Cranial Therapy

24 June, 2011 (20:53) | Other | By: Health news

Although pain and function were not measured, most participants reported an enhanced relaxation response after treatment.

The cranial therapy was associated with changes in NO levels in exhaled breath. The level of NO increased from 13.3 +/- 2.09 (SD) to 15.0 +/- 2.95 (SD) ppb (P=0.001, based upon the paired t tests of the subjects). The median level of NO before the cranial therapy was 13.0 ppb (ranging from 8 to 17 ppb); after cranial therapy, it was 16.0 ppb (ranging from 6 to 18 ppb).

Although pain and function were not measured, most participants reported an enhanced relaxation response after treatment; the most relaxed participants were those with the highest post-treatment exhaled NO levels.

Practice Implications
This study is the first to explore the physiological effect of cranial therapy on NO production. These finding are significant, especially since we are increasingly learning of the important role that NO plays in various aspects of health. It is also a big step for the cranial community, because despite having a long, rich history and an immense archive of anecdotal evidence, cranial therapy lacks substantial clinical research studies. Currently an explanation of how cranial therapy can produce an increase in exhaled NO levels remains theoretical.

Traditionally, elevated exhaled NO levels have been closely associated with chronic pulmonary conditions such as asthma. This is why it was so vital to choose participants who were qualified as “healthy adults.” Since there were no asthmatic participants, and those with post-treatment elevated levels of NO reported an enhanced relaxation response, I would hypothesize that there is an intimate connection between naturally increasing the body’s ability to produce NO and being able to decrease the devastating effects that stress has on the body. The article also states that this therapy could be a key adjunct in the prevention of coronary artery disease (CAD) and diabetes—both of which damage epithelial lining of blood vessels (indicative of low NO production). When lowered NO levels allow damage to the blood vessels to occur, the endothelium is less able to produce the necessary amount of NO, thus facilitating further endothelial damage. This, over time, can manifest into serious pathological conditions. Given the noninvasive nature of the procedure, this cranial therapy could potentially be an incredible asset to those treating such conditions.

Since the 1990s, NO has been aggressively studied—its relationship to cardiovascular health only discovered in 1998—and it has been found that too little NO, as seen in CAD and diabetic cases, can have a damaging effect, but too much can also be detrimental. In the instance of an excess of NO, further research to examine whether this cranial maneuver may have a modulating effect on NO levels would be interesting, as colleagues in the cranial field have reported positive results with asthmatic patients.

Although this study is small and uncontrolled, which is not typically the type of study highlighted in this column, these findings are relevant to clinical practice. NO is, as we’ve seen, a critical component in maintaining health. In the clinical field, NO and its precursors are being utilized in a variety of ways, ranging from treatment of pulmonary vascular disease in pediatrics, to pain associated with angina, to erectile dysfunction. It’s also becoming a staple for preventative and anti-aging protocols.

We’ve long known that there are noninvasive, effective methods of increasing NO levels, whether through supplementing with arginine or even regular exercise, but until now there has not been a physical modality that has shown a possible systemic increase in NO. These findings also suggest that various healthcare providers and readers of this column may, in addition to their current prevention or treatment protocols, begin to incorporate this type of cranial therapy into their practice.

Change is Good, Right?

23 June, 2011 (20:24) | Health Care | By: Health news

The dietary supplement world is awaiting some critical guidance regarding new dietary ingredients from the FDA due to arrive by the end of June 2011. In anticipation of this guidance, chatter in the industry has increased, and this has even made the news. An article published in the Salt Lake Tribune on May 1, 2011 focused on this anticipated communication.

One of the provisions that Congress included in the Dietary Supplement Health and Education Act (DSHEA) addresses the safety of new dietary ingredients. This provision gives the FDA the right and responsibility to review new dietary ingredients for safety prior to their being marketed in dietary supplements. “New” is defined as any dietary supplement ingredient that was not marketed in the United States before October 15, 1994. It is the manufacturer’s responsibility to make this determination, and if new, submit a new dietary ingredient (NDI) application to document the safety of the new ingredient. If the FDA does not respond within 75 days after the application is submitted, the manufacturer can introduce the ingredient to the marketplace. It is important to note that a “successful” NDI submission does not mean that FDA has confirmed that the ingredient is safe for its intended use.

Despite the growth in the number of natural products since 1994, Daniel Fabricant, the director of the FDA’s Division of Dietary Supplement Programs, reported that the FDA has received only 700 new dietary ingredient applications since 1994, out of an estimated 60,000 dietary ingredients in use. One of the reasons for this is that, in the absence of clear guidelines, the industry has been confused about what to submit. The FDA guidance expected by the end of June should clear up this confusion. And that is where the change is likely to start happening.

The requirements to prove safety may be quite onerous for smaller companies.

Depending on the requirements to demonstrate safety, hundreds to thousands of products may in be jeopardy of discontinued sales until their safety is proven. The requirements will also affect the introduction of new ingredients into the marketplace. This includes both advanced technology ingredients and botanical ingredients from other parts of the world (if not marketed for use prior to 1994). The requirements to prove safety may be quite onerous for smaller companies. A somewhat similar situation has recently taken place in the European Union. In the EU, the 7-year transition period set out in the 2004 Herbal Directive (2004/24/EC) has expired. This means that, as of May 1, 2011, only medicinal products that have been registered or authorized can remain on the shelves. A manufacturer who wishes to register a traditional herbal medicinal product must provide documentation showing that the product is safe for its intended uses. They must also provide evidence that the product has been used safely for at least 30 years, 15 of them in the EU. Although this legislation is different than the NDI requirement in the United States, the intent and approach is quite similar. Smaller herbal manufacturers in the EU are already voicing their concerns about their ability to comply with these requirements. This is, in part due to the scope of the documentation necessary to establish safety. Whether the clarified NDI requirements will present a similar challenge to smaller manufacturers in the United States remains to be seen.

Dietary supplement manufacturers are watchful of events in the EU as they await the NDI guidance. The implications to availability, and potentially cost, of affected dietary ingredients are yet to be determined. If a product is found to contain an NDI that does not have an application filed, that product is considered adulterated and will likely be removed from commerce. It’s possible that the FDA could require retailers and healthcare practitioners to pull thousands of products off the shelves as it determines the safety of these new dietary ingredients. This will also trigger remedial action on the part of the manufacturer. Despite the potential implications, most manufacturers are eager for NDI clarification. Ultimately, this guidance is what the industry has been asking for since 1994. Defining these requirements should help manufacturers submit what the FDA requires. This, in turn, will provide greater assurance of safety to dietary supplement users. Getting there may be somewhat painful, but the destination should be worth it.

Prunes Act as Laxatives

23 June, 2011 (17:52) | Other | By: Health news

Study Medication
Subjects received either prunes or psyllium to provide 6 grams per day of fiber for 3 weeks. After a 1-week washout period, therapies were switched.

Outcome Measures
The test subjects maintained a daily symptom and stool diary in which they tracked number of complete spontaneous bowel movements per week, global relief of constipation, stool consistency, straining, tolerability, and taste.

Key Findings
The number of complete spontaneous bowel movements per week (primary outcome measure) and stool consistency scores improved significantly (P<0.05) with dried plums when compared to psyllium.
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Practice Implications
Prunes work. That is, prunes appear to do exactly what everyone has always thought they do; they act as a mild laxative. Although some would think this action is obvious, this study by Attaluri et al may be among the first human clinical trials published in the peer-reviewed literature that demonstrates prunes’ efficacy.

The results of a 2002 clinical trial comparing the effects of prunes versus dried apples on factors that affect bone density “suggest that dried plums may exert positive effects on bone in postmenopausal women.”1 Though the results were favorable, they did not confirm whether prunes act as laxatives.

Two 2010 studies hinted that prunes might act as stool softeners. Both studies compared eating prunes as a snack against cookies. A June 2010 paper that appeared in the journal Appetite informed us that prunes were more effective than sugar cookies at suppressing hunger and creating a sense of satiety.3 A September 2010 article in the Journal of the American Dietary Association reported that snacking on prunes lowered triglyceride levels more than sugar cookies and mentioned a tendency for prunes to soften stools.

Few experienced practitioners or consumers will view these data as new. Instead most will be surprised that this study had to be done in the first place.

There is another paper involving prunes that is worth noting. Appearing in the Journal of the American College of Nutrition in 2007, a review paper compared the effect of eating prunes against eating berries or other fruits on serum antioxidant capacity (AOC). While data from a series of clinical trials “demonstrated that consumption of certain berries and fruits such as blueberries, mixed grape and kiwifruit “increased plasma AOC,” eating prunes or drinking prune juice did not alter measured levels of antioxidant capacity.

With the publication of the current Attaluri et al study, the use of prunes as a laxative has taken the first step away from being the product of “old wives’ tales” (OWT) toward the realm of evidence based medicine (EBM). Adherents of EBM may now prescribe prunes to patients suffering from constipation with less fear of criticism. It should be pointed out that there are weaknesses to this current study: It was single not double-blinded, participants were overwhelmingly female, little is known regarding the etiology of participants’ constipation, and obviously, one study is far from conclusive.

This new advancement in medicine does have an element of the absurd to it. Few experienced practitioners or consumers will view these data as new. Instead most will be surprised that this study had to be done in the first place; the action of prunes on the human digestive tract is self-evident.

The attraction that many us have to EBM, and our resultant desire to find support for therapies in published studies, meta-analyses, or—the Holy Grail of all papers—the Cochrane Reviews, on the surface seems both reasonable and commendable but may become an obstruction to achieving best patient outcomes.

Until now, the evidence suggested we employ psyllium seed fiber as it is more efficacious than sodium docusate.6 Yet practitioners who rely on anecdote, commonsense, and the data obtained via OWT have been using prunes to soften and increase stool frequency all along.

This story about prunes brings to mind how my colleague Steve Austin, ND, when writing years ago about breast cancer, pointed out the distinction between type 1 and type 2 errors in statistics and how different medical professions put greater emphasis on preventing one form of error over the other. For a medical oncologist who prescribes chemotherapy, the demand is to be sure the drugs will have benefit against the cancer. One needs to be certain the drugs will bring benefit as the side effects are so great.7 For naturopathic doctors who employ nontoxic therapies, in this case prunes, the demands should be the opposite. If there is a chance a therapy may help, then we should be interested in trying it: the classic ‘it won’t hurt and it might help’ view of practice.

As for prunes, however, we can now prescribe them with confidence; they have officially graduated from unproven OWT to the trustworthy EBM.

Fecal Flora Transplantation In the Treatment of Colonic and Metabolic Disease

22 June, 2011 (21:15) | Other | By: Health news

Ten patients undergoing “fecal bacteriotherapy,” or what in the United States is often termed “fecal transplantation.” In this process the bowel is cleansed with antibiotics and then fecal suspensions from healthy donors are administered daily. In this study the first infusion was administered through a colonoscpe and subsequent doses were given over a 60-minute period through a nasal jejunal tube or via enemas. Bowel flora was analyzed at 4, 8, and 24 weeks post-initial infusion and compared with the initial infused donor fecal suspension to determine whether the donor flora had become a stable microbiota of the feces.
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Key Findings
At each of the post-infusion intervals in which sample were evaluated, “the bacterial populations in the patients’ fecal samples consisted predominantly of bacteria derived from the healthy donor samples. … This is a landmark study and suggests that the manipulation of the colonic microbiota is effective and holds promise for new therapies in the treatment of colonic or metabolic disease.”

Fecal transplantation is not a new. Case reports describing this technique date back at least to the late 1950s. A report by Eiseman el al published in 1958 is credited as the first to describe using fecal enemas, in this case for treatment of pseudomembranous enterocolitis.

This is a landmark study and suggests that the manipulation of the colonic microbiota is effective and holds promise for new therapies in the treatment of colonic or metabolic disease.

Since that time there have been a number of reports using donor stool delivered both rectally or via nasogastric tubes. Most of these reports focus on treating recalcitrant Clostridium difficile infection.

Two other reports on fecal transplantation were published in the same September issue of the Journal of Clinical Gastroenterology as the Grehan et al study. They are of almost equal significance as Grehan’s study and deserve specific mention.

In one, Yoon et al from Montefiore Medical Center in the Bronx reports on 12 cases of C. difficile successfully treated using donor feces transplanted into the colon through colonoscopy. The second paper by Rohlke et al reports on 19 patients again with C. difficile treated with fecal transplantation delivered via colonoscopes. The treatment was successful in all 19 patients treated, and the patients remained disease-free on follow-up of 6 months to 4 years.

This therapy may be beneficial for treating other types disease besides gastroenteritis.

Borody et al reported striking results in a small trial using fecal transplantation therapy to treat ulcerative colitis (UC) in 2003. They treated 6 patients with “severe, recurrent symptoms and UC had been confirmed on colonoscopy and histology.” Utilizing “retention enemas … repeated daily for 5 days, complete reversal of symptoms was achieved in all patients by 4 months … by which time all other UC medications had been ceased. At 1 to 13 years …, there was no clinical, colonoscopic, or histologic evidence of UC in any patient.”

Borody is currently recruiting participants for a trial using fecal transplants to treat patients with Parkinson’s disease.12

At a conference in September 2010, Anne Vrieze and colleagues described the results after transplanting fecal flora from lean donors into patients with metabolic syndrome. Their study was a double-blind, randomized, controlled trial. Starting with 18 male subjects with newly diagnosed metabolic syndrome, half received fecal material from lean male donors and half were implanted with their own feces to serve as controls. At the conclusion of the study, fasting triglyceride levels in those subjects who received donor feces were significantly reduced. No effect was seen in the control group re-instilled with their own feces. Peripheral and hepatic insulin sensitivity significantly improved after 6 weeks in the experimental group but not in the control group.

Current knowledge suggests that the intestinal community of bacterial flora contains at least 1 x 1014 bacteria made up of from 500 to 1,000 different species of anaerobic bacteria.14 Clearly our current methodology of testing these using agar culture media to identify only a handful of species and treating with several limited strains of ‘probiotics’ may be too simple an approach to achieve lasting benefit. Fecal transplantation, although sounding to be primitive, may in fact be a more sophisticated option and have the ability to duplicate a healthy bowel ecosystem in the unwell. As unappealing as it may sound, this may prove to be a useful therapy in coming years.

Glucosamine: Bottom Line Monograph. Interactions

22 June, 2011 (16:43) | Medications | By: Health news

Most herbs and supplements have not been thoroughly tested for interactions with other herbs, supplements, drugs, or foods. The interactions listed below are based on reports in scientific publications, laboratory experiments, or traditional use. You should always read product labels. If you have a medical condition, or are taking other drugs, herbs, or supplements, you should speak with a qualified healthcare provider before starting a new therapy.

Interactions with Drugs

  • In theory, glucosamine may decrease the effectiveness of insulin or other drugs used to control blood sugar levels. However, there is limited human research to suggest that glucosamine may not have significant effects on blood sugar. Nonetheless, caution is advised when using insulin or drugs for diabetes by mouth. Patients with diabetes or hypoglycemia should be monitored closely by a qualified healthcare provider, and medication adjustments may be necessary. Based on limited evidence, the combination of glucosamine with diuretics (water pills), such as furosemide (Lasix®), may cause an increased risk of glucosamine side effects.
  • In theory, glucosamine may increase the risk of bleeding when taken with drugs that increase the risk of bleeding. Some examples include aspirin, anticoagulants (“blood thinners”) such as warfarin (Coumadin®) or heparin, anti-platelet drugs such as clopidogrel (Plavix®), and non-steroidal anti-inflammatory drugs such as ibuprofen (Motrin®, Advil®) or naproxen (Naprosyn®, Aleve®).
  • Interactions with Herbs and Dietary Supplements

  • In theory, glucosamine may decrease the effectiveness of herbs or supplements that lower blood sugar levels. Caution is advised when using herbs or supplements that may alter blood sugar.
  • Based on limited human study, side effects of glucosamine may be increased when used at the same time as diuretic herbs or supplements.
  • In theory, glucosamine may increase the risk of bleeding when taken with herbs and supplements that are believed to increase the risk of bleeding
  • There are preliminary reports that use of glucosamine with vitamin C, bromelain, chondroitin sulfate, or manganese may lead to increased beneficial glucosamine effects on osteoarthritis. Simultaneous use with fish oil may have additive beneficial effects in the treatment of psoriasis, based on preliminary research.
  • Glucosamine: Bottom Line Monograph. Safety

    21 June, 2011 (21:22) | Medications | By: Health news

    The U.S. Food and Drug Administration does not strictly regulate herbs and supplements. There is no guarantee of strength, purity or safety of products, and effects may vary. You should always read product labels. If you have a medical condition, or are taking other drugs, herbs, or supplements, you should speak with a qualified healthcare provider before starting a new therapy. Consult a healthcare provider immediately if you experience side effects.

    Since glucosamine can be made from the shells of shrimp, crab, and other shellfish, people with shellfish allergy or iodine hypersensitivity may have an allergic reaction to glucosamine products. However, some research suggests that there is not enough shrimp allergen in glucosamine supplements to trigger reactions in patients who are allergic to shrimp. Nevertheless, caution is warranted. A serious hypersensitivity reaction including throat swelling has been reported with glucosamine sulfate. There are reported cases suggesting a link between glucosamine/chondroitin products and asthma exacerbations.

    Side Effects and Warnings
    In most human studies, glucosamine sulfate has been well tolerated for 30 to 90 days.
    Side effects may include upset stomach, drowsiness, insomnia, headache, skin reactions, sun sensitivity, and nail toughening. There are rare reports of abdominal pain, loss of appetite, vomiting, nausea, flatulence (gas), constipation, heartburn, and diarrhea. Based on several human cases, temporary increases in blood pressure and heart rate, as well as palpitations, may occur with glucosamine/chondroitin products. Based on animal research, glucosamine theoretically may increase the risk for eye cataract formation.
    It remains unclear if glucosamine alters blood sugar levels. Several human studies suggest that glucosamine taken by mouth has no effects on blood sugar, while other research reports mixed effects on insulin. When glucosamine is injected, it appears to cause insulin resistance and endothelial dysfunction. Preliminary studies show no effect on mean hemoglobin A1c concentrations in patients with type 2 diabetes mellitus. Caution is advised in patients with diabetes or hypoglycemia and in those taking drugs, herbs, or supplements that affect blood sugar. Serum glucose levels may need to be monitored by a healthcare provider and medication adjustments may be necessary.
    In theory glucosamine may increase the risk of bleeding. Caution is advised in patients with bleeding disorders or taking drugs that may increase the risk of bleeding. Dosing adjustments may be necessary.
    In several human cases, abnormally high amounts of protein were found in the urine of patients receiving glucosamine/chondroitin products. The clinical meaning of this is unclear. Glucosamine is removed from the body mainly in the urine, and elimination of glucosamine from the body is delayed in people with reduced kidney function. Acute interstitial nephritis, a condition that causes the kidneys to become swollen and possibly dysfunctional, has been reported in a patient taking glucosamine. Increased blood levels of creatine phosphokinase may occur with glucosamine/chondroitin, which may be due to impurities in some products. This may alter certain laboratory tests measured by healthcare providers.
    Early data suggest that glucosamine may modulate the immune system, although the clinical relevance of this is not clear.
    One patient developed liver inflammation (acute cholestatic hepatitis) after taking glucosamine forte.

    Pregnancy and Breastfeeding
    Glucosamine is not recommended during pregnancy or breastfeeding due to lack of scientific evidence.

    Glucosamine: Bottom Line Monograph

    21 June, 2011 (16:53) | Medications | By: Health news

    The below uses are based on tradition, scientific theories, or limited research. They often have not been thoroughly tested in humans, and safety and effectiveness have not always been proven. Some of these conditions are potentially serious, and should be evaluated by a qualified healthcare provider. There may be other proposed uses that are not listed below.
    AIDS, athletic injuries, back pain, bleeding esophageal varices (blood vessels in the esophagus), cancer, congestive heart failure, depression, fibromyalgia, kidney stones, migraine headache, immunosuppression, osteoporosis, pain, psoriasis, skin rejuvenation, spondylosis deformans (growth of bony spurs on the spine), topical hypopigmenting agent (combination product containing multiple ingredients), wound healing

    The below doses are based on scientific research, publications, traditional use, or expert opinion. Many herbs and supplements have not been thoroughly tested, and safety and effectiveness may not be proven. Brands may be made differently, with variable ingredients, even within the same brand. The below doses may not apply to all products. You should read product labels, and discuss doses with a qualified healthcare provider before starting therapy.

    Adults (18 years and older)
    In most available studies, 500 milligrams of glucosamine sulfate has been taken by mouth as tablets or capsules three times daily for 30 to 90 days. Once daily dosing as 1.5 grams (1,500 milligrams) has also been used. Limited research has used 1,500 milligrams daily as a crystalline powder for oral solution or 500 milligrams of glucosamine hydrochloride three times daily. Dosing of 20 milligrams per kilogram of body weight daily has also been recommended in some publications. One study used a dose of 2,000 milligrams per day for 12 weeks.
    Another kind of glucosamine that has been used is a topical form in combination with chondroitin for a four-week period. Safety and effectiveness of these formulations are not clearly proven.
    Glucosamine hydrochloride provides more glucosamine than glucosamine sulfate, although this difference likely does not matter when products are prepared to provide a total of 500 milligrams of glucosamine per tablet.

    Children (younger than 18 years)
    There is not enough scientific evidence to recommend the use of glucosamine in children.
    Research in children has shown that there could be a relationship between the ingestion of MSM (methylsulfonylmethane) and autism; whether it is beneficial or harmful is unclear. MSM is often marketed with glucosamine as a dietary supplement and at this time should be avoided in children.

    Emerson Ecologics

    20 June, 2011 (21:28) | Health Care | By: Health news

    Message From Emerson Ecologics: The Healthcare Practitioners’ Preferred Distributor of Professional Supplements
    Emerson Ecologics is proud to be the leading provider of professional-grade nutritional supplements to the integrative healthcare community. Obtaining that recognition didn’t just happen overnight; it has been earned. For more than 30 years, Emerson has provided confidence and peace of mind to healthcare practitioners and their patients. We strive to maintain that trust and exceed the expectations of our customers every day.
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    A broad offering of 20,000 products from more than 250 of the world’s top nutritional supplement manufacturers ensures we are the single source for all a professional’s needs. Placing one convenient order for multiple brands is one simple step to reducing your carbon footprint. Emerson’s real advantage, however, is in the service solutions we offer. By lessening the administrative burden for a practice or clinic, we enable an office to streamline its business practices and focus on what doctors do best—provide high-quality, personalized care to patients.

    Since 1980, Emerson has not only worked to seamlessly and efficiently bring professional nutritional supplements to practitioners, we have also been fully committed to sharing the industry’s focus on safety and quality. We take this commitment very seriously and developed the Emerson Quality Programâ„ (EQP) to provide you a better vantage point into making informed decisions about the products you recommend.

    As healthcare continues to evolve and patients seek a more proactive and balanced approach to their overall health, we will be here to fully support the healthcare community in providing care. Emerson Ecologics is committed to being the one-stop source for products you can trust, resources you need, and services you deserve.

    Quality: The Confidence for Recommending the Best
    Emerson Ecologics recognizes that high-quality manufacturing practices are central to the success of the dietary supplement industry. With ongoing concerns continually raised about contaminants, such as heavy metals, it is increasingly important for practitioners to be able to reliably secure information about the quality of supplements. A majority of manufacturers voluntarily apply for third-party quality certification to validate their manufacturing practices for product purity, identity, and potency; however, this information is not readily accessible to healthcare practitioners, and so the EQP was created.

    The EQP is a one-of-a-kind, quality assurance program that showcases the quality practices of its participating manufacturers. Voluntary participants provide detailed data on FDA cGMP compliance, raw materials, and finished product testing, which is then scrutinized and verified by Emerson; manufacturers that meet or exceed Emerson’s quality standards are awarded the distinction of EQP Partner, EQP Silver Partner, or EQP Gold Partner. These partners understand quality as an integral part of their business and epitomize a commitment to quality manufacturing that goes above and beyond, representing some of the best quality practices in the industry.
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    All this information is compiled into an easy-to-use online tool at to provide practitioners and their patients what they need to make informed supplement decisions. Practitioners are able to access information to assist them in evaluating potency, bioavailability, and certainty of material identity and purity. The goal of the EQP is not only to recognize manufacturers that continue to raise our industry’s standards, but most importantly to give practitioners the information to confidently recommend and trust the source of supplements for their patients.

    Finasteride’s Effect on Prostate Cancer. Part 2

    20 June, 2011 (15:04) | Prostate cancer | By: Health news

    A major limitation of this sero-epidemiological study is based on the fact that fatal prostate cancer takes many years from formation until death occurs. The question is whether the fatty acid content of a man’s blood on two days out of the thousands of days over those years is a reliable measure of his average fatty acid status. Another limitation is that the researchers did not take into account the impact of vitamin E, selenium, lycopene, cruciferous vegetables, meat and dairy intake.

    EPA and DHA are hypothesized to reduce cancer risk in general through their anti-inflammatory and immunomodulatory properties, and by affected cell permeability, gene expression, and signal transduction. The effects of omega-3s on these pathways in prostate carcinogenesis are not fully understood. There is no known mechanism by which EPA or DHA would be procarcinogenic, nor is there any evidence suggesting anticancer properties of trans-fats.

    Genetic and molecular studies of high-grade prostate intraepithelial neoplasia have indicated that loss of heterozygosity is prominent and that certain oncogenes are expressed. What causes the expression of these oncogenes? What downregulates their expression?
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    Androgenic hormones are necessary for prostate growth and development. It is not surprising that polymorphic variants of genes involved in androgen action may affect PCa risk. African Americans, who have higher PCa risks than Asians, have androgen-receptor polymorphisms that result in their increased predisposition. 5-alpha reductase variants also may respond differently to inhibition by finasteride.

    The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables.

    Accumulated epidemiologic evidence implicates the environment as the major contributor to the development of most prostate cancers. PCa incidence has wide geographic variation, with high rates in the US and Western Europe and low rates in Asia. African Americans have very high PCa risks. The geographic variation can be explained best by lifestyle, as Asian immigrants to North America have higher PCa risks. The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables. Total fat intake, animal fat intake, and consumption of red meats are associated with increased PCa risk.3 Ingestion of 2-amino-1-methyl-6-phenylimidazopyridine, one of the hererocyclic amine carcinogens that appear in “well-done” red meats, leads to PCa in rats. Consumption of dairy products also increases PCa risk.

    Consumption of lycopene, cruciferous vegetables, vitamin E and selenium reduce PCa risk.
    The role of genetics in identifying individuals at high risk for prostate cancer are in their infancy, but epidemiologic studies support the concept that genetic risk plays a role, and clinical studies support the observation that early prostate cancer in some individuals is highly aggressive, while in the majority it is indolent. Linking these two factors should identify a population of men in whom screening, early detection, and chemoprevention agents can be intensively directed. In the meantime, the take-home message of this study was expressed by the chief author: “Overall, the beneficial effects of eating fish to prevent heart disease outweigh any harm related to prostate cancer risk.”

    Finasteride’s Effect on Prostate Cancer

    18 June, 2011 (21:57) | Prostate cancer | By: Health news

    A 7-year, randomized, placebo-controlled trial that tested whether the 5 alpha-reductase inhibitor, finasteride, reduces prostate cancer (PCa) risk. Over the course of the study, men underwent annual prostate-specific antigen (PSA) and digital rectal examination (DRE) testing. Men who had an abnormal DRE or PSA>/= 4.0 ng/mL were recommended for prostate biopsy. At the end of the study, all men who had not been diagnosed with PCa were requested to undergo a prostate biopsy.

    A case-control study was nested within the Prostate Cancer Prevention Trial. Serum phospholipid levels were compared from 1,809 men with biopsy-confirmed invasive prostate cancer and 1,809 men (controls) who were disease-free at the end-of-study biopsy. Controls were frequency matched to cases on distributions of age (+/- 5 years), treatment group (finasteride/placebo), and a first-degree relative with PCa, and they were oversampled for nonwhites.

    18,882 men age 55 or older were randomized to receive finasteride or placebo.

    Study Medication
    Subjects received finasteride 5 mg/day.

    Outcome Measures
    Serum samples were collected at years 1 and 4 and pooled to reduce intraindividual variability of the phospholipid fatty acid assay. Calculations were made of eicosapentaenoic acid (EPA) + docsahexaenoic acid (DHA) as a measure of total long chain omega02 fatty acids; linoleic + arachidonic acids as a measure of total omega-6 fatty acids; total trans-fatty acids (TFA) 18:1; total TFA 16; and total TFA 18:2.

    The primary outcome measure was the distribution of serum phospholipid fatty acids by percent of total among PCa cases and controls, stratified by prostate cancer grade.

    Key Findings
    Levels of DHA were higher among high-grade cases compared with controls. Levels of TFA 18:1 and 18:2 were significantly lower among high-grade cases compared with controls. There were no other significant differences of the remaining phospholipids between control and cancer groups. EPA was not associated with risk of high-grade PCa, and associations were similar for EPA+DHA to that of DHA alone.

    Practice Implications
    Epidemiologic, animal model, and in vitro studies indicate that omega-3 fatty acids, lycopene, and selenium are chemopreventive for PCa. The findings of this study run counter to what the investigators hypothesized, which was that omega-6 and TFAs would be positively and omega-3 fatty acids inversely associated with PCa risk. Although unexpected, the authors cite several other studies that are consistent with their results, and the possibility exists that there may be an inverse association of fish consumption with late stage or fatal prostate cancer. It is important to keep in mind, however, that it was only DHA, and only high-grade prostate cancer, where an increased risk of PCa risk was found. Replication in more studies is needed before any conclusive recommendations can be made.

    Fish Oil Improves Chemotherapy Effects in Lung Cancer Patients

    18 June, 2011 (17:28) | Cancer | By: Health news

    Forty-six patients with a diagnosis of non-small cell lung cancer (NSCLC) completed the study. All patients received a standard first line chemotherapy regime (carboplatin with either vinerelbine or gemcitabine). The standard of care (SOC) arm (n=31) received only the chemotherapeutic agents; the fish oil (FO) arm (n=15) consumed 2.5 grams EPA/DHA per day in addition to their chemotherapy. Study duration was one year.

    Outcome Measures
    Assessments were made using imaging and clinical examination. Measures included response rate (complete response + partial response) and clinical benefit (complete response + partial response + stable disease divided by the number of patients).
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    Key Findings
    Overall favorable response rate in the FO group was more than double that of the SOC group (60% vs. 25.8%, P= 0.008). Clinical benefit was also higher in the FO group vs. SOC group (80% vs. 41.8%, P= 0.2). There was a trend toward improved survival at the 1-year point in the FO group as well (60% vs. 38.7%, P= 0.15). Lastly, dose limiting toxicities did not differ between the two groups (P=0.46).

    Clinical Implications
    Previous studies in vitro and in vivo have shown omega-3 fatty acids may increase the cytotoxicity of chemotherapy agents.1,2 While such preliminary evidence points to potentiation of chemotherapy, there is little clinical trial data to date to substantiate these claims. The current abstract strengthens the body of evidence that suggests EPA/DHA may sensitize cancer cells to the cytotoxic effects of chemotherapeutics. It is also the first to demonstrate this effect in NSCLC patients specifically.

    While this study used a platinum-based chemotherapeutic and either gemcitabine or navelbine, the effect may not be dependent on the specific chemotherapy agents used. There was a phase II study of metastatic breast cancer patients receiving anthracycline based chemotherapy and 1.8 grams/day of DHA from an algal source. Dosing began 7–10 days before the start of chemotherapy and continued throughout. In addition to overall survival, this study assessed DHA incorporation into phospholipids and found that incorporation varied greatly between individuals. Only those considered “high incorporators” had an increase in overall survival.3 One hypothesis of how omega-3 fatty acids may potentiate cytotoxic agents is through increasing the oxidative potential of the phospholipid bilayer. Increased overall survival only in those womenwho were “high incorporators” of DHA supports this hypothesis.

    This bolsters the case for inclusion of omega-3 fatty acids in all patients with NSCLC undergoing chemotherapy.
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    Earlier studies in rodents suggested DHA may convert chemo-resistive mammary tumors to chemosensitive and radiosensitive tumors. The chemosensitization was nullified when alpha-tocopherol was given concomitantly, again supporting the role of lipid peroxidation as the mechanism of action. Other mechanisms of chemosensitization that have been proposed include influencing signaling proteins such as Ras, Akt, and Her2neu, altering expression or function of apoptotic proteins, affecting survival factors such as NF-KappaB, or increasing drug uptake or activation.5

    It should be noted that the best-evidenced use of fish oil supplementation in integrative cancer care is not for chemo-sensitization but as an anti-cachectic agent.6 In regard to lung cancer specifically, one study showed that patients with sarcopenia (muscle wasting) have significantly less plasma EPA, DHA, and total fatty acids after 2.5 months of chemotherapy. Another study of patients with lung cancer given fish oil in supplement form showed improved appetite, less fatigue, and lowered C-reactive protein. In a separate publication, the authors of the current abstract showed that muscle mass was better preserved in NSCLC patients who consumed 2.2 grams of EPA//DHA during treatment versus those just receiving standard of care. While preservation of muscle mass is enough reason to recommend supplementation with EPA/DHA in NSCLC patients, the current study suggests response rates and overall survival may also benefit. Certainly, this bolsters the case for inclusion of omega-3 fatty acids in all patients with NSCLC undergoing chemotherapy.

    Study Limitations
    This is a small study of only 46 participants. Nonetheless, it did reach statistical significance. There was no placebo used in the group that did not take fish oil. A placebo control would strengthen the findings considerably, as it is possible that those patients healthy enough to swallow addition pills would be expected to have longer survival as well.

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