Imagine a single item that could thoroughly clean your home, wash your clothes, purify the air you breathe, protect you against tained food, and defend you and your family from a criminal attack.
While such an amazing entity doesn’t exist in stores, it can be found in every cell of your body. It’s a tripeptide named glutathione (pronounced glue-ta-thigh-own) and it is arguably the body’s most powerful antioxidant. It was discovered more than a century ago, but still laguishes in the shadows of mainstream medicine.
Glutathione functions as an antioxidant and an antitoxin, protecting us from the ravages of our increasingly toxic environment and our own foibles. In addition, it is a protector of our immune defense system and a promoter of efficient blood flow and production, ……..” From GLUTATHIONE, Your Best Defense Against Aging, Cellular Damage and Disease, Dr. Robert H. Keller, MD, MS, FACP, AAHIVS
Monday, February 23, 2009
Wednesday, February 11, 2009
Healing Crisis
The first thing that happened when my dad started on the glutathione accelerator supplement was he went through a healing crisis. It never sounds good when you put the crises word with any other word but this was actually a good thing. Hence the word HEALING. It was either the very next day after he started it or the day after that he was unable to ambulate when we tried to get him up in the morning. He was slurring his words and had a fever. His blood sugar was up also. I did panic somewhat. But I soon remembered what someone had explained to me to be a healing crisis. They had actually told me about it because they expected I could go through it.
I started to call the doctor but decided I would monitor the situation closely first. I checked his blood sugar and temperature every 2 hours even throughout the night. His temperature never got above 102 degrees and I gave him extra insulin as needed. The next morning all symptoms of the previous day were gone. No temp and his blood sugar was back down. I called the friend who had educated me on the healing crises and explained what had happened. She told me that Dr. Keller (formulator of the glutathione accelerator) advised his patients to back down on the amount they took for a few days and slowly start to work back up to the full dose. I did exactly as she related.
Once dad was up to the full dose again (only about a week’s time) I began to notice my father was urinating regularly again. I am not sure what exactly happened to my father in that department down there with his enlarged prostate and all but I can tell you when the man started urinating again like a normal adult I knew things were changing.
His skin also began to get some color too it. Like maybe he had been outside and gotten some sun only he hadn’t. He seemed to have more strength and stamina. He even began talking more. If you remember he hadn’t talked much at all when I got him. He did some hand gesturing but if and when he spoke you couldn’t tell what he was saying. His blood sugars that had been out of control even with a diabetic diet suddenly became more manageable. But the proof was in the pudding so to speak a few days after a doctor’s office visit. For the first time ever, the doctor’s office called me after they got his results from his blood work back. The nurse told me to not give him any more of the cholesterol medication I had been giving him since before I got him because they were sending a new prescription. Same drug but the amount was CUT IN HALF! If I wasn’t sure things were getting better for dad I was then.
As the months passed he started communicating more and more. It didn’t take long and the father I thought I would never be able to go to and have a real conversation with was back! He was mentally back!! He could talk to me and reason. His voice was clearer even. This was most unexpected but an answer to my prayers!
I started to call the doctor but decided I would monitor the situation closely first. I checked his blood sugar and temperature every 2 hours even throughout the night. His temperature never got above 102 degrees and I gave him extra insulin as needed. The next morning all symptoms of the previous day were gone. No temp and his blood sugar was back down. I called the friend who had educated me on the healing crises and explained what had happened. She told me that Dr. Keller (formulator of the glutathione accelerator) advised his patients to back down on the amount they took for a few days and slowly start to work back up to the full dose. I did exactly as she related.
Once dad was up to the full dose again (only about a week’s time) I began to notice my father was urinating regularly again. I am not sure what exactly happened to my father in that department down there with his enlarged prostate and all but I can tell you when the man started urinating again like a normal adult I knew things were changing.
His skin also began to get some color too it. Like maybe he had been outside and gotten some sun only he hadn’t. He seemed to have more strength and stamina. He even began talking more. If you remember he hadn’t talked much at all when I got him. He did some hand gesturing but if and when he spoke you couldn’t tell what he was saying. His blood sugars that had been out of control even with a diabetic diet suddenly became more manageable. But the proof was in the pudding so to speak a few days after a doctor’s office visit. For the first time ever, the doctor’s office called me after they got his results from his blood work back. The nurse told me to not give him any more of the cholesterol medication I had been giving him since before I got him because they were sending a new prescription. Same drug but the amount was CUT IN HALF! If I wasn’t sure things were getting better for dad I was then.
As the months passed he started communicating more and more. It didn’t take long and the father I thought I would never be able to go to and have a real conversation with was back! He was mentally back!! He could talk to me and reason. His voice was clearer even. This was most unexpected but an answer to my prayers!
Tuesday, February 10, 2009
The Fires Within
TIME
In Partnership with CNN
Monday, Feb. 23, 2004
The Fires Within
By Christine Gorman; Alice Park; Kristina Dell
What does a stubbed toe or a splinter in a finger have to do with your risk of developing Alzheimer's disease, suffering a heart attack or succumbing to colon cancer? More than you might think. As scientists delve deeper into the fundamental causes of those and other illnesses, they are starting to see links to an age-old immunological defense mechanism called inflammation--the same biological process that turns the tissue around a splinter red and causes swelling in an injured toe. If they are right--and the evidence is starting to look pretty good--it could radically change doctors' concept of what makes us sick. It could also prove a bonanza to pharmaceutical companies looking for new ways to keep us well.
Most of the time, inflammation is a lifesaver that enables our bodies to fend off various disease-causing bacteria, viruses and parasites. (Yes, even in the industrialized world, we are constantly bombarded by pathogens.) The instant any of these potentially deadly microbes slips into the body, inflammation marshals a defensive attack that lays waste to both invader and any tissue it may have infected. Then just as quickly, the process subsides and healing begins.
Every once in a while, however, the whole feverish production doesn't shut down on cue. Sometimes the problem is a genetic predisposition; other times something like smoking or high blood pressure keeps the process going. In any event, inflammation becomes chronic rather than transitory. When that occurs, the body turns on itself--like an ornery child who can't resist picking a scab--with aftereffects that seem to underlie a wide variety of diseases.
Suddenly, inflammation has become one of the hottest areas of medical research. Hardly a week goes by without the publication of yet another study uncovering a new way that chronic inflammation does harm to the body. It destabilizes cholesterol deposits in the coronary arteries, leading to heart attacks and potentially even strokes. It chews up nerve cells in the brains of Alzheimer's victims. It may even foster the proliferation of abnormal cells and facilitate their transformation into cancer. In other words, chronic inflammation may be the engine that drives many of the most feared illnesses of middle and old age.
This concept is so intriguing because it suggests a new and possibly much simpler way of warding off disease. Instead of different treatments for, say, heart disease, Alzheimer's and colon cancer, there might be a single, inflammation-reducing remedy that would prevent all three.
Chronic inflammation also fascinates scientists because it indicates that our bodies may have, from an evolutionary perspective, become victims of their own success. "We evolved as a species because of our ability to fight off microbial invaders," says Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Women's Hospital in Boston. "The strategies our bodies used for survival were important in a time when we didn't have processing plants to purify our water, when we didn't have sewers to protect us."
But now that we are living longer, those same inflammatory strategies are more likely to slip beyond our control. Making matters worse, it appears that many of the attributes of a Western lifestyle--such as a diet high in sugars and saturated fats, accompanied by little or no exercise--also make it easier for the body to become inflamed.
At least that's the theory. For now, most of the evidence is circumstantial. (A few researchers think chronic inflammation can in some cases be good for you.) But that hasn't stopped doctors from testing the anti-inflammatory drugs that are already on pharmacy shelves to see if they have any broader benefits. What they've found is encouraging:
--In 2000 researchers concluded that patients who take Celebrex, a prescription drug from Pfizer that was originally designed to treat inflammation in arthritis, are less likely to develop intestinal polyps--abnormal growths that can become cancerous. Now there are dozens of clinical trials of Celebrex, testing, among other things, whether the medication can also prevent breast cancer, delay memory loss or slow the progression of the devastating neurodegenerative disorder known as Lou Gehrig's disease.
--As cardiologists gain more experience prescribing cholesterol-lowering statins, they are discovering that the drugs are more effective at preventing heart attacks than anyone expected. It turns out that statins don't just lower cholesterol levels; they also reduce inflammation. Now statins are being tested for their anti-inflammatory effects on Alzheimer's disease and sickle-cell anemia.
--DeCode Genetics, an Icelandic biotech firm, announced last week that it is launching a pilot study to test whether an anti-inflammatory drug that was under development for use in treating asthma might work to prevent heart attacks.
--Of course the granddaddy of all anti-inflammatories is aspirin, and millions of Americans already take it to prevent heart attacks. But evidence is growing that it may also fight colon cancer and even Alzheimer's by reducing inflammation in the digestive tract and the brain.
This new view of inflammation is changing the way some scientists do medical research. "Virtually our entire R.-and-D. effort is [now] focused on inflammation and cancer," says Dr. Robert Tepper, president of research and development at Millennium Pharmaceuticals in Cambridge, Mass. In medical schools across the U.S., cardiologists, rheumatologists, oncologists, allergists and neurologists are all suddenly talking to one another--and they're discovering that they're looking at the same thing. The speed with which researchers are jumping on the inflammation bandwagon is breathtaking. Just a few years ago, "nobody was interested in this stuff," says Dr. Paul Ridker, a cardiologist at Brigham and Women's Hospital who has done some of the groundbreaking work in the area. "Now the whole field of inflammation research is about to explode."
To understand better what all the excitement is about, it helps to know a little about the basic immunological response, a cascade of events triggered whenever the body is subjected to trauma or injury. As soon as that splinter slices into your finger, for example, specialized sentinel cells prestationed throughout the body alert the immune system to the presence of any bacteria that might have come along for the ride. Some of those cells, called mast cells, release a chemical called histamine that makes nearby capillaries leaky. This allows small amounts of plasma to pour out, slowing down invading bacteria, and prepares the way for other faraway immune defenders to easily enter the fray. Meanwhile, another group of sentinels, called macrophages, begin an immediate counterattack and release more chemicals, called cytokines, which signal for reinforcements. Soon, wave after wave of immune cells flood the site, destroying pathogens and damaged tissue alike--there's no carrying the wounded off the battlefield in this war. (No wonder the ancient Romans likened inflammation to being on fire.)
Doctors call this generalized response to practically any kind of attack innate immunity. Even the bodies of animals as primitive as starfish defend themselves this way. But higher organisms have also developed a more precision-guided defense system that helps direct and intensify the innate response and creates specialized antibodies, custom-made to target specific kinds of bacteria or viruses. This so-called learned immunity is what enables drug companies to develop vaccines against diseases like smallpox and the flu. Working in tandem, the innate and learned immunological defenses fight pitched battles until all the invading germs are annihilated. In a final flurry of activity, a last wave of cytokines is released, the inflammatory process recedes, and healing begins.
Problems begin when, for one reason or another, the inflammatory process persists and becomes chronic; the final effects are varied and depend a lot on where in the body the runaway reaction takes hold. Among the first to recognize the broader implications were heart doctors who noticed that inflammation seems to play a key role in cardiovascular disease.
IS YOUR HEART ON FIRE?
Not long ago, most doctors thought of heart attacks as primarily a plumbing problem. Over the years, fatty deposits would slowly build up on the insides of major coronary arteries until they grew so big that they cut off the supply of blood to a vital part of the heart. A complex molecule called LDL, the so-called bad cholesterol, provided the raw material for these deposits. Clearly anyone with high LDL levels was at greater risk of developing heart disease.
There's just one problem with that explanation: sometimes it's dead wrong. Indeed, half of all heart attacks occur in people with normal cholesterol levels. Not only that, as imaging techniques improved, doctors found, much to their surprise, that the most dangerous plaques weren't necessarily all that large. Something that hadn't yet been identified was causing those deposits to burst, triggering massive clots that cut off the coronary blood supply. In the 1990s, Ridker became convinced that some sort of inflammatory reaction was responsible for the bursting plaques, and he set about trying to prove it.
To test his hunch, Ridker needed a simple blood test that could serve as a marker for chronic inflammation. He settled on Creactive protein (CRP), a molecule produced by the liver in response to an inflammatory signal. During an acute illness, like a severe bacterial infection, levels of CRP quickly shoot from less than 10 mg/L to 1,000 mg/L or more. But Ridker was more interested in the low levels of CRP--less than 10 mg/L--that he found in otherwise healthy people and that indicated only a slightly elevated inflammation level. Indeed, the difference between normal and elevated is so small that it must be measured by a specially designed assay called a high-sensitivity CRP test.
By 1997, Ridker and his colleagues at Brigham and Women's had shown that healthy middle-aged men with the highest CRP levels were three times as likely to suffer a heart attack in the next six years as were those with the lowest CRP levels. Eventually, inflammation experts determined that having a CRP reading of 3.0 mg/L or higher can triple your risk of heart disease. The danger seems even greater in women than in men. By contrast, folks with extremely low levels of CRP, less than 0.5 mg/L, rarely have heart attacks.
Physicians still don't know for sure how inflammation might cause a plaque to burst. But they have a theory. As the level of LDL cholesterol increases in the blood, they speculate, some of it seeps into the lining of the coronary arteries and gets stuck there. Macrophages, alerted to the presence of something that doesn't belong, come in and try to clean out the cholesterol. If, for whatever reason, the cytokine signals begin ramping up the inflammatory process instead of notching it down, the plaque becomes unstable. "This is not about replacing cholesterol as a risk factor," Ridker says. "Cholesterol deposits, high blood pressure, smoking--all contribute to the development of underlying plaques. What inflammation seems to contribute is the propensity of those plaques to rupture and cause a heart attack. If there is only inflammation but no underlying heart disease, then there is no problem."
At this point, cardiologists are still not ready to recommend that the general population be screened for inflammation levels. But there's a growing consensus that CRP should be measured in those with a moderately elevated risk of developing cardiovascular disease. At the very least, a high CRP level might tip the balance in favor of more aggressive therapy with treatments--such as aspirin and statins--that are already known to work.
A NEW VIEW OF DIABETES
Before Dr. Frederick Banting and his colleagues at the University of Toronto isolated insulin in the 1920s, doctors tried to treat diabetes with high doses of salicylates, a group of aspirin-like compounds. (They were desperate and also tried morphine and heroin.) Sure enough, the salicylate approach reduced sugar levels, but at a high price: side effects included a constant ringing in the ears, headaches and dizziness. Today's treatments for diabetes are much safer and generally work by replacing insulin, boosting its production or helping the body make more efficient use of the hormone. But researchers over the past few years have been re-examining the salicylate approach for new clues about how diabetes develops.
What they have discovered is a complex interplay between inflammation, insulin and fat--either in the diet or in large folds under the skin. (Indeed, fat cells behave a lot like immune cells, spewing out inflammatory cytokines, particularly as you gain weight.) Where inflammation fits into this scenario--as either a cause or an effect--remains unclear. But the case for a central role is getting stronger. Dr. Steve Shoelson, a senior investigator at the Joslin Diabetes Center in Boston, has bred a strain of mice whose fat cells are supercharged inflammation factories. The mice become less efficient at using insulin and go on to develop diabetes. "We can reproduce the whole syndrome just by inciting inflammation," Shoelson says.
That suggests that a well-timed intervention in the inflammatory process might reverse some of the effects of diabetes. Some of the drugs that are already used to treat the disorder, like metformin, may work because they also dampen the inflammation response. In addition, preliminary research suggests that high CRP levels may indicate a greater risk of diabetes. But it's too early to say whether reducing CRP levels will actually keep diabetes at bay.
CANCER: THE WOUND THAT NEVER HEALS
Back in the 1860s, renowned pathologist Rudolf Virchow speculated that cancerous tumors arise at the site of chronic inflammation. A century later, oncologists paid more attention to the role that various genetic mutations play in promoting abnormal growths that eventually become malignant. Now researchers are exploring the possibility that mutation and inflammation are mutually reinforcing processes that, left unchecked, can transform normal cells into potentially deadly tumors.
How might that happen? One of the most potent weapons produced by macrophages and other inflammatory cells are the so-called oxygen free radicals. These highly reactive molecules destroy just about anything that crosses their path--particularly DNA. A glancing blow that damages but doesn't destroy a cell could lead to a genetic mutation that allows it to keep on growing and dividing. The abnormal growth is still not a tumor, says Lisa Coussens, a cancer biologist at the Comprehensive Cancer Center at the University of California, San Francisco. But to the immune system, it looks very much like a wound that needs to be fixed. "When immune cells get called in, they bring growth factors and a whole slew of proteins that call other inflammatory cells," Coussens explains. "Those things come in and go 'heal, heal, heal.' But instead of healing, you're 'feeding, feeding, feeding.'"
Sometimes the reason for the initial inflammatory cycle is obvious--as with chronic heartburn, which continually bathes the lining of the esophagus with stomach acid, predisposing a person to esophageal cancer. Other times, it's less clear. Scientists are exploring the role of an enzyme called cyclo-oxygenase 2 (COX-2) in the development of colon cancer. COX-2 is yet another protein produced by the body during inflammation.
Over the past few years, researchers have shown that folks who take daily doses of aspirin--which is known to block COX2--are less likely to develop precancerous growths called polyps. The problem with aspirin, however, is that it can also cause internal bleeding. Then in 2000, researchers showed that Celebrex, another COX-2 inhibitor that is less likely than aspirin to cause bleeding, also reduces the number of polyps in the large intestine.
So, should you be taking Celebrex to prevent colon cancer? It's still too early to say. Clearly COX-2 is one of the factors in colon cancer. "But I don't think it's the exclusive answer," says Ray DuBois, director of cancer prevention at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn. "There are a lot of other components that need to be explored."
ASPIRIN FOR ALZHEIMER'S DISEASE?
When doctors treating Alzheimer's patients took a closer look at who seemed to be succumbing to the disease, they uncovered a tantalizing clue: those who were already taking anti-inflammatory drugs for arthritis or heart disease tended to develop the disorder later than those who weren't. Perhaps the immune system mistakenly saw the characteristic plaques and tangles that build up in the brains of Alzheimer's patients as damaged tissue that needed to be cleared out. If so, the ensuing inflammatory reaction was doing more harm than good. Blocking it with anti-inflammatories might limit, or at least delay, any damage to cognitive functions.
The most likely culprits this time around are the glial cells, whose job is to nourish and communicate with the neurons. Researchers have discovered that glial cells can also act a lot like the mast cells of the skin, producing inflammatory cytokines that call additional immune cells into action. "The glial cells are trying to return the brain to a normal state," explains Linda Van Eldik, a neurobiologist at Northwestern University Feinberg School of Medicine in Chicago. "But for some reason, in neurodegenerative diseases like Alzheimer's, the process seems to be out of control. You get chronic glial activation, which results in an inflammatory state."
It appears that some people are more sensitive to plaques and tangles than others. Perhaps they have a genetic predisposition. Or perhaps a long-running bacterial infection, like gum disease, keeps the internal fires burning and tips the balance toward chronic inflammation.
Preliminary research suggests that low-dose aspirin and fish-oil capsules--both of which are known to reduce inflammatory cytokines--seem to reduce a person's risk of Alzheimer's disease. Unfortunately, most of these preventive measures need to be started well before any neurological problems develop. "What we've learned with dementia is that it's very hard to improve people who already have it," says Dr. Ernst Schaefer, a professor of medicine and nutrition at Tuft's Friedman School of Nutrition in Boston. "But it may be possible to stabilize people and to prevent disease."
WHEN THE BODY ATTACKS ITSELF
No doctors have more experience treating chronic inflammation than the physicians who specialize in rheumatoid arthritis, multiple sclerosis, lupus and other autoimmune disorders. For decades these diseases have provided the clearest example of a body at war with itself. But the spark that fuels their internal destruction doesn't come from excess cholesterol deposits or a stubborn bacterial infection. Instead, in a bizarre twist of fate, the body's supersophisticated, learned immunological defenses mistakenly direct an inflammatory attack against healthy cells in such places as the joints, nerves and connective tissue.
Over the past few years, powerful drugs like Remicade and Enbrel, which target specific inflammatory cytokines, have worked wonders against rheumatoid arthritis and other autoimmune disorders. But as often happens in medicine, the drugs have also created some problems. Patients who take Remicade, for example, are slightly more likely to develop tuberculosis; the same inflammatory cytokines that attacked their joints, it seems, also protected them against TB.
Inflammation may be more of a problem in the earlier stages of autoimmune diseases like multiple sclerosis. So much tissue is eventually destroyed that nerve damage becomes permanent. "Your initial goal is to keep the immune response in check, but then you have to ask how you encourage regrowth of damaged tissue," says Dr. Stephen Reingold, vice president for research programs at the National Multiple Sclerosis Society. It could take decades to figure that one out.
ASTHMA WITHOUT ALLERGIES?
One of the most intriguing questions in immunology today is why everyone doesn't suffer from asthma. After all, the air we breathe is full of germs, viruses and other irritants. Since half of the 17 million Americans with asthma are hypersensitive to common substances like cat dander or pollen, it stands to reason that their allergic reactions trigger the chronic inflammation in their bodies. Yet the people who develop asthma as adults--one of the most rapidly growing segments of the population--often don't have allergies. Doctors still don't know what's driving their disease, but the signs of inflammation are every bit as present in their lungs.
Many treatments for asthma are designed to control inflammation, although they still don't cure the disease. "It may mean that the inflammatory hypothesis is not entirely correct or the drugs that we use to treat inflammation aren't fully potent," says Dr. Stephen Wasserman, an allergist at the University of California at San Diego. "There are a lot of gaps to fill in."
Everywhere they turn, doctors are finding evidence that inflammation plays a larger role in chronic diseases than they thought. But that doesn't necessarily mean they know what to do about it. "We're in a quandary right now," says Dr. Gailen Marshall, an immunologist at the University of Texas Medical School at Houston. "We're advancing the idea to heighten awareness. But we really can't recommend specific treatments yet."
That may soon change. Researchers are looking beyond aspirin and other multipurpose medications to experimental drugs that block inflammation more precisely. Any day now, Genentech is expecting a decision from the FDA on its colon-cancer drug, Avastin, which targets one of the growth factors released by the body as inflammation gives way to healing. Millennium Pharmaceuticals is testing a different kind of drug, called Velcade, which has already been approved for treating multiple myeloma, against lung cancer and other malignancies. But there is a sense that much more basic research into the nature of inflammation needs to be done before scientists understand how best to limit the damage in chronic diseases.
In the meantime, there are things we all can do to dampen our inflammatory fires. Some of the advice may sound terribly familiar, but we have fresh reasons to follow through. Losing weight induces those fat cells--remember them?--to produce fewer cytokines. So does regular exercise, 30 minutes a day most days of the week. Flossing your teeth combats gum disease, another source of chronic inflammation. Fruits, vegetables and fish are full of substances that disable free radicals.
So if you want to stop inflammation, get off that couch, head to the green market and try not to stub your toe on the way.
--With reporting by Dan Cray/Los Angeles
With reporting by Dan Cray/Los Angeles; Christine Gorman and Kristina Dell
Find this article at:
http://www.time.com/time/magazine/article/0,9171,993419,00.html
Copyright � 2007 Time Inc. All rights reserved.
In Partnership with CNN
Monday, Feb. 23, 2004
The Fires Within
By Christine Gorman; Alice Park; Kristina Dell
What does a stubbed toe or a splinter in a finger have to do with your risk of developing Alzheimer's disease, suffering a heart attack or succumbing to colon cancer? More than you might think. As scientists delve deeper into the fundamental causes of those and other illnesses, they are starting to see links to an age-old immunological defense mechanism called inflammation--the same biological process that turns the tissue around a splinter red and causes swelling in an injured toe. If they are right--and the evidence is starting to look pretty good--it could radically change doctors' concept of what makes us sick. It could also prove a bonanza to pharmaceutical companies looking for new ways to keep us well.
Most of the time, inflammation is a lifesaver that enables our bodies to fend off various disease-causing bacteria, viruses and parasites. (Yes, even in the industrialized world, we are constantly bombarded by pathogens.) The instant any of these potentially deadly microbes slips into the body, inflammation marshals a defensive attack that lays waste to both invader and any tissue it may have infected. Then just as quickly, the process subsides and healing begins.
Every once in a while, however, the whole feverish production doesn't shut down on cue. Sometimes the problem is a genetic predisposition; other times something like smoking or high blood pressure keeps the process going. In any event, inflammation becomes chronic rather than transitory. When that occurs, the body turns on itself--like an ornery child who can't resist picking a scab--with aftereffects that seem to underlie a wide variety of diseases.
Suddenly, inflammation has become one of the hottest areas of medical research. Hardly a week goes by without the publication of yet another study uncovering a new way that chronic inflammation does harm to the body. It destabilizes cholesterol deposits in the coronary arteries, leading to heart attacks and potentially even strokes. It chews up nerve cells in the brains of Alzheimer's victims. It may even foster the proliferation of abnormal cells and facilitate their transformation into cancer. In other words, chronic inflammation may be the engine that drives many of the most feared illnesses of middle and old age.
This concept is so intriguing because it suggests a new and possibly much simpler way of warding off disease. Instead of different treatments for, say, heart disease, Alzheimer's and colon cancer, there might be a single, inflammation-reducing remedy that would prevent all three.
Chronic inflammation also fascinates scientists because it indicates that our bodies may have, from an evolutionary perspective, become victims of their own success. "We evolved as a species because of our ability to fight off microbial invaders," says Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Women's Hospital in Boston. "The strategies our bodies used for survival were important in a time when we didn't have processing plants to purify our water, when we didn't have sewers to protect us."
But now that we are living longer, those same inflammatory strategies are more likely to slip beyond our control. Making matters worse, it appears that many of the attributes of a Western lifestyle--such as a diet high in sugars and saturated fats, accompanied by little or no exercise--also make it easier for the body to become inflamed.
At least that's the theory. For now, most of the evidence is circumstantial. (A few researchers think chronic inflammation can in some cases be good for you.) But that hasn't stopped doctors from testing the anti-inflammatory drugs that are already on pharmacy shelves to see if they have any broader benefits. What they've found is encouraging:
--In 2000 researchers concluded that patients who take Celebrex, a prescription drug from Pfizer that was originally designed to treat inflammation in arthritis, are less likely to develop intestinal polyps--abnormal growths that can become cancerous. Now there are dozens of clinical trials of Celebrex, testing, among other things, whether the medication can also prevent breast cancer, delay memory loss or slow the progression of the devastating neurodegenerative disorder known as Lou Gehrig's disease.
--As cardiologists gain more experience prescribing cholesterol-lowering statins, they are discovering that the drugs are more effective at preventing heart attacks than anyone expected. It turns out that statins don't just lower cholesterol levels; they also reduce inflammation. Now statins are being tested for their anti-inflammatory effects on Alzheimer's disease and sickle-cell anemia.
--DeCode Genetics, an Icelandic biotech firm, announced last week that it is launching a pilot study to test whether an anti-inflammatory drug that was under development for use in treating asthma might work to prevent heart attacks.
--Of course the granddaddy of all anti-inflammatories is aspirin, and millions of Americans already take it to prevent heart attacks. But evidence is growing that it may also fight colon cancer and even Alzheimer's by reducing inflammation in the digestive tract and the brain.
This new view of inflammation is changing the way some scientists do medical research. "Virtually our entire R.-and-D. effort is [now] focused on inflammation and cancer," says Dr. Robert Tepper, president of research and development at Millennium Pharmaceuticals in Cambridge, Mass. In medical schools across the U.S., cardiologists, rheumatologists, oncologists, allergists and neurologists are all suddenly talking to one another--and they're discovering that they're looking at the same thing. The speed with which researchers are jumping on the inflammation bandwagon is breathtaking. Just a few years ago, "nobody was interested in this stuff," says Dr. Paul Ridker, a cardiologist at Brigham and Women's Hospital who has done some of the groundbreaking work in the area. "Now the whole field of inflammation research is about to explode."
To understand better what all the excitement is about, it helps to know a little about the basic immunological response, a cascade of events triggered whenever the body is subjected to trauma or injury. As soon as that splinter slices into your finger, for example, specialized sentinel cells prestationed throughout the body alert the immune system to the presence of any bacteria that might have come along for the ride. Some of those cells, called mast cells, release a chemical called histamine that makes nearby capillaries leaky. This allows small amounts of plasma to pour out, slowing down invading bacteria, and prepares the way for other faraway immune defenders to easily enter the fray. Meanwhile, another group of sentinels, called macrophages, begin an immediate counterattack and release more chemicals, called cytokines, which signal for reinforcements. Soon, wave after wave of immune cells flood the site, destroying pathogens and damaged tissue alike--there's no carrying the wounded off the battlefield in this war. (No wonder the ancient Romans likened inflammation to being on fire.)
Doctors call this generalized response to practically any kind of attack innate immunity. Even the bodies of animals as primitive as starfish defend themselves this way. But higher organisms have also developed a more precision-guided defense system that helps direct and intensify the innate response and creates specialized antibodies, custom-made to target specific kinds of bacteria or viruses. This so-called learned immunity is what enables drug companies to develop vaccines against diseases like smallpox and the flu. Working in tandem, the innate and learned immunological defenses fight pitched battles until all the invading germs are annihilated. In a final flurry of activity, a last wave of cytokines is released, the inflammatory process recedes, and healing begins.
Problems begin when, for one reason or another, the inflammatory process persists and becomes chronic; the final effects are varied and depend a lot on where in the body the runaway reaction takes hold. Among the first to recognize the broader implications were heart doctors who noticed that inflammation seems to play a key role in cardiovascular disease.
IS YOUR HEART ON FIRE?
Not long ago, most doctors thought of heart attacks as primarily a plumbing problem. Over the years, fatty deposits would slowly build up on the insides of major coronary arteries until they grew so big that they cut off the supply of blood to a vital part of the heart. A complex molecule called LDL, the so-called bad cholesterol, provided the raw material for these deposits. Clearly anyone with high LDL levels was at greater risk of developing heart disease.
There's just one problem with that explanation: sometimes it's dead wrong. Indeed, half of all heart attacks occur in people with normal cholesterol levels. Not only that, as imaging techniques improved, doctors found, much to their surprise, that the most dangerous plaques weren't necessarily all that large. Something that hadn't yet been identified was causing those deposits to burst, triggering massive clots that cut off the coronary blood supply. In the 1990s, Ridker became convinced that some sort of inflammatory reaction was responsible for the bursting plaques, and he set about trying to prove it.
To test his hunch, Ridker needed a simple blood test that could serve as a marker for chronic inflammation. He settled on Creactive protein (CRP), a molecule produced by the liver in response to an inflammatory signal. During an acute illness, like a severe bacterial infection, levels of CRP quickly shoot from less than 10 mg/L to 1,000 mg/L or more. But Ridker was more interested in the low levels of CRP--less than 10 mg/L--that he found in otherwise healthy people and that indicated only a slightly elevated inflammation level. Indeed, the difference between normal and elevated is so small that it must be measured by a specially designed assay called a high-sensitivity CRP test.
By 1997, Ridker and his colleagues at Brigham and Women's had shown that healthy middle-aged men with the highest CRP levels were three times as likely to suffer a heart attack in the next six years as were those with the lowest CRP levels. Eventually, inflammation experts determined that having a CRP reading of 3.0 mg/L or higher can triple your risk of heart disease. The danger seems even greater in women than in men. By contrast, folks with extremely low levels of CRP, less than 0.5 mg/L, rarely have heart attacks.
Physicians still don't know for sure how inflammation might cause a plaque to burst. But they have a theory. As the level of LDL cholesterol increases in the blood, they speculate, some of it seeps into the lining of the coronary arteries and gets stuck there. Macrophages, alerted to the presence of something that doesn't belong, come in and try to clean out the cholesterol. If, for whatever reason, the cytokine signals begin ramping up the inflammatory process instead of notching it down, the plaque becomes unstable. "This is not about replacing cholesterol as a risk factor," Ridker says. "Cholesterol deposits, high blood pressure, smoking--all contribute to the development of underlying plaques. What inflammation seems to contribute is the propensity of those plaques to rupture and cause a heart attack. If there is only inflammation but no underlying heart disease, then there is no problem."
At this point, cardiologists are still not ready to recommend that the general population be screened for inflammation levels. But there's a growing consensus that CRP should be measured in those with a moderately elevated risk of developing cardiovascular disease. At the very least, a high CRP level might tip the balance in favor of more aggressive therapy with treatments--such as aspirin and statins--that are already known to work.
A NEW VIEW OF DIABETES
Before Dr. Frederick Banting and his colleagues at the University of Toronto isolated insulin in the 1920s, doctors tried to treat diabetes with high doses of salicylates, a group of aspirin-like compounds. (They were desperate and also tried morphine and heroin.) Sure enough, the salicylate approach reduced sugar levels, but at a high price: side effects included a constant ringing in the ears, headaches and dizziness. Today's treatments for diabetes are much safer and generally work by replacing insulin, boosting its production or helping the body make more efficient use of the hormone. But researchers over the past few years have been re-examining the salicylate approach for new clues about how diabetes develops.
What they have discovered is a complex interplay between inflammation, insulin and fat--either in the diet or in large folds under the skin. (Indeed, fat cells behave a lot like immune cells, spewing out inflammatory cytokines, particularly as you gain weight.) Where inflammation fits into this scenario--as either a cause or an effect--remains unclear. But the case for a central role is getting stronger. Dr. Steve Shoelson, a senior investigator at the Joslin Diabetes Center in Boston, has bred a strain of mice whose fat cells are supercharged inflammation factories. The mice become less efficient at using insulin and go on to develop diabetes. "We can reproduce the whole syndrome just by inciting inflammation," Shoelson says.
That suggests that a well-timed intervention in the inflammatory process might reverse some of the effects of diabetes. Some of the drugs that are already used to treat the disorder, like metformin, may work because they also dampen the inflammation response. In addition, preliminary research suggests that high CRP levels may indicate a greater risk of diabetes. But it's too early to say whether reducing CRP levels will actually keep diabetes at bay.
CANCER: THE WOUND THAT NEVER HEALS
Back in the 1860s, renowned pathologist Rudolf Virchow speculated that cancerous tumors arise at the site of chronic inflammation. A century later, oncologists paid more attention to the role that various genetic mutations play in promoting abnormal growths that eventually become malignant. Now researchers are exploring the possibility that mutation and inflammation are mutually reinforcing processes that, left unchecked, can transform normal cells into potentially deadly tumors.
How might that happen? One of the most potent weapons produced by macrophages and other inflammatory cells are the so-called oxygen free radicals. These highly reactive molecules destroy just about anything that crosses their path--particularly DNA. A glancing blow that damages but doesn't destroy a cell could lead to a genetic mutation that allows it to keep on growing and dividing. The abnormal growth is still not a tumor, says Lisa Coussens, a cancer biologist at the Comprehensive Cancer Center at the University of California, San Francisco. But to the immune system, it looks very much like a wound that needs to be fixed. "When immune cells get called in, they bring growth factors and a whole slew of proteins that call other inflammatory cells," Coussens explains. "Those things come in and go 'heal, heal, heal.' But instead of healing, you're 'feeding, feeding, feeding.'"
Sometimes the reason for the initial inflammatory cycle is obvious--as with chronic heartburn, which continually bathes the lining of the esophagus with stomach acid, predisposing a person to esophageal cancer. Other times, it's less clear. Scientists are exploring the role of an enzyme called cyclo-oxygenase 2 (COX-2) in the development of colon cancer. COX-2 is yet another protein produced by the body during inflammation.
Over the past few years, researchers have shown that folks who take daily doses of aspirin--which is known to block COX2--are less likely to develop precancerous growths called polyps. The problem with aspirin, however, is that it can also cause internal bleeding. Then in 2000, researchers showed that Celebrex, another COX-2 inhibitor that is less likely than aspirin to cause bleeding, also reduces the number of polyps in the large intestine.
So, should you be taking Celebrex to prevent colon cancer? It's still too early to say. Clearly COX-2 is one of the factors in colon cancer. "But I don't think it's the exclusive answer," says Ray DuBois, director of cancer prevention at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn. "There are a lot of other components that need to be explored."
ASPIRIN FOR ALZHEIMER'S DISEASE?
When doctors treating Alzheimer's patients took a closer look at who seemed to be succumbing to the disease, they uncovered a tantalizing clue: those who were already taking anti-inflammatory drugs for arthritis or heart disease tended to develop the disorder later than those who weren't. Perhaps the immune system mistakenly saw the characteristic plaques and tangles that build up in the brains of Alzheimer's patients as damaged tissue that needed to be cleared out. If so, the ensuing inflammatory reaction was doing more harm than good. Blocking it with anti-inflammatories might limit, or at least delay, any damage to cognitive functions.
The most likely culprits this time around are the glial cells, whose job is to nourish and communicate with the neurons. Researchers have discovered that glial cells can also act a lot like the mast cells of the skin, producing inflammatory cytokines that call additional immune cells into action. "The glial cells are trying to return the brain to a normal state," explains Linda Van Eldik, a neurobiologist at Northwestern University Feinberg School of Medicine in Chicago. "But for some reason, in neurodegenerative diseases like Alzheimer's, the process seems to be out of control. You get chronic glial activation, which results in an inflammatory state."
It appears that some people are more sensitive to plaques and tangles than others. Perhaps they have a genetic predisposition. Or perhaps a long-running bacterial infection, like gum disease, keeps the internal fires burning and tips the balance toward chronic inflammation.
Preliminary research suggests that low-dose aspirin and fish-oil capsules--both of which are known to reduce inflammatory cytokines--seem to reduce a person's risk of Alzheimer's disease. Unfortunately, most of these preventive measures need to be started well before any neurological problems develop. "What we've learned with dementia is that it's very hard to improve people who already have it," says Dr. Ernst Schaefer, a professor of medicine and nutrition at Tuft's Friedman School of Nutrition in Boston. "But it may be possible to stabilize people and to prevent disease."
WHEN THE BODY ATTACKS ITSELF
No doctors have more experience treating chronic inflammation than the physicians who specialize in rheumatoid arthritis, multiple sclerosis, lupus and other autoimmune disorders. For decades these diseases have provided the clearest example of a body at war with itself. But the spark that fuels their internal destruction doesn't come from excess cholesterol deposits or a stubborn bacterial infection. Instead, in a bizarre twist of fate, the body's supersophisticated, learned immunological defenses mistakenly direct an inflammatory attack against healthy cells in such places as the joints, nerves and connective tissue.
Over the past few years, powerful drugs like Remicade and Enbrel, which target specific inflammatory cytokines, have worked wonders against rheumatoid arthritis and other autoimmune disorders. But as often happens in medicine, the drugs have also created some problems. Patients who take Remicade, for example, are slightly more likely to develop tuberculosis; the same inflammatory cytokines that attacked their joints, it seems, also protected them against TB.
Inflammation may be more of a problem in the earlier stages of autoimmune diseases like multiple sclerosis. So much tissue is eventually destroyed that nerve damage becomes permanent. "Your initial goal is to keep the immune response in check, but then you have to ask how you encourage regrowth of damaged tissue," says Dr. Stephen Reingold, vice president for research programs at the National Multiple Sclerosis Society. It could take decades to figure that one out.
ASTHMA WITHOUT ALLERGIES?
One of the most intriguing questions in immunology today is why everyone doesn't suffer from asthma. After all, the air we breathe is full of germs, viruses and other irritants. Since half of the 17 million Americans with asthma are hypersensitive to common substances like cat dander or pollen, it stands to reason that their allergic reactions trigger the chronic inflammation in their bodies. Yet the people who develop asthma as adults--one of the most rapidly growing segments of the population--often don't have allergies. Doctors still don't know what's driving their disease, but the signs of inflammation are every bit as present in their lungs.
Many treatments for asthma are designed to control inflammation, although they still don't cure the disease. "It may mean that the inflammatory hypothesis is not entirely correct or the drugs that we use to treat inflammation aren't fully potent," says Dr. Stephen Wasserman, an allergist at the University of California at San Diego. "There are a lot of gaps to fill in."
Everywhere they turn, doctors are finding evidence that inflammation plays a larger role in chronic diseases than they thought. But that doesn't necessarily mean they know what to do about it. "We're in a quandary right now," says Dr. Gailen Marshall, an immunologist at the University of Texas Medical School at Houston. "We're advancing the idea to heighten awareness. But we really can't recommend specific treatments yet."
That may soon change. Researchers are looking beyond aspirin and other multipurpose medications to experimental drugs that block inflammation more precisely. Any day now, Genentech is expecting a decision from the FDA on its colon-cancer drug, Avastin, which targets one of the growth factors released by the body as inflammation gives way to healing. Millennium Pharmaceuticals is testing a different kind of drug, called Velcade, which has already been approved for treating multiple myeloma, against lung cancer and other malignancies. But there is a sense that much more basic research into the nature of inflammation needs to be done before scientists understand how best to limit the damage in chronic diseases.
In the meantime, there are things we all can do to dampen our inflammatory fires. Some of the advice may sound terribly familiar, but we have fresh reasons to follow through. Losing weight induces those fat cells--remember them?--to produce fewer cytokines. So does regular exercise, 30 minutes a day most days of the week. Flossing your teeth combats gum disease, another source of chronic inflammation. Fruits, vegetables and fish are full of substances that disable free radicals.
So if you want to stop inflammation, get off that couch, head to the green market and try not to stub your toe on the way.
--With reporting by Dan Cray/Los Angeles
With reporting by Dan Cray/Los Angeles; Christine Gorman and Kristina Dell
Find this article at:
http://www.time.com/time/magazine/article/0,9171,993419,00.html
Copyright � 2007 Time Inc. All rights reserved.
Monday, February 9, 2009
A New Beginning
On June 7, 2007 my husband and I went to a meeting. We had been invited there by a friend who knew I had been sick and who thought he had something that could help me. No one there could know how hard it had been for me to get out of the house and attend the meeting. No one there knew I had been in bed 80% of my day for over 4 years and took 9 prescription medications practically every day just to function at all. No one knew at the age of 42 I actually felt like I was 70 years old and that I wanted to die.
One thing that was clear to everyone there, I was told, is that I was not well. (Just check out the posted picture taken at that very meeting. I do have makeup on even though I am pasty white in the picture.)
I listened to the information they had to share and although very skeptical I agreed to try it. In less than a week I was up and around and in no pain. I came out of that bed and I have never been back.
Who would have thought an all natural product could do that in 3 ½ days? Who would have thought that within 1 month I would be off all of my medications except my hormones? Who would have thought I would no longer need all the specialists I had been seeing on a regular basis? Not me….. Not me……. Not ever.
At the time of that meeting my husband was also in bed a lot He had had 3 major surgeries within 1 ½ years after having a perforated colon and almost dying. So he was in bed a lot too. Now he did manage to go to work with the help of lots of caffeine. But that’s about all he did.
He started taking it the same time I did and his energy came back as he started feeling better. I got my husband back at the same time he got his wife back.
Of course dad started on it as soon as I could get it ordered and delivered. His story will be in the next post.
One thing that was clear to everyone there, I was told, is that I was not well. (Just check out the posted picture taken at that very meeting. I do have makeup on even though I am pasty white in the picture.)
I listened to the information they had to share and although very skeptical I agreed to try it. In less than a week I was up and around and in no pain. I came out of that bed and I have never been back.
Who would have thought an all natural product could do that in 3 ½ days? Who would have thought that within 1 month I would be off all of my medications except my hormones? Who would have thought I would no longer need all the specialists I had been seeing on a regular basis? Not me….. Not me……. Not ever.
At the time of that meeting my husband was also in bed a lot He had had 3 major surgeries within 1 ½ years after having a perforated colon and almost dying. So he was in bed a lot too. Now he did manage to go to work with the help of lots of caffeine. But that’s about all he did.
He started taking it the same time I did and his energy came back as he started feeling better. I got my husband back at the same time he got his wife back.
Of course dad started on it as soon as I could get it ordered and delivered. His story will be in the next post.
Saturday, February 7, 2009
Wednesday, February 4, 2009
Feb 5 Quote
"There are multiple arbitrary divisions of medicine including: allopathic, osteopathic, chiropractic, alternative or complementary, homeopathic, naturopathic, etc. These divisions are a paradigm of the parable of the four blind men feeling and then describing an elephant. I have learned over the last quarter century that there is only one kind of medicine; THAT WHICH WORKS and it encompasses aspects from all of the arbitrary divisions." Dr. Robert Keller, MD, MS, FACP, AAHIVS
Tuesday, February 3, 2009
Dark before Light
Okay, so dad did do much better for a very long time. Instead of lying in bed all the time he was only in bed at night and for an hour nap. The rest of the time was spent sitting in his lift chair, getting help with exercises, walking around the house or outside with the help of his walker, taking a spin around the block with the sitter and of course watching television. To manage dad’s diabetes we counted carbohydrates and proteins instead of sugars. This became a very effective way to manage his blood sugars. We got very good at it. Our greatest challenge was getting him to drink enough water. It was a great chore to keep him hydrated. Everyone worked hard to get him to drink plenty of fluids.
Remember now that my little brother had said dad would not be living much longer right before turning dad over to me and that dad had been in and out of the hospital with pneumonia several times that year. For about 5 years I believe dad never spent the night in the hospital. Never even had pneumonia.
Despite all of the advancements we had made with dad though his mental state did not ever change much. It was still hard to understand him and he still didn't talk much. This was particularly hard on me. Especially in times of great distress. Nothing is harder in my opinion for a daughter to need her mom or dads support, have one in the house even and not be able to run to their arms for comfort. Oh I could go to dad but dad wasn’t there. He would be of no help. It left me with such an empty feeling. I mourned that loss many times.
At some point after those many years now dad did start to decline physically again. Bouts of physical and occupational therapy helped but his insurance wouldn’t pay forever and although my caregivers continued to keep working with dad it wasn’t the same. Something else I had noticed. He didn’t seem to urinate as much. The doctor had said there seemed to be some renal problems. I don’t think that’s uncommon for a diabetic though. We had also been having a time trying to keep his blood sugars manageable. We still had one thing to be happy about and that was no pneumonia.
During my dad’s decline I also had started having problems of my own. I myself had been diagnosed with degenerative disk disease and arthritis in my low back and neck. About 2002 I had a 4 vertebral fusion in my neck from an auto accident. I had my gallbladder removed, ankle surgery and adhesion surgery. I am positive I am leaving out a few things like terrible allergies and asthma. I had also started having migraines. They had been going on for years. I was on a preventative for the migraines. I also took a special pill when I had one and if that didn’t work took trips to the ER. My sciatic flared up so bad one time I couldn’t walk. I had no energy, hurt all the time, and spent 80% of my time in my bedroom. At age 42 I wanted to die. We were a mess. I thank God everyday for my dad’s caregivers. In truth they sometimes took care of me too.
June 17, 2007 everything changed. Everything. Dad and I would never, ever be the same. Stay tuned to see what made that change happen.
Remember now that my little brother had said dad would not be living much longer right before turning dad over to me and that dad had been in and out of the hospital with pneumonia several times that year. For about 5 years I believe dad never spent the night in the hospital. Never even had pneumonia.
Despite all of the advancements we had made with dad though his mental state did not ever change much. It was still hard to understand him and he still didn't talk much. This was particularly hard on me. Especially in times of great distress. Nothing is harder in my opinion for a daughter to need her mom or dads support, have one in the house even and not be able to run to their arms for comfort. Oh I could go to dad but dad wasn’t there. He would be of no help. It left me with such an empty feeling. I mourned that loss many times.
At some point after those many years now dad did start to decline physically again. Bouts of physical and occupational therapy helped but his insurance wouldn’t pay forever and although my caregivers continued to keep working with dad it wasn’t the same. Something else I had noticed. He didn’t seem to urinate as much. The doctor had said there seemed to be some renal problems. I don’t think that’s uncommon for a diabetic though. We had also been having a time trying to keep his blood sugars manageable. We still had one thing to be happy about and that was no pneumonia.
During my dad’s decline I also had started having problems of my own. I myself had been diagnosed with degenerative disk disease and arthritis in my low back and neck. About 2002 I had a 4 vertebral fusion in my neck from an auto accident. I had my gallbladder removed, ankle surgery and adhesion surgery. I am positive I am leaving out a few things like terrible allergies and asthma. I had also started having migraines. They had been going on for years. I was on a preventative for the migraines. I also took a special pill when I had one and if that didn’t work took trips to the ER. My sciatic flared up so bad one time I couldn’t walk. I had no energy, hurt all the time, and spent 80% of my time in my bedroom. At age 42 I wanted to die. We were a mess. I thank God everyday for my dad’s caregivers. In truth they sometimes took care of me too.
June 17, 2007 everything changed. Everything. Dad and I would never, ever be the same. Stay tuned to see what made that change happen.
Sunday, February 1, 2009
Antioxidants
"The Antioxidants you should care about are the ones
God gave you." Dr. Robert H. Keller
I Fell In Love With My Daddy Again
How did I go from thinking dad belonged in a nursing home to moving him in with my family?
There was some information missing from my last post. I failed to mention that I had fallen in love with my father again. What do I mean by falling in love with him? Well a little girl almost always adores her father. I did. I thought he hung the moon and then I grew up. The teenage angst kicked in and before I knew it I was married.
When my father moved in with me it gave me a chance to really look at him. I requested his military records. When I received them I learned he had never completed high school but had gotten his GED in the military. I also learned he did 3 tours overseas which pretty much covered my mom and dad’s whole marriage. Maybe that was why they got divorced.
This new information suddenly explained away some of my misconceptions and he hadn’t said a word (he didn’t communicate much due to his illness). I started to see my father in a different light. I began to see him as a separate individual from me. I began to see the whole picture of his life. Maybe he really had done the best he could do with what he had been given.
My heart began to soften towards my dad and I knew I needed to help him in any way I could. He was a human and he deserved to be taken care of and respected. A new relationship between father and daughter had begun to bloom.
I started doing research. Stay tuned.....
There was some information missing from my last post. I failed to mention that I had fallen in love with my father again. What do I mean by falling in love with him? Well a little girl almost always adores her father. I did. I thought he hung the moon and then I grew up. The teenage angst kicked in and before I knew it I was married.
When my father moved in with me it gave me a chance to really look at him. I requested his military records. When I received them I learned he had never completed high school but had gotten his GED in the military. I also learned he did 3 tours overseas which pretty much covered my mom and dad’s whole marriage. Maybe that was why they got divorced.
This new information suddenly explained away some of my misconceptions and he hadn’t said a word (he didn’t communicate much due to his illness). I started to see my father in a different light. I began to see him as a separate individual from me. I began to see the whole picture of his life. Maybe he really had done the best he could do with what he had been given.
My heart began to soften towards my dad and I knew I needed to help him in any way I could. He was a human and he deserved to be taken care of and respected. A new relationship between father and daughter had begun to bloom.
I started doing research. Stay tuned.....
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