This donor is a healthy carrier for a genetic disease.
Please see his Genetic Testing Summary and Acknowledgment of Genetic Risk for details

Physical

Height:
5'10"
(177 cm)
Weight:
172 lb
(78 kg)
Eye Color:
Blue
Hair:
Brown/
Straight
Skin Tone:
Light
Ancestry:
Caucasian
Blood Type:
O+
Ethnic Background:
German-Scottish/German-Welsh
Education:
MS/Civil Engineering
Occupation:
Lead Scheduler
Interests:
Climbing, Cycling, Hiking, Kayaking, Lacrosse, Running

Medical

Question Response
Have you or any of your family members been diagnosed with alcoholism or drug addiction?
If yes, relation and age affected:
No
Any dietary restrictions?
If yes, explain:
No
Do you wear glasses or contact lenses?
Are you near or far-sighted?
No
Allergies (medicines, food, pollens)?
If yes, please list substance and reaction caused:
Yes - Pollen and ragweed (raw nose and fatigue)
CMV IgG AntibodyNegative
CMV IgM AntibodyNegative
Note any comments regarding above items:N/A

Family Medical History
See list of questions asked here

Question Response
Current age or age at death 72
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 70
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Disease
Age Diagnosed
Treatment For Condition
Other
 
Underwent disc fusion surgery at age 50 to treat bulging disc
Question Response
Current age or age at death 31
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 29
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 90
Living / DeadDead
Cause of death and any treatment prior to deathOld age (passed away in sleep, specific cause unknown)
Health Problems
Disease
Age Diagnosed
Treatment For Condition
Other
 
No diagnosed health problems at time of death
Question Response
Current age or age at death 94
Living / DeadDead
Cause of death and any treatment prior to deathPneumonia
Health Problems
Disease
Age Diagnosed
Treatment For Condition
Other
 
No other diagnosed health problems at time of death
Question Response
Current age or age at death 70
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 68
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 66
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 72
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 75
Living / DeadDead
Cause of death and any treatment prior to deathStroke
Health Problems
Disease
Age Diagnosed
Treatment For Condition
Dementia or degenerative disorders
75
Was showing early signs when he died, no treatment
Question Response
Current age or age at death 90
Living / DeadDead
Cause of death and any treatment prior to deathAneurism
Health Problems
Disease
Age Diagnosed
Treatment For Condition
Osteoarthritis
75
Surgery on both hips
Question Response
Current age or age at death 75
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 70
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy
Question Response
Current age or age at death 74
Living / DeadLiving
Cause of death and any treatment prior to deathN/A
Health Problems
Healthy

Religion:

Faith None
Denomination N/A

Updates to Profile

Update AvailableN/A
Updates - PersonalN/A
Updates - MedicalUPDATE October 2025: Testing of donor 7055 identified him to have a duplication of at least 331 kb within cytogenetic band Xq22.2. See the July and October 2025 updates in the Family Medical History section for more information.
Updates - Family Medical HistoryUPDATE July 2025: Two embryos conceived by this donor have been identified to have a 1.4 Mb gain of Chr Xq22.1-q22.2 via PGTA. Egg source negative. Donor testing is pending. UPDATE Oct 2025: Subsequent testing of donor 7055 identified him to have a duplication of at least 331 kb within cytogenetic band Xq22.2. The duplicated portion of DNA identified in this donor involves six genes.One of these genes, called PLP1, is associated with a known clinical condition. Pathogenic (disease-causing) variants in the PLP1 gene cause conditions that affect the central nervous system and how the covering of nerve cells (myelin) is formed. Two examples of PLP1-related conditions include Pelizaeus Merzbacher disease (PMD) and spastic paraplegia 2 (SPG2). Patients with PMD typically start to show signs and experience symptoms in infancy or early childhood including nystagmus (involuntaryrhythmic eye movements), low muscle tone, and cognitive impairment, followed by progressive muscle stiffness and lack of coordination. Those with SPG2 tend to show similar, though milder, symptoms.Males who have a pathogenic PLP1 variant are expected to exhibit at least some features of a PLP1-related disorder, which can vary from the more severe PMD to the less severe SPG2. Duplications including the entire PLP1 gene are common among PLP1 pathogenic variants. Typically, females are not expected to show signs or experience symptoms, however skewed X-inactivation has been suggested to play a role in why some females do. Skewed X-inactivation is when one of the two X chromosomes in a female is preferentially inactivated (or turned off). If the X without the variant is turned off, signs and symptoms can be present. Some studies indicate that females who carry a PLP1 variant in families with mildly affected males are more likely toexhibit features of a PLP1-related disorder than females who carry a PLP1 variant in families with severely affected males. All female offspring of this donor will be a carrier of this duplication while no male offspring will have this duplication.The effect of this duplication is difficult to predict. The donor shows no symptoms of PMD even though he carries a duplication of the gene which generally results in signs and symptoms. His family history is negative for individuals with features PMD. Females are less likely to be affected. One healthy birth has been reported for this donor.UPDATE October 2025: Since our original notification letter, our team has spoken with both an expert on the PLP1 gene and the laboratory that performed the donor’s genetic testing (GeneDx). When experts looked more closely at the donor’s results theyfound that the donor appears to have an extra copy of only the PLP1 gene—but not the enhancer regions. According to the PLP1 expert: (1) If only the PLP1 gene is duplicated (without the enhancers), the body likely still makes the normal amount ofof protein. (2) This may explain why the donor does not have any symptoms of PMD or SPG2. (3) The expert and her team are currently studying and publishing similar cases to better understand this finding. GeneDx agrees that a duplication without the enhancer regions is unlikely to cause too much PLP1 protein, which may be why people with this type of result remain healthy. In addition, GeneDx noted that their test cannot determine exactly where this extra copy is located. If the duplication is not on the X chromosome, it could mean that any child (regardless of sex) conceived from this donor could have a 50% chance of inheriting the duplication. Even so, both the PLP1 expert and our medical geneticist believe the duplication is still most likely on the X chromosome. At this time, this explanation is considered a working theory, and more research is needed to confirm it. However, the fact that the donor remains healthy is a reassuring sign for the health of his biological children.