Prostate Cancer – Exercise Cuts Inflammatory Cytokines IL-6 & IL-8, reduces psychological distress

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American Society of Clinical Oncologists (ASCO) in Chicago yesterday report on exercise reducing psychological distress. Whether cancer outcome will be impacted is not yet known and will require study but inflammation may impact cancer progression.

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The usual treatments change metabolism, cause weight gain, “loss of lean muscle mass, change[s] lipids, increase[s] rates of diabetes, and it thins bones.”

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Exercise is even more critical in those undergoing hormone therapies.

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This was a small randomized study for seven weeks.

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Patients receiving usual care experienced a 0.08 log10 increase in pro-inflammatory interleukin-6 production, while patients treated with an exercise program experienced a 0.03 log10 decrease in IL-6 (P<0.05), said Charles Kamen, PhD, research assistant professor at the University of Rochester Medical Center in New York.

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In his oral presentation … Kamen and colleagues observed a similar relationship with another pro-inflammatory cytokine, interleukin-8. In the control patients, the researchers noted a 0.03 log10 increase compared with a 0.04 log10 decrease among the exercise group, Kamen said.

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Using the Profile of Mood States (POMS), the research team determined that psychological distress decreased 5.17 points among the exercise group but increased 2.43 points in the patients who were in the usual control group (P=0.02).

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“This study supports the use of exercise for cancer patients for reducing psychological distress and suggests a potential biological mechanism by which this improvement occurs, namely by reducing systemic inflammation,” Kamen said in his presentation….

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The POMS scores were overall significantly in favor of the exercise group, and the subscales all trended in favor of exercise, except for the anger subscale in which there was virtually no change, Kamen said.

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Radical experiment in managing pain without narcotics – Validation of years of work

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Read this story in the New York Times Business Day, May 10, 2014.

 

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It is the story of one veteran who had severe injuries. His wife now says when she sees other patients: “I can go in there and I can immediately spot people that are on narcotics or on drugs.”

 

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A Soldier’s War on Pain

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Many thanks from my heart to Barry Meier for his research into these rare pain specialists who are managing pain without narcotics, and the story of how this veteran did it.

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This validates so much of the work I’ve been toiling over since the turn of the century. This has nothing to do with blame. There is a whole new paradigm to the understanding of treating pain. But the article mentioned only those things my patients have failed, that were done before use of opioids. Physical therapy alone dates back to Greek culture and Hippocrates’ influence as the father of Western medicine and in Europe during the 1500’s. But another point was made and is important to emphasize: these therapies don’t work while someone continues taking opioids.

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Where are we now and what are the questions?

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-Only a few doctors are mentioned. We need more.

-Physicians are taught the first thing: Do no harm. But we are in a very difficult place right now. We are taught to use opioids. Little attention has been paid to research on how to treat patients once off opioids, after they have failed gabapentin, Lyrica, Cymbalta, opioids, Elavil.

-Patients don’t know that when asking for more opioids, they are actually creating more pain.

-There is less pain when you taper off opioids. That alone is often enough to help, but often more must be done.

-Who does better with a new approach?

-Insurance companies must be taught not to tie doctor’s hands with denials.

-Do we need to allow PA’s and NA’s to write their own opioids without doctor’s supervision?

-Or do we need to teach everyone, doctors and patients included, how to treat pain without opioids?

-None of us has the data that gives us greater certainty. Until then trillions of dollars are wasted creating disability and pain unknowingly.

-No I am not taking away grandmum’s small dose that she has been on for years and has been shown to improve function.

-Acute pain definitely and usually requires treatment with opioids. But chronic pain? How long do we prescribe opioids in the acute situation before we taper?

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Monster in the system – personal doctor ratings

Translation: job and hospital ratings – by the insurance system and the internet’s phoney doctor “ratings” — all those ratings partly depend on giving opioids and that colors the patient’s opinion of the doctor.

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Doctors who push opioids are more highly rated by patients. Is that what we want as a society?

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 Patients can’t be faulted.

How can they know better?

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Doctors do what they are trained to do, unaware that the opioids they prescribe actually cause more pain,  reinforcing the demand to give more opioids.

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I see better pain relief without opioids

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I will add much more on this page in the next few days, and even later adding remarkable case reports, and covering other medications seldom used, often compounded, but I wanted to get this out urgently. This is such a vast area. We all need to learn from those who are doing this work.

 

“Heavy NSAID Use Linked to Higher Dementia Risk” – Exercise, Antidepressants Both Help Neurogenesis

NSAIDs are anti-inflammatory drugs used to treat pain, inflammation, or fever.  The only NSAIDs that are NOT associated with increased risk of heart attack or arrhythmia are naproxen (Aleve) or aspirin.  Taking high doses of aspirin has a greater risk of GI bleed than naproxen, which is why I usually recommend naproxen.

Background:

Several past studies have shown NSAIDs delay or prevent dementia, but there have been contradictory results.  Last year Neurology published a study of 49,349 patients’ usage ranging from ≤1 year to ≥7 years done at Boston University and Bedford VA. They showed long term use of NSAIDs protects against Alzheimers:

Compared with no NSAID use, the relative risk of Alzheimer’s disease decreased from 0.98 for ≤1 year of use (95% CI 0.95 to 1.00) to 0.76 for >5 years of use (95% CI 0.68 to 0.85).

Among patients who specifically cited use of ibuprofen, the risk of Alzheimer’s disease declined from 1.03 (95% CI 1.00 to 1.06) to 0.56 (95% CI 0.42 to 0.75).

Ibuprofen came out ahead in that study perhaps because it is the most commonly used.

They also sought to answer whether NSAIDs known to suppress Aβ1-42 amyloid would more likely protect .  Aβ1-42 amyloid is a major component of plaques found in Alzheimer’s Disease.

Aβ1-42 amyloid suppressors include ibuprofen, diclofenac, flurbiprofen — but as for suppressing Alzheimer’s, these were found to be no different than other NSAIDs, putting that theory to rest.

Risk of dementia and Alzheimer’s Disease with prior exposure to NSAIDs in an elderly community-based cohort:

This new study by Breitner  et al, from the University of Washington School of Medicine was published online April 22, 2009, before the print edition in Neurology.  

Their outcome contradicts earlier protective studies possibly because they started with an older cohort, healthy adults 65 and older, which “could be enriched for cases [of Alzheimer’s] that would otherwise have appeared earlier.”

They prospectively followed 2,736 persons in a Seattle health plan.  Before starting the study, they reviewed pharmacy records as much as 17 years earlier.

Findings:

12.8% of the study participants [were] heavy NSAID users at baseline. Heavy use was defined as taking 500 or more standard daily doses over a two-year period.

Another 3.9% of participants became heavy users during follow-up.

Ibuprofen, naproxen, indomethacin, and sulindac accounted for about 80% of all NSAIDs used.

Through follow-up, 476 participants developed dementia; for 356 of them, it was Alzheimer’s disease.

After controlling for age, gender, education, APOE status, hypertension, diabetes, obesity, osteoarthritis, and physical activity, the risk of developing all-cause dementia was 66% higher among heavy users than among those with little or no NSAID use (HR 1.66, 95% CI 1.24 to 2.24).

The risk of developing Alzheimer’s disease was 57% higher (HR 1.57, 95% CI 1.10 to 2.23).

Strengths of the study: the community-based sample, biennial assessment of dementia, rigorous exposure classification, and large numbers of dementia cases, outweigh the limitations.

Limitations:  lack of generalizability to a younger patient population, the lack of exact dosing information, and the possibility of bias from unmeasured confounders.

Can we draw conclusions on one study alone? We know that exercise is protective against Alzheimer’s Disease and pain may have prevented this older age group from being active. Though they did control for that, this research needs to be supported by further studies. What is helpful is to remain as active as you can.  Keep and maintain every bit of function you can and get help for depression and anxiety as they may profoundly affect memory, morbidity and mortality.  For a review of the literature on the morbidity and mortality of stress and mood, refer to my post on Cognitive Behavioral Therapy and the importance of a positive outlook.

The brain makes new neurons – neurogenesis.  I will write more in the future on exercise, mood, stress, brain atrophy and memory loss.   Exercise improves depression and anxiety, and exercise stimulates neurogenesis.  It appears that the action of antidepressants also may be to stimulate neurogenesis.  Chronic low back pain has been reported to cause brain atrophy.  Chronic depression leads to brain atrophy and memory loss with atrophy occurring in the hippocampus, the area essential for memory.  This important publication from Vancouver reviews the topic in great detail and proposes a hypothesis:  Antidepressant effects of exercise: Evidence for an adult-neurogenesis hypothesis?

Further medication is being tested to reduce neuronal cell death that leads to Alzheimer’s Disease, using a very simple compound that blocks free radicals and inflammation.  More on this later.

The material on this site is for informational purposes only, and

is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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