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Sperm DNA Damage & Fatherhood
There’s DNA damage and sperm DNA damage. While all systemic side effects are important including:
- Inflammation (read more 1)
- premature aging, senescence (read more 2)
- DNA damage, (read more 3)
- Treatment-induced secondary cancer (read more 4)
the chemotherapy and/or radiation that cause sperm DNA damage potentially causes damage that can effect multiple people and generations.
I know this because when I underwent local radiation to my iliac crest in early 1995 at the age of 35, I developed a number of short, long-term and late stage side effects. At my radiation oncologist’s suggestion, I postponed radiation long enough to save some of my sperm. My son Alex will turn 25 this September.
Saving and freezing sperm is a high risk solution to this problem. I know that I got lucky.
My point and the point of the research linked and excerpted below is that cancer patients must understand short, long-term and late stage side effects and try to anticipate problems as best they can.
To learn more about testicular cancer- click now
Fertility is an important issue for cancer patients and survivors- read more
- Stem Cell Transplant- Multiple Myeloma- Freeze Sperm
- AYA, Pediatric Cancer Survivors
- Multiple Myeloma Side Effect- Infertility
- Cost of Surviving AYA Cancer- Suleika Jaouad
To learn more about fertility issues and cancer, scroll down the page, post a question or comment and I will reply to you ASAP.
Hang in there,
David Emerson
- Cancer Survivor
- Cancer Coach
- Director PeopleBeatingCancer
- https://www.nature.com/articles/s41392-021-00658-5
- https://www.jci.org/articles/view/158452
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3672181/
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435077/
Fatherhood and Sperm DNA Damage in Testicular Cancer Patients
“Survivors must overcome anxiety and fears about reduced fertility and possible pregnancy-related risks as well as health effects in offspring. There is thus a growing awareness of the need for reproductive counseling of cancer survivors…
The sperm cell has three options: (a) repair the damage, (b) activate the apoptotic process, causing cell death, or (c) tolerate the damage, resulting in mutations which could be transmitted to future generations (2, 34, 35). However, mature sperm are incapable of repairing DNA damage, as translation and transcription activities are silenced in the later stages of spermatogenesis (34)…
From a clinical perspective, sperm DNA damage, including chromatin fragmentation, has been associated with impaired spermatogenesis and infertility and can have negative consequences on the reproductive process (43–46), including recurrent pregnancy loss (RPL) (47).
Various studies have investigated the relationship between sperm DNA damage and reproductive outcome. Studies of natural fertility highlighted that sperm DNA damage is associated with a prolonged time to pregnancy (48) as well as a low probability of achieving natural pregnancy (49). Several studies also reported an association between low pregnancy rates in ART and DNA damage (50). Moreover, various authors found a significant correlation between DNA fragmentation and pregnancy loss after IVF or ICSI (OR 2.37) (51–53)…
Different factors, especially leukocytospermia (60, 61), smoking, obesity and other lifestyles (62–64), age (65, 66), male accessory gland infections (67), varicocele (68), and neoplastic diseases (69–72), may be correlated with increased sperm DNA damage, with a consequent impact on male fertility. Iatrogenic causes, above all the chemo- and radiotherapies used to treat cancer, can also have effects on spermatogenesis and consequently on the sperm chromatin (43, 73, 74)…
To date, there is little literature information on the damage suffered by sperm DNA after exposure to antineoplastic treatments. Above all, the duration, extent and biological significance of their effects on chromatin integrity and the time necessary to repair such damage are not yet known…
Post-treatment
Antineoplastic therapies are an important cause of sperm DNA damage. Interest in the toxic effects of these therapies on embryonic development has generally focused on the mother, while the paternal aspect has often been underestimated. Few studies have investigated male-mediated teratogenicity (130–132), but above all the little information that is available provides conflicting evidence of the sperm chromatin damage induced by these treatments.
Radiotherapy and chemotherapy have a damaging effect on reproductive function through both cytological and molecular effects. The negative effects include impaired spermatogenesis, resulting in oligozoospermia or azoospermia (72, 133), and an increase in aneuploidies for up to 18–24 months after the end of the therapy (134–136). Most chemotherapeutic agents are cytotoxic for cells in a given phase of the cell cycle. Furthermore, the testicle is one of the most radiosensitive tissues and is vulnerable to damage from both direct radiation or, more commonly, the scattering of radiation during the treatment of adjacent tissues (137)…
Effects on Offspring
The incidence of any effects in the offspring of fathers treated with antineoplastic therapies was not always investigated by the various studies and the evidence in the literature is highly contradictory. Unlike in children born to mothers with a previous diagnosis of cancer, some Danish multicentre and register studies did not find any increased risk of congenital or genetic abnormalities in the children of male cancer survivors treated with chemotherapy or radiotherapy (151, 152, 156–158) and did not find any increased risk of perinatal death, low birth weight or preterm birth (155).
In contrast, Magelssen et al. found an increased incidence of congenital abnormalities in firstborn infants fathered after the cancer diagnosis, regardless of whether or not ART was used (153). The abnormalities reported in this study were observed after various types of treatment and up to 15–20 years after diagnosis, even if they were not correlated with any specific antineoplastic treatment…
Given that measurable sperm nuclear damage has been demonstrated for both RT and CT, especially in the first 12–24 months after the end of treatment, it is reasonable to suppose that malformations and early abortions occurring in this time period can probably be attributed to the effects of the treatment on sperm DNA. This aspect should thus be discussed openly with the patient, to enable the protection of the patient’s future fertility through cryopreservation of semen or testicular tissue before beginning any treatment (Table 3A)…