatigue at a given intensity/duration. When glucose levels/glycogen stores are not sufficient to keep muscle (along with free fatty acids, primarily in the form of PUFAs) from being catabolized to fuel the activity, performance of the activity will suffer or stop altogether.
And if you think about it, it's simply another ingenious example of the body trying to survive. The body believes that fuel is scarce. It has no idea you could simply stop at the next convenience store and buy a coke or, better yet, some o.j. But since you won't stop, you body stops you. Or slows you down--anything it can do to spare the body's limited resources. And it has a lot of built in safeguards at play in these conditions just in case. From the production of serotonin (not the happy hormone you've been led to believe) to the inhibition of glucose utilization via the Randle Cycle, the body's gonna win this one. So you can live to ride another day.
And this time, maybe you'll fuel yourself appropriately.
Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model
Clinical investigations have highlighted a biological link between reduced brain glucose metabolism and Alzheimer’s disease (AD). Previous studies showed that glucose deprivation may influence amyloid beta formation in vivo but no data are available on the effect that this condition might have on tau protein metabolism. In the current paper, we investigated the effect of glucose deficit on tau phosphorylation, memory and learning, and synaptic function in a transgenic mouse model of tauopathy, the h-tau mice. Compared with controls, h-tau mice with brain glucose deficit showed significant memory impairments, reduction of synaptic long-term potentiation, increased tau phosphorylation, which was mediated by the activation of P38 MAPK Kinase pathway. We believe our studies demonstrate for the first time that reduced glucose availability in the central nervous system directly triggers behavioral deficits by promoting the development of tau neuropathology and synaptic dysfunction. Since restoring brain glucose levels and metabolism could afford the opportunity to positively influence the entire AD phenotype, this approach should be considered as a novel and viable therapy for preventing and/or halting the disease progression.
“Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model” by E Lauretti, J-G Li, A Di Meco & D Praticò in Translational Psychiatry. Published online January 31 2017 doi:10.1038/tp.2016.296
Original source found here: http://www.nature.com/tp/journal/v7/n1/full/tp2016296a.html
Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms
AIM: To investigate the effect of reducing dietary fiber on patients with idiopathic constipation.
METHODS: Sixty-three cases of idiopathic constipation presenting between May 2008 and May 2010 were enrolled into the study after colonoscopy excluded an organic cause of the constipation. Patients with previous colon surgery or a medical cause of their constipation were excluded. All patients were given an explanation on the role of fiber in the gastrointestinal tract. They were then asked to go on a no fiber diet for 2 wk. Thereafter, they were asked to reduce the amount of dietary fiber intake to a level that they found acceptable. Dietary fiber intake, symptoms of constipation, difficulty in evacuation of stools, anal bleeding, abdominal bloating or abdominal pain were recorded at 1 and 6 mo.
RESULTS: The median age of the patients (16 male, 47 female) was 47 years (range, 20-80 years). At 6 mo, 41 patients remained on a no fiber diet, 16 on a reduced fiber diet, and 6 resumed their high fiber diet for religious or personal reasons. Patients who stopped or reduced dietary fiber had significant improvement in their symptoms while those who continued on a high fiber diet had no change.Of those who stopped fiber completely, the bowel frequency increased from one motion in 3.75 d (± 1.59 d) to one motion in 1.0 d (± 0.0 d) (P < 0.001); those with reduced fiber intake had increased bowel frequency from a mean of one motion per 4.19 d (± 2.09 d) to one motion per 1.9 d (± 1.21 d) on a reduced fiber diet (P < 0.001); those who remained on a high fiber diet continued to have a mean of one motion per 6.83 d (± 1.03 d) before and after consultation. For no fiber, reduced fiber and high fiber groups, respectively, symptoms of bloating were present in 0%, 31.3% and 100% (P < 0.001) and straining to pass stools occurred in 0%, 43.8% and 100% (P < 0.001).
CONCLUSION: Idiopathic constipation and its associated symptoms can be effectively reduced by stopping or even lowering the intake of dietary fiber.
INTRODUCTION: Lack of fiber in the diet was first postulated in 1971 as the cause of diseases such as diverticulosis, hemorrhoids and colorectal cancer. Since then, partly due to widespread media publicity, it is now widely accepted that dietary fiber is a necessary component of a healthy diet and is required for normal bowel movement[2-5]. It is popularly used in the management of constipation by the public and by many doctors. Insoluble fiber is known to increase stool weight and decrease colonic transit time[6,7]. Fiber is said to aid in water retention in the colon and results in stools that are less dry and easier to evacuate. However, the reality is that stool moisture content remains at 70%-75% regardless of the amount of fiber and water consumed[7,8].
There is recent evidence that low fiber intake does not equate to constipation. Patients with chronic constipation also have similar fiber intake to controls[10-13]. Patients with chronic constipation may also have worsening symptoms when dietary fiber intake is increased. Another study found that lactulose was more effective in easing constipation when compared with fiber.
It has also been our experience that many patients with constipation are already consuming a large amount of fiber before they seek medical attention.
We therefore carried out a prospective longitudinal case study to investigate the effect of decreasing dietary fiber in patients with idiopathic constipation.
MATERIALS AND METHODS: Constipation was defined clinically in patients who presented either with symptoms of straining to expel bulky large stools or a bowel frequency of less than one motion per 3 d over a period of at least 3 mo. Patients who presented to the clinic with symptoms of constipation, abdominal distension, pain or bloating, difficulty in evacuation with or without symptoms of rectal bleeding were considered for the study. For the purpose of this study, we did not distinguish between slow colonic transit type or obstructed defecation type of constipation nor did we attempt to classify the patients according to irritable bowel syndrome subtypes. All the patients underwent colonoscopy to exclude colonic lesions. Patients who had colorectal cancer, previous colonic surgery, melanosis coli or thyroid disorders were excluded. Patients with anal conditions such as severe prolapsed hemorrhoids, chronic anal fissure or any other condition that required surgery were also excluded.
Sixty-three consecutive patients after normal colonoscopy were enrolled into the study from May 2008 to May 2010. Each patient was to act as their own control. The physiology of the gastrointestinal tract and the bulking effects of dietary fiber were explained to the patients[16,17]. Patients were then instructed to completely stop their intake of dietary fiber, including vegetables, cereals, fruits, wholemeal bread and brown rice for 2 wk. Those who were vegetarians were asked to eat white rice instead of unpolished rice, white bread instead of whole meal bread, and to take processed bean products for protein. They were to continue their normal quantities of carbohydrates and proteins. Sieved fruit juices and clear vegetable soups were allowed. Patients were instructed not to take any laxatives during these 2 wk. After 2 wk, patients were asked to continue on with as little fiber in their diet as they were comfortable with for the long term. Patients were followed up at 1 mo and 6 mo intervals and final results were analyzed at 6 mo.
Data collected included age, sex, general dietary fiber intake, symptoms of constipation, difficulty in evacuation of stools, anal bleeding, abdominal bloating or abdominal pain. Constipation was recorded as the interval in days between bowel movements. Difficulty in evacuation was a subjective measure and patients were asked to choose from one of 3 degrees (no straining, occasional or moderate straining and severe straining or straining most of the time).
RESULTS: There were 16 males (25.6%) and 47 (74.4%) females, median age 47 years (range, 20-80 years) included in the study. At the commencement of the study, all patients were already on a high fiber diet or taking fiber supplements. After 2 wk of a no fiber diet, patients were asked to continue on as little fiber in the diet as they were able to follow if this were to give them relief from their symptoms.
At 6 mo, 41 patients continued on a no fiber diet and 16 were on a reduced fiber diet. The remaining 6 patients continued on a high fiber diet for various reasons including being vegetarians or inability to stop consuming dietary fiber for religious or personal reasons.
The median age of patients who stayed on a no fiber diet was 46 years (range, 21-80 years), on a reduced fiber diet was 45 years (range, 20-65 years) and on a high fiber diet was 59 years (range, 28-75 years). There was no statistical significant difference in age between the 3 groups. There was also no statistical difference in sex between the 3 groups.
At 6 mo follow-up, the interval between bowel movements decreased with the reduction in fiber intake (P < 0.001). Forty one patients who completely stopped fiber intake had their bowel frequency increased from one motion in 3.75 d (± 1.59 d) to one motion in 1.0 d (± 0.00 d) (P < 0.001). Of 16 patients who reduced their dietary fiber intake, 12 patients had daily bowel movement, 3 had one bowel movement every 2 to 3 d and one had a bowel movement every 4 to 6 d, giving one motion per 1.9 d (± 1.21 d) on a reduced fiber diet compared with 1 motion per 4.19 d (± 2.09 d) on a high fiber diet (P < 0.001). There was no change in the frequency of bowel movement for patients who continued with high dietary fiber intake, with one motion per 6.83 d (± 1.03 d) before and after consultation (P = 1.00).
There was also a difference between the groups in the proportion of patients with associated symptoms. For symptoms of bloating, all of those on a high fiber diet continued to be symptomatic, while only 31.3% in the reduced fiber group and none of the no fiber group had symptoms.
With regards to straining, all those on a no fiber no longer had to strain to pass stools. Of those who reduced dietary fiber, 7 of 16 showed improvement while the symptoms remain unchanged in those who remained on a high fiber diet (P < 0.001 between groups).
Symptoms of abdominal pain only improved in patients who stopped fiber completely while those who continued on a high fiber diet or reduced fiber diet did not show any improvement (Table (Table2).2). In addition, those on a no dietary fiber diet no longer had symptoms of anal bleeding.
DISCUSSION: This study has confirmed that the previous strongly-held belief that the application of dietary fiber to help constipation is but a myth. Our study shows a very strong correlation between improving constipation and its associated symptoms after stopping dietary fiber intake. However whilst there was no significant difference between the mean age of the 3 groups with different post-consultation dietary fiber intake, older patients seemed less likely to stop dietary fiber, although this did not reach significance. We did not survey the actual reasons for resuming dietary fiber. The clinical impression during consultation however was that some of these patients were vegetarians, some felt uneasy not eating any fiber, whilst others could not completely discontinue fiber due to constant media and peer pressure to increase dietary fiber.
Constipation is often mistaken by the layman as the state of not passing stool, with the subsequent false notion that making more feces will allow easier defecation. In truth, constipation refers to the difficulty in evacuating a rectum packed with feces, and easier defecation cannot possibly be affected by increasing dietary fiber which increases bulky feces. In this paper, we looked at constipation both as the number of days before each motion as well as the ease of defecation.
It is well known that increasing dietary fiber increases fecal bulk and volume. Therefore in patients where there is already difficulty in expelling large fecal boluses through the anal sphincter, it is illogical to actually expect that bigger or more feces will ameliorate this problem. More and bulkier fecal matter can only aggravate the difficulty by making the stools even bigger and bulkier. Several reviews and a meta-analysis had already shown that dietary fiber does not improve constipation in patients with irritable bowel diseases[18-21].
The role of dietary fiber in constipation is analogous to cars in traffic congestion. The only way to alleviate slow traffic would be to decrease the number of cars and to evacuate the remaining cars quickly. Should we add more cars, the congestion would only be worsened. Similarly, in patients with idiopathic constipation and a colon packed with feces, reduction in dietary fiber would reduce fecal bulk and volume and make evacuation of the smaller and thinner feces easier. Adding dietary fiber would only add to the bulk and volume and thus make evacuation even more difficult.
Whilst it is often stated in physiology textbooks that bulking agents improve peristalsis, there is no proof of this in practice nor experimentally. Regardless of the food ingested, small intestinal and right mid colonic contents are fluid and all ingestible dietary fiber is suspended therein. Dietary fiber, therefore, cannot act as solid boluses for the initiation of peristalsis. In fact, dietary fiber had been shown to retard peristalsis and hold up gaseous expulsion in human experiments.
Dietary fiber is also associated with increased bloatedness and abdominal discomfort. Insoluble fiber was reported to worsen the clinical outcome of abdominal pain and constipation[18-20]. In our recent study, patients who followed a diet with no or less dietary fiber intake showed a significant improvement, not just in their constipation, but also in their bloatedness. Patients who completely stopped consuming dietary fiber no longer suffered from abdominal bloatedness and pain. These symptoms are caused by the fermentation of dietary fiber by colonic bacteria, which produces hydrogen, carbon dioxide and methane. Gases that are trapped by peristaltic colon exert pressure on the walls, causing the abdominal pain experienced by patients. This was previously observed in a prior study on younger patients, when dietary fiber had been shown not to be effective in the management of children with recurrent abdominal pain or bloating.
Stools only become well-formed in the sigmoid colon and rectum and by this time, especially in constipated subjects, more stools result in more evacuation problems. It is not logical to increase both the volume and size of stool in patients with idiopathic constipation and indeed for anybody with difficulty in passing stools, e.g., due to anismus or anal spasm from anal stricture, fissure or pelvic outlet disorders. We have shown that decreasing the bulk and volume of feces immediately enables the easier evacuation of smaller and thinner stools through the anal sphincter mechanism. This eliminates the need to strain in passing stools, and prevents the tearing of the anal sphincter and bleeding due to large and bulky fecal loads. None of our patients experienced anal bleeding or straining following complete abstinence from dietary fiber.
The results of this study should lead us to reexamine popular beliefs in benefits of dietary fiber and more studies should be undertaken to confirm or repudiate these results.
In conclusion, contrary to popularly held beliefs, reducing or stopping dietary fiber intake improves constipation and its associated symptoms.
Original Source found here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435786/
Mov Disord. 2015 Apr;30(4):552-9. doi: 10.1002/mds.26152. Epub 2015 Jan 14. Statins, plasma cholesterol, and risk of Parkinson's disease: a prospective study.
Previous findings on the association of statins, plasma lipids, and Parkinson's disease (PD) are confounded by the fact that statins also affect lipid profiles. We prospectively examined plasma lipids and statin use in relation to PD in the Atherosclerosis Risk in Communities (ARIC) Study. Statin use and plasma lipids were assessed at baseline (visit 1, 1987-89) and at three triennial visits thereafter (visits 2-4) until 1998. Potential PD cases were identified from multiple sources and validated where possible. The primary analysis was limited to incident PD cases diagnosed between 1998 and 2008. Odds ratios and 95% confidence intervals were derived from multivariate logistic regression models. Statin use was rare at baseline (0.57%) but increased to 11.2% at visit 4. During this time frame, total-cholesterol levels decreased, particularly among statin users. Fifty-six PD cases were identified after 1998. Statin use before 1998 was associated with significantly higher PD risk after 1998 (odds ratio = 2.39, 95% confidence interval 1.11-5.13) after adjusting for total cholesterol and other confounders. Conversely, higher total cholesterol was associated with lower risk for PD after adjustment for statin usage and confounders. Compared with the lowest tertile of average total cholesterol, the odds ratios for PD were 0.56 (0.30-1.04) for the second and 0.43 (0.22-0.87) for the third tertile (P(trend) = 0.02). Statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk.These data are inconsistent with the hypothesis that statins are protective against PD.
Original Source found here: http://www.ncbi.nlm.nih.gov/pubmed/25639598
Vegetarianism can lead to heart disease and cancer
By Sarah Knapton 2:38 PM Wednesday Mar 30, 2016
Long term vegetarianism can lead to genetic mutations that raise the risk of heart disease and cancer, scientists have found.
Populations who have had a primarily vegetarian diet for generations were found to be far more likely to carry DNA that makes them susceptible to inflammation.
Scientists in the US believe that the mutation occurred to make it easier for vegetarians to absorb essential fatty acids from plants.
But it has the knock-on effect of boosting the production of arachidonic acid, which is known to increase inflammatory disease and cancer. When coupled with a diet high in vegetable oils - such as sunflower oil - the mutated gene quickly turns fatty acids into dangerous arachidonic acid.
The finding may help explain previous research which found vegetarian populations are nearly 40 per cent more likely to suffer colorectal cancer than meat eaters, a finding that has puzzled doctors because eating red meat is known to raise the risk.
Researchers from CornellUniversity in the US compared hundreds of genomes from a primarily vegetarian population in Pune, India to traditional meat-eating people in Kansas and found there was a significant genetic difference.
"Those whose ancestry derives from vegetarians are more likely to carry genetics that more rapidly metabolise plant fatty acids," said Tom Brenna, Professor of Human Nutrition at Cornell.
"In such individuals, vegetable oils will be converted to the more pro-inflammatory arachidonic acid, increasing the risk for chronic inflammation that is implicated in the development of heart disease, and exacerbates cancer. The mutation appeared in the human genome long ago, and has been passed down through the human family."
To make the problem worse, the mutation also hinders the production of beneficial Omega 3 fatty acid which is protective against heart disease. Although it may not have mattered when the mutation first developed, since the industrial revolution there has been a major shift in diets away from Omega 3 - found in fish and nuts - to less healthy Omega 6 fats - found in vegetable oils.
"Changes in the dietary Omega 6 to Omega 3 balance may contribute to the increase in chronic disease seen in some developing countries," added Dr Brenna. "The message for vegetarians is simple. Use vegetable oils that are low in omega-6 linoleic acid such as olive oil." (I would add that avoidance of PUFAs in general is a good strategy, replacing them in the diet with saturated fat from quality sources).
The mutation is called rs66698963 and is found in the FADS2 gene which controls the production of fatty acids in the body.
Previous studies have shown that vegetarianism and veganism can lead to problems with fertility by lowering sperm counts. (Nature doesn’t want to perpetuate weakness. Thus, anytime one’s vitality sinks below the level where one can positively contribute to the gene pool, the ability to procreate is compromised or lost entirely).
Separate research from Harvard University also found that a diet high in fruit and vegetables may impact fertility because men are consuming high quantities of pesticides.
Many vegetarians also struggle to get enough protein, iron, vitamin D, vitamin B12 and calcium which are essential for health. One study found that vegetarians had approximately five percent lower bone-mineral density (BMD) than non-vegetarians.
However other research suggests vegetarianism lowers the risk of diabetes, stroke and obesity.
The new research was published in the journal Molecular Biology and Evolution
Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid
Long chain polyunsaturated fatty acids (LCPUFA) are bioactive components of membrane phospholipids and serve as substrates for signaling molecules. LCPUFA can be obtained directly from animal foods or synthesized endogenously from 18 carbon precursors via the FADS2 coded enzyme. Vegans rely almost exclusively on endogenous synthesis to generate LCPUFA and we hypothesized that an adaptive genetic polymorphism would confer advantage. The rs66698963 polymorphism, a 22 bp insertion-deletion within FADS2, is associated with basal FADS1 expression, and coordinated induction of FADS1 and FADS2 in vitro. Here we determined rs66698963 genotype frequencies from 234 individuals of a primarily vegetarian Indian population and 311 individuals from the U.S. A much higher I/I genotype frequency was found in Indians (68%) than in the U.S. (18%). Analysis using 1000 Genomes Project data confirmed our observation, revealing a global I/I genotype of 70% in South Asians, 53% in Africans, 29% in East Asians, and 17% in Europeans. Tests based on population divergence, site frequency spectrum and long-range haplotype consistently point to positive selection encompassing rs66698963 in South Asian, African and some East Asian populations. Basal plasma phospholipid arachidonic acid status was 8% greater in I/I compared to D/D individuals. The biochemical pathway product-precursor difference, arachidonic acid minus linoleic acid, was 31% and 13% greater for I/I and I/D compared to D/D, respectively. Our study is consistent with previous in vitro data suggesting that the insertion allele enhances n-6 LCPUFA synthesis and may confer an adaptive advantage in South Asians because of the traditional plant-based diet practice.
That the FDA considers carrageenan safe—all I can say is WOW! Then it must be. After all, their track record is exemplary! Aspartame, artificial colors, Olestra…No harm there. And it’s gotta be tough to get their approval. I explore this subject here:
Yet I wonder—have they ever “approved” of a product before issuing a recall?
Fen-Phen—24 yrs on the market despite heart disease and other pulmonary problems.
DES—37 yrs on the market when in 1971 it was connected to a rare tumor that kept appearing in the daughters of women who had taken it. The FDA only banned DES prescriptions to women because no such problems have been found in men.
Baycol—4 yrs on the market is reportedly responsible for more than 100,000 deaths
Vioxx—5 yrs on the market and then found to be responsible for increased risk of heart attack and stroke.
Read more: The Ten Worst Drug Recalls In The History Of The FDA – 24/7 Wall St. http://247wallst.com/2010/12/10/the-ten-worst-drug-recalls-in-the-history-of-the-fda/#ixzz2Qle0DSL6
But back to Carrageenan—maybe some of the below reading from the FDA’s own website would interest you:
There it clearly states that “significant abnormalities appear to be induced in the anaphase figures of human embryoic lung cells in tissue culture at dosages that are slightly above average daily human intake. It is of further concern that parenterally administered carrageenan is reported to inhibit the activity of complement, excert cytotoxic effects on macrophases, suppress delayed hypersensitivity reactions in some tuberculin sensitive animals, activate factors causing procoagulant activity in human blood platelets, increase vascular permeabiltiy, and liberate kinin in vitro, all of which point to the possibility of the generation of toxic effects that could cause adverse responses followint the oral consumption of carrageenan if, during pregnancy or in the presence of infectious challenge or metabolic disorder, appropriate amounts of carrageenan should be absorbed from the gastrointestinal tract.”
And so my readers may read Dr. Tobacman’s position, you can find a 2012 letter along with attached studies here: http://www.cornucopia.org/DrTobacmanComment_toNOSB.pdf
Or the following studies by others:
Pathol Biol (Paris). 1979 Dec;27(10):615-26. [Biological and pharmacological effects of carrageenan (author’s transl)]. [Article in French] Roch-Arveiller M, Giroud JP. Carrageenan is sulfated polysaccharide which has been extensively used as emulsifier and thickening agent in the food industry, for its ability to induce acute inflammation in pharmacology and for its selectively toxic effect for macrophages in immunology. Carrageenan is a complex substance which displays various biological properties. The authors have shown the extent of these actions and reviewed the latest investigations on this subject.
J Allergy Clin Immunol. 1995 May;95(5 Pt 1):933-6. Anaphylaxis to carrageenan: a pseudo-latex allergy. Tarlo SM, Dolovich J, Listgarten C. Toronto Hospital, Western Division, Ontario, Canada. BACKGROUND: Anaphylactic reactions during a barium enema have been attributed to allergy to latex on the barium enema device. The observation of anaphylaxis during barium enema without latex exposure or latex allergy led to the performance of an allergy skin test to the barium enema solution. METHODS: Individual components of the barium enema solution were obtained for double-blind skin testing. A RAST to identify specific IgE antibodies to the skin test active agent was established. RESULTS: Carrageenan, a component of the barium enema solution, produced positive reactions to allergy skin test and RAST. Gastrointestinal symptoms for which the patient was being investigated by the barium enema subsequently disappeared with a diet free of carrageenan. CONCLUSIONS: Carrageenan is a previously unreported cause of anaphylaxis during barium enema. It is an allergen widely distributed in common foods and potentially could account for some symptoms related to milk products or baby formula.
Food Addit Contam. 1989 Oct-Dec;6(4):425-36. Intestinal uptake and immunological effects of carrageenan–current concepts. Nicklin S, Miller K. Carrageenans are a group of high molecular weight sulphated polygalactans which find extensive use in the food industry as thickening, gelling and protein-suspending agents. Although there is no evidence to suggest that the persorption of small amounts of carrageenans across the intestinal barrier poses an acute toxic hazard, they are known to be biologically active in a number of physiological systems and extended oral administration in laboratory animals has been shown to modify both in vivo and in vitro immune competence. Whereas this effect could be attributed to carrageenan having a selective toxic effect on antigen-processing macrophages, additional studies suggest that macrophages can also influence immune responses by the timed release of immunoregulatory mediators. Evidence in support of this comes from in vitro studies which demonstrate that carrageenan-treated macrophages can, depending on conditions and time of administration, release either stimulatory or inhibitory factors. The former is known to be the immunostimulatory agent interleukin 1 (IL-1). The inhibitory factor, which is produced at an early stage following exposure to non-toxic doses of carrageenans, has yet to be formally identified but it is believed to be a prostaglandin because of its specific mode of action and short biological half-life. At present it is impossible to relate these studies to the human situation. Although it is established that carrageenans can cross the intestinal barrier of experimental animals, there is no evidence to suggest that the limited uptake that may occur in man in any way interferes with normal immune competence. Nevertheless, increased exposure may occur in the neonate during weaning, and adults and children following allergic reactions and episodes of gastrointestinal disease. Further studies under such conditions now seem warranted in order to elucidate the possible immunological consequences which may be associated with enhanced uptake of carrageenans in vulnerable groups.
Environ Health Perspect. 2001 October; 109(10): 983–994. Review of harmful gastrointestinal effects of carrageenan in animal experiments. J K Tobacman In this article I review the association between exposure to carrageenan and the occurrence of colonic ulcerations and gastrointestinal neoplasms in animal models. Although the International Agency for Research on Cancer in 1982 identified sufficient evidence for the carcinogenicity of degraded carrageenan in animals to regard it as posing a carcinogenic risk to humans, carrageenan is still used widely as a thickener, stabilizer, and texturizer in a variety of processed foods prevalent in the Western diet. I reviewed experimental data pertaining to carrageenan’s effects with particular attention to the occurrence of ulcerations and neoplasms in association with exposure to carrageenan. In addition, I reviewed from established sources mechanisms for production of degraded carrageenan from undegraded or native carrageenan and data with regard to carrageenan intake. Review of these data demonstrated that exposure to undegraded as well as to degraded carrageenan was associated with the occurrence of intestinal ulcerations and neoplasms. This association may be attributed to contamination of undegraded carrageenan by components of low molecular weight, spontaneous metabolism of undegraded carrageenan by acid hydrolysis under conditions of normal digestion, or the interactions with intestinal bacteria. Although in 1972, the U.S. Food and Drug Administration considered restricting dietary carrageenan to an average molecular weight > 100,000, this resolution did not prevail, and no subsequent regulation has restricted use. Because of the acknowledged carcinogenic properties of degraded carrageenan in animal models and the cancer-promoting effects of undegraded carrageenan in experimental models, the widespread use of carrageenan in the Western diet should be reconsidered.
Food Chem Toxicol. 1990 Dec;28(12):807-11. The effects of carrageenan on drug-metabolizing enzyme system activities in the guinea-pig. Pintauro SJ, Gilbert SW. Carrageenans are seaweed extracts comprising high molecular weight sulphated polygalactosides. They are used in foods at concentrations of up to 2.5% as thickening and gelling agents. When degraded to lower molecular weight forms, they have been shown to induce ulcerative colitis and colon cancer in laboratory animals. Furthermore, undegraded carrageenan (CG) has been shown to promote azoxymethane and methylnitrosourea initiated carcinogenesis, but the promotion mechanism is unclear. To determine if this mechanism involves alterations of tissue drug-metabolizing enzyme system (DMES) activities, six groups of five guinea-pigs each were administered 0.2% kappa undegraded, 0.2% i undegraded, 1% kappa degraded or 1% i degraded CG, or control solutions in the drinking-water for 8 wk. Microsomal and cytosolic DMES activities of the liver, small intestine and colon were determined. The kappa undegraded CG group exhibited significant (P less than 0.05) increases in small intestine cytochrome P-450 levels and benzo[a]pyrene hydroxylase activities. These data suggest that undegraded CG may selectively induce DMES activities in the small intestine mucosa.
J Pharm Pharmacol. 1989 Jun;41(6):423-6. Rapid production of ulcerative disease of the colon in newly-weaned guinea-pigs by degraded carrageenan. Marcus AJ, Marcus SN, Marcus R, Watt J. In a dose-response study, degraded carrageenan (Eucheuma spinosum) was supplied in the drinking fluid at 1.2 and 3% concentrations over two weeks to young adult guinea-pigs. Ulceration of the large bowel was produced in 100% of animals, the severity and extent of damage probably being dose-related. In a time-course study, 3% degraded carrageenan solution supplied to newly-weaned guinea-pigs produced in 100% of animals ulceration in the caecum by four days and in the ascending colon by seven days. The onset of ulceration occurred as early as the second day. This model is convenient and economic for the screening of drugs of potential therapeutic value in human ulcerative colitis.
Gut. 1971 Feb;12(2):164-71. Carrageenan-induced ulceration of the large intestine in the guinea pig. Watt J, Marcus R. A 5% aqueous solution of degraded carrageenan derived from the red seaweed Eucheuma spinosum was fed to guinea pigs in their drinking water over a period of 20-45 days. Occult blood in the faeces and multiple ulcers in the caecum, colon and rectum occurred in 100% of animals by the 30th day. The clinical and pathological features bear a close resemblance to human ulcerative colitis. The method provides a simple experimental model for the study of various aspects of the pathology of ulcerative lesions in the large intestine as well as the effects of therapeutic agents.
Int J Exp Pathol. 1992 Aug;73(4):515-26. The pre-ulcerative phase of carrageenan-induced colonic ulceration in the guinea-pig. Marcus SN, Marcus AJ, Marcus R, Ewen SW, Watt J. The pre-ulcerative phase of carrageenan-induced colonic ulceration was investigated in guinea-pigs supplied 3% degraded carrageenan as an aqueous solution as drinking fluid for 2 or 3 days during which no ulceration of the bowel was observed with the naked eye or dissecting microscope. Mucosal microscopic changes, from caecum to rectum, were multifocal and included cellular infiltrates, dilatation of glands, crypt abscesses, micro-ulcers and sulphated polysaccharide in the lamina propria. Sulphated polysaccharide was also demonstrated histologically for the first time within the surface epithelium and showed ultrastructural features similar to carrageenan. The results indicate that colonic epithelium in the guinea-pig is capable of macromolecular absorption. Carrageenan, a highly active polyanionic electrolyte, within the surface epithelial cells is most likely a primary factor in the breakdown of mucosal integrity. Macromolecular absorption causing enteropathy of the large bowel is a new pathophysiological concept which may have implications in man, particularly in the pathology of large bowel disease.
Methods Achiev Exp Pathol. 1975;7:56-71. Experimental ulcerative disease of the colon. Watt J, Marcus R. The oral administration to guinea-pigs of an aqueous solution of carrageenan derived from the red seaweed, Eucheuma spinosum, provides a useful, readily available experimental model for the study of ulcerative disease of the colon. Two types of ulcerative disease can be produced within a 4-6 week period, viz., ulceration localised mainly to the caecum by using 1% undegraded carrageenan in the drinking fluid, and extensive ulceration involving caecum, colon, and rectum by using 5% degraded carrageenan. Ulceration is probably due to the local action of carrageenan in the bowel.
J Natl Cancer Inst. 1977 Apr;58(4):1171-2. Promotion of incidence of adenovirus type 12 transplantable tumors by carrageenan, a specific antimacrophage agent. Lotzová E, Richie ER. Carrageenan, a sulfated polygalactose with known macrophage-toxic properties, was used to ascertain the role of macrophages in resistance to adenovirus type 12 transplantable tumors. A single ip injection of 5 or 10 mg carrageenan led to increased incidence and more rapid growth of tumors in C3H mice. Carrageenan was most effective if given 1 day before tumor inoculation; the effectiveness decreased with increasing intervals before or after tumor cell injection. The macrophage stabilizer poly-2-vinylpyridine N-oxide injected sc (150 mg/kg) 1 day before carrageenan was given reduced the incidence of tumors. These data lend further support to the importance of macrophages in tumor immunity.
Biomedicine. 1975 Sep;22(5):387-92. Involvement of macrophages in genetic resistance to bone marrow grafts. Studies with two specific antimacrophage agents, carrageenan and silica. Lotzova E, Gallagher MT, Trentin JJ. Carrageenans and silica, agents toxic for macrophages, were used in this study to examine the role of macrophages in resistance of irradiated mice to inbred parental and rat bone marrow grafts. Administration of 2.5 mg of carrageenans or 2.5-5 mg of silica particles intravenously to prospective graft recipients resulted in a prompt abrogation of hybrid and xenogeneic resistance. The macrophage stabilizer poly-2-vinylpyridine N-oxide (PVNO) injected subcutaneously in the dose of 150 mg/kg, 24 hr before silica prevented or reduced the suppression of resistance. PVNO, however, did not antagonize the suppression of resistance by carrageenen, horse anti-mouse thymocyte serum and cyclophosphamide. These results suggest that a) a subpopulation is involved in marrow graft rejection by irradiated mice; b) carrageenan and silica apparently act on macrophages by different mechanisms c) horse anti-mouse thymocyte serum and cyclophosphamide may act on cells other than macrophages or they act on macrophages by a different mechanism than silica, to resistance to bone marrow transplantation.
Agents Actions. 1981 May;11(3):265-73. Carrageenan: a review of its effects on the immune system. Thomson AW, Fowler EF. Carrageenans (kappa, lambda and iota) are sulphated polysaccharides isolated from marine algae that can markedly suppress immune responses both in vivo and in vitro. Impairment of complement activity and humoral responses to T-dependent antigens, depression of cell-mediated immunity, prolongation of graft survival and potentiation of tumour growth by carrageenans have been reported. The mechanism responsible for carrageenan-induced immune suppression is believed to be its selective cytopathic effect on macrophages. This property of carrageenan has led to its adoption as a tool for analysing the role of these cells in the induction and expression of immune reactivity. Systemic administration of carrageenan may, however, induce disseminated intravascular coagulation and inflict damage on both the liver and kidney. This is an important consideration in the interpretation of the effects of carrageenan in vivo and precludes its use as a clinical immune suppressant.
Biomedicine. 1978 May-Jun;28(3):148-52. Carrageenan and the immune response. Thomson AW. Since the biological effects of carrageenan were reviewed in 1972 by Di Rosa it has become clear from a large number of reports that this algal polysaccharide markedly influences immune responses. Profound suppression of immunity evidenced by impaired antibody production, graft rejection, delayed hypersensitivity and anti-tumour immunity, has been observed in carrageenan-treated animals and the immunodepressive ability of carrageenan confirmed by in vitro studies. Efforts at analysis of carrageenan-induced immune suppression have focussed on the selective cytotoxic effect of this agent on mononuclear phagocytes. Faith in the ability of carrageenan to eliminate those cells has led to its use in examination of the role played by mononuclear phagocytes in various aspects of immune reactivity. This review documents and discusses the effects of carrageenan on immune responses and assesses the value of carrageenan as a useful tool in both current and future work aimed at broadening our knowledge of mechanisms underlying immune reactions.
Biomedicine. 1976 May;24(2):102-6. Evaluation of carrageenan as an immunosuppressive agent and mediator of intravascular coagulation. Thomson AW, Wilson AR, Cruickshank WJ, Horne CH. Carrageenan suppressed antibody responses to SRBC in mice and rats, measured in terms of splenic IgM PFC production. The effect, in mice, was dependent on dose and on the temporal relationship between treatment and antigen administration. Carrageenan was found to alter the time course of the PFC response and also to produce disseminated intravascular coagulation. Some correlation between the observed effects and the use of chemically distinct carrageenans was found. The possible mode of actio2n of carrageenan is discussed in the light of these, and other findings.
J Pathol. 1980 Sep;132(1):63-79. Histological and ultrastructural changes following carrageenan injection in the mouse. Fowler EF, Simpson JG, Thomson AW. Mice were injected intravenously with either uncharacterised potassium carrageenan or purified iota carrageenan and tissue was examined by light and electron microscopy 1 hr and 24 hr later. The survival of animals injected with these carrageenans was monitored over a 6-month period. Histological examination of liver and kidney was carried out on animals which died during this time and in the surviving mice at 28 weeks. Histological and ultrastructural evidence of disseminated intravascular coagulation was observed within 24 hr of carrageenan injection. The changes were more severe in animals given potassium carrageenan. Electro-microscopic examination of liver revealed carrageenan within membrane-bound vacuoles in Küpffer cells. These cells were largely unaffected by phagocytosis of iota carrageenan but uptake of potassium carrageenan resulted in marked ultrastructural changes and occasional damage to adjacent hepatocytes. Mice given potassium carrageenan had the poorer long-term survival and many animals in this group showed chronic renal damage with features which suggested obstructive nephropathy. A smaller proportion of mice injected with iota carrageenan displayed similar changes. There was no evidence of long-term hepatotoxicity in either group although both types of carrageenan persisted within liver macrophages for at least 6 months after injection.
Am J Pathol. 1971 Aug;64(2):387-404. Spectrum and possible mechanism of carrageenan cytotoxicity. Catanzaro PJ, Schwartz HJ, Graham RC Jr. Carrageenan, a sulfated polygalactose which suppresses established delayed hypersensitivity in vivo, is shown to be cytotoxic to macrophages but not to lymphocytes in vitro. This cytotoxicity depends on the carrageenan concentration and degree of lysosomal differentiation but is independent of serum. Survival of macrophages in the presence of carrageenan can be enhanced temporarily by corticosteroids. Ultrastructural studies reveal that carrageenan is readily taken up by macrophages and stored in lysosomes, which subsequently swell and rupture, apparently resulting in cell death. The presence of corticosteroids temporarily retards lysosome swelling. It is suggested that carrageenan may exert its cytotoxic effect by causing osmotic rupture of lysosomes. The possible immunologic significance of these findings is discussed.
Cancer Lett. 1978 Mar;4(3):171-6. Induction by degraded carrageenan of colorectal tumors in rats. Ashi KW, Inagaki T, Fujimoto Y, Fukuda Y. Degraded carrageenan derived from the red seaweed Eucheuma spinosum was given to Sprague—Dawley rats through the diet, in drinking water or by stomach tube for up to 24 months. Carrageenan-induced squamous cell carcinomas, adenocarcinomas and adenomas in the colorectum were observed. Some rats had metastases to the regional lymph nodes of squamous cell carcinomas. These results show that degraded carrageenan is carcinogenic to the colorectum of the rat.
Toxicol Lett. 1981 Jun-Jul;8(4-5):207-12. Effect of degraded carrageenan on the intestine in germfree rats. Hirono I, Sumi Y, Kuhara K, Miyakawa M. The role of intestinal bacterial flora in display of the effect of degraded carrageenan was investigated by feeding 9 germfree and 12 conventional female Wistar rats on diet containing 10% carrageenan for 63 days. Animals were sacrificed 7, 20, 35, and 63 days after the start of feeding and histological changes induced by carrageenan were studied. The germfree rats showed mucosal lesions, such as macrophage aggregates, erosion, and squamous metaplasia of the large intestine, and these lesions were more extensive than those in the conventional rats. Therefore, it was concluded that bacterial flora are not essential for display of the biological effects of degraded carrageenan.
Food Chem Toxicol. 1987 Feb;25(2):113-8. Intestinal permeability changes in rodents: a possible mechanism for degraded carrageenan-induced colitis. Delahunty T, Recher L, Hollander D. Rats and guinea-pigs were treated with degraded carrageenan (50 g/litre in the drinking-water) and their intestinal permeability was studied at weekly intervals over the last 4 wk of the test period by determining the recovery of orally administered tracer doses of [3H]polyethylene glycol (PEG-900) or D-[3H]mannitol in 16-hr urine collections. A freely diffusible dye, Azure A, was administered simultaneously to compensate for non-intestinal factors that could modify renal excretion. Animals were killed after a total treatment period of 5 months for rats and 6 wk for guinea-pigs. After 3 wk of carrageenan treatment, excretion of PEG-900 (expressed as a ratio of the Azure A excretion) in guinea-pigs showed a statistically significant increase over that in the control group. At autopsy, the caeca showed numerous macroscopically visible erosions of the entire mucosal surface and histological examination showed ulcerations largely in the mucosa with abscesses in the crypts. Although no such histological changes were seen in the intestines of the treated rats, even after 5 months, a statistically significant increase in PEG-900 excretion was again found compared with the control group. This increase did not occur when deoxycholate was administered with the carrageenan solution. No effect of carrageenan treatment on mucosal permeability to D-[3H]mannitol was demonstrated in either species. The results suggest that degraded carrageenan-induced colitis could be a result of increased intestinal permeability, since ingestion of this polysaccharide by rats increased PEG-900 absorption without causing mucosal damage.
Cancer Detect Prev. 1981;4(1-4):129-34. Harmful effects of carrageenan fed to animals. Watt J, Marcus R. An increased number of reports have appeared in the literature describing the harmful effects of degraded and undegraded carrageenan supplied to several animal species in their diet or drinking fluid. The harmful effects include foetal toxicity, teratogenicity, birth defects, pulmonary lesions, hepatomegaly, prolonged storage in Kupffer cells, ulcerative disease of the large bowel with hyperplastic, metaplastic, and polypoidal mucosal changes, enhancement of neoplasia by carcinogens, and, more ominously, colorectal carcinoma. Degraded carrageenan as a drug or food additive has been restricted in the United States by the FDA, but undegraded carrageenan is still widely used throughout the world as a food additive. Its harmful effects in animals are almost certainly associated with its degradation during passage through the gastrointestinal tract. There is a need for extreme caution in the use of carrageenan or carrageenan-like products as food additives in our diet, and particularly in slimming recipes.
Food and Cosmetics Toxicology Volume 14, Issue 2, 1976, Pages 85-93 Carrageenan: The effect of molecular weight and polymer type on its uptake, excretion and degradation in animals K.A. Pittmana, L. Golberga, F. Coulstona A variety of τ-, κ- and λ-carrageenans was given to guinea-pigs, monkeys and rats, either in the drinking-water, by gavage or in the diet. Faecal and liver samples were examined qualitatively by gel electrophoresis, to determine any changes in the apparent molecular weight of carrageenans after administration. Quantitative measurements of carrageenans were carried out on samples of liver and urine. That there was little or no absorption of carrageenans of high molecular weight was evidenced by the absence of carrageenan from the livers of guinea-pigs or rats or from the urine of guinea-pigs or monkeys. By contrast, substantial amounts of carrageenan were found in the livers of guinea-pigs and rats given low-molecular-weight carrageenans (Mn ⩽ 40,000). Intermediate amounts of carrageenan were found in livers of animals given carrageenans ranging in Mn between 40,000 and 150,000. Urinary excretion of carrageenan was limited to low-molecular-weight material (Mn ⩽ 20.000). Qualitative and quantitative evidence indicated that there was an upper limit to the size of carrageenan molecules absorbed, but estimates of this upper limit ranged from 10,000 to 85.000 depending upon the analytical approach. Absorption of carrageenan from the drinking-water may differ qualitatively from absorption from the diet. Analysis of faecal samples by gel electrophoresis showed that degradation of high-molecular-weight carrageenan had occurred, either in the gut or in the faeces.
Cancer Letters Volume 14, Issue 3, December 1981, Pages 267-272 A study on carcinogenesis induced by degraded carrageenan arising from squamous metaplasia of the rat colorectum Yasuyuki Oohashi, Tomonori Ishioka, Kazuo Wakabayashi, Noriyuki Kuwabara We have undertaken studies on carcinogenesis arising from precancerous lesions, such as squamous metaplasia and ulcerative lesions of the rat colorectum, after termination of degraded carrageenan administration. Rates of tumor incidence in groups that were given a 10% diet of degraded carrageenan for 2, 6 and 9 months were 5 rats out of 39 (12.8%), 8 out of 42 (19.0%) and 17 out of 42 (40.5%), respectively. The colorectal squamous metaplasia persisted in all rats and progressed irreversibly. Degraded carrageenan was deposited not only in the colorectal propria mucosa, but also in the other reticuloendothelial organs. These results show that, even with short-term degraded carrageenan administration, degraded carrageenan is carcinogenic to the colorectum of the rat after a prolonged period.
Cancer Res. 1997 Jul 15;57(14):2823-6. Filament disassembly and loss of mammary myoepithelial cells after exposure to lambda-carrageenan. Tobacman JK. Carrageenans are naturally occurring sulfated polysaccharides, widely used in commercial food preparation to improve the texture of processed foods. Because of their ubiquity in the diet and their observed preneoplastic effects in intestinal cells, their impact on human mammary myoepithelial cells in tissue culture was studied. At concentrations as low as 0.00014%, lambda-carrageenan was associated with disassembly of filaments with reduced immunostaining for vimentin, alpha-smooth muscle-specific actin, and gelsolin; increased staining for cytokeratin 14; and cell death. The absence of mammary myoepithelial cells is associated with invasive mammary malignancy; hence, the destruction of these cells in tissue culture by a low concentration of a widely used food additive suggests a dietary mechanism for mammary carcinogenesis not considered previously.
Acta Pathol Microbiol Scand A. 1980 May;88(3):135-41. Stereomicroscopic and histologic changes in the colon of guinea pigs fed degraded carrageenan. Olsen PS, Poulsen SS. A colitis-like state induced in Guinea Pigs fed degraded carrageenan orally. By means of a combined semimacroscopic and histologic technique the course of the disease was followed during 28 days. The changes were primarily seen and became most prominent in the caecum. The first lesions were observed following 24 hours of treatment as small rounded foci initially with degenerative changes and inflammation in the surface epithelium, later forming superficial focal ulcerations. Ulcerative changes gradually progressed during the experiment, forming linear and later large, geographical ulcerations. Topographically the ulcerative process was strongly related to the larger submucosal vessels. Nonulcerated parts of the mucosa were not changed until following 7-14 days of treatment. The mucosa became bulging, granulated and finally villus-like. Accumulation of macrophages was found under the surface epithelium after 7-17 days. Possible pathogenetic mechanisms are discussed, especially the development of the early lesions and the significance of the macrotphages.
Teratology. 1981 Apr;23(2):273-8. Teratogenic effect of lambda-carrageenan on the chick embryo. Monis B, Rovasio RA. Carrageenans are widely used as food additives. Thus, it seemed of interest to test their possible teratogenic action. For this purpose, 530 chick eggs were injected in the yolk sac with 0.1 ml of a solution of 0.1% lambda-carrageenan in 0.9% sodium chloride. As controls, 286 eggs were injected with 0.1 ml of 9.0% sodium chloride. In addition, 284 eggs received no treatment. After incubation for 48–50 hours at 39 degrees C, embryos were fixed, cleared, and observed with a stereoscopic microscope. The frequency of abnormal embryos in the group receiving lambda-carrageenan was higher than in the controls (p less than 0.04). Partial duplication of the body, abnormal flexures of the trunk, anencephaly, a severely malformed brain, thickening of the neural tube wall, an irregular neural tube lumen with segmentary occlusion and a reduction in crown-rump length and number of somites were distinctly seen in the lambda-carrageenan-injected group. Moreover, the average number of anomalies per embryo in the lambda-carrageenan-injected group was nearly twice that in the controls. Present data indicate that lambda-carrageenan has teratogenic effects on early stages of the development of the chick embryo.
Let me know if I can provide more reading material for you. In the meantime, I would strongly urge you to stop listening to your government while ignoring what your body is trying to tell you. Paying attention here just may save your health.
The more health claims made about a food, the worse it is for you.
In the case the dairy industry, the above statement is nothing less than spot on (shameless plug, I'll admit). Sick cows fed everything under the sun other than the grass they were designed to eat are not the ideal source for your dairy consumption. And if the producers opt to then pasteurize or homogenize or in some shape or form bastardize that dairy, then what was once an incredibly healthy source of nutrition soon becomes udderly unrecognizable as a food.
However, organic, grass-fed cows (and sheep, goats, etc) raised the way nature intended can produce quality dairy products which are extremely beneficial for health. Sufficient quantities of bio-available calcium (i.e. animal sources for those of us who aren't ruminant herbivores) keep parathyroid hormone low while also increasing the likelihood of tryptophan converting to niacin rather than serotonin (and that should make the health conscious happy). It also helps maintain a favorable calcium to phosphorous ratio in the diet, without which blood pressure, inflammation, and even tumor growth are often increased. Calcium also down regulates the production of adrenalin. Oh--and it's involved in muscle contraction and is an essential component in the electrical conduction system of the heart, too.
But does dairy cause mucus production?
Quite simply--yes. In those who are sensitive to it, dairy can create an immune response in the body...just like any and every food someone eats that isn't conducive to their specific digestive capabilities.
As one study from the journal Medical Hypotheses states:
Excessive milk consumption has a long association with increased respiratory tract mucus production and asthma. Such an association cannot be explained using a conventional allergic paradigm and there is limited medical evidence showing causality. In the human colon, β-casomorphin-7 (β-CM-7), an exorphin derived from the breakdown of A1 milk, stimulates mucus production from gut MUC5AC glands. In the presence of inflammation similar mucus overproduction from respiratory tract MUC5AC glands characterises many respiratory tract diseases. β-CM-7 from the blood stream could stimulate the production and secretion of mucus production from these respiratory glands. Such a hypothesis could be tested in vitro using quantitative RT-PCR to show that the addition of β-CM-7 into an incubation medium of respiratory goblet cells elicits an increase in MUC5AC mRNA and by identifying β-CM-7 in the blood of asthmatic patients. This association may not necessarily be simply cause and effect as the person has to be consuming A1 milk, β-CM-7 must pass into the systemic circulation and the tissues have to be actively inflamed. These prerequisites could explain why only a subgroup of the population, who have increased respiratory tract mucus production, find that many of their symptoms, including asthma, improve on a dairy elimination diet.
So I guess it depend on who you are and what you've done to your digestive capacity via nutrition and lifestyle practices. Let me 'splain:
Oftentimes an inability to digest/assimilate dairy begins secondary to another offending agent. Gluten is a prime suspect. Alcohol and medicinal drugs are also common culprits. Anything which is a stress to the biological system has the potential to inflame the gut wall (for more on this subject, see the Seesaw of Sickness in my book, Spot On: Nutrition found here: http://triumphtraining.com/collections/books/products/spot-on-nutrition). This microtrauma to the intestine causes tiny holes to form, allowing food particles to pass into the bloodstream undigested. The body then creates antibodies to that particular food, potentially causing you to have an immune response to whatever you’re eating. Additionally, the constant inflammation causes what's termed villous atrophy. Lining the wall of your intestines, you have little finger like projections called villi. These, in turn, have tiny little microvilli covering them--you have about 200 million per square millimeter. The job of the microvilli is to help you assimilate nutrition from your food by producing various enzymes. One of these enzymes, in the case of our current discussion, is lactase--the enzyme you need to do anything with the lactose in dairy. No micromilli equals limited lactase (and other digestive enzymes) which limits your ability to consume dairy without suffering ill effects.
Of course, raw dairy typically comes with the exact enzymes one needs to safely and effectively consume it. But pasteurization destroys all those enzymes along with most if not all of the heat-sensitive nutrients. This is one reason why folks who are "lactose intolerant" often do fine when eating raw dairy. These people also typically fare better with full fat dairy instead of skim or low fat versions which will have more lactose per serving than the unadulterated milk products. Sheep and goat dairy are often better tolerated than diary from cow (ask if you wanna know why); and still others are sensitive to the form--doing fine with hard cheeses or yogurt yet having trouble with milk. Lastly, quantity and frequency of exposure are also factors which need to be considered in regards to how a person reacts to dairy. While the healthy digestive system should be able to handle just about anything that's thrown at it or in it (up to a point), the sad truth is most of us have done such damage to ourselves that we need to do some serious rehab of the gut wall and our health in general before we're able to eat whatever we want.
And, personally, I think that level of consciousness--even if forced upon us due to digestive complaints or otherwise--is actually a blessing. It's a painful signal that we're moving in the wrong direction, and it's time to redirect.
For those who need their academic mind satisfied, I've included a couple of studies below. N = 1, however, so I suggest you experiment on you to find what works best for your specific biochemistry.
http://www.ncbi.nlm.nih.gov/pubmed/2154152In the first of three studies investigating the widely held belief that "milk produces mucus," 60 volunteers were challenged with rhinovirus-2, and daily respiratory symptoms and milk and dairy product intake records were kept over a 10-day period. Nasal secretion weights were obtained by weighing tissues collected and sealed immediately after use. Information was obtained on 51 subjects, yielding 510 person-days of observation. Subjects consumed zero to 11 glasses of milk per day (mean, 2.7; SE, 0.08), and secretion weights ranged from zero to 30.4 g/day (mean, 1.1; SE, 0.1). In response to an initial questionnaire, 27.5% reported the practice of reducing intake of milk or dairy products with a cold or named milk or dairy products as bad for colds. Of the latter group, 80% stated the reason as "producing more mucus/phlegm." Milk and dairy product intake was not associated with an increase in upper or lower respiratory tract symptoms of congestion or nasal secretion weight. A trend was observed for cough, when present, to be loose with increasing milk and dairy product intake; however, this effect was not statistically significant at the 5% level. Those who believe "milk makes mucus" or reduce milk intake with colds reported significantly more cough and congestion symptoms, but they did not produce higher levels of nasal secretions. We conclude that no statistically significant overall association can be detected between milk and dairy product intake and symptoms of mucus production in healthy adults, either asymptomatic or symptomatic, with rhinovirus infection.
http://www.ncbi.nlm.nih.gov/pubmed/16373954There is a belief among some members of the public that the consumption of milk and dairy products increases the production of mucus in the respiratory system. Therefore, some who believe in this effect renounce drinking milk. According to Australian studies, subjects perceived some parameters of mucus production to change after consumption of milk and soy-based beverages, but these effects were not specific to cows' milk because the soy-based milk drink with similar sensory characteristics produced the same changes. In individuals inoculated with the common cold virus, milk intake was not associated with increased nasal secretions, symptoms of cough, nose symptoms or congestion.Nevertheless, individuals who believe in the mucus and milk theory report more respiratory symptoms after drinking milk. In some types of alternative medicine, people with bronchial asthma, a chronic inflammatory disease of the lower respiratory tract, are advised not to eat so-called mucus-forming foods, especially all kinds of dairy products. According to different investigations the consumption of milk does not seem to exacerbate the symptoms of asthma and a relationship between milk consumption and the occurrence of asthma cannot be established. However, there are a few cases documented in which people with a cow's milk allergy presented with asthma-like symptoms.
Original Source found here: http://www.smh.com.au/comment/not-eating-read-meat-wont-save-the-planet-20151214-glmxly
Not eating red meat won’t save the planet
Asa Wahlquist Published: December 14, 2015 - 9:00PM
Comment: The future of protein is not meat It sounds so easy: stop eating red meat to lower greenhouse gas emissions. But nature is far more complicated than that.
There are three critical questions you need to ask before cutting beef and lamb out of your diet for environmental reasons: what will happen to the grasslands that cattle and sheep graze; how will alternate protein be produced; and what will the greenhouse consequences of that production be?
About 60 per cent of the world's agricultural land is grasslands, land that is too poor and too dry to be cropped. In Australia, about 70 per cent of the country is grassland. The only way food can be produced from grasslands is by grazing ruminants. Mammals cannot digest grass, but ruminants have special stomachs filled with grass-digesting bacteria. The problem is those bacteria produce methane, which the ruminant burps out.
Methane is a potent greenhouse gas with a rating 25 times that of carbon dioxide over 100 years, although it has a lifetime of 9 to 12 years in the atmosphere.
The experience worldwide is that if cattle are removed from grasslands, the original ruminants re-establish themselves, or ferals invade.
In Australia the main ferals are goats, as well as camels in drier regions. Contrary to popular belief, kangaroos do produce methane, although the actual quantities, and their alternate pathways for digesting cellulose from grass, are the subject of ongoing research. Even termites produce methane: they are responsible for about three per cent of Australia's greenhouse gas emissions.
What if everyone did go vegetarian and the grasslands were not grazed at all? In Australia, they would most likely burn. Bushfire accounts for about 3 per cent of Australia's net greenhouse gas emissions.
The argument overseas focuses largely on the huge quantities of grain, that could otherwise be consumed by humans, that are fed to livestock. This is a practice that is indefensible on environmental grounds. In Australia, most cattle and all sheep are grassfed. Dairy cattle are usually given supplementary feed, which is mostly forage or hay with some grain.
If you decide not to eat meat, where are you going to get your protein, and what are the greenhouse gas consequences? Soy beans, chickpeas, lentils - all the high-protein legumes - are crops that are grown on cleared land, land that is ploughed, fertilised, planted, irrigated and harvested by greenhouse-gas producing machines.
Australia is at its limit of land that can be cleared for cropping, and is in the process of reducing irrigation in its food bowl, the Murray-Darling basin. And talking of irrigation, under Australian conditions soybeans need almost as much water as cotton. Australia produces roughly 15 per cent of the soybeans that it consumes, although much of that is used in stock feed.
Pigs and chickens are monogastric and as a result produce a small fraction, per kilo, of the methane produced by ruminants. Unlike cattle they cannot live on grass. In traditional farm situations they were fed on crop residues and waste, but now significant quantities of grains are grown to feed them.
Meat protein substitutes, ranging from tofu to synthetic meat, are all highly processed and that means more greenhouse gas production.
Estimating methane production is a tricky business. There are a number of figures for the percentage of greenhouse gas emissions agriculture is responsible for, and they are getting better. On Monday, the CSIRO announced methane emissions from Australian cattle were actually 24 per cent lower than previously thought.
Critics of meat consumption like to compare ruminant-produced methane with transport emissions. But fossil fuels are releasing carbon that was sequestered hundreds of millions of years ago that will never be replaced. The methane burped by a cow comes from carbon sequestered in the grass during the last growing season. If that grass keeps growing, or produces seedlings, carbon will be sequestered again next season.
There is no comparison: burning fossil fuels is a one-way street. The methane produced by ruminants is a natural part of an ancient life cycle.
Asa Wahlquist is a rural journalist.
This story was found at: http://www.smh.com.au/comment/not-eating-red-meat-won8217t-save-the-planet-20151214-glmxly.html
Original Source found here: http://mobile.nytimes.com/2013/12/17/health/a-lifelong-fight-against-trans-fat.html?_r=0
By MELANIE WARNER
December 16, 2013
In 1957, a fledgling nutrition scientist at the University of Illinois persuaded a hospital to give him samples of arteries from patients who had died of heart attacks.
When he analyzed them, he made a startling discovery. Not surprisingly, the diseased arteries were filled with fat — but it was a specific kind of fat. The artificial fatty acids called trans fats, which come from the hydrogen-treated oils used in processed foods like margarine, had crowded out other types of fatty acids.
The scientist, Fred Kummerow, followed up with a study that found troubling amounts of artery-clogging plaque in pigs given a diet heavy in artificial fats. He became a pioneer of trans-fat research, one of the first scientists to assert a link between heart disease and processed foods.
Now, Dr. Kummerow (KOO-mer-ow) is still active at age 99, living a few blocks from the university, where he runs a small laboratory. And he continues to come to contrarian conclusions about fat and heart disease.
In the past two years, he has published four papers in peer-reviewed scientific journals, two of them devoted to another major culprit he has singled out as responsible for atherosclerosis, or the hardening of the arteries: an excess of polyunsaturated vegetable oils like soybean, corn and sunflower — exactly the types of fats Americans have been urged to consume for the past several decades.
The problem, he says, is not LDL, the “bad cholesterol” widely considered to be the major cause of heart disease. What matters is whether the cholesterol and fat residing in those LDL particles have been oxidized. (Technically, LDL is not cholesterol, but particles containing cholesterol, along with fatty acids and protein.)
“Cholesterol has nothing to do with heart disease, except if it’s oxidized,” Dr. Kummerow said. Oxidation is a chemical process that happens widely in the body, contributing to aging and the development of degenerative and chronic diseases. Dr. Kummerow contends that the high temperatures used in commercial frying cause inherently unstable polyunsaturated oils to oxidize, and that these oxidized fatty acids become a destructive part of LDL particles. Even when not oxidized by frying, soybean and corn oils can oxidize inside the body.
If true, the hypothesis might explain why studies have found that half of all heart disease patients have normal or low levels of LDL.
“You can have fine levels of LDL and still be in trouble if a lot of that LDL is oxidized,” Dr. Kummerow said.
This leads him to a controversial conclusion: that the saturated fat in butter, cheese and meats does not contribute to the clogging of arteries — and in fact is beneficial in moderate amounts in the context of a healthy diet (lots of fruits, vegetables, whole grains and other fresh, unprocessed foods).
His own diet attests to that. Along with fruits, vegetables and whole grains, he eats red meat several times a week and drinks whole milk daily.
He cannot remember the last time he ate anything deep-fried. He has never used margarine, and instead scrambles eggs in butter every morning. He calls eggs one of nature’s most perfect foods, something he has been preaching since the 1970s, when the consumption of cholesterol-laden eggs was thought to be a one-way ticket to heart disease.
“Eggs have all of the nine amino acids you need to build cells, plus important vitamins and minerals,” he said. “It’s crazy to just eat egg whites. Not a good practice at all.”
Dr. Robert H. Eckel, an endocrinologist and former president of the American Heart Association, agreed that oxidized LDL was far worse than nonoxidized LDL in terms of creating plaque.
But he disputed Dr. Kummerow’s contention that saturated fats are benign and that polyunsaturated vegetable oils promote heart disease. “There are studies that clearly show a substitution of saturated fats with polyunsaturated fats leads to a reduction in cardiovascular disease,” said Dr. Eckel, a professor at the University of Colorado.
“Oxidation is something that consumers can detect,” he said. “Therefore, it is in everyone’s best interest to control it.”
The long arc of Fred Kummerow’s life and career illustrates the frustratingly slow pace of science and the ways in which scientific conformity can hinder the search for answers. Born in Germany just after World War I broke out, he moved to Milwaukee with his family when he was 9. His father, who worked at a cement block factory, did not have the money to send him to college, so Dr. Kummerow worked full time at a drug distribution company while attending the University of Wisconsin in the evenings. After he earned a Ph.D. in biochemistry, his first job was at Clemson University in South Carolina, where he helped prevent thousands of deaths in the South from pellagra, a disease resulting from a deficiency of vitamin B3.
His early research on trans fats was “resoundingly criticized and dismissed,” said Dr. Walter Willett, the chairman of the nutrition department at the Harvard School of Public Health, who credited Dr. Kummerow with prompting his desire to include trans fats in the Nurses’ Health Study. A 1993 finding from that study, which showed a direct link between the consumption of foods containing trans fats and heart disease in women, was a turning point in scientific and medical thinking about trans fats.
“He had great difficulty getting funding because the heart disease prevention world strongly resisted the idea that trans fats were the problem,” Dr. Willett continued. “In their view, saturated fats were the big culprit in heart disease. Anything else was a distraction from that.”
At an age when life itself is an accomplishment, Dr. Kummerow said he had no intention of stepping away from the work that has consumed him for six decades. He continues to work from home and talks daily to the two scientists who work in his lab, which receives funding from the Weston A. Price Foundation.
His wife of 70 years, Amy, died last year at age 94 from Parkinson’s disease; he has three children, three grandchildren and a great-grandchild.
He takes no medications, and his mind shows no sign of aging: He has an encyclopedic recall for names, dates and, more impressive, complex scientific concepts. After his muscles became inflamed from a blood pressure drug that he has since stopped taking, he started using a wheelchair combined with a walker.
His most significant health problem, appropriately enough, was an artery blockage at age 89 — probably a result of the inevitable effects of aging, not diet.
Bypass surgery took care of the blockage, and the fact that he now has an artery from his arm running into his heart has made him even more determined to keep working. Heart disease remains the leading cause of death for Americans, and he would like to stick around to continue funding research that will help change that.
“What I really want is to see trans fats gone finally,” he said, “and for people to eat better and have a more accurate understanding of what really causes heart disease.”
This pilot study aimed to determine if an elemental diet could be used to treat patients with active rheumatoid arthritis and to compare its effect to that of oral prednisolone.
Thirty patients with active rheumatoid arthritis were randomly allocated to 2 weeks of treatment with an elemental diet (n = 21) or oral prednisolone 15 mg/day (n = 9). Assessments of duration of early morning stiffness (EMS), pain on a 10 cm visual analog scale (VAS), the Ritchie articular index (RAI), swollen joint score, the Stanford Health Assessment Questionnaire, global patient and physician assessment, body weight, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and haemoglobin, were made at 0, 2, 4 and 6 weeks.
All clinical parameters improved in both groups (p<0.05) except the swollen joint score in the elemental diet group. An improvement of greater than 20% in EMS, VAS and RAI occurred in 72% of the elemental diet group and 78% of the prednisolone group. ESR, CRP and haemoglobin improved in the steroid group only (p<0.05).
An elemental diet for 2 weeks resulted in a clinical improvement in patients with active rheumatoid arthritis, and was as effective as a course of oral prednisolone 15 mg daily in improving subjective clinical parameters. This study supports the concept that rheumatoid arthritis may be a reaction to a food antigen(s) and that the disease process starts within the intestine.
Original Source: http://www.ncbi.nlm.nih.gov/pubmed/17308218
From the CDC website (http://www.cdc.gov/flu/protect/vaccine/thimerosal.htm):
Do the 2014-2015 seasonal flu vaccines contain thimerosal?
The Food and Drug Administration (FDA) has approved several formulations of the seasonal flu vaccine, including multi-dose vials and single-dose units. (See Table of Approved Influenza Vaccines for the U.S. 2014–2015 Season.) Since seasonal influenza vaccine is produced in large quantities for annual vaccination campaigns, some of the vaccine is produced in multi-dose vials, and contains thimerosal to safeguard against possible contamination of the vial once it is opened.
I am pro vaccine. I had all of my six children vaccinated. I believe that vaccines save millions of lives. So let me explain why I oppose the current wave of state legislation to remove parents’ right to choose whether to give their children particular vaccines.
Vaccines are big business. Pharma is a trillion dollar industry (1) with vaccines accounting for $25 billion in annual sales. (2) CDC’s decision to add a vaccine to the schedule can guarantee its manufacturer millions of customers and billions in revenue (3) with minimal advertising or marketing costs and complete immunity from lawsuits. High stakes and the seamless marriage between Big Pharma and government agencies have spawned an opaque and crooked regulatory system. Merck, one of America’s leading vaccine outfits, is currently under criminal investigation for fraudulently deceiving FDA regulators about the effectiveness of its MMR vaccine. Two whistleblowers say Merck ginned up sham studies to maintain Merck’s MMR monopoly. (4)
Big money has fueled the exponential expansion of CDC’s vaccine schedule since 1988, when Congress’ grant of immunity from lawsuits (5) suddenly transformed vaccines into paydirt. CDC recommended five pediatric vaccines when I was a boy in 1954. Today’s children cannot attend school without at least 56 doses of 14 vaccines by the time they’re 18.(6)
An insatiable pharmaceutical industry has 271 new vaccines under development in CDC’s bureaucratic pipeline (7) in hopes of boosting vaccine revenues to $100 billion by 2025. (8)The industry’s principle spokesperson, Dr. Paul Offit, says that he believes children can take as many as 10,000 vaccines. (9)
Public health may not be the sole driver of CDC decisions to mandate new vaccines. Four scathing federal studies by Congress, (10) the US Senate, (11) the HHS Inspector General, (12) and the HHS Office of Research Integrity, (13) paint CDC as a cesspool of corruption, mismanagement and dysfunction with alarming conflicts of interest suborning its research, regulatory and policymaking functions. CDC rules allow vaccine industry profiteers like Dr. Offit to serve on advisory boards that add new vaccines to the schedule. In a typical example, Offit in 1999 sat on the CDC’s vaccine advisory committee and voted to add the rotavirus vaccine to CDC’s schedule paving the way for him to make a fortune on his own rotavirus vaccine. (14) Offit and his business partners sold the royalties to his rotavirus vaccine patent to Merck in 2006 for $182 million. (15) Offit told Newsweek, “It was like winning the lottery!” (16) A 2009 HHS Inspector General’s report found that as many as 97% of the individuals who sit on the CDC advisory boards that approve vaccines may have similar conflicts. In addition to lucrative business partnerships with Merck, Offit holds a $1.5 million research chair, funded by Merck, at Children’s Hospital in Philadelphia. (17) From this industry sinecure, he broadcasts vaccine industry propaganda and annually publishes books urging unlimited vaccinations and vilifying safe-vaccine advocates. (18) (19)
The corruption has also poisoned CDC’s immunization safety office, the research arm that tests vaccines for safety and efficacy. In August 2014, seventeen year CDC veteran, Dr. William Thompson, who is author of the principal study cited by CDC to exculpate mercury preserved vaccines from the autism link, invoked whistleblower protection, and turned extensive agency files over to Congress. (20)Thompson, who is still employed at CDC, says that for the past decade his superiors have pressured him and his fellow scientists to lie and manipulate data about the safety of the mercury based preservative, thimerosal, to conceal its causative link to a suite of brain injuries, including autism. (21) (22)
Thimerosal is 50% ethylmercury which is far more toxic and persistent in the brain than the highly regulated methylmercury in fish. (23) Hundreds of peer reviewed studies by leading government and university scientists show that thimerosal, is a devastating brain poison linked to neurological disorders now epidemic in American children.My book, Thimerosal: Let the Science Speak, (24) is a summary of these studies, (25) which CDC and its credulous journalists swear don’t exist. Although Thompson’s CDC and vaccine industry colleagues have created nine patently fraudulent and thoroughly discredited epidemiological studies to defend thimerosal, no published study shows thimerosal to be safe. (26)
The common canard that US autism rates rose after drug makers removed most thimerosal from pediatric vaccines in 2003 is wrong. That same year, CDC added flu shots containing massive doses of thimerosal to the pediatric schedule. (27) As a result, children today can get nearly as much mercury exposure as children did from all pediatric vaccines combined in the decade prior to 2003. (28) Worse, thimerosal, for the first time, is being given to pregnant women in flu shots. (29) Furthermore, CDC’s current autism numbers are for children born in 2002, when kids were still getting thimerosal in their pediatric vaccines. The best science suggests that thimerosal’s complete removal from vaccines is likely to prompt a significant decline in autism. For example, a 2013 CDC study in JAMA Pediatrics shows a 33% drop in autism spectrum disorder in Denmark following the 1992 removal of thimerosal from Danish vaccines. (30) That paper is among 37 peer reviewed studies linking thimerosal to the autism epidemic. (31)
Thimerosal has precipitated a journalistic as well as a public health crisis. Big Pharma pumps over $3.5 billion annually into TV, newspapers and other advertising, targeting news departments, which have become vehicles for pharmaceutical sales and propaganda platforms for the industry. Television and print outlets feature spokespeople like Dr. Offit – without identifying their industry ties - while censoring criticisms of vaccine safety and excluding the voices of informed vaccine safety advocates. Busy journalists parrot the deceptive talking points dispensed by government and pharma officials rather than reading the science themselves. Unable to argue the science, they bully, pillory and demonize vaccine safety advocates as “anti-vax”, “anti-science” and far worse. The unwillingness of the press to scrutinize CDC has emboldened both industry and agency to follow the lowest paths of easy profit and bureaucratic preservation.
The measles scare was classic disaster capitalism with media outlets dutifully stoking public hysteria on editorial pages and throughout the 24 hour broadcast cycle. With Dr. Offit leading the charge, CDC, drug makers and industry funded front groups parlayed a garden variety annual measles outbreak into a national tidal wave of state legislation to ban religious and philosophical vaccine exemptions. The national media frenzy over 159 measles cases (32) left little room for attention to the the autism cataclysm which has debilitated 1 million American children since the pandemic began in 1989, (33) with 27,000 new cases annually. CDC refuses to call autism an “epidemic”. In defiance of hard science, and common sense, CDC and Offit have launched a denial campaign to gull reporters into believing the autism plague is an illusion created by better diagnosis. (34) (35) (36)
Big Pharma is among the nation’s largest political donors giving $31 million last year to national political candidates. (37) It spends more on political lobbying than any other industry, $3.0 billion from 1998 to 2014 (38) – double the amount spent by oil and gas and four times as much as defense and aerospace lobbyists. (39) By February, state legislators in 36 states were pushing through over one hundred new laws to end philosophical and religious vaccine exemptions. Many of those state lawmakers are also on the industry payroll. (40) You can see how much money bill sponsors from your state took from Big Pharma on http://www.maplight.org.
Normally plaintiffs’ tort lawyers would provide a powerful check and balance to keep vaccines safe and effective and regulators and policymakers honest. But Pharma’s dirty money has brought the industry immunity from lawsuits for vaccine injury no matter how dangerous the product. An obliging Congress disposed of the Seventh Amendment right to jury trial making it impossible for vaccine injured plaintiffs to sue pharmaceutical companies for selling unsafe vaccines. (41) That’s right! No Class Actions. No discovery. No depositions and little financial incentive for the industry to make vaccines safer.
Vaccine industry money has neutralized virtually all of the checks and balances that once stood between a rapacious pharmaceutical industry and our children. With the research, regulatory and policymaking agencies captured, the courts closed to the public, the lawyers disarmed, the politicians on retainer and the media subverted, there is no one left to stand between a greedy industry and vulnerable children, except parents. Now Big Pharma’s game plan is to remove parental informed consent rights from that equation and force vaccine hesitant parents to inject their children with potentially risky vaccines which the Supreme Court has called “unavoidably unsafe”. (42)
Ending exemptions is premature until we have a functioning regulatory agency and a transparent process. The best way to insure full vaccine coverage is for the vaccine program to win back public trust by ending its corrupt financial ties with a profit-making industry.
To educate yourselves about CDC corruption and the truth about vaccine science, download the movie Trace Amounts (43) and insist your legislators watch it before voting on any of these bills.
26 Methodological Issues and Evidence of Malfeasance in Research Purporting to Show Thimerosal in Vaccines is Safe, Dr. Brian Hooker et al. 2014. www.hindawi.com/journals/bmri/2014/247218 (Critique of six epidemological studies cited by CDC to exculpate thimerosal)
35http://www.ncbi.nlm.nih.gov/pubmed/19234401 (In contrast to the unsupported statement by Gerber and Offit, this paper from the UC Davis MIND Institute shows true increases in autism levels, far beyond that possible through “broadening diagnostic criteria and increased awareness”)
40http://maplight.org/california/legislator/1397-richard-pan (This link gives an example of industry donations to state lawmakers, i.e., the campaign funding profile of Dr. Richard Pan, a state senator who is heavily supported by the health care industry and is leading the charge to remove parental vaccine consent rights in California)
Abstract Background Epidemiological and animal-based studies have suggested that prenatal and postnatal fluoride exposure has adverse effects on neurodevelopment. The aim of this study was to examine the relationship between exposure to fluoridated water and Attention-Deficit Hyperactivity Disorder (ADHD) prevalence among children and adolescents in the United States.
Methods Data on ADHD prevalence among 4-17 year olds collected in 2003, 2007 and 2011 as part of the National Survey of Children’s Health, and state water fluoridation prevalence from the Centers for Disease Control and Prevention (CDC) collected between 1992 and 2008 were utilized.
Results State prevalence of artificial water fluoridation in 1992 significantly positively predicted state prevalence of ADHD in 2003, 2007 and 2011, even after controlling for socioeconomic status. A multivariate regression analysis showed that after socioeconomic status was controlled each 1% increase in artificial fluoridation prevalence in 1992 was associated with approximately 67,000 to 131,000 additional ADHD diagnoses from 2003 to 2011.Overall state water fluoridation prevalence (not distinguishing between fluoridation types) was also significantly positively correlated with state prevalence of ADHD for all but one year examined.
Conclusions Parents reported higher rates of medically-diagnosed ADHD in their children in states in which a greater proportion of people receive fluoridated water from public water supplies. The relationship between fluoride exposure and ADHD warrants future study.
What are your thoughts on calorie counting? I've always been against it and understand a 'calorie doesn't equal a calorie' ideology from Paul Chek. Though all I ever see nutritionists go on about for weight loss is to ensure you are on a calorie deficit. Again which I've always taught has many more hormonal problems long term. Interested in your thoughts on the whole matter even tho the question is rather vague. Thanks.
I speak more about this in my latest book (http://triumphtraining.com/collections/books/products/spot-on-nutrition), but I think it's a slippery slope. Most foods worth eating don't have a label. And the USDA allows for a 20% margin of error in both calories and nutrition in a food. So while I think it can prove insightful when people track what and how much they actually consume in the short term, it's not like the human digestive system is the same as a combustion engine. As I say in my book, "the impact a given amount of food has on a person's physiology is predicated less on the total calories in that food and more on the total of what that person has done to themselves via nutrition and lifestyle choices." My experience has shown that many people don't eat enough. But since they're so metabolically damaged for the reasons mentioned in my book and otherwise, their scales and their health both move in the wrong direction.
Need some advice, 3rd week in a row since changing from chemicals on ride to organic snacks and water/honey/salt that I've had difficult cycle rides. Started out great today and burnt up with leg and hip cramps at mile 40, by mile 50 very little leg power.
My Response With His Answers:
What was breakfast? Freshly made organic fruit smoothie with gelatin and milk, half a bagel with peanut butter
What was dinner the night before? Lasagna
What was dinner 2 nights before? Steak, baked potato, zucchini
We could really look at the whole week, but those are the most important meals.
Are you pre-ex stretching? Not for a long period but focused on legs, arms, back, stomach
Have you been fit on the bike? Matt Cole fit me when I bought my Parlee from him in early 2014
Where were the cramps exactly? Started in Thighs then hamstrings and worked it’s way to hips
How much time before your pre-ride meal and the start of the ride? 45 minutes
How soon do you eat once you start? Drank a bottle ever hour with water, salt, honey, started eating buffalo bites, organic blocks within 45 minutes of ride
Is VW suffering, too, or is it just you? Just me, thank God, VW is rocking it on this nutrition and on the bike/run
--I'd nix the bagel or at least the PB--the PUFA content in it inhibits the body's ability to utilize glucose (stored and brought in at dinner and bfast) as well O2 and it's also pro-inflammatory.
--noodles are gluten, I assume, and sub-optimal for those with opposable thumbs.
--beautiful--more/less what I'd do with some fruit or quality dessert at the end!
--good--just use reps before.
--most folks (especially triathletes) are quad dominant. Learning to utilize the hammies will help so the quads don't overwork, then get tight, then force the hammies to overwork, the the whole kinetic chain falls apart.
--you may find that you do better with a longer time period between the end of the last feeding and the start of training. As soon as exercise begins, blood flow to the digestive system is compromised and any calories/nutrition you could have derived from the food in the stomach becomes unavailable (or less so, depending on intensity and several other factors).
--looks pretty good. If the organic blocks are homemade, you should be fine. If commercial, look out for sunflower oil or another PUFA which would inhibit glucose utilization.
--good to know, and I'm glad (but not surprised). Now we just need to dial you in. And I hope my responses help.
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and 'heme A', and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.
Original source: http://www.ncbi.nlm.nih.gov/pubmed/25655639