DRUG UPDATES

  Cardiovascular Risks with Anti-Inflammatory Drugs (BMJ. 2011 Jan 11;342:c7086. doi: 10.1136/bmj.c7086.)

Abstract: DATA SOURCES: Bibliographic databases, conference proceedings, study registers, the Food and Drug Administration website, reference lists of relevant articles, and reports citing relevant articles through the Science Citation Index (last update July 2009). Manufacturers of celecoxib and lumiracoxib provided additional data.

DATA SYNTHESIS: 31 trials in 116?429 patients with more than 115?000 patient years of follow-up were included. Patients were allocated to naproxen, ibuprofen, diclofenac, celecoxib, etoricoxib, rofecoxib, lumiracoxib, or placebo. Compared with placebo, rofecoxib was associated with the highest risk of myocardial infarction (rate ratio 2.12, 95% credibility interval 1.26 to 3.56), followed by lumiracoxib (2.00, 0.71 to 6.21). Ibuprofen was associated with the highest risk of stroke (3.36, 1.00 to 11.6), followed by diclofenac (2.86, 1.09 to 8.36). Etoricoxib (4.07, 1.23 to 15.7) and diclofenac (3.98, 1.48 to 12.7) were associated with the highest risk of cardiovascular death.

CONCLUSIONS: Although uncertainty remains, little evidence exists to suggest that any of the investigated drugs are safe in cardiovascular terms. Naproxen seemed least harmful. Cardiovascular risk needs to be taken into account when prescribing any non-steroidal anti-inflammatory drug. PMID: 21224324

Toxicity of Antineoplastic Drugs (Medscape: Hazardous Drugs in Healthcare, Thomas H. Connor, PhD, Posted: 03/07/201)

The toxicity of antineoplastic drugs in patients has been well-known since their introduction in the 1940s and 1950s.^[1] Because most antineoplastic medications have nonselective mechanisms of action, these agents affect noncancerous cells as well as cancerous cells, resulting in numerous adverse effects. When secondary cancers began to develop in patients treated with these drugs, concern was raised that healthcare workers also could be at risk for harmful effects from antineoplastic agents as a result of occupational exposure.^[2]

FDA Approves New Drug for Melonma (Webmd)

Yervoy is a biologic therapy. It’s a kind of man-made antibody (a monoclonal antibody) that blocks a crucial switch on immune cells called CTLA-4. Cancers use this switch to turn off the body’s anticancer immune responses.

Most drugs like this come with possibly severe side effects, and Yervoy is no exception. The drug can provoke powerful autoimmune reactions in which the immune system attacks normal cells in the body. In clinical trials, nearly 13% of patients taking Yervoy had severe or fatal autoimmune reactions.

Common side effects resulting from such autoimmune reactions linked to Yervoy include fatigue, diarrhea, skin rash, hormone deficiencies, and colitis (inflammation of the intestines).

NUTRIGENOMICS

Krill Oil Effects Brain Signals In Obese Subjects (Nutrition and Metabolism)

Notes: Endocannabinioids effect appetiate, pain, mood and memory.

We have previously shown that krill oil (KO), more efficiently than fish oil, was able to downregulate the endocannabinoid system in different tissues of obese zucker rats.

We therefore aimed at investigating whether an intake of 2 g/d of either KO or menhaden oil (MO), which provides 309 mg/d of EPA/DHA 2:1 and 390 mg/d of EPA/DHA 1:1 respectively, or olive oil (OO) for four weeks, is able to modify plasma endocannabinoids in overweight and obese subjects. The results confirmed data in the literature describing increased levels of endocannabinoids in overweight and obese with respect to normo-weight subjects. KO, but not MO or OO, was able to significantly decrease 2-arachidonoylglycerol (2-AG), although only in obese subjects. In addition, the decrease of 2-AG was correlated to the plasma n-6/n-3 phospholipid long chain polyunsaturated fatty acid (LCPUFA) ratio. These data show for the first time in humans that relatively low doses of LCPUFA n-3 as KO can significantly decrease plasma 2-AG levels in obese subjects in relation to decrease of plasma phospholipid n-6/n-3 LCPUFA ratio. This effect is not linked to changes of metabolic syndrome parameters but is most likely due to a decrease of 2-AG biosynthesis caused by the replacement of 2-AG ultimate precursor, arachidonic acid, with n-3 PUFAs, as previously described in obese Zucker rats.

Cocoa and Chocolate for Heart Health (VitalChoice)

Eating dark chocolate exerted beneficial influences over the enzyme targeted by blood pressure drugs, called angiotensin-converting enzyme or ACE. Confirming that this effect on genes that control ACE had a practical impact, dark chocolate also lowered blood pressure in the people participating in the clinical portion of the study. And in the test tube portion of the new study, cocoa polyphenols raised levels of nitric oxide (NO) in human endothelial cells – an effect that usually causes arteries to relax and dilate. Interestingly, the degree of inhibition of the AC enzyme depended on the volunteers’ individual “genotype” or genetic profile. People can have one of three genotypes related to angiotensin-converting enzyme ACE, called D/D, I/D, and I/I, distributed about equally across the human population. Three hours after consuming dark chocolate, ACE was inhibited by 21 percent in people with the I/I genotype, and by 28 percent in people with the D/D genotype.

HEALTH

Lavender Essential Oil is Antifungal (Science Daily)

Scientists from the University of Coimbra in Portugal distilled lavender oil from the Lavandula viridis L’Hér shrub that grows in southern Portugal. The oil was tested against a range of pathogenic fungi and was found to be lethal to a range of skin-pathogenic strains, known as dermatophytes, as well as various species of Candida. Dermatophytes cause infections of the skin, hair and nails as they use the keratin within these tissues to obtain nutrients. They are responsible for conditions such as Athletes’ foot, ringworm and can also lead to scalp and nail infections. Candida species coexist with most healthy individuals without causing problems but may cause mucocutaneous candidosis — or thrush — in some people. In immunocompromised patients, Candida species are able to cause serious infection if the fungal cells escape into the blood stream.

Help for Migraines (Ultrawellness)

Worse, migraines are hard to treat and very difficult to prevent with conventional approaches. There are a host of preventive drugs — calcium channel blockers, beta-blockers, anti-seizure medications, antidepressants, and more –which work poorly, if at all, and are accompanied by frequent side effects. Some doctors are now even using Botox to paralyze neck muscles in the hopes of easing migraines. There is also a new class of medication called triptans (like Imitrex, Maxalt, and Zomig) that can stop a migraine once it starts. Though these have made migraine sufferers handle the attacks better, they also have serious potential side effects, including strokes, and are expensive. Still other treatments can lead to addiction or dependence. Not a pretty picture. And for many, none of these treatments work very well or at all. The problem with migraines is the same one we see so often in medicine: We treat the symptoms, not the cause. We only deal with the effects of something and not the underlying 7 keys to UltraWellness. But using Functional Medicine I have been able to get nearly 100 percent of my patients migraine free within days to weeks!

More Research on Bad Brain Effects & Cell Phones (JAMA. 2011 Feb 23;305(8):808-13.)

It seems that more cell use brings more glucose to the brain, creating more opportunity for inflammation and free radical damage. This could be a biochemical mechanism for a link with brain tumors and cell phones. Cancer thrives on glucose.

Abstract CONTEXT: The dramatic increase in use of cellular telephones has generated concern about possible negative effects of radiofrequency signals delivered to the brain. However, whether acute cell phone exposure affects the human brain is unclear.

OBJECTIVE: To evaluate if acute cell phone exposure affects brain glucose metabolism, a marker of brain activity. DESIGN, SETTING, AND PARTICIPANTS: Randomized crossover study conducted between January 1 and December 31, 2009, at a single US laboratory among 47 healthy participants recruited from the community. Cell phones were placed on the left and right ears and positron emission tomography with ((18)F)fluorodeoxyglucose injection was used to measure brain glucose metabolism twice, once with the right cell phone activated (sound muted) for 50 minutes (“on” condition) and once with both cell phones deactivated (“off” condition). Statistical parametric mapping was used to compare metabolism between on and off conditions using paired t tests, and Pearson linear correlations were used to verify the association of metabolism and estimated amplitude of radiofrequency-modulated electromagnetic waves emitted by the cell phone. Clusters with at least 1000 voxels (volume >8 cm(3)) and P < .05 (corrected for multiple comparisons) were considered significant. CONCLUSIONS: In healthy participants and compared with no exposure, 50-minute cell phone exposure was associated with increased brain glucose metabolism in the region closest to the antenna. This finding is of unknown clinical significance. PMID: 21343580 [PubMed – indexed for MEDLINE]

Why Soda is Addictive (Neuroimage. 2008 Feb 15;39(4):1559-69. Epub 2007 Nov 19.) It seems that artificial sweetners don’t stimulate the dopamine (reward center) of the brain as strongly as sucrose, making you feel not as satified and wanting more.

Abstract: Animal models suggest that sucrose activates taste afferents differently than non-caloric sweeteners. Little information exists how artificial sweeteners engage central taste pathways in the human brain. We assessed sucrose and sucralose taste pleasantness across a concentration gradient in 12 healthy control women and applied 10% sucrose and matched sucralose during functional magnet resonance imaging. The results indicate that (1) both sucrose and sucralose activate functionally connected primary taste pathways; (2) taste pleasantness predicts left insula response; (3) sucrose elicits a stronger brain response in the anterior insula, frontal operculum, striatum and anterior cingulate, compared to sucralose; (4) only sucrose, but not sucralose, stimulation engages dopaminergic midbrain areas in relation to the behavioral pleasantness response. Thus, brain response distinguishes the caloric from the non-caloric sweetener, although the conscious mind could not. This could have important implications on how effective artificial sweeteners are in their ability to substitute sugar intake. PMID: 18096409

The Dangers of Gluten (Ultrawellness)

A recent large study in the Journal of the American Medical Association found that people with diagnosed, undiagnosed, and “latent” celiac disease or gluten sensitivity had a higher risk of death, mostly from heart disease and cancer. (i) This study looked at almost 30,00 patients from 1969 to 2008 and examined deaths in three groups: Those with full-blown celiac disease, those with inflammation of their intestine but not full-blown celiac disease, and those with latent celiac disease or gluten sensitivity (elevated gluten antibodies but negative intestinal biopsy). The findings were dramatic. There was a 39 percent increased risk of death in those with celiac disease, 72 percent increased risk in those with gut inflammation related to gluten, and 35 percent increased risk in those with gluten sensitivity but no celiac disease.

This is ground-breaking research that proves you don’t have to have full-blown celiac disease with a positive intestinal biopsy (which is what conventional thinking tells us) to have serious health problems and complications–even death–from eating gluten. Yet an estimated 99 percent of people who have a problem with eating gluten don’t even know it. They ascribe their ill health or symptoms to something else–not gluten sensitivity, which is 100 percent curable.

Gluten Sensitivity: One Cause, Many Diseases: A review paper in The New England Journal of Medicine listed 55 “diseases” that can be caused by eating gluten. (iv) These include osteoporosis, irritable bowel disease, inflammatory bowel disease, anemia, cancer, fatigue, canker sores, (v) and rheumatoid arthritis, lupus, multiple sclerosis, and almost all other autoimmune diseases. Gluten is also linked to many psychiatric (vi) and neurological diseases, including anxiety, depression, (vii) schizophrenia, (viii) dementia, (ix) migraines, epilepsy, and neuropathy (nerve damage). (x) It has also been linked to autism.(ix)

Healthy Bones Mean Skinner Bodies (BetterBones Osteoblast)

As it turns out, our skeletons aren’t simply the support structure for movement — they’re also endocrine organs, and they produce at least two hormones. One of these bone hormones, osteocalcin, signals the body to enhance insulin production and sensitivity, and to reduce intra-abdominal fat. To make a long story short, healthy bones undergoing normal bone turnover produce osteocalcin, which helps keep blood sugar and insulin sensitivity at normal, healthy levels while simultaneously reducing fat stores — and that helps lower your risk of obesity and related diseases, including diabetes. Researchers have found, in fact, that many people with Type 2 diabetes also have low osteocalcin levels,4 and it’s been suggested that helping people with diabetes to produce more osteocalcin could become a way of improving their health

Columbia News publishes findings on bone health and blood sugar:

The researchers found that osteocalcin, a protein made only by bone-forming cells (osteoblasts), was not a mere structural protein, but rather a hormone with totally unanticipated and crucial functions. Osteocalcin directs the pancreas’ beta cells, which produce the body’s supply of insulin, to produce more insulin. At the same time, osteocalcin directs fat cells to release a hormone called adiponectin, which improves insulin sensitivity. This discovery showed for the first time that one hormone has a synergistic function in regulating insulin secretion and insulin sensitivity, and that this coordinating signal comes from the skeleton. Additionally, osteocalcin enhances the production of insulin-producing beta cells, which is considered one of the best, but currently unattainable, strategies to treat diabetes.

Pop & Pounds (Dr. Mercola)

Here’s how Dr. Ralston and a colleague explain the basics in a review paper published last year (Ralston NV, Raymond LJ 2010). We’ve broken out the key points in this bulleted list:

• Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity.
• Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets.
• Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms.
• It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues.
• Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity.
• Because Hg’s binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis.
• This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm.
• However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern.

Arsenic in Our Playgrounds? (Orion Magazine)

That is, until I discovered that, like many of its kind, the school’s beloved play structure?—with its wooden gangway, turrets, and tunnels?—was made out of pressure-treated lumber, which, at the time, contained arsenic, a carcinogen. A bladder carcinogen, in fact. I am a bladder cancer survivor. I am familiar with this particular disease and all the ongoing medical surveillance it requires. So, after a lot of research and discussion, we eventually decided to move our daughter to a different nursery school. The risk of doing nothing just seemed too high. 

There seem to be four big lessons arising from the frontiers of pediatric neurotoxicology. The first is that the developing brain is more vulnerable than the adult brain, and the timing of exposure can determine whether and how severe the damage might be. ..

The second lesson is that neurotoxicants can act in concert with each other. Prenatal exposure to lead contributes to the risk of ADHD, as does exposure to tobacco smoke. Both together, however, create a higher risk than either one alone. These findings indicate that neurotoxicants need to be regulated as a group rather than one by one.

The third is that elements of a child’s social and nutritional environment can also be toxic to the development of cognition and can magnify the effects of exposure to chemical toxicants. Poverty and family stress are particularly detrimental. Attention deficit disorder is more prevalent among poor children, as are learning disabilities…

And fourth, maybe not surprisingly, is that the chemicals designed to act as neurological poisons?—?the organophosphate pesticides?—?truly do so. And at levels common among children. Frequently used in fruit and vegetable farming, organophosphate insecticides kill by attacking the nervous systems of insect pests. They have the same effect in humans: organophosphates interfere with the recycling of the neurotransmitter acetylcholine, one of the messaging signals that flow between neurons. Mounting evidence collected among various populations of children?—?