Muscle and cancer - It is not getting old that is the problem, it is getting weaker!

I saw this get picked up in a few places but no one was linking to the actual study.  The takeaway message is that building and maintaining muscle strength is vital to all for overall health and this extends to surviving cancer.  It is not getting old that is the problem, it is getting weaker!

Researchers studied patients with advanced melanoma to understand the illness as it related to muscle strength. They looked at CT scans of the psoas muscle in order to measure core muscle density. The authors then correlated the core muscle density with the risk of metastasis, or spreading of the cancer. 

Patients with higher muscle density were found to have significantly better survival rates and less metastasis.  The authors concluded that decreased muscle density was an important predictor in the outcome of the disease. Furthermore, they stated that “frailty, not age, was associated with decreased disease-free survival.”

Here is theabstract

Sarcopenia as a Prognostic Factor among Patients with Stage III Melanoma.

Abstract

BACKGROUND: Several hypotheses proposed to explain the worse prognosis for older melanoma patients include different tumor biology and diminished host response. If the latter were true, then biologic frailty, and not age, should be an independent prognostic factor in melanoma.

METHODS: Our prospective institutional review board (IRB)-approved database was queried for stage III patients with computed tomography (CT) scans at time of lymph node dissection (LND). Psoas area (PA) and density (PD) were determined in semi-automated fashion. Kaplan-Meier (K-M) survival estimates and Cox proportional-hazard models were used to determine PA and PD impact on survival and surgical complications.

RESULTS: Among 101 stage III patients, PD was significantly associated with both disease-free survival (DFS) (P = 0.04) and distant disease-free survival (DDFS) (P = 0.0002). Cox multivariate modeling incorporating thickness, age, ulceration, and N stage showed highly significant association with PD and both DFS and DDFS. DDFS was significantly associated with Breslow thickness (P = 0.04), number of positive nodes (P = 0.001), ulceration (P = 0.04), and decreasing muscle density (P = 0.01), with hazard ratio of 0.55 [95% confidence interval (CI) 0.35-0.87]. PD also correlated with surgical complications, with odds ratio (OR) of 1.081 [95% CI 1.016-1.150, P = 0.01]. 

CONCLUSIONS: Decreased psoas muscle density on CT, an objective measure of frailty, was as important a predictor of outcome as tumor factors in a cohort of stage III melanoma patients. On multivariate analysis, frailty, not age, was associated with decreased disease-free survival and distant disease-free survival, and higher rate of surgical complications.

Avoid ibuprofen if you want to grow muscle?

Well that heading is just to promote some interest, but to be honest it does have something to do with this post.  I spotted this bit of research reported yesterday, about how muscles get the signal to grow.  Developing and retaining muscle is not just an issue for bodybuilders or athletes, it is essential to health as we grow old.

The story in EurekaAlert explains:

We take it for granted, but the fact that our muscles grow when we work them makes them rather unique. Now, researchers have identified a key ingredient needed for that bulking up to take place. A factor produced in working muscle fibers apparently tells surrounding muscle stem cell "higher ups" that it's time to multiply and join in, according to a study in the January Cell Metabolism, a Cell Press journal.

The research identifies this factor as "serum response factor (Srf)" which  translates the mechanical signal of work into a chemical one.

Srf works through a network of genes, including one known as Cox2. That raises the intriguing possibility that commonly used Cox2 inhibitors—think ibuprofen—might work against muscle growth or recovery, Sotiropoulos notes.

The research is available here:

Srf-Dependent Paracrine Signals Produced by Myofibers Control Satellite Cell-Mediated Skeletal Muscle Hypertrophy

Adult skeletal muscles adapt their fiber size to workload. We show that serum response factor (Srf) is required for satellite cell-mediated hypertrophic muscle growth. Deletion of Srf from myofibers and not satellite cells blunts overload-induced hypertrophy, and impairs satellite cell proliferation and recruitment to pre-existing fibers. We reveal a gene network in which Srf within myofibers modulates interleukin-6 and cyclooxygenase-2/interleukin-4 expressions and therefore exerts a paracrine control of satellite cell functions. In Srf-deleted muscles, in vivo overexpression of interleukin-6 is sufficient to restore satellite cell proliferation but not satellite cell fusion and overall growth. In contrast cyclooxygenase-2/interleukin-4 overexpression rescue satellite cell recruitment and muscle growth without affecting satellite cell proliferation, identifying altered fusion as the limiting cellular event. These findings unravel a role for Srf in the translation of mechanical cues applied to myofibers into paracrine signals, which in turn will modulate satellite cell functions and support muscle growth.

Ok so how do I apply this to get massive?

Muscle Anatomy

I am getting addicted to the Khan Academy.  Their stuff on biology is amazing.