Frequently asked questions

GMRI has received a number of questions about our remarkable case reports associated with healing prayer. Check below to see if your question has already been addressed:

Romez et al., 2021, Juvenile Macular Degeneration

Q: You claim the patient likely had autosomal recessive Stargardt’s disease, but the patient had an identical twin sister who did not have it. As this is a disease with a genetic basis, and a single-gene disease in particular, doesn’t this mean that the patient could not have had autosomal recessive Stargardt’s disease?

A: The reasoning here is that IF the patient did have Stargardt’s, THEN her monozygotic twin sister must have had it also. This claim rests on the assumption that recessive single gene disorders, where both disease alleles are present, must necessarily cause the disease, and specifically in the case of autosomal recessive Stargardt’s.  Thus we might think that the fact that the twin did not have the disease is evidence that the patient also could not have had the disease, in which case our conclusions in the paper that our patient COULD have had Stargardt’s (without absolutely ruling out other maculopathies), might not stand.

For the possibility of autosomal recessive Stargardt’s disease to stand in this case, it is necessary to demonstrate specifically that patients with BOTH disease alleles SPECIFICALLY for autosomal recessive Stargardt’s disease may nevertheless not have the disease phenotype, thus accounting for our patient’s monozygotic twin without the disease.  In support of this claim, the abstract of Hoyng et al. (1996) says regarding recessive Stargardt’s disease: “We have identified one 45-year-old nonpenetrant individual who carries two [recessive Stargardt’s] disease alleles.”  Heath Jeffrey et al. (2022) analyzed 39 individuals who had been genotyped to verify that they had BOTH autosomal recessive Stargardt’s disease alleles, and in their Table 1, they report two individuals who did NOT have the Stargardt’s phenotype, despite the fact that their siblings, who also had both disease alleles, did have evidence of disease. On page 1552 of Heath Jeffrey et al. (2022), they report that the age of onset in just their 37 patient cohort ranged up to age 82. Thus it is very plausible that the age of onset can vary up to and beyond one’s lifespan, meaning that some individuals with both disease alleles may never in their long lifetimes show evidence of disease. Furthermore, even within siblings, the discordance in the age of onset in just this cohort of 37 patients was observed to vary up to and beyond 32 years, with no upper bound. Thus it is entirely consistent that our patient had autosomal recessive Stargardt’s disease, despite the fact that her monozygotic twin did not. 


Heath Jeffery, R. C., Thompson, J. A., Lo, J., Lamey, T. M., McLaren, T. L., de Roach, J. N., Azamanov, D. N., McAllister, I. L., Constable, I. J., & Chen, F. K. (2022). SIBLING CONCORDANCE IN SYMPTOM ONSET AND ATROPHY GROWTH RATES IN STARGARDT DISEASE USING ULTRA-WIDEFIELD FUNDUS AUTOFLUORESCENCE. Retina, 42(8), 1545–1559.

Hoyng, C. B., Poppelaars, F., van de Pol, T. J. R., Kremer, H., Pinckers, A. J. L. G., Deutman, A. F., & Cremers, F. P. M. (1996). Genetic fine mapping of the gene for recessive Stargardt disease. Human Genetics, 98(4), 500–504.

Q: It looks like there is only one record of an eye exam diagnosing Juvenile Macular Degeneration in 1960. Maybe the diagnosis is uncertain and could reflect a psychosomatic (conversion) disorder?

A: Please see supplementary Figure S3 in the paper. In it, there is another eye exam of January 29, 1971, in which the physician examines the eyes and reports “Degeneration and scarring of macula in both eyes”. Note that this organic disease was observed and re-confirmed over ten years after the original examination. In addition, the report states “legally blind”. This examination was carried out as verification that she was eligible to attend the state school for the blind. From these multiple original examination records, there can be no doubt that the patient had extensive organic disease of the macula over a more than ten year period, and which accounts for the severe vision impairment. To see the records, go to, scroll down to the Appendix, and click on the supplementary material file. In cases with longstanding documented organic disease, a purely psychosomatic diagnosis does not fit. For example, if someone presents with complaints of pain in the arm, and an x-ray shows a fractured ulna, we would not diagnose it as purely psychosomatic pain.

Q: The ophthalmologist in 1960 said that there are dense areas of atrophy in each eye, but Stargardt’s disease affects the whole macula, so perhaps it is not Stargardt’s disease.

A: Stargardt’s disease typically affects the whole macula, and the areas surrounding the affected fovea typically display pisciform flecks, known as fundus flavimaculatus. However, some patients present only with foveal atrophy. In one case series, 14 out of 67 patients with Stargardt’s did not have flecks (Noble & Carr, 1979). Furthermore, the patient’s exam in 1971 finds degeneration and scarring of the macula. Thus the diagnosis remains consistent with Stargardt’s disease. 

Noble, K. G., & Carr, R. E. (1979). Stargardt’s Disease and Fundus Flavimaculatus. Archives of Ophthalmology, 97(7), 1281–1285.

Q: In the photos of Figure 2, there is an artifact on the retina. Doesn’t this mean that what the ophthalmologist saw in 1960 is still present, despite her restored eyesight, so it could not have been the cause of the blindness?

A: If you read the caption of Figure 2 closely, you will see that the artifact is from the camera lens, not a feature on the back of the eyes.  The macular lesion(s) at the time she was examined in c. 1960 must have been substantial enough to convince the Mayo clinic ophthalmologist that they were responsible for her very poor visual acuity.  The small lesions on recent retinal photographs show very small lesions (excluding the optical artifacts) which suggest that the prior macular lesions essentially resolved with just a small residual lesion/leftover.  Her recent visual acuities also are consistent with those small left over lesions.

Q: The time course of vision loss does not fit that of Stargardt’s disease. Typically the cause of vision loss is a slow buildup of lipofuscin in the eyes over some years.

A: A paper by Hayasaka et al. (1993) is entitled “Initial rapid decrease in visual acuity in siblings with Stargardt’s disease.”  The abstract states that “Two siblings with Stargardt’s disease who had an initial rapid decrease in visual acuity were reported. The 8-year-old boy and his 5-year-old sister experienced a bilateral visual decrease within a period of 3 months… Stargardt’s disease should be included in the list of conditions showing rapid decrease in visual acuity.”  Likewise, Fishman et al. (1987) review earlier findings that rapid deterioration is sometimes observed, including 12 out of a 24 patient cohort who lost vision within a 3-month period (Moloney et al., 1983; Pearce, 1975). Moloney et al. (1983) notes that “In three of ten patients with Stargardt’s disease, the visual loss had occurred within a one-week period.” The references for these papers are below. These are peer-reviewed papers that demonstrate that vision loss from Stargardt’s disease can occur within a one-week period. Our patient’s vision loss fits within this range of time frames, so appeals to the lipofuscin buildup dynamics cannot withstand the empirical observations about the actual time course of vision loss in Stargardt’s disease.

Fishman, G. A., Farber, M., Patel, B. S., & Derlacki, D. J. (1987). Visual Acuity Loss in Patients with Stargardt’s Macular Dystrophy. Ophthalmology, 94(7), 809–814.

Hayasaka, S., Kurome, H., Noda, S., & Mihara, M. (1993). Initial rapid decrease in visual acuity in siblings with Stargardt’s disease. Japanese Journal of Ophthalmology, 37(4), 485–489.

Moloney, J. B. M., Mooney, D. J., & O’Connor, M. A. (1983). Retinal Function in Stargardt’s Disease and Fundus Flavimaculatus. American Journal of Ophthalmology, 96(1), 57–65.

Q: If the patient lost her vision in 1959, why was she not seen by an ophthalmologist until June of 1960?

A: We do not know. People in the late 1950s or early 1960s may have delayed seeking medical treatment for various reasons of access, finances, or other constraints.

Romez et al., 2019, Gastroparesis

Q: After the healing, the doctor notes that “it is difficult to explain his years of intolerance to oral feeding after his Nissen fundoplication, but this has apparently resolved”. Doesn’t this mean that the diagnosis of gastroparesis is in doubt, and that the gastroparesis could have resolved quickly after birth, leaving only a psychosomatic difficulty with swallowing after the first months?

A: The difficulty refers to explaining the etiology, not the diagnosis. The diagnosis of gastroparesis was made shortly after birth and reconfirmed repeatedly in the patient’s charts:

2002,  26 Sept: “A 7-5/12th-year-old boy with a gastroparesis (intestinal motility disorder) and gastrostomy tube.”

2003, 24 Feb: “Problem: 1. Gastroparesis and probable intestinal motility disorder”

2003, 25 June: “Problems: 1. Gastroparesis and probable intestinal motility disorder / 2. Mild developmental delay / 3. Gastrostomy and jejunostomy”

2007, 23 July: “Assessment: Patient active problem list / Diagnoses / Gastric Motor function disorder”

2008, 30 June:  “Chronic pseudo-obstruction syndrome / Gastric Paresis”

2009, 16 July: “Patient Active Problem List / Diagnoses / Gastric Motor Function Disorder”

Also the entire rationale for the G-tube and J-tube insertions was that the severe lack of gastric emptying persisted despite the Nissen fundoplication and pyloroplasty. This is precisely characteristic of gastroparesis. The J-tube is necessary for providing food directly to the small intestine, bypassing the stomach, because the stomach is unable to contract and thereby pass food into the small intestine. The G-tube is necessary for removing accidentally swallowed food or normal secretions of the stomach, because otherwise due to the lack of stomach contractions, the food will remain in the stomach indefinitely and cause discomfort.

Q: You noted that the patient was given Zantac and elsewhere noted the patient was given ranitidine. Did you not know that these are generic and brand names for the same medication?

A: We reported the medical records as we received them. Doctors sometimes allow generic medication and sometimes specify that only the brand name must be given, not the generic.

Q: The details of the medication given to treat the gastroparesis (Reglan) are only given in the supplementary material, not in the main text. Are the authors hiding, or not aware of, the supplementary material? 

A: We authored both the main text and the supplementary materials, so we are aware of both. Journals typically place word limits on material in the main text, which means some of the important details must nevertheless be relegated to the supplementary material. We urge all readers to read both the main text and the supplementary material to find answers to their questions.