Travis Sky Ingersoll, PH.D., MSW, M.ED. - Social Work & Sexual Health Education/Consulting/Research
My Blog

What exactly is PMS? And why do women taking the pill still have to deal with it?

What exactly is premenstrual syndrome? A syndrome is a group of symptoms that
occur together, and in the case of PMS those symptoms are in relation to the female
menstrual cycle. With PMS, physical symptoms may include cramps, dizziness,
backache, fatigue, nausea, a tingling in the extremities, abdominal bloating, breast
tenderness, breast swelling, change in appetite, thirst, edema, and increased body weight.
Psychoemotional symptoms may include anxiety, tension, irritability, depression, mood
swings, crying spells, decreased interest, insomnia, feeling out of control, and an
inability to concentrate (Backstrom et al., 2003; Hatcher, 2004; Jones & Lopez, 2006).
For women whose PMS symptoms have a significant, negative impact on their daily life,
a diagnosis of premenstrual dysphoric disorder (PMDD) could be made according to the
criteria set by the American Psychiatric Association’s DSM-IV (1994).

How many women suffer from premenstrual syndrome? According to Jones and
Lopez (2006) around 70% - 90% of U.S. women suffer from some kind of physical and/or
emotional symptoms associated with their menstrual cycle. Around 20% to 30%
experience moderate to severe PMS, while another 1% - 10% are debilitated by the
severity of their symptoms (Hatcher et al., 2004).

What mechanisms cause premenstrual syndrome? The truth of the matter is that
nobody really knows what the exact mechanisms underlying many of the symptoms
associated with PMS are. However there are a number of researched-backed theories
which offer some insight on this physiological/psychoemotional phenomenon. PMS is
understood as a result of various neurochemical and physiological interactions that take
place due to the cyclic dispersal of gonadotropins. Due to the interactions between the
brain and secreted hormones, it is generally agreed that the ovaries, and in particular the
corpus luteum, are at the root of PMS (Backstrom et al., 2003; Freeman et al., 2001;
Jones & Lopez, 2006).

The corpus luteum forms in the follicular cavity left by the expelled egg during
ovulation. This process occurs during the second half of the menstrual cycle. Lutenizing
hormone (LH) peaks during ovulation and is understood to be the primary compound
responsible for the formation and function of the corpus luteum, which is to secrete
progesterone and estradiol (Jones & Lopez, 2006). The hormones secreted prime the
uterus for the possible implantation of a fertilized ovum. If the egg is not fertilized the
corpus luteum disintegrates, during which time PMS symptoms also disappear (Freeman
et al., 2001). If however, fertilization does occur, the corpus luteum continues producing
progesterone and estradiol until the developing embryo takes over the process of
hormone secretion. Research has found that during anovulatory cycles, such as those
induced by the use of some oral contraceptives, or for any other reason, the corpus
luteum is not formed and PMS symptoms are either improved or absent (Hamarback &
Backstom, 1988; Mortola, Girton, & Fisher, 1991).

Estradiol, progesterone and progesterone metabolites appear to be the primary
catalysts for experiencing PMS in susceptible women. I mention PMS susceptibility
due to the fact that not every woman will ever experience PMS, and research has shown
no difference in progesterone and estradiol levels between women who suffer from PMS
and those who do not (Backstrom et al., 2003). With regard to PMS, levels of estradiol
and progestogens appear to affect the GABA and serotonin systems, but also have been
shown to influence norepinephrine and endorphin production (Jones & Lopez, 2006).
How this gonadotropin influence on the GABA system and serotonin levels works to
produce symptoms of PMS is not completely understood yet. However, when women
suffering from PMS are given selective serotonin reuptake inhibitors (SSRIs), a
significant decrease in PMS symptoms is produced (Kouri, E. M. & Halbreich, U., 1997).

What treatment options are available for PMS? As was mentioned, SSRIs have
been shown to be effective in treating the psychoemotional symptoms of PMS, and have
been shown to improve some women’s physical symptoms as well (Hatcher et al., 2004).
Of course the specific kind of SSRI used, such as fluoxetine (Prozac), alprazolam
(Xanax), or sertraline, would impact the specific symptoms alleviated. With regard to
dosage, SSRIs have been found to be effective when taken continuously, but also can be
taken in a cyclic manner, such as only during the last 14 days of the menstrual cycle (Backstrom et al., 2003; Hatcher et al., 2004). However, one of the most common side
effects of using SSRIs is sexual dysfunction.

Another route in the treatment of PMS is administering high doses of gonadotrophinreleasing hormone (GnRH) agonists (Jones & Lopez, 2006). The use of GnRH agonists result in extremely low progesterone and estrogen blood serum levels, thereby causing a reduction in the secretion of follicle-stimulating hormone (FSH) and LH by the pituitary gland (Freeman et al., 2001). Due to the reduction of FSH and LH, anovulation and amenorrhoea result. Anovulation means not ovulating, while amenorrhoea refers to a cease of menstruation. Both physiological and psychoemotional symptoms are alleviated using this method of treatment. The primary drawbacks of using GnRH agonists in the treatment of PMS are a loss of bone density, possible impairment in cognitive
functioning, and postmenopausal symptoms (Backstrom et al., 2003).

Surgical oophorectomy is yet another option. Performing an oophorectomy means that
the ovaries are completely removed. Although this treatment method for PMS is drastic
and should only be used when all other options have been exhausted, substantial
reduction of symptoms have been documented (Backstom et al., 2003).

It should be mentioned that many of the treatment options being reviewed are intended
to treat severe forms of PMS, there are many less-drastic options available as well.
Exercise and dietary manipulations have also been shown to reduce symptoms for those
experiencing mild forms of PMS. Minimizing consumables such as alcohol, caffeine,
sugar and salt have been found to help (Jones & Lopez, 2006). Vitamin therapy has also
shown promise. In particular, vitamin B6 has shown to produce significant improvement
in PMS symptoms (Abraham & Hargrove, 1980). However, other studies have indicated
no such improvement using vitamin B6 (London & Bradley, 1991). Of course there’s
always Midol.

In addition there has also been research pointing to the effectiveness of an extract of
the chaste tree or chasteberry. In a randomized, placebo controlled study by Schellenberg
(2001), 178 women who experience PMS were either given a chasteberry tablet or a
placebo pill once daily. Participants taking the chasteberry tablets communicated a
significant improvement in PMS symptoms on 5 of the 6 self-assessment items.
Alleviated symptoms included irritability, anger, mood-alteration, headache and breast
swelling. The only symptom not relieved was bloating (Huddleston & Jackson, 2001).

To begin to answer the question posed at the beginning of this paper, we will now
review the use of oral contraceptives in the treatment of PMS. Theoretically, oral
contraceptives should decrease PMS symptoms since they inhibit ovulation. This is
accomplished by giving the female body a constant, and somewhat elevated, dose of
estrogen, progesterone, or a combination of both (Jones & Lopez, 2006). Estrogen
inhibits ovulation, while progesterone thins the endometrium and thickens cervical
mucous (Hatcher et al., 2004). However, simply inhibiting ovulation does not appear to
be the cure-all for PMS sufferers.

Research has found that oral contraceptives containing estrogen are often effective in
alleviating physical symptoms, but not psychoemotional symptoms, and add insult to
injury by decreasing sexual interest (Backstrom et al., 2003; Graham & Sherwin, 1992).
Progesterone-only contraceptives all seem to result in negative mood changes and
physical symptoms (Backstrom et al., 2003). In general various treatments using
estrogens and progestogens have produced inconsistent results with regard to alleviating
PMS symptoms (Bancroft & Rennie, 1993; Hatcher et al., 2004; Jones & Lopez, 2006).

What role do oral contraceptives play in the experience of PMS? Evidence from
studies examining the effects of postmenopausal, or post-oophorectomy hormone
replacement therapy (HRT), point to a primarily neurochemical basis for PMS
(Backstrom et al., 2003; Casper et al., 1990). Literature indicates an interaction between
hormones and the brain’s response systems. Women with a history of PMS, who had
undergone both a surgical oophorectomy and a hysterectomy, could be safely be given
estrogen-only replacement therapy without experiencing a reoccurrence of symptoms
(Feeman et al., 2001).

With regard to GnRH agonist therapy, women whose symptoms improved
significantly all suffered a re-occurrence of PMS when estrogen and progesterone replacement therapy was administered (Mortola, Girton, & Fischer, 1991; Mezrow et al., 1994). It is the combination of estrogen and progestin that appears responsible for the experience of symptoms associated with PMS. Estrogen alone does not appear to create PMS symptoms. The question then is, why not just use estrogen only pills? There is, in fact, a very good reason not to. Due to the strong correlation between estrogen replacement
therapy (ERT) and endometrial cancer, adding progestogen is advised due to studies
indicating that its addition significantly decreases the risk for such cancers (Jones &
Lopez).

In conclusion, PMS symptoms are not solely the result of hormonal fluctuations due to
a woman’s menstrual cycle. This is why women with a history of PMS still experience
symptoms even when their hormonal systems are kept in contraceptive-based homeostasis and they are not ovulating. The mechanisms producing PMS are much more complex than that. The experience of PMS is due to the way in which certain women’s bodies process
neurochemical agents, in particular a combination of estrogen and progesterone.
However there does seem to be a degree of psychosomatic influence indicated by high
placebo response rates in many studies on the treatment of PMS and PMDD (Freeman &
Rickels, 1999; Freeman et al., 2001; Yonkers, Clark & Trivedi, 1997).

Is the end of menstruation and PMS in the foreseeable future? With recent
advances in oral contraceptive technology, such a possibility may already be a reality. As
far as eliminating menstruation, there are already a few products on the market such as
Seasonale that can be taken for 84 consecutive days. After the 84 days of taking the pill,
seven days of placebo pills are given to promote a progesterone cycle withdrawal bleed.
Even in the light of side effects such as spotting, in 2004 sales for Seasonale were around
$87 million (George, 2005).

Two new oral contraceptives, Anya and Belara both promise to give women complete
choice over menstruation. Both can be taken 365 days a year without the need for
placebos. Unless the user wants to experience a withdrawal bleed, which they could for a
variety of reasons, they do not have to (Bitzer, 2005; George, 2005). Although both Anya
and Belara claim to lessen, or even eliminate symptoms associated with PMS, further
research is needed to ascertain whether both forms of contraceptive can actually live up
to that claim. As we have learned, simply producing a state of anovulation and
amenorrhea does not necessarily translate into an absence of PMS. Although our
understanding of PMS continues to advance, it is evident that we still have a lot to learn.

References

Abraham, G. E., & Hargrove, J. T. (1980). Effect of vitamin B6 on premenstrual
symptomatology in women with premenstrual tension syndrome: A double-blind
crossover study. Infertility, 3, 155-165.

American Psychiatric Association (1994). Diagnostic and statistical manual of mental
disorders (4th ed.), 714-718, Washington, DC: American Psychiatric Association.

Backstrom, T., Andreen, L., Birzniece, V., Bjorn, I., Johansson, I., Nordenstam-Haghjo,
M., Nyberg, S., Sundstrom-Poromaa, Wahlstrom, G., Wang, M., & Zhu, D. (2003).
The role of hormones and hormonal treatments in premenstrual syndrome. CNS
Drugs, 17, 5, 325-342.

Bancroft, J., Rennie, D. (1993). The impact of oral contraceptives on the experience of
perimenstrual mood, clumsiness, food craving and other symptoms. Journal of
Psychosomatic Research, 37, 195-202.

Bitzer, J. (2005). Belara - proven benefits in daily practice. The European Journal of
Contraception and Reproductive Health Care, 10(supplement 1), 19-25.

Casper, R. F., Hearn, M. T. (1990). The effect of hysterectomy and bilateral
oophorectomy in women with severe premenstrual syndrome. American Journal of
Obstetrics and Gynecology, 162, 105-109.

Freeman, E. W., Kroll, R., Rapkin, A., Pearstein, T., Brown, C., Parsey, K., Zhang, P.,

Patel, H., & Foegh, M. (2001). Evaluation of a unique oral contraceptive in the
treatment of premenstrual dysphoric disorder. Journal of Women’s Health & Gender
Based Medicine, 10, 6, 561-569.

George, L, (2005). The end of menstruation. Maclean’s, 118, 50, 40-46.

Graham, C. A., & Sherwin, B. B. (1992). A prospective treatment study of premenstrual
symptoms using a triphasic oral contraceptive. Journal of Psychosomatic Research,
36, 257-266.

Hamarback, S., & Backstrom, T. (1988). Induced anovulation as treatment of
premenstrual tension syndrome: A double-blind cross-over study with GnRH-agonist
versus placebo. Acta Obstet Gynecol Scandinavia, 67, 159-166.

Hatcher, R. A. (2004). Contraceptive technology (18th ed.) San Francisco, CA:Ardent
Media Inc.

Huddleston, M., & Jackson, E. A. (2001). Is an extract of the fruit of agnus castus
(chaste tree or chasteberry) effective for prevention of symptoms of premenstrual
syndrome (PMS)? The Journal of Family Practice, 50, 4, 298-298.

Jones, R. E., & Lopez, K. H. (2006). Human reproductive biology (3rd ed.) San Diego,
CA: Academic Press.

Kouri, E. M., Halbreich, U. (1997). State and trait serotonergic abnormalities in women
with dysphoric premenstrual syndromes. Psychopharmacological Bulletin, 33, 767
770.
London, R. S., & Bradley, L. (1991). Effect of a nutritional supplement on premenstrual
symptomatology in women with premenstrual syndrome: A double-blind longitudinal
study. Journal of the American College of Nutrition, 10, 494-494.

Mezrow, G., Shoupe, D., Spicer, D., Lobo, R., Leung, R., & Pike, M. (1994). Depot
leuprolide acetate with estrogen and progestin add-back for long-term treatment of
premenstrual syndrome. Fertility and Sterility, 62, 932-932.

Mortola, J. F., Girton, L., & Fischer, U. (1991). Successful treatment of severe
premenstrual syndrome by combined use of gonadotropin-releasing hormone agonist
and estrogen/progestin. Journal of Clinical Endocrinol Metab, 72, 252 A-F.

Schellenberg, R. (2001). Treatment for the premenstrual syndrome with agnus castus fruit
extract: Prospective, randomized, placebo controlled study. BMJ, 322, 134-137.

Sveinsdottir, H., & Backstrom, T. (2000). Menstrual cycle symptom variation in a
community sample of women using and not using oral contraceptives. Acta
Obstetricia et Gynecologica Scandinavica, 79, 9, 757-764.

























0 Comments to What exactly is PMS? And why do women taking the pill still have to deal with it?:

Comments RSS

Add a Comment

Your Name:
Email Address: (Required)
Website:
Comment:
Make your text bigger, bold, italic and more with HTML tags. We'll show you how.
Post Comment
Website Builder provided by  Vistaprint