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1948–2026

The International Society for Orthomolecular Medicine is saddened to announce the death of Tsuyoshi (Ken) Kitahara, who passed peacefully on June 1, 2026, surrounded by his family.

Ken was born in Tokyo and graduated from the University of Keio, Faculty of Law. Throughout his life, Ken lived in the United States, Europe, Singapore and Japan. He also travelled extensively as an international businessman. It was in search of psychiatric help for his son that Ken discovered orthomolecular medicine. When told that his son would never get well and would have to take drugs for the rest of his life, Ken decided this was not acceptable. An article on vitamin therapy for psychiatric disorders lead him to visit Dr. Abram Hoffer in Victoria in 2002. He received a level of support that was not available in Japan and committed his time and resources to ensuring that other people in his country had access to the knowledge that had benefited his son.

In 2003, along with Dr. Hiroyuki Abe and Dr. Osamu Mizukami, Ken established the Japanese Society for Orthomolecular Medicine (JSOM) to provide education and advocacy for the use of nutrients in medical practice. From that time, Ken became a regular attendee at the International Orthomolecular Medicine Today Conference in Canada, often accompanied by a large delegation of colleagues from Japan. He would bring the information learned at the conference back to Japan for dissemination to physicians and patients. Ken also engaged with nutraceutical manufacturers in North America, establishing supply chains to ensure access to a wide range of products and services. He was responsible for the Japanese translation of numerous English books and printed resources for orthomolecular medicine.

In 2011, Ken was inducted into the Orthomolecular Medicine Hall of Fame for his pioneering influence in Japan, introducing our work to thousands.

He will be remembered for his generosity, his strong commitment to serving others, and for his leading role in orthomolecular advocacy.

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September 20, 1938 – December 5, 2025

It is with profound sadness that we announce the passing of Dr. Hiroyuki Abe, MD, a distinguished pioneer in orthomolecular medicine and integrative cancer care, who died on December 5, 2025, at the age of 87, due to pneumonia.

Dr. Abe’s lifelong contributions to clinical medicine, research, and the advancement of nutritional therapies have left an indelible mark on our global medical community. His passion for improving patient outcomes through evidence-based, compassionate care distinguished him as a leader and mentor to countless physicians, researchers, and healthcare professionals.

Dr. Abe was a founding figure in orthomolecular and integrative oncology in Japan. After completing his medical education and surgical training, he devoted himself to advancing patient-centered medicine that combined conventional oncology with innovative supportive therapies, including high-dose intravenous vitamin C and other nutritional treatments.

In 1988, he established his medical foundation and subsequently the Tokyo Cancer Clinic, a place that became known not only for its comprehensive cancer care but also for its emphasis on quality of life and holistic patient support. Under his leadership, the Tokyo Cancer Clinic became a beacon of hope for many patients and families, offering compassionate care and multidisciplinary treatment approaches long before such models became widespread.

Dr. Abe’s influence extended beyond his clinic. He was a dedicated educator and a vocal advocate for orthomolecular medicine, tirelessly promoting the integration of nutrient-based therapies into mainstream care. He served as a board member of the IV Therapy Research Society, contributing his clinical insights, guiding research initiatives, and fostering international collaboration.

In recognition of his pioneering work and enduring impact, Dr. Abe was honored with induction into the Orthomolecular Medicine Hall of Fame, a testament to his commitment to advancing health through science, compassion, and innovation.

Those who knew Dr. Abe remember him not only for his intellectual rigor, clinical expertise, and visionary leadership, but also for his warm humanity, humility, and unwavering dedication to patients. He inspired many to think broadly about healing, to challenge convention wisely, and to serve with integrity.

Dr. Abe is survived by his family, colleagues, and a global community of practitioners whose lives and work were enriched by his example. His legacy will continue to inspire generations of clinicians and researchers devoted to integrative, patient-centered care.

We extend our deepest condolences to his family and all who had the privilege of knowing him. May his memory be a blessing and a lasting source of inspiration.

Author: Atsuo Yanagisawa, MD

Premenstrual syndrome (PMS) is a complex condition marked by psychological and physical symptoms that occur approximately two weeks before menstruation (Farahmand et al., 2017), which are linked to the luteal phase of the female menstrual cycle,  and resolve when menstruation ceases (Freeman, 2003). Globally, the pooled prevalence of PMS involving females of reproductive age is 47.8% (Gudipally & Sharma, 2023). Common psychological symptoms of PMS include irritability, crying, mood swings, and anxiety, whereas physical symptoms include headaches, breast tenderness, abdominal pain, and changes in appetite (Gudipally & Sharma, 2023).

The etiology of PMS involves hormonal fluctuations during the monthly menstrual cycle accompanied by reductions in estradiol and progesterone (Modzelewski et al., 2024). The progesterone metabolite allopregnanolone (ALLO), an allosteric modulator of the gamma-aminobutyric acid (GABA) receptor, has broad effects on the central nervous system (CNS), which explains its role in reducing PMS symptoms (Modzelewski et al., 2024). The role of ALLO in PMS is complex because it parallels the rise and fall of progesterone and peaks in the luteal phase  (Modzelewski et al., 2024).  ALLO acts specifically on GABA-A receptors, facilitating the inhibition of signaling in the brain, leading to the suppression of corticotopin-releasing hormone (CRH) from the hypothalamus, thus blunting the stress response and attenuating anxiety (Toufexis et al., 2004). Females with PMS have an abnormal stress response characterized by an inability to return to baseline following a stressor, and insufficient production of ALLO and/or reduced sensitivity of the GABA-A receptor to ALLO (di Scalea & Pearlstein, 2019). The abnormal stress response and associated ALLO dynamics underlie mood instability, anxiety, and other emotional symptoms (di Scalea & Pearlstein, 2019). Further complicating matters, women with PMS may exhibit elevated baseline ALLO levels or abnormal progesterone conversion. As blocking ALLO synthesis reduces these symptoms, altered ALLO metabolism likely plays a key role in symptom development (Modzelewski et al., 2024).

Based on the aforementioned data, it seems clinically plausible that treatment aimed at modulating ALLO production may facilitate improved sensitivity of the GABA-A receptor, thus helping with PMS symptoms. This is the precise reason why selective serotonin reuptake inhibitors (SSRIs) have been used to treat the more severe form of PMS – known as premenstrual dysphoric disorder – since SSRIs increase ALLO levels, assist in the restoration of normal GABAergic function, and augment stress resilience (di Scalea & Pearlstein, 2019).

Transdermal progesterone cream (TPC) should also be considered for reproductive-aged females experiencing PMS. Theoretically, TPC may facilitate baseline allopregnanolone (ALLO) production, mitigate issues associated with abnormal ALLO metabolism, and improve GABA-A receptor sensitivity to ALLO. This case report details a reproductive-aged female with severe PMS symptoms who experienced significant symptom alleviation following a combined regimen of TPC and micronutrients. Although micronutrients were utilized, clinical observations and patient feedback strongly suggested that TPC was the primary driver of therapeutic improvement.

Patient History and Background

A 45-year-old woman presented to my clinical practice on September 20, 2023, with a history of panic attacks and depression. Her medical history was notable for developmental trauma experienced during childhood and adolescence, stemming from the caregiving demands of her father’s cancer diagnosis. She had previously consulted a therapist for several years approximately 10 to 15 years prior, at which time psychiatric medication was prescribed but never initiated. Instead, she managed her symptoms through lifestyle modification.

The patient also reported a history of postpartum anxiety following the delivery of her baby girl during the coronavirus disease 2019 pandemic. Upon returning home, pandemic-related lockdown measures left the patient and her husband to care for the newborn without external support.

Current Symptomatology and Assessment

Over the last several years, the patient experienced seasonal depression, energy challenges, and significant mood fluctuations coinciding with her menstrual cycles. She reported episodes of acute anxiety triggered by her daughter’s distress, during which she practiced cognitive detachment (“checking out”) to maintain composure and remain available to assist her child.

Her menstrual cycles occurred every 28-30 days, with an occasional missed period every 4-5 cycles attributed to stress. Premenstrually, her mood was described as highly labile, accompanied by irritability, breast tenderness, backaches, and cravings for salt and sugar. These premenstrual changes precipitated interpersonal challenges, which increased in severity following the birth of her daughter. The family history was non-contributory to these presenting symptoms. Her medical history was significant for a diagnosis of polycystic ovarian syndrome.

Baseline Lifestyle and Interventions

The patient was not taking any prescribed medications. Her baseline regimen consisted of natural health products (NHPs), including:

• Vitamin D3: 2000 IU daily
• Vitamin B1: 100 mg occasionally
• Prenatal supplement: A comprehensive multiple vitamin and mineral formula

She reported no use of cannabis or other recreational substances, and rare alcohol consumption. Her energy level was rated between 4 and 8 out of 10 (with 10 being the best), showing frequent diurnal fluctuations. She typically retired to bed around 9:00 PM and achieved sleep onset within 10 min. However, sleep architecture was fragmented due to nocturnal childcare duties, with awakenings at 12:00 AM, 2:00 AM, and 5:00 AM. The final morning awakening occurred between 5:30 and 7:30 AM. She reported a highly supportive marriage and high relationship satisfaction.

Diagnosis and Management Plan

The patient was diagnosed with premenstrual syndrome (PMS). The initial treatment plan advised continuing the prenatal multiple vitamin and mineral supplement and vitamin D3, with additional NHPs, hormonal, and lifestyle interventions:

• B-complex: 1 capsule daily
• Magnesium bisglycinate: 400 mg at bedtime
• TPC: 20 mg applied daily on days 12 to 26 of each menstrual cycle
• Physical activity: Recommended exercise for approximately 20 minutes, 1 to 2 times weekly

Clinical Progress and Follow-Up

First Follow-Up (November 15, 2023)

At her first follow-up appointment, the patient reported an 80% improvement in her overall condition, noting that her social circle had observed a positive behavioral shift. Her premenstrual mood swings had ameliorated, and acute anxiety episodes occurred only a few times since initiating treatment.

The therapeutic plan was adjusted as follows:

• Omega-3 essential fatty acids: Added to provide 750 mg eicosapentaenoic acid (EPA) and 500 mg docosahexaenoic acid (DHA) daily.
• B-complex: Increased to two capsules daily.

Final Follow-Up (January 17, 2024)

At the final evaluation, the patient demonstrated approximately 80% adherence to the recommended NHP protocol. She reported an improved capacity for cognitive regulation, allowing her to navigate challenging mental states with greater ease without reverting to previous negative cycle patterns. She observed that missing doses of her NHPs or TPC correlated with a recurrence of negative mood states, reinforcing adherence.

The patient achieved a significant and satisfactory resolution of her previously distressing PMS symptoms. Her self-reported emotional baseline was calm and content, reflecting an overall improvement in her clinical well-being. She expressed high satisfaction with the treatment outcomes and appeared in good spirits. Given her clinical improvement, the patient deemed further follow-up appointments unnecessary.

Long-Term Patient Perspective

In a subsequent correspondence dated June 11, 2026, regarding the documentation of her case and response to TPC, the patient provided the following reflections:

Following the birth of my child, I found myself having challenging mood swings and fatigue. In Sept 2023, Dr. Prousky introduced me to bioidentical progesterone cream to help manage these symptoms. The PMS related stress began to mellow after a few months. The changes became profoundly life-changing, leading to a stability that I haven’t experienced before.

Discussion

TPC has demonstrated clinical utility in alleviating PMS symptoms in reproductive-aged women (Lee, Hanley & Hopkins, 1999). Lee, Hanley and Hopkins (1999) attribute these benefits to the correction of progesterone deficiency, which offsets relative estrogen dominance and counteracts stress-induced cortisol production. Although this hypothesis is clinically plausible, TPC may offer distinct neurosteroidogenic advantages. By bypassing first-pass hepatic metabolism, TPC avoids the rapid, sharp spikes in systemic ALLO associated with oral administration, which can paradoxically trigger mood symptoms in sensitive individuals. In contrast, TPC provides a sustained pool of parent progesterone for steady, localized ALLO conversion within the CNS, optimizing GABA-A receptor sensitivity. Consequently, TPC lessens affective PMS symptoms via stable GABAergic modulation, while simultaneously mitigating physical symptoms such as mastalgia, abdominal distress, and cephalgia by rebalancing the estrogen-to-progesterone ratio. This hormonal rebalancing also counteracts luteal water retention and bloating symptoms arising from increased plasma renin and aldosterone system activation in PMS, resulting from progesterone’s diuretic properties that facilitate renal sodium excretion (Rosenfeld et al., 2008).

Testing of serum progesterone levels before treatment was not necessary. I prescribe TPC empirically based on the clinical presentation and diagnosis of the patient. I have administered this treatment to many premenopausal, perimenopausal, menopausal, and postmenopausal patients. To my knowledge, I have had only one case in which TPC surprisingly worsened a patient’s mood. This patient was previously diagnosed with a mood disorder, was stable although her mood was low, and was not on any prescribed medication. She was also postmenopausal, for which her progesterone level would obviously be very low or deficient compared to her premenopausal level. Her mood worsened within a few weeks of taking 20 mg of TPC daily except on Sundays. Upon discontinuation of TPC, her mood returned to its low baseline state. Other than this patient, I cannot recall a single case of any patient worsening on TPC treatment.

If testing is clinically indicated, saliva testing would be the most accurate since the serum level is unreliable when determining the bioavailable progesterone level (Lee, 2003; Lee, Hanley & Hopkins, 1999). Saliva testing, on the other hand, reflects the tissue-active free progesterone value and shows an increase from regular TPC administration (Lee, 2003; Lee, Hanley & Hopkins, 1999). Once TPC is applied, the levels increase over the course of 3-4 hours, are maintained for another 3-4 hours, and then drop gradually over the course of another 3-4 hours (Lee, Hanley & Hopkins, 1999). Should saliva testing be desired, the approximate optimal range is between 0.3 and 0.5 ng/ml although 2 ng/ml can be considered the upper limit (Lee, Hanley & Hopkins, 1999). To date, I have not requisitioned any saliva testing at baseline or beyond when prescribing TPC and have not found it necessary when providing this treatment.

The route of administration is important. According to Lee, Hanley and Hopkins (1999), large doses of oral progesterone (i.e., often in the range of 100-400 mg per day) provide a very small amount (approximately 10%)  of circulating “real” progesterone (p. 356). In contrast, TPC at doses of 15-40 mg per day, provides a more physiological dose since progesterone passes through the skin and into the subcutaneous fat, gradually restoring progesterone levels to normal over the course of several months (Lee, Hanley & Hopkins, 1999). The correct dose of TPC is the dose that works for the patient (Lee, Hanley & Hopkins, 1999), but 20 mg/day often provides sufficient benefit although I have sometimes needed to increase the dose to 40 mg/day for symptom amelioration. In women of reproductive age, TPC is applied daily, usually 14-15 days prior to expected menses. I usually have my patients apply TPC at bedtime because it can assist with restorative sleep. Although TPC is usually devoid of adverse effects, in premenopausal women who have been progesterone deficient for many years, the application of TPC can sometimes cause water retention, cephalgia, breast engorgement and mastalgia. These unpleasant symptoms will abate in 2 weeks, sometimes lasting as long as 2-3 months, due to the temporary increased estrogen receptor sensitivity that can happen when progesterone deficiency is being corrected (Lee, Hanley & Hopkins, 1999).

Published evidence evaluating the clinical efficacy of progesterone in PMS is lacking. A Cochrane review included only two studies for analysis, which encompassed 280 patients between 18 and 45 years of age (Ford et al., 2012). The progesterone dose and delivery methods were different, which meant that the studies could not be combined for the meta-analysis. Based on the limited data, the trial results could not prove or disprove the clinical efficacy of progesterone as a treatment for PMS. However, none of the published studies included in the analysis used TPC as a treatment for PMS.

While there are many evidence-based orthomolecular and herbal medicine options for PMS, such as vitamin B1 (Abdollahifard et al., 2014), vitamin B6 (Ebrahimi et al., 2012; Retallick-Brown et al., 2020; Wyatt et al., 1999), magnesium (Facchinetti et al., 1991; Fathizadeh et al., 2010), calcium (Arab et al., 2020; Shobeiri et al., 2017), potassium (Okeahialam, 2017; Takacs, 1998), broad-spectrum micronutrients (Retallick-Brown et al., 2020), chasteberry extract (Csupor et al., 2019), and saffron extract (Mohammadi & Karimi, 2026), I assert that TPC is the most etiological treatment for PMS given its positive impact on ALLO dynamics, luteal phase optimization, and balancing the estrogen-to-progesterone ratio.

Limitations

The positive effects of TPC may have worked synergistically with the other recommended treatments. Since the patient had been taking micronutrients before working with me, it is more likely that the noted benefits were a consequence of TPC treatment. It is also impossible to generalize the positive benefits noted here for other patients struggling with PMS. While a significant criticism is the absence of randomized controlled trials (RCTs) evaluating TPC for PMS, the comprehensive work of the late Dr. Lee, MD., has shown this treatment to be both efficacious and safe when prescribed to patients struggling with disabling PMS symptoms. In one of Dr. Lee’s earliest volumes on natural progesterone, he reported on its clinical efficacy:

More than a decade ago, after reading of the work of of Dr. Katherina Dalton in London, who defined PMS and found success using high-dose progesterone administered as rectal suppositories, I decided to add natural progesterone cream to my treatment of patients with PMS. The results were most impressive. The majority (but not all) of these patients reported remarkable improvement in their symptoms, including the elimination of their premenstrual water retention and weight gain. I have received hundreds of phone calls and letters from women and their doctors over the past few years who report that PMS has been alleviated with the use of natural progesterone (1996, p. 231).

Conclusion

While I hope that a well-constructed RCT on TPC for PMS is conducted in the future, the positive outcome in this case is quite ordinary given my clinical experience with this treatment. TPC is safe and often effective in treating PMS. The benefits, as noted by the patient in this case, improved her PMS symptoms by 80% and afforded her life-changing stability. For interested clinicians, all references referring to the late Dr. John R. Lee, MD., is a recommended resource (Lee, 1996; Lee, 2003; Lee, Hanley & Hopkins, 1999), as is his website (https://www.johnleemd.com/).

Ethics Statement

This case report was prepared in accordance with the CARE Case Report Guidelines. Written informed consent was obtained from the patient for publication of this de-identified case report. All identifying information has been removed or altered to protect patient privacy.

Conflict of Interest Statement

The author declares no conflicts of interest related to this case report.

Funding

No external funding was received for preparation of this case report.

Author Contributions

Dr. Jonathan Prousky conceived the clinical intervention, managed the case, and prepared the manuscript.

References

Abdollahifard, S., Rahmanian Koshkaki, A., & Moazamiyanfar, R. (2014). The effects of vitamin B1 on ameliorating the premenstrual syndrome symptoms. Global journal of health science, 6(6), 144–153. https://doi.org/10.5539/gjhs.v6n6p144

Arab, A., Rafie, N., Askari, G., & Taghiabadi, M. (2020). Beneficial Role of Calcium in Premenstrual Syndrome: A Systematic Review of Current Literature. International journal of preventive medicine, 11, 156. https://doi.org/10.4103/ijpvm.IJPVM_243_19

Csupor, D., Lantos, T., Hegyi, P., Benkő, R., Viola, R., Gyöngyi, Z., Csécsei, P., Tóth, B., Vasas, A., Márta, K., Rostás, I., Szentesi, A., & Matuz, M. (2019). Vitex agnus-castus in premenstrual syndrome: A meta-analysis of double-blind randomised controlled trials. Complementary therapies in medicine, 47, 102190. https://doi.org/10.1016/j.ctim.2019.08.024

Ebrahimi, E., Khayati Motlagh, S., Nemati, S., & Tavakoli, Z. (2012). Effects of magnesium and vitamin b6 on the severity of premenstrual syndrome symptoms. Journal of caring sciences, 1(4), 183–189. https://doi.org/10.5681/jcs.2012.026

Facchinetti, F., Borella, P., Sances, G., Fioroni, L., Nappi, R. E., & Genazzani, A. R. (1991). Oral magnesium successfully relieves premenstrual mood changes. Obstetrics and gynecology, 78(2), 177–181.

Farahmand, M., Ramezani Tehrani, F., Khalili, D., Amin, G., & Negarandeh, R. (2017). Factors associated with the severity of premenstrual syndrome among Iranian college students. The journal of obstetrics and gynaecology research, 43(11), 1726–1731. https://doi.org/10.1111/jog.13439  

Fathizadeh, N., Ebrahimi, E., Valiani, M., Tavakoli, N., & Yar, M. H. (2010). Evaluating the effect of magnesium and magnesium plus vitamin B6 supplement on the severity of premenstrual syndrome. Iranian journal of nursing and midwifery research, 15(Suppl 1), 401–405.

Freeman E. W. (2003). Premenstrual syndrome and premenstrual dysphoric disorder: definitions and diagnosis. Psychoneuroendocrinology, 28 Suppl 3, 25–37. https://doi.org/10.1016/s0306-4530(03)00099-4   

Ford, O., Lethaby, A., Roberts, H., & Mol, B. W. (2012). Progesterone for premenstrual syndrome. The Cochrane database of systematic reviews, 2012(3), CD003415. https://doi.org/10.1002/14651858.CD003415.pub4

Gudipally, P. R., & Sharma, G. K. (2023). Premenstrual Syndrome. In StatPearls. StatPearls Publishing.  

Lanza di Scalea, T., & Pearlstein, T. (2019). Premenstrual Dysphoric Disorder. The Medical clinics of North America, 103(4), 613–628. https://doi.org/10.1016/j.mcna.2019.02.007  

Lee J. R. (2003). Topical progesterone. Menopause (New York, N.Y.), 10(4), 374–379. https://doi.org/10.1097/00042192-200310040-00018

Lee, J. R. (1996). What your doctor may not tell you about menopause: The breakthrough book on natural progesterone. Warner Books.

Lee, J. R., Hanley, J., & Hopkins, V. (1999). What your doctor may not tell you about premenopause: Balance your hormones and your life from thirty to fifty. Grand Central Publishing.

Modzelewski, S., Oracz, A., Żukow, X., Iłendo, K., Śledzikowka, Z., & Waszkiewicz, N. (2024). Premenstrual syndrome: new insights into etiology and review of treatment methods. Frontiers in psychiatry, 15, 1363875. https://doi.org/10.3389/fpsyt.2024.1363875  

Mohammadi, M. M., & Karimi, Z. (2026). Effect of saffron on premenstrual syndrome and dysmenorrhea: a systematic review and meta-analysis. Korean journal of family medicine, 47(1), 69–80. https://doi.org/10.4082/kjfm.24.0259

Okeahialam, B. N. (2017). Potassium treatment for premenstrual syndrome. Medical Journal of Obstetrics and Gynecology, 5(2), 1101. https://www.jscimedcentral.com/jounal-article-pdf/Medical-Journal-of-Obstetrics-and-Gynecology/obstetrics-5-1101.pdf

Retallick-Brown, H., Blampied, N., & Rucklidge, J. J. (2020). A Pilot Randomized Treatment-Controlled Trial Comparing Vitamin B6 with Broad-Spectrum Micronutrients for Premenstrual Syndrome. Journal of alternative and complementary medicine (New York, N.Y.), 26(2), 88–97. https://doi.org/10.1089/acm.2019.0305

Rosenfeld, R., Livne, D., Nevo, O., Dayan, L., Milloul, V., Lavi, S., & Jacob, G. (2008). Hormonal and volume dysregulation in women with premenstrual syndrome. Hypertension (Dallas, Tex. : 1979), 51(4), 1225–1230. https://doi.org/10.1161/HYPERTENSIONAHA.107.107136

Shobeiri, F., Araste, F. E., Ebrahimi, R., Jenabi, E., & Nazari, M. (2017). Effect of calcium on premenstrual syndrome: A double-blind randomized clinical trial. Obstetrics & gynecology science, 60(1), 100–105. https://doi.org/10.5468/ogs.2017.60.1.100

Takacs, B.E. (1998). Potassium: A new treatment for premenstrual syndrome.  J Orthomol Med, 13(4), 215-222. https://orthomolecular.org/library/jom/1998/pdf/1998-v13n04-p215.pdf

Toufexis, D. J., Davis, C., Hammond, A., & Davis, M. (2004). Progesterone attenuates corticotropin-releasing factor-enhanced but not fear-potentiated startle via the activity of its neuroactive metabolite, allopregnanolone. The Journal of neuroscience : the official journal of the Society for Neuroscience, 24(45), 10280–10287. https://doi.org/10.1523/JNEUROSCI.1386-04.2004   

Wyatt, K. M., Dimmock, P. W., Jones, P. W., & Shaughn O’Brien, P. M. (1999). Efficacy of vitamin B-6 in the treatment of premenstrual syndrome: systematic review. BMJ (Clinical research ed.), 318(7195), 1375–1381. https://doi.org/10.1136/bmj.318.7195.1375

In 1998 I published the results of a study in the Journal of Orthomolecular Medicine titled “Potassium: A New Treatment for  Premenstrual Syndrome” (Takacs, 1998). The paper described a small pilot study in which a specific protocol using potassium supplements eliminated severe premenstrual syndrome (PMS) in all participants. In 2017, a small open clinical trial using the potassium protocol for PMS was published by cardiologist Dr. Basil Okeahialam (Okeahialam, 2017), who learned of my study while on sabbatical in the United States. His study results are consistent with those I reported and concluded that potassium supplementation warranted further investigation.

Since the completion of my study, women from around the world have from time-to-time contacted me asking about the protocol. In this communication, I wish to comment on my original paper with some additional observations from my conversations with women over the past 40 years. I am not a healthcare professional. When requesting the protocol, all women are first asked to check with their doctor to ensure that potassium is medically safe for them to take.

Overall, women with severe PMS, but few complicating conditions, seem to respond well to the potassium protocol. Any lack of progress is usually traced to too low a dose of potassium or a source of phosphorus-free calcium inadvertently added into the diet. About 10% of women needed to double the dose from the one used in the original study to notice improvement.  Regardless of symptom severity, it always takes three full cycles on potassium to become free of symptoms. Potassium needs to be started very early in the first cycle to notice a difference in that cycle. One of the most interesting observations in the study group was a change in the timing of the symptoms. For the first cycle on potassium only, symptoms often extended further into the period than usual before abating.

There are always new treatments and medications being discovered and popularized. There is no way of knowing a priori which might interfere with the protocol or not. However, I have noted some conditions or medications for which the potassium protocol has not been helpful. For example, one woman with polycystic ovarian syndrome, a condition marked by hormone imbalances, did not seem to respond. Using albuterol to treat asthma, even once per month, seemed to negate benefits from potassium treatment. Commonly prescribed selective serotonin reuptake inhibitors (SSRIs), which should never be stopped abruptly, also seemed to interfere. Some individuals had positive results with the protocol by reducing SSRIs use under professional guidance. Women using hormone treatment to manage their PMS will likely need to adjust their dosage. For example, one woman in the study already using natural progesterone suppositories found that her usual dose seemed too high by her second cycle on potassium. In response, she reduced and eventually stopped hormone treatment. Her situation was complicated in that she also took levothyroxine and had severe chemical and mold sensitivities, but the potassium worked for her. Potassium-depleting situations, such as some illnesses, especially coronavirus disease, can cause temporary setbacks.

Of course, I still do not know the mechanism by which a mild-to-moderate potassium deficiency, one that is not necessarily severe enough to show up in the standard serum test, might cause PMS. I am always trying to learn more and keep my observations current in an updated potassium protocol written specifically for the woman with PMS. Should readers have questions for me, or would like a copy of the protocol, please email me.

Competing Interest

The author declares she has no competing interests.

References

Okeahialam, B. N. (2017). Potassium treatment for premenstrual syndrome. Medical Journal of Obstetrics and Gynecology, 5(2), 1101. https://www.jscimedcentral.com/jounal-article-pdf/Medical-Journal-of-Obstetrics-and-Gynecology/obstetrics-5-1101.pdf

Takacs, B.E. (1998). Potassium: A new treatment for premenstrual syndrome.  J Orthomol Med, 13(4), 215-222. https://orthomolecular.org/library/jom/1998/pdf/1998-v13n04-p215.pdf

Dear Readers of the Journal of Orthomolecular Medicine (JOM),

My editorship with JOM ended in 2017, but I never lost touch with the philosophy, community, or clinical practice of orthomolecular medicine. At that time, I simply needed to focus on other work. As luck would have it, I have now returned as Editor, and I am deeply grateful for this second opportunity to be part of something I am truly passionate about: the dissemination of clinically relevant information on the value, efficacy, and practice of orthomolecular medicine.

When Linus Pauling first coined the term orthomolecular in his seminal paper in Science (1968), it was quickly embraced by his colleague, Dr. Abram Hoffer, because it perfectly captured the essence of what Hoffer had already been researching, publishing, and practicing. The word orthomolecular not only defined his work—it also created a vital publishing and communication vehicle for clinicians in the field, allowing them to share their findings without being unfairly silenced by the dominant medical journals of the time.

Many decades later, that silencing is thankfully far less overt, though it still exists in subtle ways. Numerous journals now publish work that is orthomolecular in nature, even if it is not explicitly labeled as such. Given this evolving landscape, we at JOM have decided to refine our focus and create a unique publishing niche—one that honors the past, present, and future of orthomolecular medicine.

Moving forward, JOM will focus on case reports and case series. Our goal is to make the journal a repository of clinically relevant, experience-based knowledge that clearly demonstrates both the efficacy and the challenges of using substances normally found in the human body and brain as therapeutic tools. We want JOM to immediately support real-world clinicians by offering practical insights they can apply directly in patient care. Simply put, JOM will assist practitioners in the excellent and demanding work of evaluating and managing patients from an orthomolecular perspective, in integration with all forms of medicine.

As we begin this exciting re-engineering of JOM, we are now inviting submissions for Volume 41, Number 1. We warmly encourage your submission of case reports highlighting the therapeutic use of nutrients, vitamins, minerals, amino acids, hormones, and other biochemical substances in restoring and maintaining optimal mental and physical health.

Please note that submissions should conform to the CARE Case Report Guidelines, an internationally endorsed framework designed to increase accuracy, transparency, and the utility of published information.

As I said at the outset, I am thrilled to be back. Even more so, I am excited to help evolve the journal by publishing meaningful, clinically useful case reports and case series that truly serve our community.

Thank you again for this opportunity, and I wish you all a terrific 2026.

Sincerely,

Jonathan Prousky, ND, MSc, MA

Editor, Journal of Orthomolecular Medicine

References

Pauling L. (1968). Orthomolecular psychiatry. Varying the concentrations of substances normally present in the human body may control mental disease. Science (New York, N.Y.), 160(3825), 265–271. https://doi.org/10.1126/science.160.3825.265

“As in clinical work, it is the single case which is the stimulus for further enquiry” (Osmond, 1962, xii). This prophetic excerpt from Niacin Therapy In Psychiatry was made by the long-time collaborator of Dr. Abram Hoffer, Dr. Humphry Osmond, in reference to an astounding reversal of a schizophrenic teenager in 1952. Here is a brief description of this case:

Towards the end of May, another opportunity arose to try niacin. A seventeen-year-old boy, C. C., was admitted with an acute schizophrenic illness in February. This had started only a few days before admission. He was excited, overactive, silly and at times deluded. He responded transiently to ECT and was put on deep insulin but this had to be stopped after less than ten comas because he developed rightsided facial palsy. During the next three weeks his mental condition worsened steadily until he was lying in his bed, naked, hallucinated, lalling in an incomprehensible way, urinating and defecating where he lay. His family, who were much attached to him, were distressed about this obvious deterioration since ECT and insulin could not be given. On May 28th he was started on 5 grams of niacin and 5 grams of ascorbic acid divided into five doses daily. A chance for the better was noticed within twenty four hours and ten days later he was described as “almost normal.” A Rorschach test done within three weeks of the new treatment being given showed “some anxiety” still remaining which was hardly surprising but no perceptual anomalies. Vitamins were stopped on the 27th of June and he was watched for three weeks before leaving hospital for his home on July 21st. A follow up three years later showed that he was in good health and had finished Grade XII. He has not been in hospital since (Osmond, 1962, xi-xii).

Shortly after this clinical reversal, Dr. Hoffer and his team conducted further studies (e.g., Hoffer et al., 1957) to determine the clinical efficacy of therapeutic doses of niacin and niacinamide. These astounding results confirmed what was observed in this noted case, and have been documented meticulously by Hoffer in this journal and others for decades until his death in 2009. Imagine what life would have been like for the thousands of schizophrenic patients had Hoffer ignored the result of that single case?

On a related note, the treatment of schizophrenia was fundamentally transformed by neuroleptics – originally called major tranquilizers and now known as typical and atypical antipsychotics. While preliminary psychiatric testing of chlorpromazine (CPZ) took place at the Villejuif psychiatric hospital in Paris (Chertok, 1982, as cited in Stip, 2002), it was Drs. Delay, Deniker, and Harl who first published comprehensive reports on its use. They demonstrated that CPZ did not simply sedate agitated patients, but actively targeted psychotic symptoms like hallucinations and delusions (Delay, Deniker, & Harl, 1952, as cited in Stip, 2015), effectively launching the era of modern psychopharmacology. The rest, as they say, is history.

My late father had Parkinson’s disease (PD) and died at the age of seventy-six in 2010. For years prior to his death, the most important treatment providing quality of life benefits was Sinemet, a combination of levodopa (L-3,4-dihydroxyphenylalanine; L-DOPA) and carbidopa. By allowing more L-DOPA to enter his brain and boost dopamine production, the medication significantly lessened his tremors, stiffness, and slow movement. One can only imagine the delayed suffering that would have unfolded to the countless millions of patients globally if Dr. Walter Birkmayer had not given 50 mg of L-DOPA intravenously to patient L.S. in July 1961 (Foley, 2003). Here is an excerpt (as documented by Foley, 2003, p. 469) from the seminal paper originally written in German by Birkmayer and Hornykiewicz (1961).

The effect of a single intravenous injection of L-DOPA in Parkinson’s disease was, in short, the total abolition or the substantial reduction of akinesia. Patients who, when lying in their beds, could not sit themselves up, who could, when sitting, could not stand, or who, when standing, could not start walking, were able to accomplish these tasks with ease after L-DOPA. They walked with the normal associated swinging movements, they could even run and spring. The voiceless, aphonic speech, with its unclear, palillalic articulation, became as strong and clear as that of normal persons. The patients could, for a short period, carry out motor activities to a degree which had been thus far achieved by no other medicament. This DOPA effect reached its peak within 2-3 hours and lasted (to a lesser degree) for 24 hours.

At present, L-DOPA treatment remains the international gold standard and the most effective symptomatic treatment for PD. On a related note, there was an epidemic of encephalitis lethargica (EL), sometimes referred to as “sleeping sickness,” that spanned across the globe beginning in the winter of 1916-17, and continued into the 1930s (Hoffman & Vilensky, 2017).  EL is a neurological disorder that has acute and chronic phases, though both phases tend to be mixed, and is initially characterized by “excessive sleepiness, disorders of ocular motility, fever, and movement disorders, although virtually any neurological sign or symptom could be exhibited, with day-today, and even hour-by-hour shifts in symptomatology” (p.2247). The chronic phase, on the other hand, can last months to years, and is marked clinically by severe “parkinsonian-like signs” (p. 2247). The film Awakenings, directed by Penny Marshall, portrays the story of a neurologist, Dr. Malcolm Sayer, who brought patients with EL back to life by administering L-DOPA – albeit, for a temporary period of time – because he noted advanced Parkinsonian symptoms among his patients with EL (“Awakenings,” n.d.). This movie was based on the remarkable book with the same title by neurologist Dr. Oliver Sacks (1999), documenting his work with EL patients from around 1966 to 1969. Here is a passage from Dr. Sacks about his most famous patient from that period, Leonard, whom he had first seen in the spring of 1966 and who later exhibited a remarkable response to L-DOPA treatment:

L-DOPA was started in early March 1969 and raised by degrees to 5.0 gm. a day. Little effect was seen for two weeks, and then a sudden ‘conversion’ took place, The rigidity vanished from all his limbs, and he felt filled with an access of energy and power; he became able to write and type once again, to rise from his chair, to walk with some assistance, and to speak in a loud and clear voice – none of which had been possible since his twenty-fifth year. In the latter part of March, Mr L. enjoyed a mobility, a health, and a happiness which he had not known in thirty years. Everything about him filled him with delight: he was like a man who had awoken from a nightmare or a serious illness, or a man released from entombment or prison, who is suddenly intoxicated with the sense and beauty of everything around him (pp. 184-185).

As these historical milestones demonstrate, individual case reports remain the foundation of discovery, and form the basis of how early clinical observations on treatment can uniquely transform the routine care of patients. All medical students become acculturated into their future clinician roles because of the case report. During clerkships, internships, and residencies, medical students report on their cases and determine individualized care based on how their patients respond to treatment while under their care. It is the hope of this editor and the journal that our case reports will not only inspire work in orthomolecular medicine, but perhaps transform the routine care of patients in a manner similar to the pioneering work of these notable and brilliant clinicians.

Jonathan E. Prousky, ND, MSc, MA

Editor

References

“Awakenings.” (n.d.). In Wikipedia. Retrieved June 7, 2026, from https://en.wikipedia.org/wiki/Awakenings

Birkmayer, W., & Hornykiewicz, O. (1961). Wiener klinische Wochenschrift, 73, 787–788.

Chertok L. (1982). 30 ans après. La petite histoire de la découverte des neuroleptiques [30 years later. The story of the discovery of neuroleptics]. Annales medico-psychologiques, 140(9), 971–976.

Delay, J., Deniker, P., & Harl, J. M. (1952). Utilisation en thérapeutique psychiatrique d’une phénothiazine d’action centrale élective (4560 RP) [Therapeutic use in psychiatry of phenothiazine of central elective action (4560 RP)]. Annales medico-psychologiques, 110(2 1), 112–117.

Foley P. (2003). Beans, roots and leaves: a brief history of the pharmacological therapy of parkinsonism. Wurzburger medizinhistorische Mitteilungen, 22, 215–234. https://opus.bibliothek.uni-wuerzburg.de/files/85/dissfoley.pdf

Hoffer, A., Osmond, H., Callbeck, M., & Kahan, I. (1957). Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical & Experimental Psychopathology, 18(2), 131-158.

Hoffman, L. A., & Vilensky, J. A. (2017). Encephalitis lethargica: 100 years after the epidemic. Brain : a journal of neurology, 140(8), 2246–2251. https://doi.org/10.1093/brain/awx177

Osmond, H. (1962). Introduction. In N. Kugelmass (Ed.), Niacin therapy in psychiatry (ix-xii).  Charles C Thomas. https://ia802906.us.archive.org/1/items/in.ernet.dli.2015.145919/2015.145919.Niacin-Therapy-In-Psychiatry.pdf

Sacks, O. (1999). Awakenings. Vintage Books.

Stip E. (2015). Who pioneered the use of antipsychotics in North America? Canadian journal of psychiatry, 60(3 Suppl 2), S5–S13. https://pmc.ncbi.nlm.nih.gov/articles/PMC4418623/pdf/cjp-2015-vol60-april-supplement-s5-s13.pdf

Stip E. (2002). Happy birthday neuroleptics! 50 years later: la folie du doute. European psychiatry : the journal of the Association of European Psychiatrists, 17(3), 115–119. https://doi.org/10.1016/s0924-9338(02)00639-9