THREAD: Adhesive capsulitis: An age related symptom of metabolic syndrome and chronic low-grade inflammation?

Summary of this interesting paper of Pietrzak 2016.
https://www.ncbi.nlm.nih.gov/pubmed/26880627 

The underlying etiology of adhesive capsulitis (AC) is very poorly understood. Several hypotheses have been suggested (discussed further below). Some reviews want to abandon the term AC cause no articular adhesions are associated w/ the pathophys., however capsular adhesions are.

AC is probably overly diagnosed. Clinical diagnosis mostly consists of history, equaly restricted passive and active ER and elevation range w/ negative Rx to check for extreme OA cases, posterior dislocations, tumors, etc. that can mask as AC.

There are strong associations between AC, age, diabetes and cardiovascular diseases. Do they share a common etiology? Off to the hypotheses:

1. Metabolic Syndrome: chronic low grade inflammation

Evidence of elevated blood glucose, lipids and cholesterol have been associated with AC. In one study, apparently healthy indiv. w/ AC underwent blood tests. 23% were hyperglycaemic, 68% had high total cholesterol,...

...64% elevated LDL & 34% elevated TG. Could those pre-diabetic cases be considered secondary AC patients? What are the average blood gluc., LDL and TG levels in a 21st century western person?

Is this the new 'norm', are these cases really so different from the genpop nowadays? Or ar we just seeing floor effects of 'unreasonably low' cut-off values for 21st century? Since 30-70% (via WHO) of the European population is considered overweight.

If so - and these hypotheses are the true underlying cause - we should see an increase of AC over the years. Is this the case? (honestly don't know, anyone?)

2. Chronic low grade inflammation, autonomic dysregulation

Relative autonomic sympathetic dominance is thought to induce chronic low grade inflammation. This sympathetic dominance is measured via variables as decreased heart rate variability (HRV). Tissue biopsies show signs...

...of this chronic low grade inflammation. This low grade inflammation is associated with increased pro-inflamm cytokine production and increased sympathetic activity and neuro-immune activation. These cytokines and neuro-immune cells are found in AC.

3. Shoulder functional design and modern lifestyle

The shoulder has gotten an evolutionary design to be able to do a variety of overhead movements like throw. People nowadays might not use these kinds of ROM which might mean these structures aren't exercised or stretched...

...enough and could predispose these people for adhesions via cytokine production, sympathetic activity and a neuro-immune response in this region. They found decreased shoulder ROM in the contralateral limb as well. This might explain secondary AC after an injury in the limb.

4. CHL anatomy, synovitis, AC and psychosocial stress

The CHL is prone to 'impingement' which can result in a cascade of reactions described above.
Psychosocial stress can induce endothelial dysfunction and low grade inflammation through the same mechanisms.

"The hypothesis predicts that age matched populations over >40y w/ obesity, metabolic syndrome & decreased HRV will show sgn greater incidence of AC compared to healthy controls w/out obesity & metabolic syndrome who participate in PA to recommended standards & have nrml HRV."

Last quote is a bit of a leap I think, considering the limitations of the study and the somewhat uncertain data (correlations vs causations, confounding variables, proxy variables and whatnot).

Nonetheless, end of the thread. Thanks!