Age-related Macular Degeneration


Age-related macular degeneration is one of the commoner causes of visual impairment in the elderly. See: The pathology starts much earlier, though. The symptoms are loss of clarity in the centre of the visual field. As the disease progresses a grey smudge fills the centre of vision. There is evidence of an association with cpn. Vigorous treatment with antioxidants and mitochondrial support supplements may stop its advance.


"A combination of supplements (acetyl L-carnitine, CoQ10 and n-3 oils) was found to improve and stabilize vision in age-related macular degeneration (AMD). [Feher J et al., Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl L-carnitine, n-3 fatty acids, and coenzyme Q10. Ophthalmologica. 2005 May-Jun;219(3):154-66.] AMD is a condition with a multifactorial aetiology, one factor being possible chronic infection with Chlamydia pneumoniae [Ishida O et al., Is Chlamydia pneumoniae infection a risk factor for age related macular degeneration? Br J Ophthalmol. 2003 May;87(5):523-4; Kalayoglu MV et al., Serological association between Chlamydia pneumoniae infection and age-related macular degeneration. Arch Ophthalmol. 2003 Apr;121(4):478-82; Robman L et al., Exposure to Chlamydia pneumoniae Infection and Progression of Age-related Macular Degeneration. Am J Epidem 2005 161(11):1013-1019.] AMD is a disorder characterized by mitochondrial depletion and damage. [Feher J et al., Mitochondrial alterations of retinal pigment epithelium in age-related macular degeneration.Neurobiol Aging. 2005 Jun 22.] If the link between AMD and cpn is further ascertained, AMD may be considered a paradigm of chronic progressive infection with Chlamydia pneumoniae. Improvement following antioxidant treatment is significant." (edited excerpt from 

Very interesting, as the opthalmologist my husband saw, thought he had that problem, but the tests at the hospital said no....but he had been doing the BBD for 2 years, so maybe that helped him (same supplements).

Another abstact on AMD:

Exposure to Chlamydia pneumoniae Infection and Progression of Age-related Macular Degeneration

Authors: Robman, Luba1; Mahdi, Olaimatu2; McCarty, Catherine1; Dimitrov, Peter1; Tikellis, Gabriella1; McNeil, John3; Byrne, Gerald2; Taylor, Hugh1; Guymer, Robyn1

Source: American Journal of Epidemiology, Volume 161, Number 11, 1 June 2005, pp. 1013-1019(7)

Publisher:Oxford University Press


Recent studies have found an association between exposure to Chlamydia pneumoniae infection and risk of age-related macular degeneration (AMD). To assess a potential risk of AMD progression posed by exposure to C. pneumoniae, the authors reexamined Australian residents in 2001–2002 who were aged 51–89 years with early AMD at baseline (1992–1995). Examination included macular photography and an enzyme-linked immunosorbent assay to determine antibody titers to the elementary bodies from C. pneumoniae AR39. AMD progression was assessed quantitatively, using both coarse and fine progression steps following an international classification for AMD grading, and also qualitatively, by side-by-side comparison of baseline and follow-up macular photographs. Serologic data were available for 246 of 254 (97%) subjects. AMD progression was associated with a higher antibody titer. After adjustment for age, smoking, family history of AMD, history of cardiovascular diseases, and source study, the subjects in the upper tertiles of antibody titers were 2.1 (95% confidence interval: 0.92, 4.69), 2.6 (95% confidence interval: 1.24, 5.41), and 3.0 (95% confidence interval: 1.46, 6.37) times more at risk of progression than those in the lowest tertile, using three definitions of progression, respectively. The fact that seroreactivity to C. pneumoniae was independently associated with the risk of AMD progression suggests that C. pneumoniae infection may be an additional risk factor for AMD progression.

Document Type: Research article

DOI: 10.1093/aje/kwi130

Affiliations: 1: Centre for Eye Research Australia, University of Melbourne, Melbourne, Australia 2: Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN 3: Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia



On Stratton protocol for CFS starting 01/06 (NE Ohio, USA).


On CAP for CFS starting 01/06 (NE Ohio, USA)

Began rifampin trial 1/14/09

Currently: on intermittent


Further work on Age-related Macular degeneration, again showing an association with Chlamydia pneumoniae:

Kalayoglu MV, Bula D, Arroyo J, Gragoudas ES, D'Amico D, Miller JW. Identification of Chlamydia pneumoniae within human choroidal neovascular membranes secondary to age-related macular degeneration. Graefes Arch Clin Exp Ophthalmol. 2005 Nov;243(11):1080-90.

Abstract: Age-related macular degeneration (AMD) is a leading cause of blindness in the United States, and increasing evidence suggests that it is an inflammatory disease. The prokaryotic obligate intracellular pathogen Chlamydia pneumoniae is emerging as a novel risk factor in cardiovascular disease, and recent sero-epidemiological data suggest that C. pneumoniae infection is also associated with AMD. In this study, we examined choroidal neovascular membrane (CNV) tissue from patients with neovascular AMD for the presence of C. pneumoniae and determined whether the pathogen can dysregulate the function of key cell types in ways that can cause neovascular AMD. Nine CNV removed from patients with neovascular AMD were examined for the presence of C. pneumoniae by immunohistochemistry (IHC) and polymerase chain reaction (PCR); in addition, we performed PCR on nine non-AMD eyes, and IHC on five non-AMD CNV, seven non-AMD eyes, and one internal limiting membrane specimen. Finally, human monocyte-derived macrophages and retinal pigment epithelial (RPE) cells were exposed to C. pneumoniae and assayed in vitro for the production of pro-angiogenic immunomodulators (VEGF, IL-8, and MCP-1). C. pneumoniae was detected in four of nine AMD CNV by IHC and two of nine AMD CNV by PCR, induced VEGF production by human macrophages, and increased production of IL-8 and MCP-1 by RPE cells. In contrast, none of the 22 non-AMD specimens showed evidence for C. pneumoniae. These data indicate that a pathogen capable of inducing chronic inflammation and pro-angiogenic cytokines can be detected in some AMD CNV, and suggest that infection may contribute to the pathogenesis of AMD.

Interestingly, a new agent is coming onto the market: (Macugen, pegaptanib sodium.) It is a monoclonal antibody active against Vascular Endothelial Growth Factor. It is injected directly into the eye; a year's treatment is about £4000 ($7540) 'While not a cure, Macugen “appears to be an effective therapy� concluded the team responsible, led by Dr Evangelos Gragoudas from the Massachusetts Eye and Ear Infirmary in Boston. (London Times, 18th May 2006)


D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazole. No medication now. Morning BP typically 110/75]

My brother who is 46 was just diagnosed to something in same family as Macular degeneration

and is losing vision in one eye.  He has had 3 medical treatments but these have not stopped vision loss - I think he should be on this treatment also - I will be sending him these articles. 





On Wheldon protocol for MS since April, 2006.  LDN 1994

5oo mgs Ceftin 2 x/day, 500 mgs Zithromax, 500 mgs 2 x tini pulses,100 mg diflucan, 4.5 ldn; Wheldon protocol for MS April, 2006 to May 2008. 2008 MRI shows NO NEW DISEASE ACTIVITY, 2012 MRI no new disease activity.

David- This is a nice bit of science where it is not just the numbers of positive Cpn measures which is important, but the way they are building the links between an otherwise ubiquitous pathogen and the particulars of the disease:

"and determined whether the pathogen can dysregulate the function of key cell types in ways that can cause neovascular AMD."

Thanks for bringing it to our attention. 

On CAP's protocol for Cpn in CFS/FMS since December 2004.
Currently: 150mg INH, Doxy/Zith, Tini pulses 

"I really didn't say everything I said." Yogi Berra


CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral


Just ran across this interesting interview with one of the researchers from the study David points out on 2006-05-18 above:

Note the discussion about the link between variations in Complement Factor H and Cpn, suggesting "...patients with CFH variations may be particularly susceptible to the damaging effects of chronic infection, and an infectious organism like C. pneumoniae may be particularly effective in accelerating inflammation and driving progression of AMD in these patients".

The lead author of the study also points out "We found that C. pneumoniae infection led to increased production of vascular endothelial growth factor (VEGF)...".   I think this is an important point in linking Cpn and rosacea in that rosacea also presents itself with greatly increased VEGF production.

One other pathogen I found linked with increased VEGF was Mycobacteria (Note this study suggests that treatment decreases VEGF levels as you would hope):

Mycobacteria & VEGF

BTW, I was a little surprised to find how few pathogens seem to be linked directly with increased VEGF production since infection can lead to inflammation and inflammation can lead to increased VEGF levels.  Does anyone know why this would be the case?  Perhaps it requires chronic infections for increased VEGF levels?  


Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

 I didn't find anything new on Highwire, but there are links to several of the referenced articles available free in full-text format.



On CAP for CFS starting 01/06 (NE Ohio, USA)

Currently: doxy & zith -- continous; metronidazole -- 5 days on, 7 days off.

Get the research results you paid for: support Open Access


On CAP for CFS starting 01/06 (NE Ohio, USA)

Began rifampin trial 1/14/09

Currently: on intermittent

Eye disease linked to heart attacks.  Here is link.

Amazing to learn in this article that risk of heart attack or stroke goes up if you have Macular degeneration.   She said in tone dripping with sarcasm.

 Let's see - Macular degeneration is linked to CPN.   Cardiovascular disease is linked to CPN.  Stroke is linked to CPN.   

Daisy - Husband on CAP 5/07.   Roxithromycin, Minocycline, Rifampin, Bactrim DS, Mepron, Prednisone, Novantrone, Doxy, Azithromycin, Flagyl, Diflucan

Daisy - Husband on CAP 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MS drugs killed him.

Daisy on her own CAP 11/2012. 

And the thigh bone is linked to the hip'll get into doctor's brains eventually that prior infection with CPn is not just a coincidence in all these diseases. One hopes, anyway...

New Forest, UK. Progressive MSi dx 12/06 LDN 3/07 CAP 6/07: Wheldon version. Pulses so far #10


This is encouraging to read that there is a connection with macular degeneration and Cpn.  My mother has severe AMD (age related Macular Degeneration) and has been on the protocol for about a year now with no better results. (doctor put her on protocol for back aches and possible mild arthritis.)

A month ago, she started NAC, 2400mg daily, with Cipro and Metro pulses every othe week.  She probably also has Chronic Fatigue.  You would think after a whole year there would be some improvement. She keeps threatening to stop treatment.

One thing--the antibiotics stopped the bleeding vessel in one eye. So it shows that there is a connection. 

Hope to hear more about research findings to treat AMD. So grateful for this website.

MaloryImage removed.