For both men and women, avoid these in order to maintain your testosterone levels.: KILLER #1 SUGAR Excess sugar consumption destroys your testosterone levels. A study found that the group of males with excess sugar-sweetened beverage consumption was 2x likely to have low T KILLER #2: SEED OILS This study on 12 men showed that PUFA consumption was associated with lower testosterone. Another observational study of 209 men confirmed the same. Why are seed oils called seed oils? Because they destroy the male seed. https://pubmed.ncbi.nlm.nih.gov/9029197/ KILLER #3: OBESITY Aromatase is the key enzyme responsible for the synthesis of estrogen. Human fat tissue is a major source of estrogenic activity. A 2007 study of 1,667 men found “that each one-point increase in BMI was associated with a 2% decrease in testosterone” KILLER #4: SOY A study in 35 men showed that men drinking soy isolate when exercising led to a drop in testosterone levels. Exercise usually increases testosterone, illustrating how much soy damages men’s testosterone production. KILLER #5: DRUGS & ALCOHOL While some of the manliest men in the world consumed substantial amounts of drugs. A study showed that 2 to 3 drinks a day decreased testosterone levels by 7% in men over 3 weeks. KILLER: #6 XENOESTROGENS & PLASTICS Xenoestrogens are endocrine-disrupting chemicals that damage testosterone levels. They act like hormones, affecting your natural production. Some can even turn on a switch that upregulates estrogen production KILLER #7: GLYPHOSATE & ATRAZINE Glyphosate and Atrazine are the two most common herbicides used for commercial agriculture. Glyphosate reduced testosterone and disrupted the progression of puberty Atrazine, another widely used pesticide, turned 10% of male frogs into females. Now for some NATURAL TESTOSTERONE BOOSTERS #1: LOW-CARB DIETS Low-carb diets significantly increase testosterone compared with the Standard American diet. This could be for a few reasons, such as weight loss, nutrient density, and removal of other toxins.

In a newly published article by The Lancet (2025), the women’s health condition previously known as PCOS (Polycystic Ovary Syndrome) has been formally reclassified as ‘PMOS,’ or Polyendocrine Metabolic Ovarian Syndrome. This name change was the result of a multistep global consensus process, established through the engagement of 56 leading academic, clinical, and patient organizations, and more accurately reflects the disease’s multisystem pathophysiology. Why is the change from PCOS to PMOS so important? It was never just about the cysts. The problem with the previous name, Polycystic Ovary Syndrome, is that it placed the pathological burden on ovarian cysts, which not every woman with ‘PCOS’ even experiences, and completely overlooked the diverse endocrine and metabolic features of the condition. This narrow focus was an incredible disservice to millions of women suffering from the disease because it frequently led to delayed diagnosis, fragmented care, and significant stigma around associated symptoms like obesity and hyperandrogenism. Approximately 10% to 13% of reproductive-age women around the world are impacted by PMOS, but an estimated 70% don’t know they have it- often because their symptoms seem unrelated to a reproductive disorder. The physiological complexity of PMOS results in not just menstrual irregularities and fertility challenges, but also insulin resistance, Type II Diabetes, obesity, cardiovascular disease, sleep apnea, depression, body dysmorphia, and female-pattern baldness. Recognizing that this condition is not limited to the ovaries and expanding the diagnostic criteria is a huge step forward in improving diagnostic accuracy and women’s health care. Polyendocrine The condition involves reproductive hormones like estrogen, progesterone, and androgens (testosterone), but is not isolated to those hormones. It also involves metabolic hormones like insulin and neuroendocrine hormones like cortisol, highlighting the strong connection between PMOS and mood disorders like anxiety and depression.

Cortisol is an essential hormone. It performs many functions, including helping regulate the body’s stress response. When we are stressed, the brain sends a signal from the hypothalamus to the pituitary gland, which then signals the adrenal glands to release cortisol. Cortisol helps mobilize energy, raise blood sugar, sharpen focus, and temporarily dial down functions that are not immediately needed, like digestion and reproduction. In a healthy system, once the threat passes, cortisol drops back to baseline. When stress is chronic, from poverty, caregiving, an abusive relationship, or an awful workplace (and often there is more than one), signaling from the brain to the adrenal glands can become dysregulated. Cortisol initially stays elevated, but over time, cortisol rhythms may flatten, cortisol spikes may occur at the wrong times, or stress responses may become blunted. Think of the brain's signaling like a thermostat, and the adrenal glands as the furnace. HPA dysfunction is the equivalent of a thermostat malfunctioning: you get heat when it’s 90 degrees and the AC when it’s cold, or sometimes the furnace doesn’t respond at all. Over the years, this results in cumulative biological wear and tear that affects the cardiovascular, immune, metabolic, and brain systems, a process collectively called allostatic load. This is why chronic stress does not just feel bad; it contributes to disease and may even accelerate biological aging. Women disproportionately carry this kind of stress from caregiving, intimate partner violence, economic stress, and societal and workplace discrimination. Chronic stress, HPA-axis dysregulation, and allostatic load are associated with increased risks of cardiovascular disease, type 2 diabetes, dementia, autoimmune disease flares, depression, and all-cause mortality. Essentially, it contributes to accelerated physiologic aging across multiple organ systems. From a nutritional standpoint, magnesium, theanine, ashwagandha, lavender, among others, can be used to help relieve adrenal stress.

For a long time, women in their forties and fifties have been quietly describing a strange new pattern. Foods they have eaten for decades suddenly cause flushing or migraines. Random hives appear without warning. Fragrance triggers headaches. Sleep is disrupted by 3 a.m. heart pounding. Allergies that were once seasonal now feel year-round, and medications they used to tolerate now cause unpredictable reactions. When they raise these concerns, they are often told this is “just menopause” or “just stress.” It is rarely just menopause. What is often happening is a collision between two powerful systems: declining and fluctuating ovarian hormones and an immune system whose mast cells are exquisitely sensitive to those very hormones. A 2026 mini-review published in Frontiers in Allergy by Valerieva and colleagues finally puts a name and a framework around what so many of my patients have lived: menopause profoundly reshapes mast cell behavior, type 2 inflammation, vascular permeability, and skin barrier function, and these changes can either unmask new allergic disease or worsen what was already there. The Valerieva review synthesizes a growing body of evidence suggesting that menopause is not a passive endpoint of reproductive life but an active inflammatory and immunological transition. Estrogen and progesterone modulate mast cell activity, T helper 2 (Th2) inflammation, vascular permeability, and tissue homeostasis. As they fluctuate and decline, the clinical expression of allergic and hypersensitivity disease changes too. The authors describe distinct menopause-related patterns across nearly every allergic condition we see in the clinic: - Asthma: Postmenopausal women, especially after surgical menopause, have an increased risk of new-onset asthma, with body mass index partly mediating this risk. Estrogen receptor alpha activation can amplify type 2 inflammation through CRTh2 upregulation, contributing to asthma severity and even steroid insensitivity in some women. - Allergic and non-allergic rhinitis: Approximately 33% of postmenopausal women report chronic cough lasting longer than eight weeks, and life-long endogenous estrogen exposure has been linked to higher rates of allergic rhinitis later in life. - Anaphylaxis: Postmenopausal women more often present with cardiovascular-dominant manifestations and delayed recovery, and beta-blockers, ACE inhibitors, and NSAIDs (all common in this age group) can amplify reaction severity. - Skin allergies and urticaria: Estrogen decline thins the skin, weakens the barrier, increases mast cell reactivity, and reduces diamine oxidase activity, predisposing midlife women to atopic dermatitis, contact dermatitis, and chronic urticaria. - Drug hypersensitivity: Self-reported drug allergy rises sharply with age, and women over 55 are at higher risk. Estrogen-driven shifts in CYP enzymes (notably a reduction in CYP1A2 activity by up to 50%) alter how medications are metabolized. - Hereditary angioedema: Estrogen-containing hormone therapy can unmask or worsen attacks, while progesterone-only or non-hormonal options are typically better tolerated.

A major Danish study finds no excess mortality, even with long-term use, and signals real benefits after surgical menopause. The study, Menopausal hormone therapy and long-term mortality: nationwide, register-based cohort study, is from Denmark, where they have robust registries they can mine and produce far better observational studies than we can in America. Over 800,000 women were included, with an average follow-up of 14.3 years. Just over 100,000 women filled at least one HRT prescription, more than 15,000 took HRT for 5-10 years, and over 7,000 women had 10 or more years of HRT use. This really shows the power of well-managed databases, because these numbers are just not achievable in a clinical trial. With 12 million person-years of follow-up, the investigators found no “epidemiological evidence of excess mortality following menopausal hormone therapy use. Specifically, they did not see an increase risk for female cancer such as breast, uterine, ovaries, etc. That has been the concerns for the last 30 years is that HRT could increase the risk of certain cancers. But this study, along with several others published in the last 5 years or so, has confirmed that HRT does not cause cancer! I have to mention that HRT was done using bio-identical hormones, but not the synthetic estrogen or progesterone, which could actually increase the risk of cancer.