Vitamin D and Interstitial Cystitis
I think that interstitial cystitis (IC) must be one of the most distressing of conditions to have, and it is certainly one of the most challenging to treat. Outside the United States, it is more often called painful bladder syndrome (PBS).
IC is a condition that results in recurring discomfort or pain in the bladder and the surrounding pelvic region. The symptoms vary from person to person and even in the same individual. It can vary from an experience of mild discomfort, pressure, tenderness, to intense pain in the bladder and pelvic area. Symptoms may include an urgent need to urinate (urgency), a frequent need to urinate (frequency), or a combination of these symptoms. Both may be severe: I’ve seen people who had to urinate every ten minutes. Pain may change in intensity as the bladder fills with urine or as it empties. Women’s symptoms often get worse during menstruation, and some experience pain with vaginal intercourse. There is a good website provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), that is fairly up-to-date.
Because IC varies so much in symptoms and severity, most researchers believe that it is not one, but several diseases. There are clear links between IC and fibromyalgia, irritable bowel syndrome and chronic fatigue, and probably many other illnesses.
There is good evidence that inflammation in one pelvic organ can cause pain in other organs that share some of the same nerve supply. Inflammation of the colon may make some nerves coming from the spinal cord hyper-excitable, which in turn makes nerves running to the bladder hypersensitive. Because the same nerve plexus connects with the ovaries and uterus, it is no surprise to learn that phases of the menstrual cycle impact the way in which inflammation in one pelvic organ can cause inflammation in another.
IC appears to be becoming more common, although that is always a risky comment, because it was undoubtedly not often recognized in the past. The old teaching was that it was only something that occurred in menopausal women, but it is now being diagnosed in men as well as women, and in people as young as their late teens.
The cause of IC remains unknown, though there have been many theories: infections, allergy, autoimmunity, neurological and genetic. There have been recent claims of the discovery of responsible genes, but hey would most likely be susceptibility genes, rather than causative. Otherwise why should the rates of IC genuinely seem to be increasing? What seems clear is that the normal mucus lining of the bladder wall is damaged.
Multiple types of treatment have been tried, from medication to pelvic floor exercise, to neurological implants and homeopathy and acupuncture. The report of anything new that may help is always welcome.
So I was interested to see a report from investigators in Milan on the efficacy using a molecule that has been attracting a lot of interest recently: vitamin D. The active form of vitamin D is known as calcitriol or 1,25-dihydroxycholecalciferol (1,25(OH)2D3) that is manufactured in the kidney. Its in vivo biological effects include regulation of bone metabolism, control and modulation of the proliferation of cells and some aspects of the immune response. These characteristics have already led to therapeutic applications in osteoporosis, secondary hyperparathyroidism, and psoriasis. Many reports show beneficial effects of vitamin D in animal models of diabetes, organ graft rejection, experimental allergic encephalomyelitis, lupus nephritis, and in asthma. Despite what you may have seen in some advertisements, just taking extra vitamin D does not help, and may make matters worse: they key is to have the right form of vitamin D, that can reach and affect the right areas of the body.
The Milan team used a vitamin D3 analogue (BXL628) in a mouse model of chronic cystitis. What they found was that a specific inflammatory marker in the blood went down with treatment, and at the same time histological analysis showed a decrease in edema and white blood cell (leukocyte) infiltration in the bladder wall. This and some other biochemical evidence of what is known as “mast cell degranulation,” is very encouraging and strongly supports the potential therapeutic use of BXL628 in diseases such as human interstitial cystitis.
This is the kind of mechanism-based research that holds out enormous promise for everyone’s welfare and will help us in our goal of using science to inform the development of the next generation of treatment, health and wellness.
Women, Asthma and the Brain
There’s been a longstanding puzzle in medicine. Well actually there are lots of them, but here’s one that may be a puzzle no more.
For many years now, it’s been known that asthma is more common in women, and also that psychological stress can cause flare ups of asthma.
Many women experience “menstrual flaring:” a worsening of asthma around the time of their menstrual period. There is also a strange paradox: some women with asthma wheeze less if they take an oral contraceptive, while some non-asthmatic women begin to wheeze when they take it. In some women pregnancy makes asthma worse, and in others it affords months of relief of symptoms. Women who are obese are more likely to get asthma, presumably because their intra-abdominal fat stores are churning out inflammatory mediators.
Researchers from the University of Wisconsin have shed some important light on this link between asthma and the brain. In research published in the Proceedings of the National Academy of Sciences. In the study, six patients with mild asthma were exposed to ragweed or dust-mite extracts. The subjects were shown three different categories of words: asthma-related (e.g., "wheeze"), non-asthma negative ("loneliness") or neutral ("curtains").
Using functional magnetic resonance imaging, they showed that activity in two regions, known as the anterior cingulate cortex and the insula showed increased activity when the asthma-related words were heard compared with the other types. What is more, this enhanced activity was specifically linked to physiologic signals from the ragweed and dust-mite extracts. So being exposed to asthma-relevant emotional stimuli is associated with markers of inflammation and airway obstruction in asthmatic people exposed to an asthma-producing antigen.
In people with asthma and other stress-related conditions, these brain regions may be hyper-responsive to disease-specific emotional and physiologic signals. Taken together, these could contribute to problems that worsen the asthma, such as inflammation.
And one of the ways of making these regions of the brain hyper-responsive? Bathe them in estrogen.
That still does not explain why pregnancy and the oral contraceptive makes some women’s asthma better, and does the opposite in others. But it may just have to do with the “set point” of the cells in these regions of the brain. In the same way that we might set the thermostat in out house. An already hyper-responsive brain might be normalized and an under-active one stimulated to be over-active.
We need to do some more experiments, but these are a great start.
If you ever wheeze, have a look to see if there are stressors or hormonal events that trigger you. Whether you are being treated with homeopathy, herbals or conventional therapy, knowing when to expect trouble gives you the power to adapt you treatment when you are entering a risky time in your life.
Another Reason to Eat Your Greens
“Health requires healthy food.”
–Roger Williams (Indian-born American Chemist who did pioneering work on the Vitamin B Complex, 1893-1988)
Earlier this year several news outlets including Time picked up a story that has been causing a great deal of discussion in medical circles.
Most of us have been extolling the virtues of fruits and vegetables for decades, but it’s always nice to have an extra piece of evidence to support what we’ve been saying. The question has been how to go from large-scale epidemiological studies proving the benefits of vegetables to the inner workings of a person’s arteries.
Investigators from Wake Forest University School of Medicine in Winston-Salem, North Carolina published an important study in the Journal of Nutrition. What they did was to study genetically altered mice, who had been bred to have a very high risk of developing rapid arteriosclerosis: the formation of fatty plaques in the arterial wall that can eventually block blood flow and lead to heart attacks and stroke.
Half the mice were fed a vegetable-free diet and half the mice were fed a diet that included broccoli, green beans, corn, peas and carrots.
After 16 weeks, the researchers measured the cholesterol content in the blood vessels and estimated that plaques in the arteries of the mice were 38% smaller. Cholesterol, and particularly the “bad” cholesterols VLDL and ILDL fell markedly in the mice on the healthy diet, but these improvements were not on their own enough to explain the improvement in the blood vessels: the anti-atherogenic effects of the vegetable diet remained largely unexplained by the variation in plasma lipoproteins or body weight.
There was a 37% reduction in serum amyloid – a marker of inflammation in mice – suggesting that consuming vegetables may inhibit inflammatory activity. This is line with data from other studies indicating that fruit and vegetables should be key components of an inflammation-lowering program. This is very important: in the last twenty years it has become very clear that arteriosclerosis is intimately associated with inflammation in the arterial wall.
Many inflammatory conditions including rheumatic fever, rheumatoid arthritis, systemic lupus erythematosus and psoriasis, are all associated with an increased risk of developing arteriosclerosis.
Interestingly some years ago Dean Ornish presented evidence indicating that diet and exercise could reverse arteriosclerosis. I’ve always found Dean’s work interesting, well done and persuasive. It surprises me to see how many people remain unconvinced. This new research provides indirect support for his work.
The average person only eats three portions of fruit and vegetables a day: we should all be eating at least five, and they should be of as many different colors and types as possible: there is excellent evidence that combinations of fruits and vegetables are much better for your health than just eating one or two types.
As an aside, I must admit that I’m no fan of animal experiments: I don’t and won’t do them. And every time that I hear about them, I think that we need to say a sincere thank you to the animal kingdom for their sacrifice in helping us.
“God, in His infinite wisdom, neglected nothing and if we would eat our food without trying to improve, change or refine it, thereby destroying its life-giving elements, it would meet all requirements of the body.”
–Jethro Kloss (American Nutritionist and Writer 1863-1943)
“In fresh fruit and vegetables and nuts are all the vitamins and minerals and high grade proteins the human body needs to bring it to a state of physical perfection and to MAINTAIN it in that state indefinitely.”
–Herbert Shelton (English Evolutionary Philosopher, 1820-1903)
“Nothing will benefit human health and increase the chances for survival of life on earth as much as the evolution to a vegetarian diet.”
–Albert Einstein (German-born American Physicist and, in 1921, Winner of the Nobel Prize in Physics, 1879-1955)
Peripheral Neuropathy
Treating peripheral neuropathy can be one of the toughest problems facing a clinician. Peripheral neuropathy simply means disease affecting the peripheral nerves.
There are a great many cause of peripheral neuropathy. This is just a partial list to give you an idea of the things that a clinician has to think about before starting treatment:
- Metabolic illnesses: Diabetes mellitus; porphyria; chronic renal failure; amyloidosis and disturbances in circulating proteins
- Vitamin deficiencies: Vitamins, B1, B3, B6 and B12
- Drugs and chemicals: Alcohol; Heavy metals like arsenic, lead and mercury; organic pesticides; several drugs used in cancer chemotherapy; isoniazid; nitrofurantoin
- Infections: Lyme disease; Herpes zoster (shingles); Diphtheria; Brucellosis; Leprosy; Tetanus; Botulism
- Malignant illnesses
- Inflammatory and autoimmune illnesses: Rheumatoid arthritis; Systemic lupus erythematosus; Polyarteritis nodosa; Sarcoidosis; Guillain-Barre syndrome; Celiac disease
- Physical injury: Trauma, stretching and compression of nerves, which can include things like carpal tunnel syndrome.
- Congenital illnesses
Many causes of peripheral neuropathy, particularly diabetes, may also damage the autonomic nervous system that controls the heart, blood pressure, swallowing, intestinal and bladder function.
Neuropathic symptoms typically start in the feet, because the nerves running down there are longer and more vulnerable than the ones going to the hands.
The most common symptoms are:
- Numbness
- Tingling
- Abnormal sensations called dysesthesias
- A characteristic form of pain, called neuropathic pain or neuralgia: people usually describe it as “pins and needles,” a steady burning sensation or “electric shocks.” These pains can be difficult to describe: typically pains, like stubbing your toe or stepping on something sharp, are transmitted through pain fibers. Neuropathy also involves other neurological pathways, so that the brain receives impressions that it cannot process.
There has been a revolution in out understanding of neuropathic pain in recent years. It is now considered to be a disease rather than a symptom. Normal pain is designed to protect you: you put your foot on a hot plate and you pull it away immediately. Neuropathic pain is different: it is non-protective and it persists and therefore behaves like a disease.
Multiple different classes of medications have been shown to be effective in some people with neuropathic pain, though most are not approved for use by the Food and Drug Administration:
- Lidocaine patches and creams
- Capsaicin creams
- Opioid analgesics
- Tricyclic antidepressants
- Serotonin-norepinephrine reuptake inhibitors (SNRIs)
- Anticonvulsants: Carbamazepine; gabapentin; pregabalin
Earlier this week, data presented at the European Federation of IASP (International Association for the Study of Pain) Chapters (EFIC) indicated that an innovative combination of painkillers might hold the key to unlocking the severe and relatively untreatable pain of peripheral neuropathy.
Dr Magdi Hanna, Director of Pain Clinical Research Hub at King’s College Hospital in London, has been studying the combination of the strong opioid oxycodone (OxyContin) with gabapentin (neurontin) in over 300 patients with severe diabetic neuropathy. This combination demonstrated a significant 33% improvement on top of the best pain relief achievable using the maximum tolerated dose of gabapentin as monotherapy. The study was part funded by one of the medicine manufacturers.
This study is good news, but even in this study there were a great many people who were not helped. In another blog item, I’m going to talk about some of the unorthodox approaches that have helped some people.
Restless Legs Syndrome
Restless legs syndrome (RLS) is a common (3-15% of the population) and sometimes very unpleasant problem in which people have uncontrollable urges to move their legs. If they do not move, they will begin to feel uncomfortable, painful or odd sensations in their legs, and sometimes also in other parts of the body. The restlessness may last for minutes or even hours. Movement affords people very temporary relief. The sensations are usually between the ankle and the knees, but they can also involve the thighs. If other parts of the body are involved it always makes us question the diagnosis.
The severity of the problem is highly variable, running from a mild annoyance to an incapacitating problem. In most people the symptoms are worse when sitting or at night, and often lead to loss of sleep. Not surprisingly many people feel of exhausted and irritable during the day.
With such enormous variations in the severity of the problem, and even the parts of the legs affected, it is highly likely that RLS is a symptom of a group of illnesses.
The International Restless Legs Syndrome Study Group (IRLSSG) identified four criteria that must be present for an RLS diagnosis:
- An urge to move, usually due to uncomfortable sensations that occur primarily in the legs.
- Motor restlessness, expressed as activity, that relieves the urge to move.
- Worsening of symptoms by relaxation.
- Variability over the course of the day-night cycle, with symptoms worse in the evening and early in the night.
About 80% of the people with restless legs syndrome also suffer from a separate condition called periodic limb movements in sleep (PLMS). Periodic limb movements in sleep are involuntary jerking movements in extremities, usually the legs. You can have PLMS without having RLS, and vice versa.
RLS may start at any age, including early childhood, and is a progressive disease for a certain percentage of sufferers, although it has been known for the symptoms to disappear permanently in some sufferers. The condition runs in families; children of RLS sufferers are more likely than other people to develop RLS.
It has some similarities to a syndrome known as akathisia that occurs in people taking some medications that work in the dopamine pathways of the brain. There are some subtle ways of telling the two apart, but RLS also seems to be caused by disturbances in one of the dopamine pathways of the brain.
It has been known for many years that there is an association between RLS and iron deficiency, but this link is probably not causal: just giving iron only helps a proportion of sufferers. But because of this link, everyone with RLS should have their ferritin levels tested; ferritin levels should be at least 75 mcg for those with RLS. If it’s below this level, iron supplements may help, but they are best administered by a physician, because ferritin needs to be monitored and there are down sides to taking too much iron. In a moment I’ll tell you about some very new research on iron and RLS
Caffeine and other stimulants usually make RLS worse. Restless legs syndrome frequently occurs during pregnancy. About 15% of pregnant women develop RLS symptoms during the last few months of their pregnancy. The sensations usually stop after the woman delivers the baby.
We normally divide RLS into primary and secondary. Primary RLS usually starts before age 40 and the onset is often slow. The RLS may disappear for months, or even years. But it can be progressive and get worse as the person ages.
Secondary RLS often had a sudden onset and may be daily from the very beginning. Apart from pregnancy, secondary RLS is a result of a number of medical conditions, so it is always important to rule them out. They include:
- Iron deficiency anemia
- Macrocytic anemia due to folate or vitamin B12 deficiency
- Diabetes mellitus
- Peripheral neuropathy
- Alcohol abuse
- Some types of cancer, particularly of the lung
- Celiac disease
- Renal failure
- Inflammatory arthritis
There have been reports of associations of RLS with other illnesses, but most seem rare. Interestingly people who undergo surgery often find that RLS symptoms become worse, which may be another clue as to the cause of the problem.
An international conference entitled SLEEP 2006, the 20th Anniversary Meeting of the Associated Professional Sleep Societies took place from June 17-22, 2006 in Salt Lake City, Utah. There were a great many interesting papers this year, including several on RLS
An international group of collaborators presented the results of the first population-based pediatric RLS survey. They used the National Institutes of Health pediatric RLS diagnostic criteria and collected data from over 10,000 families. The criteria for definite RLS were met in 1.9% of 8- to 11-year-olds and in 2% of 12- to 17-year-olds. Two different papers explored the value of using a single screening question to identify possible RLS patients. Those who answered, “Yes,” then answered more detailed questions to determine whether they met the International RLS Study Group diagnostic criteria.
A single screening question can eliminate people without RLS rapidly and direct appropriate subjects to further evaluation. Two groups of researchers found a high level of sensitivity with the question, "When you try to relax in the evening or sleep at night, do you ever have unpleasant, restless feelings that can be relieved by walking or movement?"
As I mentioned, it has been known for decades that RLS may be associated with low iron, and especially with low ferritin levels. These may be present in symptomatic RLS patients during pregnancy and in people with iron-deficiency anemia and end-stage renal disease. Previous studies had suggested that supplemental iron was beneficial for RLS patients with low ferritin levels. One paper presented further evidence of the possible efficacy of supplemental iron in the treatment of selected RLS patients with a prospective, randomized, placebo-controlled, double-blind study of RLS patients with low to normal ferritin levels (15-75 mcg/L). The RLS subjects were given either placebo or iron 325 mg twice daily and were monitored with a validated RLS symptom scale. The preliminary findings showed that the iron supplementation group had significant increases in their ferritin levels and had improved quality of life compared with those on placebo; however, the interim data presented did not show a significant change in the RLS symptom score. The study is ongoing.
Treatment for RLS is based on how disruptive the symptoms are. Apart from iron, people should review their lifestyle and see what changes could be made to reduce or eliminate their RLS symptoms. These include: Finding the right level of exercise (too much worsens it, too little may trigger it)
Eliminating caffeine
Stopping smoking
Reducing alcohol intake
Several drugs have been tried for RLS: Some of the same medications used in Parkinson’s disease, benzodiazepines, anticonvulsants like carbamazepine and gabapentin.
Last month saw the publication of an important paper indicating that the medicine pramipexole, another anti-Parkinsonan drug, helps many people with RLS
In the next article I shall review some of the other approaches used by Integrated Medicine.
Psychiatric Illnesses and Fibromyalgia
There’s an interesting and important article in last month’s issue of the Journal of Clinical Psychiatry, by a group of investigators from the University of Cincinnati.
They have shed important new light on fibromyalgia. We’ve recently learned how it is linked to disturbances of the serotonin transporter, as well as anti-inflammatory proteins, and that is may respond best to the kind of comprehensive multi-leveled approaches that we use in Integrated Medicine.
The new research compared people with fibromyalgia with people with rheumatoid arthritis, and it found that fibromyalgia, but not rheumatoid, may be associated with a range of psychiatric illnesses:
- Major depressive disorder
- Bipolar disorder
- Comorbid anxiety disorders including panic disorder, social phobia, posttraumatic stress disorder and obsessive-compulsive disorder
- Eating disorders and
- Substance abuse
What was particularly important in this study was that the psychiatric problems usually preceded the onset of fibromyalgia. So it wasn’t that people were developing psychological problems because they were in chronic pain.
It’s beginning to look as if fibromyalgia is part of a larger group of disorders that all share common etiologies or causes. Family studies have indicated that fibromyalgia and mood disorders share some of the same – perhaps genetic – determinants.
The study also confirms what we have said before: fibromyalgia is not only associated with some psychiatric problems, but also with other medical disorders, several of which may also co-exist with the same psychiatric problems. They include:
- Chronic fatigue syndrome
- Irritable bowel syndrome
- Interstitial cystitis
- Multiple chemical sensitivities and
- Migraine
Not only does this research highlight the need to check people with fibromyalgia to see if they might also be struggling with a psychiatric problem, but it is helping us home in on some of the mechanisms linking these apparently separate problems.
This particular study was done mainly in white women, and the investigators knew who had fibromyalgia, so there’s more work to be done.
But if you or a loved one is struggling with fibromyalgia, it is good news to know that we are making rapid progress in unraveling this horrible illness.
Rheumatoid Arthritis: A Neurological Disease?
For more than a century, there’s has been a puzzle in rheumatology. Why is it that so many people with inflammatory arthritis get symmetrical involvement of their joints? It is very common for people to get exactly the same joints involved in both hands or in both feet.
Sometimes joints get affected by arthritis because they have already been subjected to a lot of wear and tear: that’s thought to be one of the reasons why gout most often affects the big toe. But the symmetrical pattern of arthritis is far more difficult to understand. There has been speculation for at least 30 years that this symmetry indicates neurological involvement in the disease, and there was a stimulating paper on the topic seventeen years ago, and it has been known for some time that artificially induced arthritis in one joint produces inflammatory changes in the same joint on the other side of the body.
Now investigators from the University of California at San Diego School of Medicine have published an important discovery. Rheumatoid arthritis drugs work better, at least in arthritic rats, when delivered into the central nervous system. Rheumatoid arthritis (RA) is a disease in which there is chronic inflammation, leading to joint pain and destruction. Pain and inflammation in the joints are constantly monitored by the central nervous system, and we have known for many years that the nervous system can regulate inflammation and immune responses. It was demonstrated in the 1960s that damage to certain regions in the hypothalamus of the brain could impair the work of the immune system. The scientists from San Diego focused on a protein called p38, which is involved in a number of cellular processes critical to the development of RA. Several substances that block the action of p38 are effective in animal models of arthritis and are currently being tested in clinical trials in patients with RA.
Pain and inflammation activate p38 in the brain and spinal cord, and blocking it by introducing medicines directly into the central nervous system reduces inflammation in joints.
This is important research, because it opens up new possibilities for treating an illness that can often be very difficult to treat. It may also help explain another observation. Some patients with rheumatoid arthritis who are treated with acupuncture get a reduction in joint symptoms and sometimes even repair of some of the damage to the cartilage in their joints. Experienced acupuncturists see this in about a third of patients whom they treat, so it was a surprise to see a review claiming that acupuncture did not help RA. If we see a disconnect between clinical observation and a research study, there are two options: either clinicians are deluding themselves or there’s something wrong with the research method. Interestingly, there’s recently been a great deal of discussion about the kind of research methodology that produced this negative result, prompted by a very interesting and challenging paper.
My conclusion? Acupuncture may indeed be a valuable adjunctive treatment for RA. But whether it will work on its own remains less certain.
And the best approach of all is to address the physical, psychological, social, subtle and spiritual dimensions of a person with RA. In other words, the new form of Integrated Medicine that I describe in Healing, Meaning and Purpose.
Probiotics: Caveat Emptor
You may well have heard the advice that we all need to keep the bacetria in our intestines healthy. Countless experts have recommended that, as long as we are not lactorse intolerant, we should regularly take some live yoghurt to "re-colonize" our intestines with nice friendly bacteria.
There has just been a briefing in London to warn the public that as many as half of the "probiotic" or "friendly bacteria" products on sale in the United Kingdom could be ineffective and some may even be harmful.
The experts on the panel included Professor Glen Gibson from the University of Reading who is an expert in food microbiology, and recommended sticking to products made by major manufacturers. Too many of the other productsmight not contain the numbers of bacteria advertised, and the icrobes might not survive long enough in the intestines to do much good.
The evidence that probiotics help is still far from settled, as discussed in a recent review. But there are enough reports to think that probiotics may be helpful for irritable bowel syndrome and perhaps inflammatory bowel disease.
An even newer area or interest in the use of "prebiotics:" short-chain carbohydrates that alter the composition, or metabolism, of the intestinal organisms in a beneficial way.
Make sure that if you are using a product, it comes from a reputable manufacturer, and that it contains at least 10 million bacteria. And as I said in my title, "Caveat Emptor," "Let the buyer beware."
Parkinson’s Disease, Allergies and Inflammation
The symptoms of Parkinson’s disease have been reported throughout history, but it was first described in the modern era by the great Scottish neurologist James Parkinson in 1817. Even after all these years, we still do not know all that much about what causes it. There’s an interesting study in the August issue of the journal Neurology, which is the official publication of the American Academy of Neurology.
Investigators from the Mayo Clinic used what is known as a case-control design (196 cases and 196 matched controls). What they found was that people who suffered from hay fever or allergic rhinitis, are 2.9 times more likely to develop Parkinson’s disease over a 20-year period.
The researchers did not find any association with autoimmune illnesses such as lupus, rheumatoid arthritis, pernicious anemia or vitiligo. They also did not find any association with asthma.
In addition, people who developed Parkinson’s disease used anti-inflammatory agents less frequently than controls, although this result was not statistically significant. The results may support the hypothesis that there is an inflammatory component in the causation of Parkinson’s disease.
You may ask, “Why on earth would anyone even look at a link like this?” The answer is that there have been previous reports of an association between the use of non-steroidal anti-inflammatories and lower rates of Parkinson’s disease in men but not in women and Alzheimer’s diseases.
This study does not suggest that hay fever causes Parkinson’s disease: it provides evidence for an association between the two. Parkinson’s is probably a group of illnesses with different causes. However, if chronic inflammation around the upper airways could produce inflammation in the brain, we might have a whole new way of preventing a degenerative brain disease.
In a future posting I’ll talk about some natural methods for reducing the burden of inflammation in your body.
