…directly. But in practice, the pain of arthritis limits activity and discourages exercise. The chronic pain of arthritis wears people down, contributing to depression, which is a substantial mortality risk factor. Limitations on mobility combined with disspiriting effects of pain can destroy the will to live. There is no cure for arthritis yet, but anti-inflammatories can slow its progress, and one Swiss company claims a cure in the pipeline.
The “commonsense” view of osteoarthritis is that the cartilage that lubricates our joints gradually wears down over time, and when we are old, bone grinds against bone. Ouch! In fact, the commonsense view became the medical view which dominated for many years. But is it really so commonsensical? Wearing down of the lubricant cartrilage takes place in the course of hours and days, and, in young people, it is rebuilt and replaced as fast as it is worn away. (Even the association of extreme exertion with early-onset arthritis (Sandy Koufax’s elbow, : Shaquille O’Neal’s foot) is an effect of chronic inflammation rather than physical wear.) Thirty-year-olds don’t have more arthritis than ten-year olds, but by sixty, almost everyone has symptoms of enlarged joints, degenerated disks or lumbar pain. What happens over decades is not explained by the sum of tiny deficits in repair from day to day. Rather it is changes in the metabolism (initiated by epigenetics, and mediated by signal molecules in the blood) that causes a slowing of regeneration and an acceleration of inflammatory damage.
Historically, the medical community distinguishes rheumatoid arthritis–an autoimmune disease–from osteoarthritis, which is accumulated wear on joints. The emerging view, however, is that there is no fundamental distinction between them, and that the same metabolic forces are at play in both. The symptoms were always the same, but the distinction was based etiology: osteoarthritis is almost universal in older people, whereas rheumatoid arthritis is traceable to trauma or an autoimmune condition. We know now that autoimmunity is part of human aging, an icon of the self-destruction program coded in our genes.
Spinal stenosis is a particularly painful and debilitating complication of arthritis in the spine. Inflamed bone grows until it impinges on the spinal cord, generating numbness or referred pain in the legs and compromising movement. Fibromyalgia seems to be a generalized inflammation of joints and muscles.
What can be done?
Exercise may be the best treatment. The cruel paradox is that arthritis makes exercise much less appealing, and so a vicious cycle begins.
“Patients’ fear for disease aggravation and an indefensible traditional approach of rheumatology health professionals to recommend exercise restriction may account for the inactive lifestyle of this population. It is now established that well-designed physical exercise programmes promote prolonged improvements without inducing harmful effects on disease activity and joint damage.” [ref]
Exercise may hurt, but you won’t hurt yourself with exercise. Cycling and water aerobics are often suggested, not because they are inherently better for arthritis, but because people experience less discomfort and are more likely to stick with the program.
There is no cure for arthritis, but all the emerging anti-aging technologies are expected to slow or turn back the arthritis clock.
I’ve recommended vitamin D for many reasons, especially lowering risk of cancer and preserving the immune system. In this study, vitamin D supplementation lowered incidence of arthritis by 1/3. This study found that people with high circulating levels of vitamin D in the blood had risk of arthritis lower by 2/3. Depending on your metabolism, you may need to take jumbo doses of vitamin D (10,000 – 30,000 IU) to get your blood level up above 90, which I think is ideal. (Here’s a study that looked for a protective effect of vitamin D and didn’t find any. Here’s another study that finds more tentative evidence of a benefit from high blod levels of vitamin D.)
Arthritis may also be one more reason to keep your magnesium intake high.
Glucosamine supplements have been used for more than 20 years, and are well-researched. On average, they are marginally effective, if taken in sufficient quantity of 3 or more g per day. Response varies with the individual, and glucosamine is well worth trying. One study has found a lower all-cause mortality rate in people who take glucosamine.
A dark horse worth trying is boron, a trace mineral for which there is indirect evidence for a powerful benefit [ref].
S-adenasyl methionine (SAMe) is a pro-hormone, sold by prescription in Europe, where it is used as a treatment for arthritis. Here’s a study that found SAMe worked as well as Celebrex. My opinion is that SAMe is worth trying, despite thin evidence, because side-effects of SAMe are likely to be salutory.
A study with krill oil produced the best reported results. Over the first month of treatment with 300mg/day, patients reported substantially less pain and more mobility, and their subjective experience was corroborated by a 30% drop in C-Reactive Protein (CRP) in their blood (a marker of inflammation).
Boswellia is a resin from the sap of a tree, classically known as frankincense. It is well-known for anti-inflammatory effect, and there are four well-controlled studies that show objective and subjective benefits [1, 2, 3, 4]. (References collected by Examine.com)
Curcumin (from turmeric) is the best known of the herbal anti-inflammatories. In clinical trials, it has been found to be effective, but not a magic bullet, comparable in benefit to ibuprofen. Getting an adequate dose absorbed into the bloodstream is always an issue.
Nigella sativa produced benefits for some patients. It is a tasty black seed, used in rye bread and middle-eastern cooking, known variously as charnoushka, kalonji, or black cumin seed (no relation to cumin).
Here is a review of many herbal anti-inflammatories, with explanation of the role of the signaling by NFkB as a bad actor. (Full text available from ResearchGate.) This team of distinguished Indian-Americans, with thousands of publications among them, highlights curcumin, resveratrol, tea polyphenols, genistein (soy), quercetin (onions), silymarin, guggulsterone boswellia and ashwagandha. Here is their table, including other candidates that have shown some promise in at least one study.
NSAIDs are effective. Aspirin and ibuprofen are safe but of small benefit. COX2 inhibitors (e.g. Celebrex=celecoxib) are more effective but raise the risk of heart disease. For some, the tradeoff may be worthwhile. Celebrex has been marketed by Pfizer for about 20 years, and has been the subject of commercial law suits unrelated to safety.
Steroids (esp dexamethasone) work temporarily and make you feel good for awhile, but are not a long-term solution because of side-effects from upset stomach to diabetes to depression.
Humira, Remicade, and Enbrel are more recent entries into the arthritis marketplace. They all target tumor necrosis factor (TNF) cytokines, they are all fantastically expensive, and clinical data is yet thin. Talk to your insurance company.
On the horizon
Two years ago, there was a report from a Swiss pharmaceutical claiming a cure for arthritis in mice. They combined dexamethasone with targeted immunotherapy, paradoxically using the immune system itself to attack inflamed sites [ref]. Interleukin4 is fantastically expensive, probably one motive for modifying the molecule with an antibody that would seek out inflamed target cells, so the dose can be reduced. (Of course, lowered dosage also means fewer side-effects.) The journal article and news reports from 2014 indicated that trials in humans were imminent, but I have been unable to find evidence that this has come to fruition yet. While you’re waiting, you might write to scientists at ETH, which is a sort of Swiss MIT.
The Bottom Line
As with so many aging conditions, there is no miracle cure, but there are lots of possibilities for treatments that have great benefit for a few, and small benefit for others. Until we have personalized medicine based on your genetic and epigenetic profile, there is no substitute for personal experimentation. Many of the recommendations above have beneficial side-effects, or none. Try them freely, singly or in pairs. On for a month – off for a month – on for a month – off for a month, keeping a diary of symptoms. This is a time-consuming exercise, to be sure, but the potential benefit is huge. Don’t give up if the first few treatments that you try don’t seem to be working; that’s all in the nature of the game. We’re looking for the treatment that resonates with your metabolism, and you’ll know it when you find it if you can remain objective and scientific. (That’s the purpose of the diary.)