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Pacific Fertility Center

55 Francisco Street,
Suite 500
San Francisco,
CA 94133
TEL: 888-834-3095
FAX: 415-834-3080
www.InfertilityDoctor.com
Info@PacificFertility.com



Our Promise

As a unified team, guided by the highest ethical standards, we provide our patients with the best quality, individualized, compassionate fertility care.
SCIENCE PULSE    Male Infertility: Actions That Make a Difference

Sperm are clearly sensitive to environmental conditions. It is possible, through changes in lifestyle and activity, to improve sperm health. The studies available to evaluate environmental effects are unfortunately limited, but they offer insight into sperm sensitivity and ways to optimize their performance.

Temperature The scrotum where sperm are produced is 2 degrees lower than core body temperature. Raising the temperature by a few degrees results in a decline in sperm count and motility. Men suffering from cryoptorchidism, where the testicles are located above the scrotum, closer to central body temperatures, frequently suffer from low sperm counts. Infertile men tend to have a higher scrotal temperature(1), a characteristic that seems to be genetically determined(2).

Common illnesses and every day activities can be sources of an increase in scrotal temperature. Acute fever associated with illness causes a significant decline in sperm quality(3). In one study, total sperm count decreased within two weeks after a fever and required 79 days to return to normal. The DNA component of these sperm showed high levels of DNA fragmentation. Researchers in France installed temperature sensors to nine volunteers, and recorded scrotal temperatures while driving(4). Scrotal temperature increased gradually over several hours, peaking 2.5 degrees higher at three hours. Another study showed that scrotal temperature was lowest while standing naked, and highest while clothed, seated, with legs crossed(5). Higher scrotal temperatures have been associated with use of a laptop computer(6). A group in Germany looked at scrotal temperatures with a variety of underwear(7). As expected, tight underwear increased the temperature more than loose or no underwear. The effect was most pronounced while walking and less noticeable while sitting, since sitting temperature was somewhat elevated regardless of type of underwear worn.

The common sense approach is to avoid activities which can increase scrotal and testicular temperature, use loose-fitting underwear, and provide adequate ventilation to the scrotum. Exposure to hot tubs or saunas should be avoided. Take showers rather than baths, because heat conductance is lower when the testicles are not immersed in hot water. Sitting or driving for extended periods should be minimized.

Stress The effects of stress on sperm are complex. Under conditions of extreme stress, sperm counts decline. Analyses of prisoners awaiting sentencing have shown complete suppression of spermatogenesis on testicular biopsies(8). A study of semen characteristics after the Slovenian war in 1991 showed a reduction in sperm count and motility, and a reduction in the proportion of male children born(9). In 1995 a strong earthquake of magnitude 7.2 on the Richter scale occurred in Kobe, Japan killing 5,502 people. Sperm motility declined immediately, with low motility lasting for months(10). The sperm of a man who lost his home and his father had still not recovered 10 months after the earthquake.

Stress associated with fertility therapy affects sperm and sexual function. Sperm parameters may decline in patients undergoing in vitro fertilization(11). Male fertility patients have a higher incidence of erectile dysfunction, ejaculatory disorders, loss of libido and a decrease in the frequency of intercourse(12). One study of infertility patients showed an increase in burnout in male patients(13).

Unfortunately, studies of the effect of stress reduction on sperm are rare,(14)(15) so the treatment of stress has not been conclusively shown to improve sperm parameters(16). In spite of the lack of clear data, stress reduction therapy is recommended for fertility patients and may reduce problems with sexual dysfunction.

Exercise The risk of developing male fertility problems appears to increase with the intensity of exercise. Intense exercise, such as endurance running, will lower levels of luteinizing hormone (LH) and testosterone.(17)(18) Studies of semen characteristics have shown variable results. DeSouza(19) developed the concept of a training volume threshold, in which running more than 100 km or 62.14 miles per week was associated with decreased levels of testosterone and sperm motility.

A detailed prospective study comparing competitive cyclists and triathletes with sedentary controls(20) was unable to show any suppressive effect of competitive exercise on FSH, LH, or testosterone levels. Although those with the highest levels of training had higher levels of circulating testosterone at baseline, these levels did not change with training. Competitive cyclists developed lower sperm motility during competition, however, motility values returned to normal following competition.

The best advice regarding exercise and sperm is moderation. While attempting conception, it is not advisable to undergo high intensity sports training. Good nutritional standards should be always be maintained when following an exercise program. An existing maintenance exercise program may be continued without concern for its effects on sperm.

Diet is a difficult topic to study in isolation, so fertility data is limited. A recent study of beef consumption showed that maternal consumption(21) of beef resulted in lower sperm concentrations in sons. The proportion of men with low sperm counts was three times higher in the sons of women that consumed high levels of beef. Lifestyle, pesticide exposure, and xenobiotics (chemicals found in organisms that are foreign to them) were all considered potential factors. Heterocyclic amines (carcinogenic chemicals formed from the cooking of muscle meats), which are estrogenic, may also play a role(22).

Alcohol has long been associated with male reproductive dysfunction. Impotence, infertility, and male secondary sex characteristics are all affected by chronic alcohol use. Testosterone levels are lower, sperm production is reduced, and FSH and LH levels are affected(23). A study of chronic alcoholics demonstrated low levels of pituitary and testicular hormones, and significantly decreased sperm concentration and morphology(24). Sperm chromosomes are altered in men that consume alcohol(25).

Little data exists on the moderate consumption of alcohol. Data from the Ontario Farm Family Health Study did not show an adverse effect of alcohol consumption(26). In another study, alcohol or cigarette consumption did not alter sperm parameters, but when patients both smoked and drank alcohol a significant reduction in seminal volume, sperm concentration, percentage of motile spermatozoa, and a significant increase of the nonmotile viable gametes were detected(27).

Smoking tobacco affects sperm parameters, with reduced sperm counts, motility, and morphology reported in several studies(28). Whether these changes affect the male fertility remains uncertain. According to ASRM, “The effect of smoking on male fertility is … difficult to discern. The available data do not conclusively demonstrate that smoking decreases male fertility… Few studies have or can address the question, because of the confounding effects of partner smoking habits and fecundity. Although sperm concentrations, motility, and/or morphology are often reduced compared to results observed in non-smokers, they often remain within the normal range. Nevertheless, to the extent that the zona-free hamster egg penetration test reflects the ability of sperm to successfully fertilize a human oocyte, the available evidence suggests that smoking may have adverse effects on sperm function.”

Caffeine studies have revealed inconsistent effects on sperm, with at least one study showing no effect(29). Caffeine has been used as a sperm stimulant, increasing the motility prior to insemination. There does not appear to be any substantial adverse effect of caffeine on sperm.

Common Medications The list of medications with effects on sperm is long, and worthy of review. Noteworthy medications are the SSRI anti-depressants (Cipramil, Lustral, and Effexor were the reported medications), which were associated with near-azospermia in a case report(30). Ibuprofen (Advil, Nuprin) does not seem to cause adverse effects on sperm(31).

Vaginal lubricants can interfere with sperm. FemGlide, Replens, and Astroglide lubricants demonstrated a significant decrease in motility, whereas Pre-Seed did not affect motility or DNA integrity(32).

Treatments for erectile dysfunction may have an effect on sperm motility. A significant increase in sperm progressive motility was observed after sildenafil (Viagra) administration as compared with baseline; in contrast, a significant decreased motility was observed after tadalafil (Cialis).

Antihypertensive drugs have numerous effects on sperm. Beta-blockers and diuretics have been associated with impotence. Calcium channel blockers (nifedipine, Procardia) have been associated with infertility(33). If you are on heart medications, review them with your physician.

Reports on the effects of marijuana use on sperm are conflicting. Early studies had poor controls, later studies showed reductions in testosterone and sperm quality(34) while other studies showed no effect on testosterone levels in chronic heavy smokers(35). A recent study revealed a direct effect of THC, the active ingredient in marijuana, on sperm motility and fertilization capacity(36). The conclusion of the study was that “the use of THC as a recreational drug may impair crucial sperm functions and adversely affect male fertility, especially in those who are already on the borderline of infertility.”

Conclusion Sperm are a biological substance, produced in a complex interplay of genetic predisposition, specific temperature and pH, and in association with specific cells and secretions. If the system is insulted, problems will often arise. The sheer numbers of sperm in an ejaculate provide a wide margin for maintaining fertility even after such insults occur, but repeated attacks on the reproductive system can ultimately result in male fertility problems.

 Philip Chenette, MD

Philip E. Chenette, MD, has spent over a decade specializing in the treatment of patients with complex infertility diagnoses, especially in women with decreased ovarian reserve and women over 40. As a member of the International Society for Stem Cell Research, he is working to apply the concepts of stem cell therapy to help couples have healthy children. His expertise is recognized by peers who repeatedly select him as “Best Doctor” in national surveys.

References:

  1. Zorgniotti, A.W. and Sealfon, A.I. (1988) Measurement of intrascrotal temperature in normal and subfertile men. J. Reprod. Fertil., 82, 563–566.
  2. Hjollund, N., Storgaard, L., et al. (2002) Correlation of scrotal temperature in twins: Brief Communication. Human Reproduction, 17(7):1837-1838.
  3. Sergerue, D.E.S.S., et al., (2007) High risk of temporary alteration of semen parameters after recent acute febrile illness. Fertil Steril, In press.
  4. Bujan L, et al. (2000) Increase in scrotal temperature in car drivers. Human Reprod 15, 1355–1357.
  5. Mieusset, R. et al., (2007). Effect of posture and clothing on scrotal temperature in fertile men. J Androl. 28(1):170-175.
  6. Sheynkin, Y., et al., (2006) Increase in scrotal temperature in laptop computer users. Human Reproduction. 20(2):452-455.
  7. Jung, A., et al. (2005) Influence of the type of undertrousers and physical activity on scrotal temperature. Human Reproduction. 20(4):1022-1027.
  8. Steve, H. (1952) Der ein Fluss de nerven System auf ban und Fatigkeit des Geschlechtorgane des Menschen. Theim, Stuttgart.
  9. Zorn, B et al., (2002) Decline in sex ratio after 10-day war in Slovenia. Human Reproduction.17(12):3173-3177.
  10. Fukuda, M, et al. (1996) Kobe earthquake and reduced sperm motility. Human reproduction. 11(6):1244-1246.
  11. Clarke R.N., et al., (1999) Relationship between psychological stress and semen quality among in vitro fertilization patients. Human Reproduction. 14(3):753-758.
  12. Lenzi, et al. (2003) Stress, sexual dysfunctions, and male infertility. J Endocrin Invest. 26(3 Suppl):72-6.
  13. Sheiner, et al., (2002) Potential association between male infertility and occupational psychological stress. J Occup Environ Med. 44(12):1093-1099.
  14. Pook, M, et al. (1999). Coping with infertility: distress and changes in sperm quality. Human Reproduction. 14(6):1487-1492.
  15. Tuschen-Caffier B, Florin I, Krause W, Pook M. (1999) Cognitive-behavioural therapy for idiopathic infertile couples. Psychother Psychosom 68:15–21.
  16. Campagne, D.M., (2006) Should fertilization treatment start with reducing stress? Human Reproduction. 21(7):1651-1658.
  17. Wheeler, G. D., et al. (1991) Endurance training decreases serum testosterone levels in men without change in luteinizing hormone pulsatile release. J. Clin. Endocrinol. Metab. 72: 422–425.
  18. Arce, J. C., et al. (1993) Subclinical alterations in hormone and semen profile in athletes. Fertil. Steril. 59: 398–404.
  19. De Souza, M. J., et al. (1991) Gonadal hormones and semen quality in male runners. A volume threshold effect of endurance training. Int. J. Sports Med. 15: 383–391.
  20. Lucia, A, et al. (1996) Reproductive function in male endurance athletes: sperm analysis and hormonal profile. J Applied Physiology. 81:2627-2636.
  21. Swan SH et al (2007) Semen quality of fertile US males in relation to their mothers' beef consumption during pregnancy. Human Reproduction. 22(6):1497-1502.
  22. Cho E, Chen WY, Hunter DJ, et al. (2006) Red meat intake and risk of breast cancer among premenopausal women. Arch Intern Med 166:2253–9.
  23. Emanuele, MA et al. (1998) Alcohol’s effects on male reproduction. Alcohol Health and Research World. 22:195-201.
  24. Muthusami, KR et a;, (2005) Effect of chronic alcoholism on male fertility hormones and semen quality. Fertility and Sterility. 84(4):919-924.
  25. Robbins, WA, et al. (2005) Effect of lifestyle exposures on sperm aneuploidy. Cytogenetic & Genome Research. 111(3-4):371-7.
  26. Curtis KM, et al. (1997) Effects of cigarette smoking, caffeine consumption, and alcohol intake on fecundability. Am J Epidemiol. 146(1):32-41.
  27. Martini, AC, et al. (2004) Effects of alcohol and cigarette consumption on human seminal quality. Fertility Sterility. 82(2):374-377.
  28. Vine MF. (1996) Smoking and male reproduction: a review. Int J Androl.19:323–337.
  29. Klonoff-Cohen, H, et al. (2002) A prospective study of the effects of female and male caffeine consumption on the reproductive endpoints of IVF and gamete intra-Fallopian transfer. Human Reproduction. 17(7):1746-1754.
  30. Tanrikut C, Schlegel PN (2006) Antidepressant-associated changes in semen parameters. Fertil Steril. 86(3):S14.
  31. Robinson, N, et al. (2005). Regular Use of Ibuprofen Does Not Affect Semen Analysis Parameters, Need for ICSI, or ART Clinical Pregnancy Rate. Fertility and Sterility (84): S14.
  32. Agarwal A, et al., (2007) Effect of vaginal lubricants on sperm motility and chromatin integrity: a prospective comparative study. Fertil Steril. In press.
  33. Hershlag A, et al. (1995) Pregnancy following discontinuation of a calcium channel blocker in the male partner. Human Reproduction. 10(3):599-606.
  34. Kolodny RC, et al. (1974) Depression of plasma testosterone with acute administration. In: Braude MC, Szara S editor. The pharmacology of marijuana. New York: Raven Press; p. 217–225.
  35. Mendelson JH, et al. (1974). Plasma testosterone levels before, during and after chronic marihuana smoking. N Engl J Med. 291:1051–1055.
  36. Whan, LB, et al., (2006) Effects of delta-9-tetrahydrocannabinol, the primary psychoactive cannabinoid in marijuana, on human sperm function in vitro. Fertil. Steril. 85(3):653-660.

               
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  The American Society for Reproductive Medicine (ASRM) is the largest organization in the United States for medical professionals in the field of Reproductive Endocrinology and Infertility. In 2002, ASRM published medical and psychological guidelines for ovum donation. The psychological recommendations for donors are general guidelines for addressing moral, ethical and psychosocial issues that may confront ovum donors. Included are standards for what should be included in a psychosocial screening of donors and reasons to exclude donors. A few of the objective reasons for donor exclusion include known substance abuse, positive family history of heritable psychiatric disorders such as schizophrenia or bipolar disorder, or instability in donors’ lives. To determine “inclusion” I take a psychosocial history and administer a psychological test that informs me about the donor’s personality profile, including just how much they are trying to impress me - the “fake good” factor. I am also assessing motivation to donate and the donor’s “need” versus “desire for” the compensation. Stability, stress levels, and reproductive history are also part of an ASRM assessment of donors.

Although I would like to base my entire decision on objective information, much of my decision on donor acceptance must, in fact, be based on intuition. Throughout my 25 years as a therapist, I have found that my intuition is quite accurate, but it is not fool proof.

There is one major controversy in the field that may hinder a psychotherapist’s ability to screen donors. That is the hotly debated topic on compensation of donors. In August 2000, the Ethics Committee of The American Society for Reproductive Medicine concluded that there is no consensus on the precise payment that oocyte donors should receive. It was suggested, “sums of $5,000 or more require justification and sums above $10,000 go beyond what is appropriate.” Due to costs of living and the scarcity of available donors, there are significant regional variations that affect these rates.

The Society for Assisted Reproductive Technology (SART) has attempted to assist clinics and patients by creating a list of Egg Donor Agencies that have signed an agreement stating that they will abide by the Ethics Committee Guidelines governing the compensation of egg donors.

The debate centers on the fact that donors could feel undue inducement and exploitation in the process if the fee is so high as to be coercive. Part of the job of the mental health professional is to provide donors with informed consent. Might donors conceal pertinent medical information that could be important for themselves or offspring if the monetary incentive is so high? Will donors discount risks to themselves? How can the donor actually give informed consent about the medical procedure and pay attention to the risks if $$ signs are floating before their eyes?

Ethicists and some in the field of women’s health advocacy express concern “that lucrative payments are enticing young women with credit-card debt and steep tuition bills to sell eggs without seriously evaluating the risks.” Can the payment cloud someone’s judgment and can we assess that? How much is too much? Where is that line?

When I began working with PFC in 1998, we were paying first time egg donors $2,500. Nine years later, the compensation is $6,500 for a first time donor and $7,000 for any subsequent donations. Even adjusted for inflation, the payment is rising at a phenomenal rate. Competition, supply and demand govern these rises.

As part of my objective/intuitive approach to interviewing donors, I discuss money with them. What would she use the compensation for? How does she support herself? What kind and how much debt does she have? While $25,000 in student loans points to a person’s drive toward positive goals, the same amount in credit card debt speaks to me of impulsive behavior. How much have they educated themselves on ovum donation? Whom have they talked with about their desires? Do they have their own children? Are they science majors who may be more likely to view gametes as DNA and not their own children? Are their answers well thought out?

My goal is to provide the recipients of donated eggs with intelligent, healthy, and thoughtful young women who understand the implications of ovum donation both for themselves and for the recipients. Donors who are motivated by the “need” for money are more likely to provide inaccurate information on their applications, or leave out information that could be pertinent to the recipients or their offspring. It is my job and the job of the Egg Donor Agency to determine motivation.

Although impossible to attain, we would all like donors to be motivated altruistically. We may diminish altruism by making the donation about eggs for money. However, I believe we can increase altruism by helping the donors to have a greater understanding of who the recipients are and what their struggles have been.

Peggy Orlin, MFT

Ms. Orlin served as 2006-7 chair of ASRM’s Executive Committee of the Mental Health Professional Group, is a member of Resolve’s National Mental Health Advisory Board. She co-teaches PFC’s Mind/Body workshops.

To register for the September 8th Mind/Body@PFC Workshop, please phone 415-834-3095.

               
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  Pacific Fertility Center Team
Left to Right: Front: Philip Chenette, MD, Isabelle Ryan, MD, Carolyn Givens, MD
Back: Joe Conaghan, PhD, Carl Herbert, MD, Eldon Schriock, MD

Question:

How do I decide which one of your “Shared Risk” plans is best for me?

Answer:

It is estimated that there are approximately 2 million infertile patients in the US. Approximately 1.5 million will seek treatment. Of these, about 750 K conceive with standard treatment and 750 K remain infertile. Of the 750 K who remain infertile, 50 K adopt, 50 K undergo IVF, and 650 K drop out of treatment. Only about ¼ to ¹/3 of infertile patients see a Reproductive Endocrinologist; most patients are only treated by gynecologists. The remaining ¹/3 don’t seek treatment because they believe that they can’t afford it, and ¹/ 3 don’t proceed to adequate treatment secondarily to financial barriers.

Given these daunting statistics, we understand that it is important for IVF clinics to help maximize access to all levels of fertility care, by sharing the financial burden and the risk of an IVF cycle. With these goals in mind, PFC offers two “shared risk” financial plans to our patients. We call our two plans: the Refund Plan and the Option 2 Plan.

When engaged with you in a shared risk plan, we are indicating that if you meet the appropriate medical criteria, we feel confident that we have a reasonable chance to help you achieve your goal of parenthood, and we are therefore willing to share in the financial risk associated with IVF. Sharing in the financial risk of treatment is a statement of confidence in our ability to help you overcome infertility.

As physicians, we are often asked by our patients to recommend a financial plan. Each patient’s case is different, and choosing the best plan for you has to do with your own comfort level in taking financial risk, dovetailed with your emotional comfort and commitment to treatment. These levels of comfort can only be addressed on a personal and individual level.

Some general questions to consider in analyzing the plans are the following:
  • What are your estimated chances of success with your fresh embryo transfer?
  • What are the chances of having any frozen embryos?
  • What are your estimated chances of success with your frozen embryos?
  • If you are not pregnant with this IVF cycle, would you want to proceed to another IVF cycle?
  • If you do not become pregnant after a treatment cycle, would you rather receive a refund and then decide on the next steps for treatment?

Depending on the answers to these questions, you can begin to define which financial plan may make the most sense. For patients who want some financial buffer if their cycle is not successful, the Refund Plan may be the best choice. It allows you to receive a refund and then decide if the next steps will be to do nothing more, to continue treatment, or to use the refund for other options such as adoption. For those who are ready to commit to a second IVF cycle attempt if the first cycle is not successful, the Option 2 Plan may be the preferred choice. This plan provides the option of 2 cycles for only a little more cost than a single cycle. In general, the Option 2 Plan is for those whose chances of having frozen embryos is less—making the probability of needing a second fresh IVF cycle greater. At PFC, we have two financial coordinators dedicated to providing all the information about costs which can then help you to make these important decisions.

As in any financial decision, there is no right or wrong answer, but only an answer which best fits your particular situation. This decision is then matched with your personal comfort level in sharing risk. For some patients, neither of these plans may seem appealing, and the Single Cycle Plan (pay for services as provided) will be most appropriate. For patients with insurance coverage for IVF, the Single Cycle plan is the only option.

While Pacific Fertility Center can not choose a financial plan for you, if you need more information about your specific fertility situation before deciding on a “shared risk” plan, please do not hesitate to discuss this with your physician or your financial coordinator.

 Isabelle Ryan, MD


               
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