• Dallas Hit Hard by West Nile Virus
• Make Your Own!
• Judge Says State of Georgia to Pay for Makena Rather than Compounded 17P
• Retinopathy in Blacks Starts at Lower Levels of HbA1c Than in Whites
• Inky Mycobacteria
• Obesity and Colorectal Adenomas Go Together
• How Obesity, Diabetes, and Infection Interact After Total Joint Replacement
• Shifting Causes of Peptic Ulcer Disease
• Statin Use and Diabetes — Weighing Risks and Benefits
• Breast Cancer Tied to Omega Imbalance … Again
• R Ratings for Movies with Smoking?
• ACE Inhibitor Use Lowers Risks for Pneumonia
• Trans Fat Content of Fast-Food Purchases in New York City Has Declined
MM: Illinois has not been missed by West Nile this year. Recent reports indicate that 2012 may be the worst year in our state for this virus since 2002 and unfortunately there is almost an 8% death rate secondary to depleted or suppressed immune systems in those who have been exposed to the virus. Are human vaccines the answer? I think not. Is improving the state of the overall immune system the answer? I think yes! Vitamin D-3, probiotics and omega-3 fish oil or Krill oil are viable first steps in improving the immune system. When people say that they can’t afford these supplements, I have to ask myself, can you truly afford not to take them? Ask your Pharmacist at Mark Drugs for more information and guidance with these and other nutritional support products.
Dallas Hit Hard by West Nile Virus
The city of Dallas has declared a state of emergency due to the high number of West Nile virus infections — 465 so far this year, with 17 deaths, Reuters reports.
This year is on pace to be a record year for West Nile, with nearly 700 cases, the highest mid-August count since the virus was first detected in this country in 1999. A CDC map also shows high disease activity in California, Louisiana, Mississippi, Oklahoma, and South Dakota.
http://www.reuters.com/article/2012/08/15/us-usa-health-westnile-idUSBRE87E0ZO20120815
http://www.cdc.gov/ncidod/dvbid/westnile/index.htm
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MM: Once again I am including an article that exposes my inner geek/nerd. This is an exciting method of drug delivery to a specific site of action that may be initiated and essentially time released by light stimulation. There may be other mini robots coming along in the not too distant future that do not rely on just the circulatory system to transport them to their destination but are at least partially self-propelled to reach their target(s). These can also be stimulated and controlled by different forms of light. Keep your eyes open as this new technology continues to appear. It could only be a matter of time before this approach becomes household knowledge. Very cool stuff!
Make Your Own!
We may be one step closer to producing drugs in the right place at the right time in the body, avoiding the collateral damage of untargeted treatments. The new method involves packaging the molecular machinery for making proteins into a membraned capsule and controlling the generation of a protein at any time with a trigger of light.
These nano-sized "protein factories" use lipids to encapsulate polymerase and other substances necessary for protein production from E. coli, along with a DNA plasmid containing a gene of interest. To block transcription until the right moment, they added a DNA "photo-labile cage" to the plasmid that is cleaved by exposure to UV light.
http://the-scientist.com/2012/08/13/next-generation-in-vivo-drug-factories/
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MM: It’s pretty sad when a judge makes a decision that he knows is so bad that he immediately covers his tracks by making the drug company post a bond to cover his ruling being overturned. This is an example of government and the courts sticking their noses into an area that they are not sufficiently educated in nor appropriately equipped to deal with.
Judge Says State of Georgia to Pay for Makena Rather than Compounded 17P
U.S. District Judge Charles Pannell granted a victory to K-V Pharmaceutical Co. by ordering the state of Georgia to provide Medicaid coverage for their pricey drug, Makena. State officials had argued that readily available compounded 17P costs far less and has no major safety issues. They accused K-V of seeking a court order that would let the company gouge taxpayers and consumers, as the compounded drug costs up to $20 per injection and K-V has said it has agreements for Makena's use in other states for rebated rates of less than $300 per injection.
Pannell said the key difference is that Makena has FDA approval and the compounded drug does not. "Because the court finds that the FDA drug approval process means something," Pannell wrote, the state has an "upside-down policy" because it is covering a drug that is not FDA-approved and not covering one that is. Pannell also ordered K-V to post a bond to cover the cost difference between Medicaid coverage of Makena and the compounded drug, in case his ruling is overturned on appeal.
http://www.ajc.com/news/atlanta/judge-orders-drug-for-1496467.html
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Retinopathy in Blacks Starts at Lower Levels of HbA1c Than in Whites
Although blacks generally have higher glycated hemoglobin levels than whites at the same blood glucose levels, they develop retinopathy at lower HbA1c levels than whites, an Annals of Internal Medicine study finds. The authors say this difference in retinopathy risk argues against setting higher diagnostic levels of HbA1c for blacks.
Researchers examined U.S. NHANES data on over 3000 people. They found that after adjustment for such factors as hypertension and BMI, higher risks for retinopathy started at HbA1c levels of 6.0% and higher in whites, but at levels of 5.5% and higher in blacks. The reasons underlying the risk difference are unknown.
The authors conclude that their results "suggest that the HbA1c levels at which the risk for prevalent retinopathy begins to increase are lower in black adults than in white adults, arguing against a higher HbA1c diagnostic cutoff for blacks."
http://annals.org/article.aspx?articleid=1305508
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N Engl J Med 2012 Aug 22
Inky Mycobacteria
Consider infection when rash develops in a tattoo.
Tattooing inks may be contaminated with infectious agents. An epidemic of cutaneous Mycobacterium chelonae infections occurred in Rochester, New York, in the fall of 2011. Data obtained for analysis included interviews with patients, histopathological analysis of skin biopsy specimens, acid-fast bacteria smears, microbial cultures, antimicrobial sensitivity testing, DNA sequencing, pulse-field gel electrophoresis, cultures of ink, assessment of source water and faucets at tattoo parlors, and investigations of the ink manufacturer.
Within 3 months, 19 persons (13 men) developed a "rash" in their new tattoos associated with the "painting" of grey tattoos by a single tattoo artist. The tattoo parlor utilized "best practices," using sterile instruments, disposable gloves, ink from single-use containers, and providing appropriate aftercare. M. cheloniae was isolated in 14 patients and confirmed by DNA sequencing. Investigations implicated a premixed ink as the infecting media. Organisms were isolated from the grey tattoo inks obtained not only from this tattoo parlor but also from unopened bottles from the manufacturer. Antimicrobial sensitivities were similar in the two patients tested; the organisms were sensitive to clarithromycin, doxycycline, and linezolid.
Comment: This is one of many reports implicating microbial contamination of tattoos as a cause of skin and subcutaneous infections by M. chelonae. I have four conclusions: (1) Rash in a tattoo may arise from infection rather than allergy to a component. (2) If a biopsy of the rash reveals granulomatous inflammation, it may indicate infection rather than allergy to a component. (3) Contamination of ink can occur during its manufacture, so the practices of tattoo artists may be blameless. (4) Tattoo? No, thank you.
— Mark V. Dahl, MD Published in Journal Watch Dermatology August 24, 2012
Citation(s): Kennedy BS et al. Outbreak of Mycobacterium chelonae infection associated with tattoo ink. N Engl J Med 2012 Aug 22; [e-pub ahead of print].
(http://dx.doi.org/10.1056/NEJMoa1205114)
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Am J Gastroenterol 2012 Aug; 107:1175
Obesity and Colorectal Adenomas Go Together
Body-mass index was positively correlated with prevalence of colorectal adenoma.
Numerous studies have identified obesity, diabetes mellitus, and metabolic syndrome as risk factors for colorectal adenomas, but none to date has quantified the association between body-mass index (BMI) and prevalence of colorectal adenomas.
In a meta-analysis of 23 studies involving 105,190 participants, patients with BMI 
25 had a higher prevalence of colorectal adenoma than those with BMI <25 (odds ratio, 1.24; P<0.01). Multivariate analysis demonstrated a dose-response relationship between BMI and prevalence of colorectal adenoma.
Comment: Guidelines for colorectal cancer screening do not take into account factors such as obesity, diabetes, and cigarette smoking, each of which is an established risk factor for adenomas and colorectal cancer. The guidelines are unlikely to be revised in the near future. In my opinion, postpolypectomy surveillance colonoscopy intervals should not be changed for any of these factors. However, clinicians encountering patients aged 
40 with these risk factors can reasonably consider initiation of colorectal cancer screening before age 50 or diagnostic colonoscopy for indications that would otherwise be considered relatively minor, such as anal bleeding (blood on the toilet paper only) or change in bowel habit.
— Douglas K. Rex, MD Published in Journal Watch Gastroenterology August 24, 2012
Citation(s): Okabayashi K et al. Body mass index category as a risk factor for colorectal adenomas: A systematic review and meta-analysis. Am J Gastroenterol 2012 Aug; 107:1175.
http://www.ncbi.nlm.nih.gov/pubmed/22733302?dopt=Abstract
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J Bone Joint Surg Am 2012 Jul 18; 94:e1011
How Obesity, Diabetes, and Infection Interact After Total Joint Replacement!
Periprosthetic infection was associated with severe obesity and, to a lesser extent, diabetes.
Some orthopedists insist that patients with diabetes have tight glycemic control before they undergo total hip or knee replacement, presumably to prevent postoperative infection. To examine the interplay between diabetes and obesity as risk factors for periprosthetic joint infection, Finnish researchers analyzed a single-center database of 7181 primary hip or knee replacement operations. Both deep incisional infections and joint (or joint space) infections that occurred during the first postoperative year were counted.
The overall incidence of infection was 0.7% (52 cases). After multivariate analysis with adjustment for diabetes, body-mass index (BMI), and several other variables, periprosthetic infection was associated significantly with both severe obesity (odds ratio, 6.4) and diabetes (OR, 2.3). The incidence of infection was zero in diabetic patients with BMIs <25 kg/m2 and was between 1% and 2% in diabetic patients with BMIs between 25 and 40. In patients with both diabetes and BMI 
40, the incidence of infection was much higher — 10%.
Comment: In this study, severe obesity was associated more strongly with periprosthetic infection than was diabetes; when both factors were present, risk was substantially higher. The data presented in this study were insufficient to determine whether poor glycemic control among diabetic patients was an additional risk factor for infection. Moreover, controlled trials have not been performed to determine whether tightening glycemic control before or after orthopedic surgery improves postoperative outcomes.
— Allan S. Brett, MD Published in Journal Watch General Medicine August 16, 2012
Citation(s): Jämsen E et al. Obesity, diabetes, and preoperative hyperglycemia as predictors of periprosthetic joint infection: A single-center analysis of 7181 primary hip and knee replacements for osteoarthritis. J Bone Joint Surg Am 2012 Jul 18; 94:e1011.
(http://jbjs.org/article.aspx?volume=94&page=e1011)
http://www.ncbi.nlm.nih.gov/pubmed/22810408?dopt=Abstract
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Aliment Pharmacol Ther 2012 Jul; 36:48
Shifting Causes of Peptic Ulcer Disease
An observational study supports prior findings of less PUD attributed to H. pylori infection and more attributed to use of NSAIDs, particularly aspirin.
The main causes of peptic ulcer disease (PUD) are Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAIDs), including low-dose aspirin (LDA). As the prevalence of H. pylori decreases in developed countries, the percentage of PUD attributable to NSAIDs or other (often idiopathic) causes is increasing.
To further investigate this trend, researchers identified patients with PUD diagnosed by endoscopy between 2005 and 2010 at a tertiary referral hospital in the U.K. They collected data on their pre-endoscopy use of NSAIDs and LDA (
325 mg/day) via patient interviews and hospital records. H. pylori infection status was determined from biopsy testing, if available, or serology testing.
Of 386 patients with PUD, 220 (57%) had used NSAIDs, with 112 (51%) using LDA only. The frequency of H. pylori infection was 57% overall, but was higher among patients with duodenal ulcers versus gastric ulcers (66% vs. 47) and among LDA users than users of any NSAID (61% vs. 52%). The prevalence of non-NSAID, non-H. pylori PUD was 12%. Patients using LDA were older than patients using other NSAIDs.
Comment: The authors conclude that these results are consistent with studies showing the declining role of H. pylori and ascendant role of NSAIDs in the etiology of PUD in developed countries. However, interpretation of these results is limited by the observational study design and use of comparison data from >10 years ago. Moreover, the independent contributions of LDA and H. pylori could not be assessed because of the high prevalence of H. pylori in the LDA group. The higher rate of H. pylori in LDA users than other NSAID users may represent a cohort effect, as both LDA use and prevalence of H. pylori increase with age. The overall prevalence of H. pylori (57%) is lower than in previous studies, but is still higher than in other countries, such as the U.S. The high number of patients taking LDA confirms prior findings that even low doses of aspirin carry a risk for PUD (JW Gastroenterol Jan 31 2006).
— David J. Bjorkman, MD, MSPH (HSA), SM (Epid.) Published in Journal Watch Gastroenterology August 3, 2012
Citation(s): Musumba C et al. The relative contribution of NSAIDs and Helicobacter pylori to the aetiology of endoscopically-diagnosed peptic ulcer disease: Observations from a tertiary referral hospital in the UK between 2005 and 2010. Aliment Pharmacol Ther 2012 Jul; 36:48
http://www.ncbi.nlm.nih.gov/pubmed/22554233?dopt=Abstract
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J Am Coll Cardiol 2012 Aug 2
Statin Use and Diabetes — Weighing Risks and Benefits
In high-risk patients, statin benefits clearly outweigh harms.
Clinical trials have suggested a modest excess of diabetes among statin users, and the FDA recently issued new guidance on this subject. But how do the risks and benefits of statins stack up in clinical practice? In an analysis from Taiwan, patients who received statins for 
30 days from 2000 to 2003 were matched with statin-naive patients. Patients with diabetes or histories of myocardial infarction (MI) or revascularization were excluded (patients with coronary heart disease were not excluded).
After median follow-up of 7.2 years, annual diabetes incidence was slightly, but statistically significantly, higher among statin users than among matched controls (2.4% vs. 2.1%). However, major adverse clinical events such as MI, stroke, or in-hospital death were significantly less common among statin users, driven mostly by lower rates of MI and in-hospital death. Risk–benefit analysis was favorable for statin use in high-risk patients (HR, 0.89) and for secondary prevention (HR, 0.89), but not in low-risk patients (no risk factors or hypertension only).
Comment: Although this is a retrospective analysis of an administrative research database, these findings make sense. They confirm excess risk for diabetes among statin users but suggest that benefits outweigh harms in higher-risk patients. Based on their findings, the authors do suggest caution in extending statin therapy to low-risk individuals, as has been advocated recently (JW Gen Med Jun 12 2012).
— Kirsten E. Fleischmann, MD, MPH Published in Journal Watch General Medicine August 23, 2012
Citation(s): Wang K-L et al. Statins, risk of diabetes, and implications on outcomes in the general population. J Am Coll Cardiol 2012 Aug 2; [e-pub ahead of print].
(http://dx.doi.org/10.1016/j.jacc.2012.05.019)
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http://www.imakenews.com/eletra/mod_print_view.cfm?this_id=2506457&u=
vitalchoiceseafood&show_issue_date=F&issue_id=000606977&lid=blssmNq&uid=b1h1R7NC
Breast Cancer Tied to Omega Imbalance … Again
Study adds details about the impacts of dietary omega-3 and omega-6 fats in premenopausal women of various weights
by Craig Weatherby
Evidence that the omega-3 fats in fish tend to discourage cancer growth continues to mount. People use the two “long-chain” omega-3s found in fish (EPA and DHA) in their cell membranes for critical immune, brain, eye, and metabolic functions. They must either get EPA and DHA from fish and/or fish oil, or make them (very inefficiently) from the small amounts of the “short-chain” omega-3 (ALA) found in certain plant foods. For more on this topic, see our Omega-3 Facts & Sources page.
Cancer risk tied to America’s omega imbalance
Last year, scientists from Penn State University College of Medicine analyzed the existing cell, animal, and population studies … and concluded that omega-3s generally discourage breast cancer. As they wrote, “preclinical data have been, in general, more supportive of a protective effect of omega-3 fatty acids on breast cancer …”. (Signori C et al. 2011) And accumulating evidence suggests that the “omega imbalance” in the standard American diet may be an even bigger problem.
For example, a study of 56,007 French women found breast cancer risk lowest among those whose estimated omega-3 intake placed in the top one-fifth. And the authors found the risk of breast cancer highest among the women whose estimated omega-6 intake placed in the top one-fifth (Thiébaut AC et al. 2009). This was just one of a number of population studies indicating that cancer risk is raised by imbalanced intakes of omega-3s and omega-6s ... as much or more than by diets low in omega-3s (Chajes V et al. 2002; Saadatian-Elahi M et al. 2002; Goodstine SL et al. 2003; Kuriki K et al. 2007; Shannon J et al. 2007; Sonestedt E et al. 2008; Bougnoux P et al. 2009).
To review some of this research, see “Breast Cancer and Omega-3s: More Encouraging Evidence”, “Breast Cancer Linked to Low Vitamin D and Omega-3 Levels”, and “Omega-3s May Fight Breast Cancer Fatigue”.
The studies that haven’t detected a protective effect from dietary omega-3s have generally failed to take omega-6 intake into account … and thereby do a serious disservice. We covered this glaring flaw in study design – and some savvy researchers’ recognition of it – in “Breast Cancer Study Questions Omega-3s’ Preventive Power but Overlooks Context”.
Now, scientists have again linked increased breast cancer risk to diets providing too few omega-3s in relation to omega-6s. And their study added important details about the varying effects of omega imbalances among obese, lean, and premenopausal women.
International study links breast cancer to the omega imbalance
Researchers from International Agency for Research on Cancer in Lyon, France conducted a “case-control” study among 2,074 premenopausal Mexican women (Maillard V et al. 2012).
Among these women, 1,000 had breast cancer and 1,074 were cancer-free “controls”, matched to the cancer cases by age, health care system, and region. The results supported those of prior studies, and added nuances:
- Overall, there was no link between higher omega-3 intake and reduced breast cancer risk.
- Higher omega-3 intakes were linked to a 42 percent drop in breast cancer risk among obese women.
- Higher omega-6 intakes were linked to a 92 percent rise in breast cancer risk among obese and lean women.
- Higher omega-3 intakes were not linked to a lower risk of breast cancer among normal-weight or overweight women.
Obesity is defined as having a body mass index (BMI) of 30 kg/m2, overweight is defined as a BMI of 25 to 29.9 kg/m2 and normal body weight is defined as a BMI between 18.5 and 25 kg/m2. The researchers came to these conclusions (Maillard V et al. 2012):
“Obesity status may affect the association between omega-3 intake and breast cancer risk. The underlying mechanisms may be related to decreased inflammation and improved adipokine and estrogen levels induced by omega-3 [content] in adipose tissue in obese women.”
(Adipokines – such as adiponectin, leptin, and resistin – are hormone-like signaling proteins secreted by fatty adipose tissue. They play crucial roles in promoting or suppressing appetite and fat accumulation.) And they offered some logical advice: “Increased intake of omega-3 polyunsaturated fatty acids should be recommended [in women] … in particular in obese women.” (Maillard V et al. 2012) We hope that public health officials and the media will begin to echo that precautionary advice … which appears risk-free and would yield ancillary heart, eye, and brain health benefits. Leading researchers into the roles of dietary fatty acids – such as William Lands, Ph.D., Joe Hibbeln, M.D., and the late, great Ralph Holman, Ph.D. – agree that the existing evidence points to an inescapable conclusion.
The risks of the standard American diet stem as much from its extreme “omega imbalance> http://vitalchoice.com/shop/pc/viewPrd.asp?idproduct=1421&idcategory=756 <” as its excess of sugars, starches, and processed/refined foods.
To learn more, see “America’s Sickening ‘Omega Imbalance’”, “Using our Omega 3/6 Balance Scores”, and the Omega-3 / Omega-6 Balance section of our news archive.
Sources: Alfano CM, Imayama I, Neuhouser ML, Kiecolt-Glaser JK, Wilder Smith A, Meeske K, McTiernan A, Bernstein L, Baumgartner KB, Ulrich CM, Ballard-Barbash R. Fatigue, Inflammation, and ω-3 and ω-6 Fatty Acid Intake Among Breast Cancer Survivors. J Clin Oncol. 2012 Mar 12. [Epub ahead of print]. Baracos VE, Mazurak VC, Ma DW. n-3 Polyunsaturated fatty acids throughout the cancer trajectory: influence on disease incidence, progression, response to therapy and cancer-associated cachexia. Nutr Res Rev. 2004 Dec;17(2):177-92. Bougnoux P, Hajjaji N, Maheo K, Couet C, Chevalier S. Fatty acids and breast cancer: sensitization to treatments and prevention of metastatic re-growth. Prog Lipid Res. 2010 Jan;49(1):76-86. Epub 2009 Aug 26. Review. Goodstine SL, Zheng T, Holford TR, Ward BA, Carter D, Owens PH, Mayne ST. Dietary (n-3)/(n-6) fatty acid ratio: possible relationship to premenopausal but not postmenopausal breast cancer risk in U.S. women. J Nutr. 2003 May;133(5):1409-14. Kuriki K, Hirose K, Wakai K, Matsuo K, Ito H, Suzuki T, Hiraki A, Saito T, Iwata H, Tatematsu M, Tajima K. Breast cancer risk and erythrocyte compositions of n-3 highly unsaturated fatty acids in Japanese. Int J Cancer. 2007 Jul 15;121(2):377-85. Maillard V, Bougnoux P, Ferrari P, Jourdan ML, Pinault M, Lavillonniere F, Body G, Le Floch O, Chajès V, Torres-Mejía G, Biessy C, Ortega-Olvera C, Angeles-Llerenas A, Ferrari P, Lazcano-Ponce E, Romieu I. ω-3 and ω-6 Polyunsaturated fatty acid intakes and the risk of breast cancer in Mexican women: impact of obesity status. Cancer Epidemiol Biomarkers Prev. 2012 Feb;21(2):319-26. Epub 2011 Dec 22. doi:10.1158/1055-9965. Chajes V. N-3 and N-6 fatty acids in breast adipose tissue and relative risk of breast cancer in a case-control study in Tours, France. Int J Cancer. 2002 Mar 1;98(1):78-83. Saadatian-Elahi M, Toniolo P, Ferrari P, Goudable J, Akhmedkhanov A, Zeleniuch-Jacquotte A, Riboli E. Serum fatty acids and risk of breast cancer in a nested case-control study of the New York University Women's Health Study. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1353-60. Sala-Vila A, Calder PC. Update on the relationship of fish intake with prostate, breast, and colorectal cancers. Crit Rev Food Sci Nutr. 2011 Oct-Nov;51(9):855-71. Review. Shannon J, King IB, Moshofsky R, Lampe JW, Gao DL, Ray RM, Thomas DB.Erythrocyte fatty acids and breast cancer risk: a case-control study in Shanghai, China.Am J Clin Nutr. 2007 Apr;85(4):1090-7. Signori C, El-Bayoumy K, Russo J, Thompson HJ, Richie JP, Hartman TJ, Manni A. Chemoprevention of breast cancer by fish oil in preclinical models: trials and tribulations. Cancer Res. 2011 Oct 1;71(19):6091-6. Epub 2011 Sep 20. Review. Sonestedt E, Ericson U, Gullberg B, Skog K, Olsson H, Wirfält E. Do both heterocyclic amines and omega-6 polyunsaturated fatty acids contribute to the incidence of breast cancer in postmenopausal women of the Malmö diet and cancer cohort? Int J Cancer. 2008 Oct 1;123(7):1637-43. Spencer L, Mann C, Metcalfe M, Webb M, Pollard C, Spencer D, Berry D, Steward W, Dennison A. The effect of omega-3 FAs on tumour angiogenesis and their therapeutic potential. Eur J Cancer. 2009 Aug;45(12):2077-86. Epub 2009 Jun 1. Review. Thiébaut AC, Chajès V, Gerber M, Boutron-Ruault MC, Joulin V, Lenoir G, Berrino F, Riboli E, Bénichou J, Clavel-Chapelon F. Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer. Int J Cancer. 2009 Feb 15;124(4):924-31. Wendel M, Heller AR. Anticancer actions of omega-3 fatty acids--current state and future perspectives. Anticancer Agents Med Chem. 2009 May;9(4):457-70. Review.
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Pediatrics 2012 Aug; 130:228.
R Ratings for Movies with Smoking?
Smoking in PG-13 movies was as strongly linked to onset of youth smoking as smoking in R-rated films.
The 2012 Surgeon General's Report concludes that a causal relation exists between exposure to smoking in movies and initiation of smoking in youth, but does the portrayal of smoking alone or the context in which it occurs underlie the association? Investigators examined this question using data from a longitudinal cohort study of 6522 adolescents (age range, 10–14 years) recruited in 2003 and surveyed every 8 months for 2 years (JW Pediatr Adolesc Med Apr 4 2012).
Exposure to smoking in the movies was determined by calculating the number of times a character handled or used tobacco or tobacco use was depicted in the background of movies that adolescents reported to have seen from a random sample of the top 100 U.S. box office hits. The median movie smoking exposure from PG-13 movies was nearly three times higher than in R-rated movies (275 vs. 93 occurrences) because of the higher viewership of PG-13 movies. However, the adjusted hazard ratios for onset of smoking for every 500 occurrences of smoking exposure were comparable for PG-13 and R-rated movies (adjusted hazard ratio, 1.49 vs. 1.33; P=0.458).
Comment: These results support the conclusion that exposure to smoking itself in movies rather than other characteristics of R-rated movies (e.g., alcohol and other drug use or sexual content) underlies the link between smoking in movies and initiation of smoking among youth. The authors estimate that assigning an R rating to all movies with smoking could reduce adolescent smoking onset by 20%. This change in ratings might motivate production companies to eliminate smoking from films they market primarily to youth audiences.
— Alain Joffe, MD, MPH, FAAP Published in Journal Watch Pediatrics and Adolescent Medicine August 22, 2012
Citation(s): Sargent JD et al. Influence of motion picture rating on adolescent response to movie smoking. Pediatrics 2012 Aug; 130:228.
http://www.ncbi.nlm.nih.gov/pubmed/22778305?dopt=Abstract
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MM: Here is an example of an annoying side effect (dry, hacking cough) that will frequently preclude treatment with a medication that may actually confer some benefit. As pharmacists, we are taught that if the coughing from these medications is not too annoying, then continue with the use of the drug. I always felt that advice was an excuse to justify an earlier treatment plan. Now, it appears that there may be more to that approach.
BMJ 2012 Jul 11; 345:e4260
ACE Inhibitor Use Lowers Risks for Pneumonia
A meta-analysis showed that angiotensin-converting–enzyme inhibitors, but not angiotensin-receptor blockers, lowered risk.
Many patients (as many as one third) who take angiotensin-converting–enzyme (ACE) inhibitors develop coughs. However, an enhanced cough reflex might lower risk for pneumonia. In this meta-analysis of 37 studies (18 randomized trials, 11 cohort studies, and 8 case-control studies), investigators evaluated the association between use of ACE inhibitors or angiotensin-receptor blockers (ARBs) and risk for pneumonia.
Overall, use of ACE inhibitors was associated with a significant 34% lower risk for pneumonia compared with no use of ACE inhibitors and a significant 30% lower risk for pneumonia compared with ARB use. Subgroup analyses of patients with stroke or heart failure yielded similar results. Finally, use of ACE inhibitors compared with no use was associated with a significant 27% lower risk for pneumonia-related death.
Comment: In this study, ACE inhibitor use was associated with attenuation of risks for pneumonia and pneumonia-related death. The authors suggest that "patients taking ACE inhibitors who develop cough should, providing that cough is tolerable, persist with treatment." Although this suggestion is reasonable (especially because ACE inhibitors confer considerable cardiovascular benefit), many patients with ACE inhibitor–related cough find this side effect too annoying or disruptive to continue taking the drug.
— Paul S. Mueller, MD, MPH, FACP Published in Journal Watch General Medicine August 2, 2012
Citation(s): Caldeira D et al. Risk of pneumonia associated with use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers: Systematic review and meta-analysis. BMJ 2012 Jul 11; 345:e4260.
(http://dx.doi.org/10.1136/bmj.e4260)
http://www.ncbi.nlm.nih.gov/pubmed/22786934?dopt=Abstract
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MM: I think that the government has already stuck its head into our business more that it should but I find it interesting that a population as large and diverse as that of NYC could be affected to such an extent in its purchasing habits as what appears to have happened here. Would policies rather than laws have the same degree of effect? Its worth investigating further.
Ann Intern Med 2012 Jul 17; 157:81
Trans Fat Content of Fast-Food Purchases in New York City Has Declined
A 2008 regulation affected what fast-food consumers eat.
Ingestion of trans fats is associated strongly with cardiovascular disease. In 2008, New York City restricted use of partially hydrogenated vegetable oils, a major contributor to dietary trans fat, in restaurants. In a cross-sectional study, which was conducted before and after implementation of the regulation, researchers assessed how this regulation affected trans fat and saturated fat contents in almost 15000 fast-food purchases.
From 2007 to 2009, mean trans fat content per purchase decreased from 2.9 g to 0.5 g. The greatest decline in trans fat content was found in hamburger chain restaurants, and the smallest decline was seen in fried chicken chain restaurants. Although mean saturated fat content per purchase increased slightly, mean trans plus saturated fat decreased by 1.9 g.
Comment: Through regulation, New York City significantly lowered the trans fat content of fast food. To achieve similar results nationwide, federal regulation would be required.
— Jamaluddin Moloo, MD, MPH Published in Journal Watch General Medicine August 21, 2012
Citation(s): Angell SY et al. Change in trans fatty acid content of fast-food purchases associated with New York City's restaurant regulation: A pre–post study. Ann Intern Med 2012 Jul 17; 157:81.
(http://annals.org/article.aspx?volume=157&page=81)
http://www.ncbi.nlm.nih.gov/pubmed/22801670?dopt=Abstract
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