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Friday, February 25, 2011

Malaria Drug for Frontotemporal Degeneration - Research Article

 This research article is copied directly from the Dementia Weekly web site:

Munich/Bonn - Scientists at the German Center for Neurodegenerative Diseases (DZNE) and the Ludwig-Maximilians Universität Munich have found a promising approach for a possible treatment of so-called frontotemporal dementia, an Alzheimer-like form of dementia.

Chloroquine increased progranulin
Frontotemporal dementia is caused by a breakdown of nerve cells in the frontal and temporal region of the brain (fronto-temporal lobe), which leads to, among other symptoms, a change in personality and behavior. The cause of some forms of frontotemporal dementia is a genetically determined reduction of a hormone-like growth factor, progranulin.

Scientists working with Dr. Anja Capell and Prof. Christian Haass have now shown that various drugs that are already on the market to treat malaria, angina pectoris or heart rhythm disturbances can increase the production of progranulin. Accordingly, these drugs are good candidates for treatment of this specific form of frontotemporal dementia. The work was published in the online edition of the scientific journal "Journal of Neuroscience" on February 2, 2011.

Progranulin is needed in the human brain as a protective factor for sensitive nerve cells. Not enough progranulin, therefore, results in a progressive neuronal cell death. Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17. As for almost every other gene, there are also two copies of the progranulin gene in the cell. In patients with progranulin dependent frontotemporal dementia, one of the two copies is defective, leading to a 50% reduction in progranulin levels. To rescue the lack of progranulin, the Munich researchers tested various substances for their ability to stimulate the remaining progranulin production and identified a drug called bafilomycin (BafA1). They then examined the molecular mechanism underlying the impact of BafA1 on progranulin more closely. Growth factors such as progranulin are produced in cellular membrane inclusions, known as vesicles. BafA1 has an alkalizing effect on these vesicles: After administration of BafA1 the interior of the vesicles is less acidic – and this increases the production of progranulin.

This observation encouraged the researchers to investigate further alkalizing substances for their ability to raise progranulin levels. Among the substances that passed the test were three drugs that are already on the market to treat various diseases: a medication for angina pectoris (bepridil), one for heart rhythm problems (amiodarone) and the widely used malaria drug chloroquine. Chloroquine increased the progranulin level not only in experiments with mouse cells to normal, but also in cells from patients with the defective progranulin gene.

In a clinical study in collaboration with the University of London, the team of Prof. Haass and Dr. Capell will now investigate whether chloroquine actually helps against progranulin dependent frontotemporal dementia. The human studies can be started very soon, as chloroquine has been used on countless patients, so that serious side effects are not to be expected. Even though the Munich scientists are optimistic, Prof. Haass warns against exaggerated hopes. “Experience shows that the step from cell and animal models to the patient is always connected with considerable difficulties. It will take several years until we know, whether chloroquine can be used as therapy for progranulin dependent frontotemporal dementia,” says Haass.

 Comments are welcome.

Tuesday, February 15, 2011

Cellular inclusions - Some Basic Chemistry Of Tauopathy

The estimated amount of glucose required to support the functions of the human brain each day, expressed in  M&M's is : 250.     ~Harpers, October 1989.
~Personally I like the green ones.

Ubiquitin with Lysine tags for destructio
Unlike Alzheimer's disease, the brain tissue of people with FTD - most probably my brain -  does not show plaques and rarely shows tangles. (Some FTD forms actually show both tangles and inclusions and are called "mixed dementia", and some have no inclusions at all, but the symptoms are indistinguishable) Brain tissue from patients with FTD often show cellular inclusions - clumps of protein that build up within brain cells (neurons). The classical cellular inclusion, named a “Pick body” nearly one-hundred years ago, stains positively for a protein called tau. Tau is a protein involved in stabilizing microtubules, proteins that support the structure and shape of neurons. These microtubules are what makes a brain brain-shaped instead of a puddle of fatty goo. About 40% of people with FTD have these tau-positive inclusions. Frontotemporal dementia was once known as "Pick's disease because of the "Picks bodies." The rest have Tau-negative inclusions, or no visible inclusions at all.

The second type of cellular inclusion found in people with frontotemporal dementia is made up of two other proteins called ubiquitin and TDP-43. These inclusions Tau-negative because when the cells are stained to make Tau inclusions visible they are not present. Ubiquitin is a protein that is involved with clearing waste products from the cell, while TDP-43 is a protein involved with making proteins from the instructions contained in DNA. Nearly all patients with FTD and amyotrophic lateral sclerosis (ALS), and most patients with semantic dementia, show these ubiquitin-TDP-43 inclusions.

Ubiquitin is a small regulatory protein that has been found in almost all tissues (ubiquitously) of eukaryotic organisms. Among other functions, it directs proteins to recycling.
Phosphorylated Serene
Ubiquitin binds to proteins and labels them for destruction. The ubiquitin tag directs proteins to the proteasome, which is an organelle in the cell that degrades and recycles unneeded proteins. This discovery won the Nobel Prize for chemistry in 2004. Ubiquitin tags can also direct proteins to other locations in the cell, where they control other protein and cell mechanisms. Now ya know.

TAR DNA-binding protein 43 (TDP-43), is a cellular protein which in humans is encoded by the TARDBP gene. TARDBP was originally identified as a transcriptional repressor that binds to chromosomally integrated TAR DNA and represses HIV-1 transcription. It was also reported to regulate alternate splicing of the CFTR gene and the apoA-II gene. Later it was discovered that hyper-phosphorylated, ubiquitinated and cleaved form of TARDBP, known as pathologic TDP43, is the major disease protein in ubiquitin-positive, tau-, and alpha-synuclein-negative frontotemporal dementia (FTLD-U) and in Amyotrophic lateral sclerosis (ALS). Elevated levels of the TDP-43 protein have also been identified in individuals diagnosed with chronic traumatic encephalopathy, a condition that often mimics ALS and that has been associated with athletes who have experienced multiple concussions and other types of head injury.

The term "frontotemporal lobar degeneration" (FTLD) is used to describe the specific pathological diseases that result in FTD syndromes. These pathological diseases are distinguished by the specific proteins found within the neuronal inclusions. Most FTLD subtypes are either:

   1. FTLD-tau, which includes Pick’s disease, corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), all of which show tau-containing inclusions or
   2. FTLD-TDP, which includes several subtypes in which TDP-43 containing inclusions are seen. None of them have been given any kool names yet as far as I can find.

Here are 3 main histological subtypes found at post-mortem:
  • tau inclusions (Pick's disease, MAPT mutations, corticobasal degeneration, progressive supranuclear palsy)
  • ubiquitin positive (tau-negative) inclusions - in the majority of cases that have this type of pathology the ubiquitinated inclusions contain a protein called TDP-43. There are four subtypes of this type of pathology described in the recent consensus criteria by Cairns et al.: type 1 with neurites predominantly, type 2 with cytoplasmic inclusions predominantly; type 3 with intranuclear inclusions and type 4 associated with VCP mutations. Not all ubiquitin-positive, tau negative cases stain for TDP-43 e.g. the CHMP2B cases but also other cases: many of these have been very recently recognized to contain the protein FUS.
  •  Dementia lacking distinctive histology (DLDH) - no inclusions - a rare and controversial entity - new analyses have allowed many cases to be reclassified into one of the positively-defined subgroups.
Note that all variations of FTD are classed as Tauopathies at this time, even though some forms seem to have no Tau inclusions. That is probably because Ubiquitinopathies sounds like something that is everywhere. Just my guess, but this nomenclature ids likely to change in the future. It is likely that the current cluster of diseases included as FTD will be split apart according to their underlying chemistry.
    Phosphorolyzation is important in protein degradation.
    Proteasome from above. Colorized.
    • In the late 1990s, it was recognized that phosphorylation of some proteins causes them to be degraded by the ATP-dependent ubiquitin/proteasome pathway. These target proteins become substrates for particular E3 ubiquitin ligases only when they are phosphorylated. The main function of the proteasome is to degrade unneeded or damaged proteins by proteolysis, a chemical reaction that breaks peptide bonds.
    Phosphorylation is a chemically complex process, but in Tauopathies the issue is that it turns on and off the activity of proteins - which is what it usually does - but with FTD it occurs in the brain cells. phosphorylation has many purposes, not just tagging proteins for transport. But, if a protein is phosphorylized at a certain site on its chain, or maybe several sites, it is marked to be transported away for recycling. If this chemical marking, or tagging, gets screwed up somehow, the proteins may accumulate, and clump together. They may even fold in half, and form tangles. There are many steps in the chemical pathway where phosphorylation is necessary, and something can go wrong at any one of them.

    This is just a very basic and simple overview. There is a lot more information and research on these brain chemistries. This is just a starting point. To find out more details just Google some of the terms like phosphorylation, tauopathies, TDP-43, and ubiquitin. If that doesn't give you a headache, nothing will.

    So, in a couple places I mention that something can go wrong in these complex chemical pathways. Maybe you are wondering things like: What can go wrong? Is there anything I can do to prevent it? Is there anything I can do to reverse it? Here is what I think about that.

    What can go wrong? Lotsa suff! First a gene could mutate, or activate, and start producing broken proteins. If a protein is missing the place where a phosphorylation-tag would be attached, that protein cannot be tagged, or possibly activated, or deactivated. Or a free radical could attach to the place where the phosphorylation-tag should go, and block the protein from being tagged, or activated, or deactivated. Toxins and chemicals can also interfere with normal brain chemistry. Pesticides and some food additives, among others, have been shown to interfere with how the brain works. Those are just a few examples.

    Is there anything I can do to prevent it? Maybe. If its genetic, probably not much can be done without some form of gene-therapy. As for those pesky free-radicals, yes! This is where all of those anti-oxidants come into play. Just about any and every one of them is beneficial. What they do is to attach to the free radical ions floating around, and bind them up so they cannot attach to anything else and screw up the normal healthy chemistry. My personal approach is to mix up the anti-oxidants in my diet and with supplements. I figure that some will be better at cleaning up certain types of ions than others, and that over time a good healthy mix will suppress all of the pesky things. Just my theory, but a healthy diet with some well-chosen supplements isn't going to hurt anything. Neither will trying to avoid and limit exposure to food additives, and other toxic substances.

    Is there anything I can do to reverse it? This is the big unknown. So far I have seen a few very preliminary research studies which have shown some promise. Check out the post on, of all things, pomegranate juice. Some medications are showing some promise also, but none are yet approved for use. The biggest issue I see with reversing the process is that the Tau inclusions are insoluble under normal circumstances. There is some promising research about dissolving Tau. The following is a short item from a very recent study:  : Tau, a microtubule associated protein, aggregates into intracellular paired helical filaments (PHFs) by an unknown mechanism in Alzheimer's disease (AD) and other tauopathies. A contributing factor may be a failure to metabolize free cytosolic tau within the neuron. The buildup of tau may then drive the aggregation process through mass action. Therefore, proteases that normally degrade tau are of great interest. A recent genetic screen identified puromycin-sensitive aminopeptidase (PSA) as a potent modifier of tau-induced pathology and suggested PSA as a possible tau-degrading enzyme. Again, there is hope.

    When they figure this one all out, we will be home free - if we still have enough brain cells left alive to matter by that time. Until then, I am trying to at least slow or stop as much of the progression as possible by trying to make sure my brain cells have what is necessary to carry on healthy chemical reactions, and guessing what to do, take, and eat to promote these healthy reactions. For information on what medications I am taking follow the "drugs" tab at the top of the blog's home page.

    Everything here is my account of what happened to me, or my interpretation of stuff, except what I copied from somewhere else. Wikepedia is a constant source of information. Every case of FTD is different. Keep in mind as you read this that the person who wrote this has dementia. That would be ME.
    Medical Disclaimer.

    Questions and comments are welcome.

        Monday, February 14, 2011

        Is It Or Isn't It bvFTD?

        Sensitivity of current criteria for the diagnosis of behavioral variant frontotemporal dementia


          Background: Diagnosis of behavioral variant frontotemporal dementia (bvFTD) relies on criteria that are constraining and potentially ambiguous. Some features are open to clinical interpretation and their prevalence unknown. This study investigated the sensitivity of current diagnostic criteria in a large group of patients with bvFTD.

          Methods: Forty-five patients with clear evidence of bvFTD as judged by progressive clinical decline (>3 years) with marked frontal features and significant frontal brain atrophy on brain MRI were included. Thirty-two have died; pathologic confirmation of frontotemporal lobar degeneration was found in all 18 coming to autopsy. We established the prevalence of core and supportive diagnostic features at presentation and with disease progression.

          Results: Only 25/45 patients (56%) showed all five core features necessary for a diagnosis of bvFTD at initial presentation and 33/45 (73%) as their disease progressed. Two core features, emotional blunting and loss of insight, were never observed in 25% and 13% of cases. Executive dysfunction, hyperorality, mental inflexibility, and distractibility were the only supportive features present in >50% of cases at initial presentation. Although not a diagnostic feature, impaired activities of daily living was present in 33/45 patients (73%).

          Conclusions: Strict application of the criteria misses a significant proportion of patients. Many supportive features have low prevalence and are clinically not useful. Revision of the criteria to include level of certainty (definite, probable, possible) dependent on the number of features present and the presence of ancillary information (e.g., brain atrophy, neuropsychological abnormalities, impaired activities of daily living) is encouraged.

          O. Piguet, PhD, M. Hornberger, PhD, B. P. Shelley, MBBS, MD, DM, C. M. Kipps, MD, PhD and J. R. Hodges, MD, FRCP. Sensitivity of current criteria for the diagnosis of behavioral variant frontotemporal dementia. Neurology 2009;72:732-737

          Comments and questions are welcome.

          Tuesday, February 8, 2011

          Metformin and Dementia - The Good, The Bad, and The Ugly

          Metformin ...a commonly prescribed drug to control blood sugar might increase the risk of Alzheimer’s disease.

          Metformin ...a common diabetic drug may help in fighting brain disorders like Alzheimer's or dementia

          This is creepy, but says it all!
          Late last year a friend and reader of this blog suggested I look into the drug Metformin as possibly being beneficial in treating FTD. It was published all over the place that Metformin was a possible cure for Alzheimer's - even Time Magazine picked up the story. Well, it made for nice headlines, but after a couple months of digging more deeply into the actual research I am left a little confused, and very skeptical. To be sure you really have to dig deep to get a clear picture. If you were to Google "Metformin + Dementia" the results returned are overwhelmingly positive. If you Google "Metformin+increased amyloid" they are overwhelmingly negative.

          The way I see it, in my own demented mind, is that the research needs to be interpreted very conservatively when it comes to pointing a finger at Metformin as either a cause or a cure. It is probably neither. When I delved into the actual chemistry it appears that it is Insulin, rather than Metformin, that is causing the actual beneficial effects observed. Metformin serves to manipulate the uptake and activity of Insulin in the brain, and influences the utilization of glucose in the process. It all comes back to the original hypothesis that Amyloid and Tau overproduction and phosphorylization is a byproduct of brain cells being starved for nutrition, and overproducing those substances in a last-gasp effort at survival. That is just my oversimplified summary-interpretation of what is going on based on the result that Metformin alone causes an increase in amyloid, and Metformin along with Insulin reduces amyloid.

          More likely to be of benefit than Metformin, is another class of related drugs used to treat diabetes. A research study suggested that a certain class of diabetes drug, commonly called a glitazone, might lower the risk of Alzheimer’s in people with diabetes. Pilot studies in small groups of patients have hinted that the drugs may be of some help, and the National Institute on Aging is sponsoring research in this area

          In the study, researchers used the records of 142,328 patients in the Veterans Affairs system who did not have dementia but were just starting to take a glitazone or insulin. They tracked the patients for six years. Compared with those using insulin, among the patients who took pioglitazone (Actos) or rosiglitazone (Avandia), there were nearly 20 percent fewer cases of Alzheimer’s. The glitazones had a similar advantage over another diabetes drug, metformin.

          Glitazones lower blood sugar by helping the body to use insulin more efficiently, so that less insulin is needed. The drugs may also lower inflammation. It is interesting that the study directly compares against Metformin, and as far as I can tell was never widely reported. It makes me wonder if there is a money trail to follow somewhere in all of this. That is a lot of people, but it is just looking at data not actually manipulating any variables or comparing drugs in a double-blind study which would be more conclusive, so again, a conservative approach is my course.

          So, here is an interesting question. I took Metformin without Insulin for several years. I developed FTD. Could that be the cause? Did Metformin cause my condition? It is as good of a working hypotheses as any for me right now. At least as good as blaming it on Albino Brain-Chiggers!

          There are many, many interesting articles both pro and con on the subject of Metformin and FTD and Alzheimer's, but below is the one I found most readable, and even-handed. Though this mentions Alzheimer's, there are also studies out there makinbg similar links to FTD due to the similar brain chemistry.  I have copied the article in it's entirety, even the video, as well as provided the link to the original article at the end.

          Here it is:
          Research published today is suggesting that a commonly prescribed drug to control blood sugar might increase the risk of Alzheimer’s disease. But, as this ScienCentral News video explains, it also suggests that using the drug in combination with insulin might reduce the risk.

          Interviewees: Francesca Fang-Liao,University of Tennessee School of Medicine and Huaxi Xu, Burnham Institute for Medical Research and Gregory Brewer, Southern Illinois University School of Medicine
          Produced by Joyce Gramza– Edited by James Eagan
          Copyright © ScienCentral, Inc
          Clinical Implications?
          Besides well-known complications like nerve damage, people with type 2 diabetes also have twice the normal risk of Alzheimer’s disease. In fact, some researchers even describe Alzheimer’s as a "type 3" diabetes.
          So Alzheimer’s researchers at San Diego’s Burnham Institute for Medical Research tested the effects of diabetes treatments on brain cells. They found that metformin, a drug commonly-prescribed to diabetics and prediabetics (those at risk of becoming diabetic), can more than double the production of amyloid-beta, or a-beta, the protein that forms toxic brain plaques in Alzheimer’s.

          Francesca Fang-Liao, Huaxi Xu and their team saw this increase in a-beta after treating brain cells in the lab with metformin. However, the effect was reversed when they added insulin. As they wrote in the Proceedings of the National Academy of Sciences, they also confirmed both findings in the brains of mice given metformin, or metformin plus insulin.

          "Based on the chemical structure of metformin, it doesn’t look to be able to cross the blood brain barrier," says Liao, who is now at the University of Tennessee School of Medicine. "However… when we gave metformin in the drinking water [of mice] we found that after one or two days it reached to the brain, accumulating there in significant concentrations.

          "We found that (for the metformin-only mice) the a-beta level had been greatly increased in the brain, particularly in both the cortical area and the hippocampal area. Those are the regions that are mostly affected in the Alzheimer’s disease patient," she explains.
          "We believe that this work has probably significant implications in the current medication prescribed to the diabetic patient," says Liao.

          Adds Xu, "If you are a patient with diabetes, you already have a higher chances of getting Alzheimer’s disease than normal people. If you take metformin alone, you further increase the chance of getting Alzheimer’s disease."

          Xu says the protective role of insulin against Alzheimer’s was suggested by his previous work in collaboration with 2000 Nobel laureate Paul Greengard.

          Memory Effects?
          But other Alzheimer’s experts are more cautious. Southern Illinois University School of Medicine’s Gregory Brewer says the study is "intriguing and raises a red flag of caution about metformin. But on the other hand, the missing link in the paper is the fact that their studies did not show any problems or measure any problems with memory."

          Brewer, who holds an endowed Chair in Alzheimer’s disease research, points out that a-beta is produced in very tiny amounts in our cells throughout our lifetime, and that some researchers think small amounts of a-beta may actually be required for learning and memory.

          "What we don’t know is whether those levels were toxic to the brain cells that they were studying," Brewer says. He says that if further research does reveal memory problems in mice that get metformin alone, it’s good news that combination therapy appears to be a solution.

          But in the meantime, "the complications from diabetes are more severe than from Alzheimer’s disease… if you don’t treat the diabetes, you’ll die much sooner." Brewer adds that a healthy diet and exercise are known to be beneficial in both diabetes and Alzheimer’s disease.

          Liao and Xu say they are now working on behavioral and memory testing in the mice, but point out that other research is already hinting that insulin may reduce diabetics’ risk of Alzheimer’s.

          They point to a human study published in December 2008 in which researchers led by Michal Beeri at Mount Sinai School of Medicine compared brain autopsy findings of diabetic patients against the patients’ treatment records.

          "They found that the patients’ brain from the single therapy has shown much more dramatic Alzheimer’s disease pathology than the patient that had taken combination drugs," explains Liao. "So that’s kind of supporting our observation. However, they haven’t collected enough patients which have been taking metformin specifically… as a single agent."

          Liao says collecting and comparing that information in large numbers of patients would take major effort and funding, and hopes one of the outcomes of their work will be to call attention to the need for such a study.

          Add Insulin?
          Liao says that thanks to previous research by Xu and others, more doctors are already prescribing insulin along with metformin for treating diabetes.

          "Indeed, in the clinical setting, insulin has been brought into the treatment more and more frequently nowadays, even in the prediabetic setting, in addition to metformin," she says. "I would say that would be a good trend."

          The researchers agree with Brewer that a-beta itself remains a subject of controversy among Alzheimer’s researchers.

          "Whether the human body or human cell needs a certain level of a-beta protein for normal function is still under great debate in the Alzheimer’s field," says Xu. But, he says, researchers in the field do agree that "over-production of this a-beta protein, by any abnormal process associated with genetic reasons or environmental factors, is bad for the human being."

          This research was published in the Proceedings of the National Academy of Sciences early online edition the week of February 23, 2009, and was funded by the National Institutes of Health and the Alzheimer’s Association.

          Here is the link to the original article: Diabetes Drug Linked To Alzheimer’s

          The Good: Metformin may help dementia
          The Bad: Metformin may cause dementia
          The Ugly: I took Metformin, and have been diagnosed with dementia. Maybe I have Albino Brain-Chiggers.

          So... for now I am only going to take Metformin when and if my blood sugar goes awry, and then only for a short duration. Until more research is done to prove if Metformin is a cause or cure I must place it into the category of interesting, informative, and investigative.

          I would like to give a special 'Thank you!" to Kevin for starting me down this path of research, which led me to something which I do think will be of help, and that is the substitution of some ketones for glucose to circumvent the insulin resistance causing an energy utilization deficiency in the brain. I found that while researching this ...and so it goes. There will be more on that in a later post.

          Everything here is my account of what happened to me, or my interpretation of stuff, except what I copied from somewhere else. Every case of FTD is different. Keep in mind as you read this that the person who wrote this has dementia. That would be ME.
          Medical Disclaimer.

          Comments are welcome.

          Wednesday, February 2, 2011

          Happy Groundhog ...errr - Kroozer the Skunk Day!

          Kroozer did NOT see his shadow. Spring is just around the corner! Yay!

          Kroozer is already back in his warm little bed snuggled up sound asleep. Kroozer made it very clear that he was not amused by his little excursion into the snow this morning.

          Snowface! WTF?

          Awright! Can I go in now? You've had your fun.

          Kroozer just Kroozin along in the snow...

          Happy Groundhog Day!

          "This is one time where television really fails to capture the true excitement of a large squirrel predicting the weather."              ~Phil Conners from the movie Groundhog Day

          Groundhog Day is my favorite holiday. When I say this people invariably give me a strange look and ask me "Why?". Since as a reader of this blog you are probably asking the same thing, I shall explain. No, this is not a symptom of dementia, and is not related to bvFTD. It has nothing to do with Pick's Disease, or Frontotemporal Lobal Degeneration. If you are looking for something like that, you will be disappointed. If you are wondering why someone with dementia is writing about a furry little marmot, read on. Groundhog Day is, and always has been, the best holiday ever.

          Here is why:
          First, nobody important like a President or anybody died on Groundhog Day.

          Second, it isn't some crazy religious holiday to start a war, or kill anybody, or blow anything up over.

          Third, no wars have been started, won, or lost, on Groundhog Day.

          Fourth, nobody controversial was born on Groundhog Day.

          Fifth, this is the big one, so get ready. It is all about a cute, cuddly little animal predicting the coming of Spring. No pressure on the animal because Spring will come in 6 weeks no matter what. At the end of the day, unlike Thanksgiving where the star of the holiday gets to be dinner, the fat little groundhog gets to go back to bed and cuddle up all warm and cozy until Spring. How kool is that?

          So that is why I love Groundhog Day. It looks to the future. It signals the end to these awful Ohio winters. Did I mention that it is snowing outside as I write this. The storm has been named by the weathertainment folks on the news shows as "The Groundhog Day Blizzard". Well, the groundhogs don't care! Neither do I. Spring will be here in 6 weeks because this is the day halfway between Winter and Spring. Duh! What a coincidence!

          Anyway, the Groundhog, also known as a Woodchuck, Whistle Pig, Marmot, and "Frakkin Varmint", isn't the only critter who can predict the weather. In "Jolly Old England" it was usually bears or badgers who did the dirty deed. Groundhogs are native to the United States, so we can thank the German immigrants to Pennsylvania for carrying on the tradition. I did a little research on the history of this wonderful holiday, and want to share a little of what I found. Hopefully I will convince at least a few to elevate the importance of this great day. Hey! I have dementia. What do I know?

          Anyway - The groundhog and badger were not the only animals that have been used to predict spring. Other Europeans used the bear or hedgehog--but in any case the honor belonged to a creature that hibernated. (I nominate a certain Skunk!) Anyway, the animals emergence symbolized the imminent arrival of spring.

          Traditionally, the groundhog is supposed to awaken on February 2, Groundhog Day, and come up out of his burrow. If he sees his shadow, he will return to the burrow for six more weeks of winter. If he doesn’t see his shadow, he remains outside and starts his year, because he knows that spring has arrived early.

          Well - Duh! Spring always arrives on or near March 21, so whether the groundhog decides to return to his den or remain above ground, the fact is spring will always come in six more weeks.

          The Roman-Catholic Church borrowed the holiday and called it Candlemass. Candlemas occurs 40 days after Christmas. Traditionally the Western term "Candlemas" (or Candle Mass) referred to the practice whereby a priest on 2 February blessed beeswax candles for use throughout the year, some of which were distributed to the faithful for use in the home. In Poland the feast is called Święto Matki Bożej Gromnicznej (Święto, "Holiday" + Matka Boska, "Mother of God" + Gromnica, "Thunder"). This name refers to the candles that are blessed on this day and called gromnicy, since these candles are lit during (thunder) storms and placed in windows to ward off the storm.

          The following is supposed to be related to the whole Groundhog seeing his shadow thing which seems to have gotten way out of hand in one certain town in Pennsylvania. I wish I would have stopped in there when I was Elk Hunting, but we were tired, and it was an hour out of our way. This is translated from English (chuckle) from around the year "really a long time ago".

          As the light grows longer
          The cold grows stronger
          If Candlemas be fair and bright
          Winter will have another flight
          If Candlemas be cloud and rain
          Winter will be gone and not come again
          A farmer should on Candlemas day
          Have half his corn and half his hay
          On Candlemas day if thorns hang a drop
          You can be sure of a good pea crop

          More importantly it is a gauge on how one should ration the Winter food stores. If you have less than half of your food left today, you are going to be really hungry before the snow melts. I don't really like peas very much, so I don't care about that part and am not going out to check any thorns. Last time I planted peas in my garden the rabbits ate them as soon as they came up. Good bunnies! Saved me from having to eat peas! Har!

          So, way before all of that there was was this Celtic Goddess Brigid. Goddess! She is one of the "Old Ones", and of course she was sainted in human form as St Briged by those crafty-Catholics. Just remember no matter how cute that Groundhog looks, she was here first. Her British and continental counterpart Brigantia seems to have been the Celtic equivalent of the Roman Minerva and the Greek Athena, goddesses with very similar functions and apparently embodying the same concept of 'elevated state', whether physical or psychological. (Minerva is especially kool, and a sexy  Heinlein computer/woman too!)

          Brigid is the goddess of all things perceived to be of relatively high dimensions such as high-rising flames, highlands, hill-forts and upland areas; and of activities and states conceived as psychologically lofty and elevated, such as wisdom, excellence, perfection, high intelligence, poetic eloquence, craftsmanship (especially blacksmithing), healing ability, druidic knowledge and skill in warfare. In the living traditions, whether seen as goddess or saint, she is largely associated with the home and hearth and is a favorite of both Pagans and Christians. A number of these associations are attested in Cormac's Glossary.

          Saint Brigid of Kildare or Brigid of Ireland (Brigit, Bridget, Bridgit, Bríd or Bride) or Mary of the Gael (Irish: Naomh Bríd) (c. 451–525) is one of Ireland's patron saints along with Saints Patrick and Columba. Irish hagiography makes her an early Irish Christian nun, abbess, and founder of several monasteries.

          A Scottish Gaelic proverb about the day is:

              Thig an nathair as an toll
              Là donn Brìde,
              Ged robh trì troighean dhen t-sneachd
              Air leac an làir.

              "The serpent will come from the hole
              On the brown Day of Bride,
              Though there should be three feet of snow
              On the flat surface of the ground." 

          Pity the serpent who pokes his head out today!

          Brigid is said to walk the earth on Imbolc eve. That is tonight! She is gonna be really, really cold! Anyway - Before going to bed, each member of the household may leave a piece of clothing or strip of cloth outside for Brigid to bless. The head of the household will smother (or "smoor") the fire and rake the ashes smooth. In the morning, they look for some kind of mark on the ashes, a sign that Brigid has passed that way in the night or morning. The clothes or strips of cloth are brought inside, and believed to now have powers of healing and protection.

          Those silly neo-Wiccans have tried to make this a holiday all about women, which they do to just about every holday, so who cares about them. Kinda cracks me up to think some might be dancing naked in circles around a sputtering fire in this blizzard. To each their own.  Groundhog Day is unisex. Groundhog Day is non-denominational. Groundhog Day is just for fun. Groundhog Day rules!

          So! Since we have a Blizzard, and all of the local Groundhog Day celebrations have been canceled, I am going to have my own. Now if you were paying attention, you would have noticed that any animal that hibernates will do as a substitute for the original Badger or Hedgehog. Did you know that skunks hibernate? Kroozer has been trying. Some days I have to wake his fat butt up so I can feed him. His is a cranky lil bugger too! I have a plan. Since I just happen to have easy access to a hibernating animal, a.k.a. Kroozer, I will wake his fat butt up tomorrow morning and pitch him off the back deck.

          If the weatherman was right Kroozer will land in a 4 foot deep snowdrift. Poof! If he sees his shadow we will have 6 more weeks of winter. If he doesn't see his shadow we will have 6 more weeks of winter. In any case, he is gonna be really pissed! Luckily I know he will forgive me for anything if I have enough Cheeze Balls. I have 2 bags in the cupboard, and I am not afraid to use them.

          I'll let ya know how this works out. Maybe it will be "Kroozer The Skunk Day" from now on. Or, maybe I will just sleep in...
          Kroozer loves Cheeze Balls!

          Comments are welcome.