Showing posts with label leukotrienes. Show all posts
Showing posts with label leukotrienes. Show all posts
Wednesday, October 28, 2015
Wisdom Wednesday: Treatment Before the Diagnosis?
This is an abbreviated case history to illustrate some of the unique features of the QA (Quintessential Applications) protocol.
A 34 four-year-old female came to my office with a chief complaint of severe pain under her left jaw. She had been to her primary care physician who thought it was a salivary gland but found no evidence of infection.
On palpation I could elicit pain but not from the salivary gland but actually from a small area just adjacent to a salivary gland. The area did not feel inflamed or abnormal in any sense, except she reacted to the pain.
Chiropractors are very good at palpation. It’s skill that is honed in school by palpating a hair through pages of Gray’s Anatomy. With practice, you can feel the distortion through about 80 pages of text. Now add 38 years of practice, palpating spines all day long.
So I was just as confused as her PCP. I could not identify the tissue from palpation.
Using the QA protocol, I looked for an injury reflex. However, Autogenic Facilitation was intact (any weak muscle strengthened when the nerve supply to that muscle was stimulated) eliminating an injury.
TL (therapy localization) to the jaw was active – if she placed her hand on the location of pain, any weak muscle became strong. Now I had a tool to evaluate her symptoms.
Next I checked to see what inflammatory pathway might be active. She was negative for prostaglandins but positive for both leukotrienes and cytokines. These pathways stimulate the immune system and when both are active can be autoimmune in nature. Typically, such cases will not respond favorably to ginger or boswellia, requiring a supplement that modulates the immune system.
Monday, March 16, 2015
Immune System Changes Tied to Chronic Fatigue Syndrome
Chronic fatigue syndrome appears to be linked to specific changes in a person’s immune system, particularly increased amounts of chemical messengers that regulate immune responses, researchers report.
The study adds to growing evidence that chronic fatigue syndrome is caused by a malfunctioning immune system, said lead author Dr. Mady Hornig. She is director of Translational Research at the Jerome L. and Dawn Greene Infectious Disease Laboratory at Columbia University’s Mailman School of Public Health, in New York City.
The immune system of a new chronic fatigue syndrome patient appears unable to shut down or reduce its response to an infection that has passed, Hornig said.
Instead, the system continues to pump out large amounts of cytokines – chemical messengers that coordinate the response of the immune system’s may cell types. However, this only seems to occur during the first 3 years of the disease.
“Their immune system is no longer resilient and able to bounce back after this cytokine surge” in response to an infection, Hornig said. “We need the system to be regulated, so it shuts off after the disease is gone, and that isn’t happening here.”
Doctors now can look for increased levels of these chemicals in the blood of patients who might have chronic fatigue syndrome, potentially aiding in their diagnosis, she said.
The new study, published February 27 in the journal Science Advances, comes on the heels of a new Institute of Medicine (IOM) report that declared chronic fatigue syndrome a “legitimate” illness that should be treated by doctors as a disease rather than an emotional problem.
Between 836,000 and 2.5 million Americans suffer from chronic fatigue syndrome, and an estimated 84 to 91% of people with the disorder are not diagnosed, according to the IOM. Chronic fatigue syndrome tends to strike people in their 40s and 50s, and occurs four times more often in women than men.
The study adds to growing evidence that chronic fatigue syndrome is caused by a malfunctioning immune system, said lead author Dr. Mady Hornig. She is director of Translational Research at the Jerome L. and Dawn Greene Infectious Disease Laboratory at Columbia University’s Mailman School of Public Health, in New York City.
The immune system of a new chronic fatigue syndrome patient appears unable to shut down or reduce its response to an infection that has passed, Hornig said.
Instead, the system continues to pump out large amounts of cytokines – chemical messengers that coordinate the response of the immune system’s may cell types. However, this only seems to occur during the first 3 years of the disease.
“Their immune system is no longer resilient and able to bounce back after this cytokine surge” in response to an infection, Hornig said. “We need the system to be regulated, so it shuts off after the disease is gone, and that isn’t happening here.”
Doctors now can look for increased levels of these chemicals in the blood of patients who might have chronic fatigue syndrome, potentially aiding in their diagnosis, she said.
The new study, published February 27 in the journal Science Advances, comes on the heels of a new Institute of Medicine (IOM) report that declared chronic fatigue syndrome a “legitimate” illness that should be treated by doctors as a disease rather than an emotional problem.
Between 836,000 and 2.5 million Americans suffer from chronic fatigue syndrome, and an estimated 84 to 91% of people with the disorder are not diagnosed, according to the IOM. Chronic fatigue syndrome tends to strike people in their 40s and 50s, and occurs four times more often in women than men.
Monday, October 6, 2014
New Clues to How Colds Can Spur Asthma Attacks
Scientists have pinpointed a molecule that may trigger potentially life-threatening asthma attacks brought on by colds.
The researchers say this finding could offer a target for new drugs to be developed to treat these attacks.
Most asthma attacks (80-90%) are caused by viruses that infected the airways, according to the British researchers. Most of these are rhinoviruses which are the main cause of the common cold.
The researchers found that a specific molecule called IL-25 may play a major role in asthma attacks caused by colds. The findings are published in the Oct. 1 issue of Science Translational Medicine.
“Our research has shown for the first time that the cells that line the airways of asthmatics are more prone to producing a small molecule called IL-25, which then appears to trigger a chain of events that causes attacks,” study co-lead author Nathan Bartlett, of the National Heart and Lung Institute at Imperial College London, said in a college news release.
“By targeting this molecule at the top of the cascade, we could potentially discover a much-needed new treatment to control this potentially life-threatening reaction in asthma sufferers,” he added.
The researchers say this finding could offer a target for new drugs to be developed to treat these attacks.
Most asthma attacks (80-90%) are caused by viruses that infected the airways, according to the British researchers. Most of these are rhinoviruses which are the main cause of the common cold.
The researchers found that a specific molecule called IL-25 may play a major role in asthma attacks caused by colds. The findings are published in the Oct. 1 issue of Science Translational Medicine.
“Our research has shown for the first time that the cells that line the airways of asthmatics are more prone to producing a small molecule called IL-25, which then appears to trigger a chain of events that causes attacks,” study co-lead author Nathan Bartlett, of the National Heart and Lung Institute at Imperial College London, said in a college news release.
“By targeting this molecule at the top of the cascade, we could potentially discover a much-needed new treatment to control this potentially life-threatening reaction in asthma sufferers,” he added.
Wednesday, September 24, 2014
Wisdom Wednesday: Chronic Low Back Pain
This new patient has been suffering from left sided sciatica for three months. About six weeks ago, he was hospitalized and treated for sciatica. During the hospital stay, he developed a perforated large intestine and had surgery, removing about a foot of large intestine and installing a colostomy bag. Subsequent surgery to remove the colostomy bag was successful. However, he developed C. difficile as a result of antibiotic therapy. After a few weeks, they were able to control the diarrhea well enough to send him home. He still has radiating pain down his left leg, his bowels are still inflamed with frequent diarrhea, and he now notes body wide aches.
Compare this history with the case of acute low back pain from last week’s Wisdom Wednesday. Obviously, this case is much more complex. On reviewing his history, he describes the pain as running down the anterior aspect of the left leg to the knee with occasional radiation into the groin. This is not the course of the sciatic nerve and, in fact, he was suffering from femoral neuralgia rather than sciatica. I have no clear information on the cause of the perforated intestine. However, I do comment on the relationship between these illnesses in my conclusions.
C. difficile kills about 1600 people in the US each year as the result of electrolyte imbalances associated with the diarrhea. It is an opportunistic infection that overgrows following the use of antibiotics. Please see my blog “Serious Diarrheal Infection in Kids Linked to Antibiotics” posted on March 14, 2014. Adults commonly develop C. difficile during hospital stays.
QA evaluation revealed impairment of Autogenic Facilitation (AF). Therapy Localization (TL) was to the surgical site of the perforated colon. This was corrected by Injury Recall Technique (IRT) restoring AF. Testing for inflammation was negative for prostaglandins, leukotrienes, cytokines, and histamine. However, nitric oxide was positive with a good response to L-glutamine, a particular probiotic (Saccharomyces boularidii), and folic acid. Challenge of the ilio-lumbar ligament was positive on the left, and after IRT correction, it returned again in weight bearing. TL was positive to the L4 vertebra, but no manipulation was performed.
Wednesday, September 17, 2014
Wisdom Wednesday: Acute Low Back Pain – A Brief Case History
This is the first in a series of typical case histories taken from my office notes. They will appear in the Wisdom Wednesday blog slot intermittently. I hope they will give the reader some insight into managing and guiding a patient through a health issue.
A 66-year old female returns to my office for the first time in six years with complaints of acute low back pain. She has been struggling with chronic bilateral knee pain and has had a couple of orthopedic opinions on treatment ranging from medication management to total joint replacement. She denies radiating pain from the back to the legs and believes the onset is related to compensating for the knee pain. She is currently on the following medications: Atenolol, Celexa, Benacar, Zyrtec, Eliquis, Prempro, Simustatin, Armour Thyroid, Flecainide and 2 baby aspirin per day. (The average American takes 4 prescription medications daily, so this patient is taking twice that amount. I commonly see patients taking 16 different prescription medications on a daily basis).
Autogenic Facilitation (AF) was intact, using a weak left gluteus medius as an indicator muscle. (This indicates no body wide injury response by the nervous system. Her body has either resolved the injury neurologically, or there was no body wide injury stimulation to begin with - the later fits her history) Oral challenge with a mix of NSAIDS resulted in strengthening of the weak muscle. A favorable response to oral challenge with fish oil was noted. (These tests indicate that her primary inflammatory response is the production of prostaglandins despite taking aspirin daily which tends to block this pathway) Challenge of the left ilio-lumbar ligament was positive in weight bearing only, corrected by Injury Recall Technique (IRT). (This is a local injury reflex and is the most common source of ongoing neurological stimulation in low back pain) Gait assessment was intact. (Despite her contention that this low back episode is the result of compensating for her knee pain, no altered gait mechanism was indicated)
Wednesday, July 30, 2014
Wisdom Wednesday: Boswellia
This is my favorite herb for personal use – it works really well for me as an anti-inflammatory compound. Boswellia or Indian frankincense is derived from the resin of Boswellia serrata. There are no known contraindications, it is deemed safe for use in pregnancy and breast feeding. However, a few people have had mild diarrhea or skin rash as an allergic reaction. I have had one case in ten years of clinical use.
The key constituents of Boswellia serrata include the boswellic acids but the resin also includes essential oil. The typical dosage is 600 to 1200mg/day of extract standardized to contain 60% boswellic acids.
I use a complex that also includes some Celery Seed fruit, ginger, and Turmeric. This combination will target leukotriene and cytokine inflammation with some benefit in reducing prostaglandin inflammation as well. Although it works in the same pathway, it does not prevent the production of leukotrienes and cytokines like ginger. It has an effect on the Vagus nerve that stimulates the breakdown of these immune inflammatory compounds in the liver.
Boswellia is extremely effective in the treatment of asthma as well. It is thought that the effect on the Vagus nerve also has a calming effect on the goblet cells lining the respiratory tract. The result is a reduction in both bronchial inflammation and mucous production in the respiratory tree.
Wednesday, July 23, 2014
Wisdom Wednesday: Ginger
Herbs are a vital aspect of my practice. When used properly, they are powerful supplements that can restore normal function quickly. My favorite herb is Ashwaganda, but my most popular herb is ginger.
Traditionally, ginger is used to treat morning sickness, nausea, motion sickness, or any digestive disturbance. It is safe for use (at recommended doses) in both pregnancy and breastfeeding.
I use ginger as an anti-inflammatory compound. Scientific research has established that ginger blocks the enzyme lipooxygenase. This enzyme is required to form leukotrienes and cytokines, common inflammatory compounds arising from the immune system. Clinically, about 40% of my new patients are producing excessive leukotrienes and/or cytokines. For a majority of them, ginger will reduce their inflammation quickly and effectively with no side effects.
Like most herbs, there are quality issues with ginger. I use a 1:2 liquid extract that is manufactured in Australia. All herbal products in Australia are produced to pharmaceutical standards by law. This is the only way I can guarantee my patients are using an effective product.
European herbal companies have similar standards that the industry has voluntarily established. In the US there are no such standards and the FDA considers herbs as food. Government food quality restricts contamination from cockroach parts and rat feces but does not address herbal quality. Therefore, in the US a product listed as ginger does not need to contain any ginger.
Wednesday, March 19, 2014
Wisdom Wednesday: Inflammation – Part 1
Regardless of what symptoms you have, inflammation is the key component. I frequently tell my patients, “if I had a magic wand and waved it to get rid of your inflammation, 80% of your symptoms would be gone.” There are several known chemical pathways for inflammation in the body. I will review the first three in this blog and cover the remainder in subsequent posts of Wisdom Wednesday.
The most common form of inflammation in the human body comes from prostaglandin production. At the site of injury, prostaglandins are released from damaged cells. The liver responds to this and releases large amounts of prostaglandins that promote systemic inflammation. That is why you often will “hurt all over” after a localized injury.
Typically musculoskeletal injuries, whether chronic or acute, will follow this prostaglandin pathway. NSAIDS (non-steroidal anti-inflammatory drugs) like Advil, Aleve, and aspirin block the prostaglandin pathways, reducing inflammation, and often providing relief. Unfortunately, they also block the prostaglandin anti-inflammatory pathways that omega 3 and omega 6 fatty acids follow. When taken for more than three days, these drugs interfere with cell membrane production and repair. With chronic use, GI bleeds, liver failure and heart attacks can occur. Several studies have documented that a minimum of 16,500 people in the US die each year from taking NSAIDS. Less than a third have any warning signals.
Omega 3 fatty acids often will block prostaglandin inflammation. I believe that the rampant inflammation seen in this country is due, in part, to omega 3 fatty acid deficiency. It is rated as the most common deficiency in America. Sometimes, omega 6 fatty acids are also necessary to block prostaglandin inflammation. However, if you have any of the attributes of metabolic syndrome (see earlier blogs), your body often will shunt the healthy omega 6 fatty acids from the anti-inflammatory pathway to make even more inflammatory prostaglandins.
A slightly less common inflammatory pathway is governed by leukotrienes and cytokines. When these chemicals are released from injury sites, they stimulate the immune system rather than the liver. The immune system then releases large amounts of leukotrienes and/or cytokines to promote systemic inflammation. This is a common occurrence in auto-immune diseases like rheumatoid arthritis, psoriasis, and Crohn’s Disease. NSAIDS have no effect on these inflammatory compounds. In fact, when NSAIDS block prostaglandins and the injury is not resolved, the body often defaults into the leukotriene/cytokine pathway. That is why NSAIDS often stop providing relief with continued use. Fortunately, leukotrienes and cytokines often will be reduced by two common herbs – ginger and boswellia.
Approximately 1500 herbs are used medicinally world wide. Of these, only 80 have had really good research. Both boswellia and ginger are part of those elite 80.
Ginger works by denaturing an enzyme called lipoxygenase. Lipoxygenase is required to form both leukotrienes and cytokines. Boswellia has an effect of the vagus nerve that results in reduced leukotrienes and cytokines. It is also often very effective in relieving asthma. In my office I prefer the ginger as it is inexpensive and easier to administer. Boswellia is quite expensive and must be taken with fat to be properly absorbed.
THE BOTTOM LINE:
If you suffer from inflammation, and I know you do, try supplementing omega 3 fatty acids. Chances are you are deficient anyway – it’s not in your diet anymore. If you have any factors associated with metabolic syndrome – central obesity, high blood pressure, high serum lipids, low thyroid function, or insulin resistance – limit your omega 6 fatty acid intake. Consider adding sesame seed oil to your diet. That will help block the conversion of healthy omega 6 fatty acids to inflammatory prostaglandins.
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