Table of Contents || Glossary || Back to MacLeod Laboratory

Chapter 1.
New Hope for Reproductive Health 2

• Helen and Arthur¹ are childless despite unflagging efforts to conceive throughout a decade of marriage.

• David and Laura, the proud parents of twin boys born within nine months of their honeymoon, waited five years before trying to expand their family; today-two years later-they are still trying, in vain.

• Rhoda and Ed have endured the heartbreak of three miscarriages in as many years, but they are determined not to abandon the goal of producing a healthy baby.

Based on reported cases alone, almost 15 percent of adult Americans experience infertility. Despite medical advances in the treatment of infertility over the last two decades, that rate has not declined. In fact, most experts believe it has risen. Meanwhile, as the population of the United States has grown since 1970, the number of infertile couples has more than doubled. At present, an estimated 9 million individuals are affected by infertility.

Typically, couples like the ones mentioned above suffer silently through this epidemic for a long time before confronting it. Once they finally do decide to seek help, most of them spend anxious months and thousands of dollars running in and out of specialists' offices and trying one fruitless treatment after another. It's an extreme exercise in pitting hope against frustration, perseverance against helplessness.

In fifteen years of practice as a pathologist and obstetrician-gynecologist at New York Hospital-Cornell Medical Center in New York City, I have examined and treated over forty thousand patients complaining of infertility. The majority of these patients have already invested years with other physicians by the time I see them. They are confused by the complicated and contradictory theories they have heard. They are exhausted by the invasive and costly tests and treatments they've undergone. And they are intimidated by all the advanced technology they've come to suspect may hold the only solution to their problem.

By contrast, what I offer my patients is a course of infertility treatment that is simple, painless, relatively inexpensive, and most important-highly effective. Putting together what I have learned from my patients' histories, from my treatment of their cases, from my own research, and from dozens of other studies performed by my colleagues in the profession, I am convinced the fundamental cause of at least half of all infertility cases is common bacterial infections. Therefore, a high percentage of these infertility cases can be easily and safely reversed with the proper combination and dosage of antibiotics.

So far, the intensive antibiotic therapy for reproductive health problems that I recommend and administer has not been institutionalized across the country. Change moves slowly in any medical field and especially in a field as sensitive as infertility treatment. Many doctors are waiting for science to provide them with more detailed information about the precise links between specific bacteria and specific infertility-related problems. Many laboratories used by doctors are not yet sophisticated enough to perform the intricate testing for bacteria that antibiotic therapy requires. Nevertheless, my antibiotic therapy is rapidly gaining attention and winning adherents. In the years to come, it promises to transform not only how medical science regards one of the most troublesome mysteries in biology but also how people in general look upon their own reproductive health care.

The revolutionary nature of antibiotic therapy in reversing infertility is most apparent in its phenomenal success rate. Overall, if no other cause of infertility besides infection can be documented, 60 percent of my infertility patients who receive this therapy go on to have trouble-free pregnancies that produce healthy babies more than double the national average for other infertility clinics of comparable size and reputation. Even in cases where antibiotic therapy doesn't completely restore fertility, it functions as a critical first step in assisting other fertility therapies. Indeed, I have used it to alleviate many reproductive health problems that fall short of outright infertility, including premenstrual syndrome (PMS) and sexually transmitted diseases (STDs).

The essential rationale behind my therapy is mercifully easy to understand. The genital tract-male or female-can host hundreds of different kinds of bacteria. Basically, I believe that certain bacteria, several of which I have specifically identified, can turn pathogenic (that is, harmful) and cause infections that directly or indirectly contribute to a couple's inability to conceive a child or to a woman's ability to carry a child full term.

For men, the result of such a bacterial infection may appear in the form of a low sperm count, sluggish sperm activity, scar tissue blocking sperm transmission, or physical destruction of the testes. For women, it may show up as cervicitis (causing stubborn vaginal discharge), endometritis (infection of the uterine lining), pelvic inflammatory disease (PID, which is characterized by extensive inflammation of any of the pelvic organs), a hormonal imbalance that upsets the ovarian cycle, or scar tissue blocking the Fallopian tubes. Some bacterial infections betray themselves by causing the victim pain or discomfort. Others do their damage without generating any symptoms at all.

Sexual intercourse is the most well established mode of transmitting bacteria from one reproductive tract to another (although I have concluded bacteria can also be transmitted vertically-that is, from mother to child during the birthing process, an issue I will discuss in Chapter 3). In the context of sexual transmission, it is the female partner who generally suffers the most, thanks to the migrating capacity of sperm. Bacteria present in the seminal fluid prior to ejaculation-or present in the cervical or vaginal milieu prior to sexual intercourse can attach themselves to sperm and "hitchhike" deep into the female partner's reproductive system, where they can colonize and jeopardize egg production, egg fertilization, and embryo implantation.

My task in reversing infertility-causing bacterial infections is multiphasic. First, I must look for clues that bacterial infection may have occurred in the history of the patient or the patient's sexual partners. Next, I must test appropriate cultures from both the patient and the patient's present partner to determine whether they harbor certain bacteria that are potentially harmful. Assuming I locate such bacteria, I must then treat both partners with a sufficiently strong antibiotic in a program of treatment lengthy enough to eradicate those bacteria. Finally, I must impose upon the couple a period of avoiding unprotected sexual intercourse until tests show that each partner's genital tract is completely clear of the suspect bacteria. At that point, I can be reasonably assured that their natural reproductive powers are on their way to restoring themselves. The high rate of post-therapy live births among my patients is testimony that my assurance is usually justified.

The Fertility Solution tells the story behind my theory about the origins of infertility; how I arrived at it, how I verified it, and how I developed my antibiotic therapy. It also demonstrates the steps I take to determine appropriate antibiotic therapies for different couples-therapies that succeed in either reversing their infertility or enabling them to derive benefit for the first time from other fertility therapies, including "fertility drug" treatments and assisted reproduction technologies such as artificial insemination and in vitro fertilization.

Before I begin this discussion, however, I must cite a few key facts about the general sociological background against which I have designed and applied my antibiotic therapy. Only then can the full value of the therapy be appreciated.

 

THE SILENT EPIDEMIC

As I indicated, the number of infertile couples in the United States has increased over two-fold in the past twenty years. Today the consensus of medical experts is that one in seven American men and women of childbearing age suffers from infertility. Either such infertile individuals have never been able to have a child, or they did produce one or more children before being rendered incapable of having another child. Why has the infertility rate continued to trend upward in the years since 1970? What bearing does this trend have on my theory about the infectious origin of reproductive health problems?

One factor responsible for the rising trend in infertility is that American men and women in general have become more sexually active, with-on a lifetime average-a greater number of sexual partners. This situation has fueled a significant spread of STDs-including, besides the well-known gonorrheal and syphilitic infections, the lesser-known infections caused by chlamydia and countless other pathogenic bacteria. Many of these infections, well known or lesser known, thrive unchecked in the victim's reproductive system because they are asymptomatic. They may not be detected until the victim, or the victim's partner, confronts the fact that he or she is unable to produce a child.

To a large extent, the introduction of convenient, reliable, and widely available birth control methods in the mid-1960s ushered in the era of sexual freedom, but some of those birth control methods came with enormous hidden costs. Aside from making a woman mistakenly believe that she was safe having frequent sex with any number of different partners, their particular operation or design (as I shall discuss later) allowed bacterial infections to penetrate farther into the user's reproductive system than they otherwise might have been able to go. I'll discuss such tragic side effects in more detail in Chapter 2.

Besides the ongoing sexual revolution and its attendant spread of disease, the other main factor contributing to the rising incidence of infertility in recent years has been the increasing trend among women to put off having a child until a later age. Their reasons are excellent: they want to wait until they've had a greater opportunity to enjoy freedom from parenting, until their relationship with their partner is more secure, until their career is more firmly established, until they can better afford the expenses associated with child rearing, or until they feel mature enough to be the nurturing kind of parent they want to be. Unfortunately, their timing is not as excellent as their reasoning.

The age bracket within which it is best for the average woman to bear a child is twenty to twenty-six. After the age of twenty-six, a woman's reproductive system begins to lose some of its efficiency and, therefore, its fertility. Today, according to the Office of Population Research at Princeton University, 25 percent of married women under the age of thirty have never had a baby by choice, compared with only 12 percent in the mid-1960s. While nine out of ten women between the ages of twenty and twenty-six are fully capable of producing a baby, the odds diminish to one out of four by the time a woman is thirty-five years old and to one out of five by the time she is forty.

In addition to suffering an inevitable natural weakening of her reproductive powers, the aging woman may be allowing an asymptomatic bacterial infection to cause increasing damage to her genital tract, to the point where she actually experiences what many doctors will diagnose as premature menopause. In my own practice, I have encountered numerous examples of this kind of bacterial damage. Fortunately, I have also been able many times to reverse the damage and restore the victim's fertility with antibiotic therapy.

 

THE PATH TO DISCOVERY

Now that I have summarized critical sociological elements relevant to infertility, I want to share with you some aspects of my personal background that led me to establish the connection between bacterial infections and infertility. It is my hope that this brief review will give you a better sense not only of the science behind this book but also of the scientist behind this book.

My fascination with the mysteries of reproductive health began when I was fifteen years old and still living in my native Hungary. My father, himself an obstetrician and gynecologist, took me into his laboratory and showed me a strange-looking tissue from the human uterus that he called fasciculus cervico angularis. He went on to take his discovery before a scientific audience and was ridiculed because no other anatomist had ever found the structure through dissection. A year later he died of Hodgkin's disease, which in those days was incurable. This sequence of events had a profound influence on me, leaving me with an overwhelming ambition to excel in medical science and a specific anatomical mystery to solve.

That ambition and that mystery carried me through six years of medical school in Hungary, a year of medical service in Austria, and after immigrating to the United States, four more years of studying pathology, including histology, cytology, and clinical chemistry, at Mount Sinai Hospital in New York City. It was during these last four years of study that I was finally able to locate the uterine structure my father had shown me long ago.

Dissecting scores of uteri, I photographed the fasciculus cervico angularis using conventional cameras and the electron microscope. Then I published two papers crediting my father's work that verified its existence. The next step was to learn the function of this unusual structure. To do this, I had to become a clinician and treat living people, and so I embarked on a residency program in obstetrics and gynecology at the New York Hospital-Cornell Medical Center in New York City.

It was at the end of this residency that an extraordinary opportunity presented itself. Dr. John MacLeod, a world-famous expert in sperm analysis and the treatment of male infertility, was about to retire, and he wanted me to take over his laboratory at New York Hospital. Accepting this challenge meant postponing indefinitely my studies of the function of the fasciculus cervico angularis, but, reassured I could continue to see female patients one day a week in my private office, I accepted.

The years since then have made me enormously glad I accepted that position. I believe that combining my training as a pathologist and experience as an obstetrician and gynecologist with expertise in semen analysis and male-related reproductive health problems has given me a uniquely comprehensive perspective on infertility. I have brought this perspective to numerous studies designed to reveal how bacterial infections compromise a couple's reproductive health, and here's what those studies have shown:

Certain bacteria in human semen can adversely affect the shape and motility of sperm. Infections of this nature can be cured with antibiotic therapy, resulting in a return of well-formed and well-functioning sperm.

In November 1977 Christine Swenson, a microbiologist, came to my laboratory for a professional consultation. I remember the date well because this short meeting was the first in a chain of events that led me to practice antibiotic therapy as I do today. Swenson was then preparing her doctoral thesis on mycoplasma, a bacterium known to cause infections in the genital tract. Some authorities had alleged that these infections might lead to infertility, but no extensive research had yet been done. I agreed to collaborate with her on an experiment to test whether the presence of mycoplasma could be easily identified and treated.

From electron microscope photographs, we knew mycoplasma could attach themselves to the tail, midpiece, or head of the spermatozoon. Most often, they bond to the tail, where they appear as little beads and cause the tail itself to coil. Our experiment involved testing semen samples from one hundred men. Swenson cultured specimens for the organism while I, working independently and unaware of her findings, studied slides of the specimens under a microscope.

Whenever I found an excess number of spermatozoa with coiled tail segments or fine beads attached to them, I postulated that Swenson's culture report would be positive. After the one hundredth specimen had been run, her culture results and my guesses were compared. It turned out my predictions were correct in 75 percent of the cases.

After we published our findings in the November 1978 edition of Fertility and Sterility, the journal of the American Fertility Society, we decided to treat a group of patients to see how their mycoplasmal infections would respond to antibiotic therapy. We began by asking both the patients and their partners to take tetracycline orally four times a day for a month. This therapy achieved a disappointingly low cure rate of 54 percent.

We repeated the experiment using a newer, broader spectrum antibiotic drug, Vibramycin, with a treatment regimen of two doses a day. This time, our cure rate was 80 percent. After therapy, the cured patients' spermatozoa were more streamlined in appearance and were moving much faster, so it was logical to conclude that the Vibramycin had removed virtually the entire bacterial load they had been carrying. It was also logical to conjecture from all our studies to date that mycoplasma may be capable of interfering with the infected male's fertility simply by reducing the speed and forward movement of the spermatozoa.

At that time, we temporarily attributed all the favorable changes we observed in semen quality after antibiotic therapy to the eradication of one organism: mycoplasma. We quickly came to realize, however, that the type of broad-spectrum antibiotics we were using against mycoplasma could also work against other, as yet, unobserved and unidentified bacteria that were also harmful.

In the years following this series of experiments, I increased the Vibramycin dosage in my therapy for mycoplasmal infections, and I complemented this treatment with three additional weeks of erythromycin. The result was a 97 percent success rate. In addition, I established that chlamydia and certain anaerobic bacteria can adversely affect spermatozoa and can be effectively treated with appropriate antibiotic therapy. I'm sure future studies will reveal other bacteria that are harmful as well, some of which my therapy may already be destroying.

One important development that arose from those early studies of mycoplasma was their influence on many other doctors across the nation. Although the dosages I recommended were exceptionally high and long lasting according to the standards set by the Physicians’ Desk Reference, these doctors began to prescribe them in their own practices. And so a movement began.

Today, my antibiotic therapy remains experimental by definition even though it is steadily becoming more and more routine in the field of reproductive health care. My answer to those doctors who continue to question the comparatively high and long-lasting dosages is this: once you accept the facts that harmful bacteria exist, that they may adversely affect fertility, that they can be eradicated only by high and long-lasting antibiotic dosages, and that patients rarely suffer any negative side effects from such dosages, then you must be consistent as well as conscientious and treat harmful bacterial infections to the point of cure.

Men whose seminal fluid is infected with harmful bacteria are far more likely to be infertile than are men whose seminal fluid is not so infected.

By the end of 1980, I had completed a two-year study involving 430 randomly selected married male patients. They were divided into five groups according to their history:

• Group A- fertile men whose wives had achieved two or more pregnancies within two months of trial and were currently pregnant.

• Group B- men from primarily (that is, no child) or secondarily (that is, no child after one or more children) infertile marriages with no history of genital-tract infection.

• Group C- men from primarily or secondarily infertile marriages with a history of nonspecific urethritis (inflammation of the urethra, a fairly common male complaint) during the last ten years.

• Group D- men from primarily or secondarily infertile marriages with a history of prostatitis (inflammation of the prostate gland, a less common, more serious male complaint) during the last ten years.

• Group E- men from primarily or secondarily infertile marriages with a history of treated gonorrhea (an even more serious reproductive health problem) during the last ten years.

Group A, the fertile group, was the control for the study, and men in this group had the least number of premarital sexual contacts among all five groups. Of the four infertile groups, group B men had the least number of premarital sexual contacts; group E, the most. I cultured semen specimens from each volunteer for bacterial isolates. The fewest isolates were found in specimens from group A men. Among the four other groups, specimens from group B men had the least amount of bacterial isolate; specimens from group E men, the most (including a high frequency of mycoplasmal and anaerobic bacteria).

The implication of these results is clear. Asymptomatic bacteria, can develop and multiply in a man's seminal fluid after he has had a clinically symptomatic or asymptomatic genital-tract infection, and these bacteria can reduce the man's fertility.

Sperm play an active role in transmitting potentially harmful bacteria throughout a woman's genital tract.

The next logical step in my investigation of the link between bacterial infections and infertility was to prove my theory that a bacterially contaminated man could infect his partner through sexual intercourse-or, more accurately, through exposure to his seminal fluid. Knowing that bacteria could attach themselves to spermatozoa, I was convinced that they could travel wherever the spermatozoa might go and, thus, that they could infect a woman's reproductive system as far up as the fallopian tubes and ovaries.

In 1982, after much creative thought, I set about replicating, under laboratory conditions, the sperm's journey through a woman's cervix, which functions as a gateway between the vagina and the uterus. Cervical mucus has always been considered an effective mechanical and immunological barrier between the bacterial flora of the vagina and the upper genital tract. Therefore, I wanted to create a milieu of cervical mucus through which contaminated sperm could swim so I could see whether the same bacteria that attached to the sperm before their journey were newly present in the cervical fluid after their journey.

First, I drew cervical mucus into sterilized microhematocrit tubes that measured 75 millimeters in length with a diameter of 1.1 millimeter. Then, I placed each filled tube upright in a small, shallow well of bacteria-laden seminal fluid, obtained from samples donated by patients visiting my laboratory for infertility consultation. To monitor the time it took the sperm to migrate throughout the microhematocrit tubes, I placed a mucus-filled tube under a microscope and immersed one end of the tube in semen.

In about an hour, the "far" end of the microhematocrit tube under the microscope showed that a significant number of sperm had arrived, so I terminated the experiment. I broke off the upper third of each microhematocrit tube and cultured the mucus inside.

In every tube that had been sub -merged in semen containing sperm, all bacteria that had originally been present in the semen (including anaerobic bacteria) could be found in the upper third of the cervical mucus, together with motile sperm. By design, I had included in the experiment some semen samples containing bacteria but no sperm, and in the upper third of the cervical mucus corresponding to these semen samples, no bacterial migration could be detected.

Thus, I established strong evidence that bacteria-contaminated sperm can carry infection into a woman's upper genital tract. My experiment also suggests that bacteria-free sperm are capable of transporting bacteria from a woman's vagina into the upper genital tract, thus enabling resident bacteria to bypass the natural barrier to "unassisted" bacteria created by the cervical milieu.

Bacterial infections can lead to infertility. The odds of infertility are dramatically reduced if an infected couple undergoes antibiotic therapy.

After completing all the studies I've described so far (as well as other studies that supported my initial findings), I still needed to forge the final links between bacterial infection and infertility and between antibiotic therapy and the reversal of infertility. I did this in 1983, when I completed a three-year follow-up study comparing the pregnancy rates of two different groups of women:

1. Women whose husbands' mycoplasma infections were successfully eradicated by antibiotic treatment, as demonstrated by a negative post-therapy semen culture.

2. Women whose husbands' mycoplasma infections were not successfully eradicated by antibiotic treatment, as indicated by the persistent presence of mycoplasma bacteria in their post-therapy cultures.

There were 161 couples in the study. All of them - husbands and wives - took 100 milligrams of doxycycline twice a day for four weeks, and in 129 cases (80 percent of the couples), the husband's mycoplasma infection was successfully eradicated. Among these 129 couples, 60 percent went on to experience a successful pregnancy, a dramatic contrast to the 5-percent pregnancy rate among the other 32 couples in the study (that is, those in which a husband's infection was not eradicated).

The results of this study were even more impressive than I thought they would be. On March 3, 1983, they were published in the New England Journal of Medicine and reported in the New York Times and various other newspapers via Associated Press; and ever since then, more and more specialists and infertile couples have turned to antibiotic therapy to prevent bacterial infections from resulting in genital-tract damage. Nevertheless, my work is far from over. Antibiotic therapy deserves to receive much more attention-not just because it has the capacity to eradicate infections, but-much more importantly-because it has the capacity to prevent them.

This book will show you how antibiotic therapy has worked for others, and it will empower you to make better, more informed decisions about your own reproductive health care. My personal hope is that the information presented here will also inspire you to anticipate problems you or your loved ones may face, and to take positive action to keep such problems from happening in the first place.

To Chapter 2: The Causes of Infertility: Facts and Fallacies
 

Table of Contents || Glossary || Back to MacLeod Laboratory