Most “super” supermoon of 2013 on June 22-23.

Full moon falls on June 23, 2013 at 11:32 UTC (6:32 a.m. CDT in the U.S.). Thus, for many, the moon appears about as full in the June 22 evening sky as it does on the evening of June 23. This full moon is not only the closest and largest full moon of the year. It also presents the moon’s closest encounter with Earth for all of 2013. The moon will not be so close again until August, 2014. In other words, it’s not just a supermoon. It’s the closest supermoon of 2013.


At United States’ time zones, the moon will turn full on June 23 at 7:32 a.m. EDT, 6:32 a.m. CDT, 5:32 a.m. MDT and 4:32 a.m. PDT.

We astronomers call this sort of close full moon a perigee full moon. The word perigeedescribes the moon’s closest point to Earth for a given month. Two years ago, when the closest and largest full moon fell on March 19, 2011, many used the term supermoon, which we’d never heard before. Last year, we heard this term again to describe the year’s closest full moon on May 6, 2012. Now the term supermoon is being used a lot. Last month’s full moon – May 24-25, 2013 – was also a supermoon. But the June full moon is even more super! In other words, the time of full moon falls even closer to the time of perigee, the moon’s closest point to Earth. The crest of the moon’s full phase in June 2013, and perigee, fall within an hour of each other.


What is a supermoon? The word supermoon didn’t come from astronomy. Instead, it came from astrology. Astrologer Richard Nolle of the website takes credit for coining the term supermoon. In 1979, he defined it as:

…a new or full moon which occurs with the moon at or near (within 90% of) its closest approach to Earth in a given orbit (perigee). In short, Earth, moon and sun are all in a line, with moon in its nearest approach to Earth.

By this definition, according to Nolle:

There are 4-6 supermoons a year on average.

That doesn’t sound very special, does it? In fact, the June 2013 full moon lines up much more closely with perigee – the moon’s closest point to Earth – than Nolle’s original definition. According to Guy Ottewell’s Astronomical Calendar 2013, the 2013 June full moon falls only 22 minutes after the moon reaches perigee, the moon’s closest point to Earth for this month and year. At perigee, the moon lies only 356,991 kilometers (221,824 miles) away. Two weeks later, on July 7, the moon will swing out to apogee – its farthest point for the month and year – at 406,490 kilometers (252,581 miles) distant.

How super is this supermoon? June 2013 presents the moon’s closest encounter with Earth until August 10, 2014, at which time the moon will be a scant 5 kilometers closer to Earth. The full moon will come even closer to Earth on September 28, 2015 (356,877 kilometers) and closer yet on November 14, 2016 (356,509 kilometers). November 2016 will feature the closest full moon until November 25, 2034! Maybe this helps you see that supermoons – while interesting – are fairly routine astronomical events.

Even the proximity of full moon with perigee isn’t all that rare. The extra-close moon in all of these years – 2011, 2012, 2013, 2014, 2015 and 2016 – finds the full moon taking place at or nearly the same hour as lunar perigee. More often than not, the closest perigee of the year comes on the one day of the year that the full moon and perigee most closely coincide. (See table below.)

Moon closest to Earth





March 19

356,575 km


May 6

356,955 km


June 23

356,991 km


August 10

356,896 km


September 28

356,877 km


November 14

356,509 km

How often is moon both full and closest to Earth? Closest full moons recur in cycles of 14 lunar (synodic) months, because 14 lunar months almost exactly equal 15 returns to perigee (moon’s closest point to Earth). A lunar month refers to the time period between successive full moons, a mean period of 29.53059 days. An anomalistic month refers to successive returns to perigee, a period of 27.55455 days. Hence:

14 x 29.53059 days = 413.428 days
15 x 27.55455 days = 413.318 days

This time period is equal to about 1 year, 1 month, and 18 days. The full moon and perigee will realign again on August 10, 2014, because the 14th full moon after the 2013 June 23 full moon will fall on that date.

Looking further into the future, the perigee full moon will come closer than 356,500 kilometers for the first time in the 21st century on November 25, 2034 (356,446 km). The closest full moon of the 21st century will fall on December 6, 2052 (356,425 km).

For the moon to come closer than 356,400 kilometers (221,457 miles) is quite a feat. In fact, this won’t happen at all in the 21st century (2001-2100) or the 22nd century (2101-2200). The last time the full moon perigee swung this close to Earth was on January 14, 1930 (356,397 km), and the next time won’t be till January 1, 2257 (356,371 km).

Will the tides be higher than usual? Yes, all full moons bring higher-than-usual tides, and perigee full moons bring the highest (and lowest) tides of all. Each month, on the day of the full moon, the moon, Earth and sun are aligned, with Earth in between. This line up creates wide-ranging tides, known as spring tides. High spring tides climb up especially high, and on the same day low tides plunge especially low.

Today’s extra-close full moon accentuates these monthly (full moon) spring tides all the more.

If you live along a coastline, watch for high tides caused by the June 23 perigee full moon – or supermoon – over the next several days. Will the high tides cause flooding? Probably not, unless a strong weather system moves into the coastline where you are. Still, keep an eye on the weather, because storms do have a large potential to accentuate high spring tides.

As a result, if you live near a coast, you’ll want to be on the lookout for higher-than-usual tides.

Because the moon – as always – shines opposite the sun in our sky at full moon, you’ll see the moon beaming all night tonight from dusk until dawn. This extra-close full moon is likely to usher in large tides along the ocean shorelines for the next several days, especially if these high tides are accompanied by strong onshore winds.

Bottom line: The full moon of June 22-23, 2013 is the closest and largest full moon of this year. By a new definition – one that has just entered the world of astronomy from astrology – many will call it a supermoon. There are three full moons in 2013 that meet the definition of a supermoon – May, June and July. But this June 22-23 full moon is the most super of the supermoons! A super-duper moon!



Atlantic Ocean to Disappear in 200 Million Years?

Europe and North America could be joined, creating new mountain chains.

A newly discovered crack in the Earth’s crust could pull North America and Europe together and cause the Atlantic Ocean to vanish in about 220 million years, scientists say.


A new map of the seafloor off the coast of Iberia—the region of Europe that includes Portugal and Spain—has revealed what could be the birth of a new subduction zone.

Subduction zones happen when tectonic plates—the large rock slabs that make up the Earth’s crust—crash into one another. The edge of the heavier plate slides, or subducts, below the lighter plate. It then melts back into the Earth’s mantle—the layer just below the crust.

The discovery of this new subduction zone, published on June 6 in the journalGeology, could signal the start of an extended cycle that fuses continents together into a single landmass—or “supercontinent”—and closes our oceans.

This breakup and reformation of supercontinents has happened at least three times during Earth’s approximately four-billion-year history.

In the far future, Earth’s continents could “look very much like the Pangea,” said study first author João Duarte, referring to a supercontinent that existed about 200 million years ago.

So what’s new? The newly discovered subduction zone is located in the Atlantic Ocean about 120 miles (200 kilometers) off the southwest coast of Portugal. It is made up of six distinct segments that together span a distance of about 186 miles (300 kilometers).

The subduction zone is actually a newly formed crack in the Eurasian plate—one of about a dozen tectonic plates that make up the Earth’s crust. The Eurasian plate contains all of Europe and most of Asia.

“In this case, the Eurasia plate is breaking in two,” said Duarte, a geoscientist at the University of Monash in Australia.

Why is it important? Scientists have long suspected that a new subduction zone was forming near the western margin of the Eurasian plate, off the coast of Portugal.

Part of the reason is that the region has been the site of significant earthquake activity, including an 8.7-magnitude quake in 1755 that devastated Lisbon.

Over the past 20 years, several scientific teams from different countries have launched research cruises to map the seafloor around the region to look for proof that a new subduction zone was forming.

As part of his research project while at the University of Lisbon, Duarte gathered together the data from all of the different mapping projects and combined them to create a new tectonic map of the seafloor off the coast of Portugal.

The updated map provided the first conclusive proof that the ocean floor off the coast of Iberia is indeed beginning to fracture, and that a new subduction zone is starting to form.

“It is not a fully developed subduction, but an embryonic one,” Duarte said.

What does this mean? The evidence collected by Duarte’s team indicate that the Eurasia plate could eventually split into separate oceanic and continental sections.

If this happens, the oceanic section—which is made of denser rock—will dive beneath the continental section. This will cause the Atlantic Ocean to shrink and pull North America and Iberia closer together.

Other studies have indicated that geologic activity in the region could also pullAfrica and Iberia together, causing the Mediterranean Sea to vanish.

“Eventually North America and Iberia will be together again, and the collision will give origin to new mountain chains like the Himalaya,” Duarte said.

What’s next? Scientists will continue to study the nascent subduction zone because it could help answer a long-lasting mystery: How do oceans—especially ones like the Atlantic that have “passive” margins that are free of fractures—start to close?

“For the first time we are seeing a [passive] Atlantic margin turn into a Pacific one,” for which subduction zones are common, Duarte said.

His team plans to continue collecting data about the crust and seafloor in the region to further investigate the subduction zone. They are also developing computer and physical models of the subduction process and plate motions.

“Understanding these processes will certainly provide new insights on how subduction zones may have initiated in the past and how oceans start to close,” Duarte said in a statement.

Source: NGC

60 Years of Research Links Gluten Grains to Schizophrenia.

Story at-a-glance

  • Research spanning 60 years shows gluten grain consumption leads to higher prevalence of both neurological and psychiatric problems, and schizophrenia in particular
  • In a recent study, researchers compared the blood work of 950 schizophrenics with 1,000 healthy controls. The odds ratio of having anti-gliadin IgG antibodies was 2.13 times higher in schizophrenics, indicating that t the least schizophrenics are more likely to experience an adverse immune response to wheat proteins
  • The discovery of antibodies to gliadin in the blood of both celiac disease patients and schizophrenics implies that the wheat protein gliadin does not break down during digestion, wheat proteins stimulate auto-immunity, and may cause your immune system to attack your nervous system
  • gluten

Does the consumption of gluten-containing grains contribute to psychiatric disorders such as schizophrenia?

Believe it or not, this question has been asked for well over 60 years by researchers who stumbled upon evidence that the removal of gluten from the diet results in improved symptoms, or conversely, that gluten grain consumption leads to higher prevalence of both neurological and psychiatric problems.

Reports of the resolution of emotional disturbances after the institution of a “gluten free” diet exist in medical literature at least as far back as 1951.1

In 1954, Sleisenger reported to have found three schizophrenics among a group of thirty-two adults with celiac disease,2 and in 1957, Bossak, Wang and Aldersberg reported discovering 5 psychotic patients among 94 patients with celiac disease.3

The initial recognition that celiac disease, or at least gluten sensitivity, occurred at a far higher prevalence among schizophrenics than the healthy, opened up the door to more elaborate investigations.

Wartime Reduction in Gluten Grain Rations Reduces Schizophrenia Prevalence

For instance, in 1966, a remarkable epidemiological study was published in The American Journal of Clinical Nutrition titled,”Wheat “Consumption” and Hospital Admissions for Schizophrenia During World War II,” which sought to confirm the possible relationship between schizophrenia and celiac disease by investigating the reported decrease in the number of admissions to mental hospitals during some wars.

The author of the study, F. C. Dohan, M.D., looked at the number of women admitted to the mental hospitals in Finland, Norway, Sweden, Canada and the United States before and after World War II. These figures were then compared to volume of wheat and rye consumed during those two periods. As Dohan explains:

“The percent change in the mean annual number of first admissions for schizophrenia to the hospital in each of the five countries from the respective pre-war mean was compared to the percent change in the “consumption” of wheat and wheat plus rye.”

The results can be view in the figure below:

As you can see above, the percent change from prewar values during World War II in the number of patients admitted to hospitals for the first time with schizophrenia in five countries was found to be significantly correlated to the percent change in the amount of wheat and wheat plus rye consumed. As gluten grain rations decreased, so did the worldwide rate of first-time admission to psychiatric institutions.

Increasing Body of Research Implicates Gluten Grains in Schizophrenia Pathogenesis

Since then, a number of studies have been published linking the consumption of gluten-containing grains to schizophrenia:

  • Schizophrenia Bulletin, 2011: Persons with schizophrenia have higher than expected titers of antibodies (7 fold increased prevalence) related to celiac disease and gluten sensitivity.4
  • Schizophrenia Research, 2010: Individual with schizophrenia have a novel immune response to gliadin distinct from those with celiac disease (i.e. absence of antibodies to the transglutaminase enzyme and the HLA-DQ2/DQ8 genetic locus of susceptibility.5
  • Acta Psychiatra Scandinavica, 2006: A review of the literature found a drastic reduction, if not full remission, of schizophrenic symptoms after initiation of gluten withdrawal has been noted in a variety of studies.6
  • Biological Psychiatry, 1984: Only two chronic schizophrenics were found among over 65,000 examined or closely observed adults in remote regions of Papua New Guinea (PNG, 1950-1967) and Malaita , Solomon Islands (1980-1981), and on Yap , Micronesia (1947-1948), who do not consume grains. Researchers noted that when these peoples became partially westernized and consumed wheat, barley beer, and rice, the prevalence reached European levels.7
  • Science, 1976: Schizophrenics maintained on a grain-free and milk-free diet challenged with gluten saw interruption of their therapeutic progress. After termination of the gluten challenge, the course of improvement was reinstated.8

New Research Confirms Gliadin-Schizophrenia Link

The latest study to confirm the gluten-schizophrenia link was published this month in the World Journal of Biological Psychiatryand titled, “Elevated gliadin antibody levels in individuals with schizophrenia.” Researchers compared the blood work of 950 schizophrenics with 1,000 healthy controls. They discovered that the odds ratio of having anti-gliadin IgG antibodies was 2.13 times higher in schizophrenics, indicating that t the least schizophrenics are more likely to experience an adverse immune response to wheat proteins.

Gliadin is the alcohol soluble complex of proteins found within what is known colloquially as gluten (the term is misleading aswheat technically contains over 23,000 different proteins, not one), and is considered the primary immunotoxic class of proteins in wheat. For instance, in celiac disease, a genetically mediated immune process unfurls where upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction that results in the destruction of the intestinal villi.

The discovery of antibodies to gliadin in the blood of both celiac disease patients and schizophrenics implies several things:

  • The Wheat Protein Gliadin Doesn’t Break Down During Digestion: Undigested wheat-derived macromolecules can act as antigens, provoking an antibody-mediated immune response, particularly if they get through the intestinal lining and into the blood. The fact that antibodies to wheat protein gliadin can be found in the blood indicates that it is not being fully broken down into constituent amino acids.
  • Wheat Proteins In the Blood Stimulate Auto-Immunity: The presence of gliadin in the blood also indicates intestinal permeability. It turns out that gliadin has been found to up-regulate the protein zonulin in the gut of those either with orwithout celiac disease, which essentially opens “pandora’s box” of intestinal permeability, and subsequent autoimmunity. In another essay, we also described the intestinal permeability generating effects of wheat lectin, also known as Wheat Germ Agglutinin (WGA) – [see Opening Pandora’s Bread Box]
  • Wheat Protein May Cause The Immune System To Attack the Nervous System: Anti-gliadin antibodies appear to cross react with neurological self-structures, which may explain how they contribute to schizophrenia. A study published in 2007 in the Journal of Immunology found that anti-gliadin antibodies bind to neuronal synapsin I, a protein found within nerve terminal of axons, which the study authors believe may explain why gliadin contributes to “neurologic complications such as neuropathy, ataxia, seizures, and neurobehavioral changes.”

Another example of anti-gliadin antibodies possibly contributing to the formation of autoantibodies against neurological self-structures is in autism.  A 2004 study in Nutritional Neuroscience found that children with autism show antibody elevations against gliadin and cerebellar (brain) proteins simultaneously. In other words, wheat proteins may simulate antibodies that cross-react, resulting in neurological damage. Learn more on the topic by reading our article: Wheat: A Missing Piece In the Autism Puzzle

Just a Problem for Schizophrenics? There Is One Surefire Way to Find Out…

A broader question is also raised by this research.  Since anti-gliadin antibodies are found in approximately 27 percent of the population, and as high as 57 percent in those suffering from neurological dysfunction of unknown causes, is it then possible that gluten-containing grains are adversely affecting the mental health of the world at large, perhaps mostly on a subclinical basis?

We actually explored this possibility in greater depth in our essay The Dark Side of Wheat, focusing on the Roman empire’s use of the wheat-based economy as a form of both cultural and biological imperialism.

Certainly we can say that wheat adversely affects the physical health of far more than present day conventional medical estimates which focus on celiac disease and food allergies to wheat. We have indexed over 200 adverse health effects of gluten-containing grains , with 20 adverse ‘modes of toxicity’ described thus far. Interestingly, top on the list is neurotoxicity, with 23 articles describing this effect available to view here: Wheat Neurotoxicity Link .

There are likely far too many variables to ever point to gluten-containing grains as a singular cause of psychiatric problems, malaise, mania, addiction, depression, schizophrenia, etc. However, one thing is sure. Your first hand experience is as valuable as a double-blind, placebo-controlled, randomized human trial. And so, if you remove them from your diet, and you feel better, and health conditions, both physical and mental, improve, then there is no better proof than that!


Statin Use Incurs Risk for Musculoskeletal Conditions.

Muscle injuries as well as myalgia and weakness might be attributable to these drugs.


Statin use has been associated with excess risk for myalgia, muscle weakness, muscle cramps, and rhabdomyolysis. Many clinicians would say the more they ask statin users about muscle conditions, the more they uncover.

In a retrospective cohort study from the military healthcare system, investigators identified about 14,000 patients who used statins for at least 90 days and 37,000 nonusers. Statin users were significantly more likely to have a wide range of cardiac risk factors and diagnoses, as well as other chronic diseases, but the investigators were able to match about 7000 patients in each group for 42 baseline characteristics. During 4.5 years of observation, the likelihood of statin users (compared with nonusers) developing one or more of a large diagnostic cluster of musculoskeletal conditions was 19% higher; risk for acute musculoskeletal injuries such as strains and sprains was 13% higher, and musculoskeletal pain was 9% more common (all between-group differences were significant). The likelihood of having osteoarthritis and other arthropathies was 7% higher (P=0.07).

Comment: The excess risk for strains, sprains, and other injuries is biologically plausible, based on the known problems of muscle weakness, concerns about associated tendinopathies, and inhibition of coenzyme Q10 synthesis (which affects muscle metabolism). Muscle conditions are of sufficient importance and prevalence to constitute an essential factor in deciding whether statin use is appropriate for a given patient.


Source: Journal Watch General Medicine







Preventing NSAID-Associated Upper Gastrointestinal Events.

Risk for symptomatic ulcer, upper gastrointestinal bleeding, or perforation was similar in patients using NSAID with high adherence to a gastroprotective agent and in those using a coxib.

Nonsteroidal anti-inflammatory drug (NSAID) use is associated with increased risk for upper gastrointestinal (UGI) events, including bleeding. This risk can be lowered by co-prescription of a gastroprotective agent (GPA) or replacement with a cyclo-oxygenase-2-selective inhibitor (coxib). So, is one approach preferable in a general population?

To investigate this issue, researchers in Europe compared the risk for a UGI event between patients taking a nonselective NSAID (nsNSAID) plus a GPA (proton-pump inhibitor, double-dosed histamine-2–receptor antagonist, or misoprostol) — with GPA compliance of 

≥80% — and patients taking a coxib. In a population-based cohort of 617,200 primary care patients aged 

≥50 years, they identified 398 case-patients with UGI events (symptomatic ulcers, upper gastrointestinal bleeding, or perforation) occurring within 60 days of the NSAID exposure and matched them with 57,568 control-patients without UGI events on age, gender, and number of risk factors for a UGI event.

The risk for a UGI event did not differ between therapy groups. Glucocorticoid use was associated with a higher risk for a UGI event in the nsNSAID group compared with the coxib group (adjusted odds ratio, 9.01; 95% confidence interval, 1.61–50.50). Nonsignificant trends toward higher risk for a UGI event were present in the coxib group with use of antiplatelet (aspirin) co-therapy and in the nsNSAID group for those with a prior UGI event. The authors concluded that concomitant use of glucocorticoids and nsNSAIDs or aspirin and coxib may warrant consideration of a different strategy.

Comment: Many studies on optimal prevention of UGI events in patients taking NSAIDs have focused on high-risk populations. This population-based study suggests that a nonselective NSAID (plus a gastroprotective agent) or a coxib is equally effective. The finding that aspirin mitigated the benefit of coxibs is consistent with other studies. Of note, patients at high risk for UGI events should be considered individually and may benefit from a more aggressive protective approach.


Source:Journal Watch Gastroenterology 

Metoclopramide plus Diphenhydramine Superior to Ketorolac for Nonmigraine Headaches.

A randomized trial found better pain relief with the antiemetic combination than with the NSAID.

Medications recommended for headache treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), prochlorperazine, metoclopramide, and caffeine. These authors compared two regimens in adult patients with recurrent headaches that did not meet definitions for migraine or cluster headache. In a randomized, double-blind study, 120 patients who presented to an academic emergency department received either intravenous metoclopramide (20 mg) plus diphenhydramine (25 mg), or intravenous ketorolac (30 mg).

After 1 hour, pain improvement was greater with the combination regimen (median improvement on an 11-point scale, 5 vs. 3 points). The combination regimen was also superior in sustained relief, requirement for rescue medications, and patient desire to receive the same treatment again.

Comment: This study joins a long list of prior studies that suggest that metoclopramide and prochlorperazine are excellent agents for headache treatment. But it would be unfortunate if we concluded from this study that there is any reason to treat benign headaches with intravenous medications. There is also no reason to use only one of these regimens. Common sense suggests that we simply treat these benign conditions with oral ibuprofen, oral prochlorperazine or metoclopramide, and perhaps also oral caffeine. Opioids and barbiturate/analgesic combinations (e.g., Fiorinal) should not be used.


Source:Journal Watch Emergency Medicine

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Google Challenges NSA Secrecy in FISA Court