Chronic Obstructive Pulmonary Disease:  Is COPD also part of the Secular trend?

 

Copyright 2012, James Michael Howard, Fayetteville, Arkansas, U.S.A.

(New: Some new support of usefulness of testosterone in COPD, below.)

I have explained the "Secular Trend," at my website and my blog.  I think one of the major problems of the secular trend is the early decrease in testosterone.  This early decrease in testosterone is the result of an early, high production of testosterone.  With time, the percentage of individuals of early, high testosterone increases within the population.  Therefore, morbidity caused by reductions in testosterone increases within this group with time.  That is, morbidity of reduced testosterone increases within the population.  I think COPD is part of this mechanism.  It is known that COPD is increasing.

A number of publications indicate that testosterone is low in COPD.  However, as far as I can determine, the authors attribute reduced testosterone to the effects of COPD.  I think COPD is caused by low testosterone.  You can do the research regarding testosterone and COPD at PubMed

It is known that blacks produce more testosterone than whites.  Therefore, in the case of reduced testosterone, blacks should exhibit less COPD than whites with time.  (In this case,  the usually used explanation of socioeconomic level is reversed.  Whites and women exhibit more COPD than blacks and males.  …see Figure 4 at “Genetics and racial, ethnic, and gender characteristics of COPD.”

The statistics, above, indicate that loss of testosterone is involved in the increase of COPD.  Therefore, I suggest COPD is part of the increased morbidity of the Secular Trend.  The findings that blacks and males exhibit some protection from COPD with age adds to my suggestion that it is loss of testosterone with age that results in chronic obstructive pulmonary disease.

NEW from “Pubmed”:

BMJ Open. 2013 Aug 13;3(8). pii: e003127. doi: 10.1136/bmjopen-2013-003127.

Endogenous testosterone level and testosterone supplementation therapy in chronic obstructive pulmonary disease (COPD): a systematic review and meta-analysis.

Atlantis E, Fahey P, Cochrane B, Wittert G, Smith S.

Source

School of Nursing and Midwifery, University of Western Sydney, Campbelltown, New South Wales, Australia.

Abstract

OBJECTIVE:

Low testosterone level may be a reversible risk factor for functional disability and deterioration in patients with chronic obstructive pulmonary disease (COPD). We sought to systematically assess the endogenous testosterone levels and effect of testosterone therapy on exercise capacity and health-related quality of life (HRQoL) outcomes in COPD patients, as well as to inform guidelines and practice.

DESIGN:

Systematic review and meta-analysis.

DATA SOURCES:

We searched PubMed, Scopus, Cochrane Library, CINAHL, Health Source Nursing and PsychINFO and the reference lists of retrieved articles published before May 2012.

INCLUSION CRITERIA:

Observational studies on endogenous testosterone levels in people with chronic lung disease compared with controls, or randomised controlled trials (RCTs) on testosterone therapy for exercise capacity and/or HRQoL outcomes in COPD patients were eligible.

DATA EXTRACTION AND ANALYSIS:

Data on the mean difference in endogenous total testosterone (TT) values, and the mean difference in exercise capacity and HRQoL values were extracted and pooled using random effects meta-analysis.

RESULTS:

Nine observational studies in 2918 men with COPD reported consistently lower levels of TT compared with controls (weighted mean difference was -3.21 nmol/L (95% CI -5.18 to -1.23)). Six RCTs in 287 participants yielded five studies on peak muscle strength and peak cardiorespiratory fitness outcomes (peak oxygen uptake (VO2) and workload) and three studies on HRQoL outcomes. Testosterone therapies significantly improved peak muscle strength (standardised mean difference (SMD) was 0.31 (95% CI 0.05 to 0.56)) and peak workload (SMD was 0.27 (95% CI 0.01 to 0.52)) compared with control conditions (all but one used placebo), but not peak VO2 (SMD was 0.21 (95% CI -0.15 to 0.56)) or HRQoL (SMD was -0.03 (95% CI -0.32 to 0.25)).

CONCLUSIONS:

Men with COPD have clinically relevant lower than normal TT levels. Insufficient evidence from short-term studies in predominately male COPD patients suggests that testosterone therapy im