Guest views are now limited to 12 pages. If you get an "Error" message, just sign in! If you need to create an account, click here.

Jump to content


  • Posts

  • Joined

  • Last visited

1 Follower

About tankdude

  • Birthday 05/08/1961

Profile Information

  • Gender
  • Location
    Helena, MT
  • Interests
    Helping others to better health - both physical and financial

Recent Profile Visitors

22,118 profile views

tankdude's Achievements


Newbie (1/14)



  1. Strangely enough - this was in the news today Pfizer denies report it hid possible Alzheimer’s breakthrough Pfizer is fighting back against a report that it hid the potential of a blockbuster drug to prevent Alzheimer’s disease in order to avoid shelling out for a “costly clinical trial.” Researchers at Pfizer in 2015 found that Enbrel, an anti-inflammatory drug used to treat rheumatoid arthritis, seemed to reduce the risk of Alzheimer’s disease by 64 percent, the Washington Post reported Tuesday. But a clinical trial on 3,000 to 4,000 patients to test the hypothesis would have cost about $80 million, according to research prepared by Pfizer’s inflammation and immunology department and seen by the Washington Post. The Washington Post noted that Enbrel was near the end of its 20-year patent life and financial incentives for further research into the drug were “diminishing.” But Pfizer contends that its decision not to pursue a study of Enbrel’s other possible uses was motivated by science and not money. “Our decision not to pursue a broader clinical trial … [was] based first and foremost on scientific rationale and not on the basis of financial incentives as the story seems to imply,” Pfizer said in a statement after the Washington Post story ran. The data was found from a review of 127,000 insurance claims completed by Pfizer employees. The group split the claims equally between people who had Alzheimer’s and those who did not. In the group of people who did not have Alzheimer’s, 302 were treated with Enbrel. Only 110 in the group with Alzheimer’s had used Enbrel, it was reported. Members of the medical community the Washington Post spoke with argued that Pfizer should have done more to publicize the potential uses of Enbrel to spur other research even if the drugmaker didn’t plan to do its own study. “Having acquired the knowledge, refusing to disclose it to those who might act upon it hides a potential benefit, and thereby wrongs and probably harms those at risk of developing Alzheimer’s by impeding research,’’ said Bobbie Farsides, professor of clinical and biomedical ethics at Brighton and Sussex Medical School in London. But not all of the people the Washington Post spoke with agreed. “I do think you have to draw some limits, and say that not every piece of information they have in their files has to be disclosed with others,’’ said Marc Rodwin, a professor at Suffolk University Law School in Boston. A source close to Pfizer told the New York Post that the drug giant publishes findings that meet the “gold standard” of medical research versus “hunches.” While researchers have been studying the role of brain inflammation in Alzheimer’s, Pfizer during a three-year internal review determined that a clinical trial was not likely to be successful because the drug doesn’t reach brain tissue. A study of 41 patients published by the American Academy of Neurology in May 2015 about potential uses for Enbrel proved to be inconclusive. “While there were some interesting trends that favored [Enbrel], there were no statistically significant changes in cognition, behavior, or global function,” according to an abstract of the researcher’s findings.
  2. It's been a while since I've posted so bear with me. Like most of mother other posts in here - this one could be a little long. I will give links to support my information - as usual. Both Alzheimer’s and psoriasis have links to a common base - oxidative stress. Quick primer on oxidative stress. As some of you know - I have a keen interest in this area as I have found it to have a role in almost all diseases. "Oxidative stress occurs when excess oxygen radicals are produced in cells, which could overwhelm the normal antioxidant capacity. When the concentration of reactive species is not controlled by internal defense mechanisms such as antioxidants (tocopherols, ascorbic acid, and glutathione) or enzymes involved in oxygen radical scavenging (catalase, peroxidase, and superoxide dismutase, SOD), oxidative damage occurs to proteins, lipids, and DNA, which could lead to cytotoxicity, genotoxicity, and even carcinogenesis when damaged (mutated) cells can proliferate. Oxidative stress could results from the following: (1) the presence of xenobiotics, (2) the activation of the immune system in response to invading microorganisms (inflammation), and (3) radiation, which makes oxidative stress a common denominator of toxicity or stress. In this chapter, the reader will find a variety of assays to measure oxidative stress and damage." More simply put - Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants. Essentially - the body is out of cellular homeostasis. If you will indulge me - let's look at Alzheimer's first. Doing search on Google Scholar with "Alzheimer's and oxidative stress" will pull up over 640,000 articles. These are citations from a few. "Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer’s disease. Examination of Alzheimer’s disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer’s disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-β-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer’s disease pathogenesis and novel therapeutic approaches." "Genetic and lifestyle-related risk factors for Alzheimer disease (AD) are associated with an increase in oxidative stress, suggesting that oxidative stress is involved at an early stage of the pathologic cascade. Moreover, oxidative stress is mechanistically and chronologically associated with other key features of AD, namely, metabolic, mitochondrial, metal, and cell-cycle abnormalities. Contrary to the commonly held notion that pathologic hallmarks of AD signify etiology, several lines of evidence now indicate that aggregation of amyloid-β and tau is a compensatory response to underlying oxidative stress. Therefore, removal of proteinaceous accumulations may treat the epiphenomenon rather than the disease and may actually enhance oxidative damage. Although some antioxidants have been shown to reduce the incidence of AD, the magnitude of the effect may be modified by individual factors such as genetic predisposition (e.g. apolipoprotein E genotype) and habitual behaviors. Because caloric restriction, exercise, and intellectual activity have been experimentally shown to promote neuronal survival through enhancement of endogenous antioxidant defenses, a combination of dietary regimen of low total calorie and rich antioxidant nutrients and maintaining physical and intellectual activities may ultimately prove to be one of the most efficacious strategies for AD prevention." One of my favorite sites kind of rolls all the information up into a bit easier to read synopsis. "Alzheimer’s disease, an age-associated dysfunction of brain cells that is degenerative in nature, is clearly connected to oxidative stress. Highly specialized brain cells are slower to replace themselves and warrant the body’s protection. The brain has mechanisms that aid this—the blood-brain barrier, for example, and the myelin sheath surrounding nerve fibers are protective of nerve cells. Damaged mitochondria in combination with chronic oxidative stress often result in the body’s inability to correct imbalances of cellular waste and toxins. Glutathione (a potent antioxidant produced by the body) plays a role in cleaning up but is ineffective without the presence of certain REDOX signaling molecules to help neutralize oxidizing free radical toxins. This deficiency, usually from sluggish, damaged mitochondria, can be genetically predisposed but may also (especially when manifest in the earlier years) result from habitual smoking, insufficient diet, and stress. Additionally, brain cells have naturally high levels of certain fatty acids, which are especially susceptible to oxidation. The vast blood supply that normally serves the brain is a key factor in the input of oxygen and nutrients and the outtake of waste. Any brief restriction of the blood supply to brain tissue is devastating, and even minor chronic deficiency of good circulation is equally debilitating to the ability of brain cells to maintain balance away from the oxidative zone."! Let's do the same thing with psoriasis. Google scholar search with "psoriasis and oxidative stress" will again yield over 52,000 results. Again - here are a excerpts from a few of the articles. "Psoriasis is a chronic inflammatory, proliferative skin disease characterized by pathological skin lesions due to various exogenous and endogenous factors. It is associated with a number of biochemical and immunological disturbances. Recently, it has been suggested that increased reactive oxygen species (ROS) production and compromised function of antioxidant system may be involved in the pathogenesis of this disease. In the present study, 90 psoriasis patients were selected. Disease severity was assessed by psoriasis area severity index score and grouped as mild, moderate and severe (each group consists of 30 subjects) and compared with 30 healthy controls. Serum levels of malondialdehyde, nitric oxide end products and the activities of antioxidant enzymes such as erythrocyte-superoxide dismutase, catalase and total antioxidant status were investigated in these groups/subjects. As compared to controls, we found severitywise significantly increased serum malondialdehyde, nitric oxide end products with decrease in erythrocyte-superoxide dismutase activity, catalase activity and total antioxidant status in patients with psoriasis suggesting worsening of the disease. It seems to be linked with the enhancement of Reactive Oxygen Species production and decreased antioxidant potential in psoriasis." "Psoriasis is a chronic immune-mediated hyperproliferative inflammatory skin disease in which a cytokine network concept is well established. Skin is a major target of oxidative stress mainly due to reactive oxygen species (ROS) originating from the environment and skin metabolism itself. Although endogenous antioxidants attenuate the harmful effects of ROS, increased or prolonged presence of free radicals can override ROS defense mechanisms and mediate numerous cellular responses that contribute to the development of a variety of skin disorders, including psoriasis. Regarding psoriasis, antioxidant strategies have proven to be beneficial therapeutics. The cellular signaling pathways such as mitogen-activated protein kinase/activator protein 1, nuclear factor κB, and Janus kinase–signal transducers and activators of transcription are known to be redox sensitive and proven to be involved in the progress of psoriasis." Again - heading to The Redox Doc - he does give a good synopsis. "Skin wraps the body in a protective shield, which itself is a living organ actively burning fuel, repairing, and replacing itself 24/7. Environmental factors such as UV light and airborne and topical toxins negatively impact skin health, prompting an adaptive response which is driven by REDOX chemistry. Oxidative damage varies by the degrees of REDOX potential of the tissue affected, since cellular repair is slowed by an imbalance of REDOX signaling molecules. Skin disorders like psoriasis, a chronic immune-mediated inflammatory condition, are also based in REDOX imbalance, since cellular signaling pathways like transcription factor Kappa B are known to rely on proper REDOX balance. While the ingestion of antioxidants has some value, it is widely known that REDOX signaling molecules provide the electron-rich REDOX molecules that endogenous antioxidants require to operate efficiently to eliminate the free-radical exposure that override cell defenses. Activate your REDOX potential with sleep, hydration, plant-based nutrition, and supplementing with REDOX molecules."! While it may seem that simpy adding more antioxidants to the diet would help alleviate oxidative stress, it's not that simple. It's all about the body being in balance and homeostasis. You actually need a certain amount of oxidants to actually make the bodies immune response work correctly. This balance is accomplished with what are knows as REDOX signaling molecules. These little molecules are one of the primary ways our body communicates it's needs and reactions - sometimes even more quickly than our nervous system. Here is a good discussion about those. Bottom line for me is the need for cellular homeostasis. Diet is a great first step - processed foods wreck havoc on the body. Whole grains, natural fats, fruits, vegetables - you've all heard it before. I also take the stabilzed REDOX supplement they talk about in the above article. I know it has helped me in many areas. Disclaimer: I am affiliated with the company the makes the REDOX supplement - so I will not give any more information about that here in the forum. I understand and appreciate Mr. Montana's forum rules and will definitely abide by them.
  3. So I have some news in the medic front with the daughter - and you can't tell me that prayer doesn't work!!! The University of Utah diagnosed her with MALS (Median arcuate ligament syndrome) - a condition in which the median arcuate ligament presses too tightly on the celiac artery (a major branch of the aorta that delivers blood to the stomach, liver, and other organs) and the nerves in the area (celiac plexus). This explained the gastric symptoms my daughter has had for the last almost 3 years - nausea, vomiting and delayed gastric emptying. It created what they called a pseudo-obstruction. As one of he diagnostic procedures they did a celiac plexus block. This can bring temporary relief from the symptoms of MALS, and helps to confirm the diagnosis for the patient and the entire medical team. We were told the chemical they use will generally wear off after 48-72 hours, but sometimes can be effective for longer because it breaks the cycle that the body has gotten itself into. Two days after the procedure - she was able to eat pasta with no issues. Last Wednesday she had a cheeseburger and fries for lunch - experienced no pain, didn't throw it up (for the first time in over 2 years) and had no major issues. She had a Cobb salad for dinner...and the doctor is taking her off of the TPN! After 10 days she is still having good results and is back to being able to eat pretty much normally! Generally smaller portions of easily digestible foods for the most part...but can still eat almost anything again. Thank You Lord! Now I know a number of you were praying for her...and I thank you SOOOO much. In my case - about a month ago I did a Novena to St. Joseph. I asked him that as Jesus' earthly father, having an understanding of how father's want to protect and nurture their children, to intercede on my daughter's behalf. I am convinced that this intercession played a hand in guiding the medical professionals. I am so grateful for this. In my's so close to a miracle I'm calling it one.
  4. We're doing OK. Daughter is pretty stable, but on total TPN for nutrition at the moment (intravenous feeds - she has a port and actually administers it to herself every night). We have an appointment at University of Utah Medical Center this month - doing some more tests. Making some headway - but its been slow. Even with all that - she has made it through her junior year of college - and just changed her major. Not a huge change - but went from pre-med to chemistry. She did some research and believes she could do better getting her master's degree in biochemistry and then apply to med school. So far, she has no student loans but that's about to change with that plan. She is still my hero. The wife had a spinal nerve stimulator implanted - but it had to be taken out 3 days later because she got a staph infection. She's healing and is going to try it again in August/September time frame. The test was great, and think this might finally get her off of the opioids she's been on for the last 2 years. For those interested - we tried the CBD oil - Topical, oral and vaped. It helps her leg tremors, but no pain relief. Overall - it could definitely be worst..but I will say, if I happen to break out in boils, I'm changing my name to Job...
  5. This is not a chawade....again...this time with feewing....
  6. So - here is some information on why the body makes to much cholesterol. The full article can be found here - Why would the body make more cholesterol than it needs? Now here’s the problem: when people eat too many sugars and starches, especially refined and high glycemic index foods, blood insulin levels can spike. When insulin spikes, it turns on HMG –CoA reductase, which tells all of the body’s cells to make more cholesterol, even if they don’t need any more. This is probably the most important reason why some people have too much cholesterol in their bloodstream. Sugars and starches can raise insulin levels, which fools the body into thinking it should grow when it doesn’t need to. This is how low glycemic index diets and low-carbohydrate diets normalize cholesterol patterns—these diets reduce insulin levels, which in turn lower HMG-CoA reductase activity. “Statin” drugs, such as Lipitor®, which are prescribed to lower cholesterol levels, work partly by interfering with the activity of HMG-CoA reductase. If your cells happen to need more cholesterol under certain circumstances, but the statin drug is blocking this critical enzyme, your cells may not be able to make cholesterol when needed. And what’s worse is that the cholesterol synthesis pathway doesn’t just make cholesterol; branches of this same pathway are responsible for synthesizing a wide variety of other important molecules, including: Vitamin A, Vitamin E, Vitamin K, and Coenzyme Q. So, you may want to think twice before you artificially interfere with this pathway by taking a statin drug. When you eat less carbohydrate, you are not artificially blocking the pathway; you are simply allowing HMG-CoA reductase to listen to other more important signals (such as cholesterol levels and growth requirements) and decide naturally when it should turn on and when it should turn off. So, to recap: refined carbohydrates speed up the cholesterol assembly line and statins slow it down. Which approach would you rather take to manage your “cholesterol problem”—taking a drug that artificially slows down this assembly line, or changing your diet so that the assembly line only runs when it’s supposed to? [Hint: Dietary changes require no monthly co-pays, and have no potentially dangerous side effects.] Chances are: if you have “high cholesterol” you do not have a cholesterol problem—you have a carbohydrate problem. Good Cholesterol and Bad Cholesterol This gets into the very complicated relationship between cholesterol blood tests and heart disease risk. This is an enormous topic that will be covered in future articles on this site, but I’ll summarize some basic points here now. When you get your cholesterol levels checked, you will see numbers for HDL and LDL, as well as triglycerides. Triglycerides are fats, so we’ll set them aside and just focus on HDL and LDL. HDL particles collect extra cholesterol from around the body and carry it back to the liver to be eliminated from the body if we don’t need it. It is typically thought of as “good cholesterol” so higher HDL levels are considered a good sign. LDL particles carry extra cholesterol made in the liver out to the rest of the cells in the body. We used to think of LDL as “bad cholesterol” so lower levels of LDL were considered a good sign. The cholesterol inside of HDL and LDL particles is exactly the same, it’s just that, for the most part, HDL is carrying it in one direction and LDL is carrying it in the opposite direction. The reason why LDL had been dubbed “bad” and HDL has been dubbed “good” is that numerous epidemiological studies (most famously, the Framingham Heart Study) told us that high LDL levels were associated with a higher risk of heart attack, and that high HDL levels were associated with a lower risk of heart attack. We used to think that HDL was good because it acted like a garbage truck, clearing evil cholesterol out of our bodies, and we used to think that LDL was bad because it burrowed its way into our coronary arteries, depositing evil cholesterol there—forming plaques and causing heart attacks. Cholesterol, Carbohydrates and Heart Disease However, this simplistic way of thinking about cholesterol and heart disease is changing before our very eyes. It turns out that it is more complicated than this. LDL, for example, exists in a variety of forms. It can be big and buoyant and “fluffy” or small and dense and oxidized (damaged). The new thinking is that small, dense,oxidized LDL may be the only type of LDL that is associated with heart disease. Therefore, instead of thinking of all LDL as “bad”, it would be more accurate to say that all LDL is not created equal—big fluffy LDL is “good” and small, dense, oxidized LDL is “bad.” Unfortunately, standard blood tests can’t tell you which type of LDL you have because it lumps all types of LDL particles together. Standard tests can only estimate how much of your cholesterol is travelling inside of LDL particles. They can’t tell you how many LDL particles you have, how big they are, how dense they are, or how oxidized they are. [For a detailed explanation of the complexities involved in interpreting cholesterol blood test results, I recommend Dr. Peter Attia’s blog] What we do know from research studies is that people who eat a diet high in refined carbohydrates tend to have a higher number of “bad” (smaller, denser, oxidized) LDL particles. This makes sense, because we know that carbohydrates are “pro-oxidants” —meaning they can cause oxidation. There is also lots of evidence telling us that refined carbohydrates can cause inflammation. Just because doctors find cholesterol inside artery-clogging plaques does not mean that cholesterol causes plaques. It is now well established that heart disease is a disease of inflammation. It is not simply that an innocent, smooth, buoyant sphere of fat and cholesterol traveling through the bloodstream decides to somehow randomly dig its way into a healthy coronary artery. The first step in the development of a vessel-clogging plaque is inflammation within the lining of the artery itself. When doctors cut into plaques they don’t just find cholesterol—they find many signs of inflammation (such as macrophages, calcium, and T cells). Wherever there is inflammation in the body, cholesterol is rushed to the scene to repair the damage—because we need cholesterol to build healthy new cells. Jumping to the conclusion that coronary artery plaques are caused by the cholesterol found inside of them is like assuming that all car accidents are caused by the ambulances that are found on the scene. Just some "food for thought" - since we were discussing diet. My take away is - limit carbrohydrates, look at anti inflammatory style diets, and look into "oxidative stress" and how to balance the redox systems in the body. Here is another good sight.!
  7. "This time around, they may just surprise us. More later. " Moscow in flames - missiles in the air! More on the 10 o'clock news....
  8. This is a reprint and expansion of something I posted quite a while back....if I may beg an indulgance - First - I would guess he is talking short tons. In other words, 2,000 pounds. I'm sure we assumed the same we learned in school - 16 ounces per pound - but that's if this is based on the Avoirdupois measurements. These are used for coarse dry weights such as grain, flour, sugar, tea, etc., and are the units of weight you likely learned about in school. The standard weight measurements used for all precious metal products are Troy ounces and pounds. All legal tender silver, gold and platinum coins are struck according to these Troy weights. Troy weights are also called Apothecary weights, due to their use with medical drugs - 1 Troy Ounce = 31.1035 grams - 1 Avoirdupois Ounce = 28.3495 grams In other words, a 1 ounce silver coin is heavier than an ounce of tea. But wait - it's about to get a bit more confusing... - 1 Troy Pound = 12 Troy Ounces (373.242 grams) - 1 Avoirdupois Pound = 16 Avoirdupois Ounces (453.592 grams) In other words, a 1 Troy pound bag of silver coins is lighter than a pound bag of rice! Thus the famous riddle - which weighs more - a pound of feathers or a pound of gold? (In case you're hazy on that - it would be the pound of feathers....) So - with this information in hand lets redo the math. 1 ton (2,000 Troy pounds) =24,000 0z t/ton 24,000 oz t X $1,284.60 (current spot bid price) = $30,830,400 /ton 30,830,400 X 96 = $2,959,718,400 - or in other words, a lot more than what's in my bank account....
  9. Sorry to hear about the heart attack FlyHi....Oh...and yeah...I'm back.....
  10. After a prolonged hiatus - I have returned! Not sure if anyone missed me or not....but let the good natured bantering and discussion resume!
  11. Actually - if we do a base of 42 ounces....and assume that we average 27 joints (base between US and CA) = that gives us approximately 1,134 cigweeds.... So - over 14 years - and using the assumption that some Guru has called it every week (to include Ramadan - which many of the gurus can't even spell) that comes out to 732 possible calls - (to include the extras with leap years) - which works out to 1.55 (rounding to 3 significant figures) joints per possible call.... Now lets assume that each joint has - on average (not sure if your a heavy roller or a big hitter) of 10 hits per joint (also makes math easy) - thats 11,134 tokes... Wait - did I just go off on a tangent? Oh wait - is this sold as dry goods or as a medicinal - should I be using Avoirdupois weights or Troy....Now I'm confused....
  12. I'm going with 42 - because ice cream has no bones....
  13. Hope Mr. Montana doesn't mind....but I'm going to redo the math because I believe he made some false assumptions - for the sake of keeping it simple. As we all know - I tend to not be so simple, but get "wrapped around the axle" at times - so with that, I will show my work. First - I would guess he is talking short tons. In other words, 2,000 pounds. I'm sure Mr. Montana in is math assumed the same we learned in school - 16 ounces per pound - but that's if this is based on the Avoirdupois measurements. These are used for coarse dry weights such as grain, flour, sugar, tea, etc., and are the units of weight you likely learned about in school. The standard weight measurements used for all precious metal products are Troy ounces and pounds. All legal tender silver, gold and platinum coins are struck according to these Troy weights. Troy weights are also called Apothecary weights, due to their use with medical drugs - 1 Troy Ounce = 31.1035 grams - 1 Avoirdupois Ounce = 28.3495 grams In other words, a 1 ounce silver coin is heavier than an ounce of tea. But wait - it's about to get a bit more confusing... - 1 Troy Pound = 12 Troy Ounces (373.242 grams) - 1 Avoirdupois Pound = 16 Avoirdupois Ounces (453.592 grams) In other words, a 1 Troy pound bag of silver coins is lighter than a pound bag of rice! Thus the famous riddle - which weighs more - a pound of feathers or a pound of gold? (In case you're hazy on that - it would be the pound of feathers....) So - with this information in hand lets redo the math. 1 ton (2,000 Troy pounds) =29,166.67 troy ounces (oz t) in gold X 6.5 = 189,583.33 troy ounces 189,583.33 oz t X $1,195.50 (current spot bid price) = $226,646,871.015 - which is a $ 20 million difference. Maybe not all that significant for a country, but it would sure make a difference in my pocket book! Today's lesson has been brought to you by the letter Zed and the number i -
  14. Understand how life gets in the way... "Life is a continuous series of seeing how quickly you can formulate plan B" - TankDude
  15. Just some thoughts. Social Security isn't an entitlement - it's something you've paid for throughout your working life. It's more of a benefit - kind of like a 401K for being a US citizen. I believe the biggest hit to the Medicaid issue actually started with the Affordable Health Care Act - and finally - so what if they impeach 45 - it didn't seem to hurt 42 much....
  • Create New...

Important Information

By using this site, you agree to our Terms of Use.