 by Ashley Jordan Ferira, PhD, RDN
Recent research from three well-known cohorts, The Nurses’ Health Study (NHS), NHS2 and Health Professionals’ Follow-Up Study (HPFS), reveals that higher magnesium intake is associated with lower risk of type 2 diabetes (T2D), particularly in diets with poor carbohydrate quality.1 Green leafy vegetables, unrefined whole grains, and nuts are richest in magnesium, while meats and milk contain a moderate amount.2 Refined foods, like carbohydrates (carb), are poor sources of magnesium. Diets with poor carb quality are characterized by higher glycemic index (GI), higher glycemic load (GL), and lower fiber intake. These poor carbs require a higher insulin demand. The typical American diet is low in vegetables and whole grains, resulting in reduced magnesium intake. The Recommended Daily Allowance (RDA) for magnesium is 310-320 mg/day for adult women and 400-420 mg/day for adult men.3 Half of the US population fails to meet their daily magnesium needs, and hypomagnesemia exists in 1/3 of adults.4-5 Magnesium is needed for normal insulin signaling; current research has linked insufficient magnesium intake to prediabetes, insulin resistance and T2D.4 Increased magnesium intake has been inversely associated with T2D risk in observational studies.6 Collaborators from Tufts University, Harvard University, and Brigham and Women’s Hospital, sought to investigate the impact of magnesium intake, from both dietary and supplemental sources, on the risk of developing T2D in subjects who had diets with poor carb quality and raised GI, GL, or low fiber intake.1 They followed three large prospective cohorts, NHS, NHS2 and HPFS (totaling over 202,700 participants). Dietary intake was quantified by validated food frequency questionnaires (FFQ) every 4 years, and T2D cases were captured via questionnaires. Over 28 years of follow-up, there were 17,130 cases of T2D. Major study findings included:1
Similar to the US population estimates, 40-50% of study participants had inadequate magnesium intake. A healthful, varied diet and supplemental magnesium (especially in diets that restrict or exclude carbohydrates, dairy or meat) are essential to ensure sufficient daily magnesium intake. Why is this Clinically Relevant?
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 Urinary Tract Infections (UTIs) aren't just a health inconvenience; they're a global epidemic, affecting millions worldwide, with Africa bearing a particularly heavy burden of 150 million cases annually. However, amidst this alarming statistic, there's a glimmer of hope: the potential of natural solutions in tackling this pervasive issue.
The UTI Epidemic: UTIs, primarily instigated by the bacterium E. coli, pose a significant health challenge, especially for women, with half experiencing at least one UTI in their lifetime. The recurring nature of UTIs complicates treatment, often rendering conventional approaches inadequate. Harnessing Nature's Arsenal: Natural ingredients offer promising avenues in UTI management: D-Mannose: A naturally occurring monosaccharide, D-mannose emerges as a formidable weapon against UTIs. Its mechanism involves binding to E. coli bacteria, impeding their attachment to bladder walls, and facilitating their expulsion via urine. Studies highlight its superiority over antibiotics in preventing recurrent UTIs. Cranberry: Famed for its anti-adhesion properties, cranberry contains proanthocyanidins that deter E. coli attachment to urinary epithelial cells, thus diminishing infection risk. Moreover, cranberry's proanthocyanidins disrupt biofilm formation, further hindering bacterial colonization. Quercetin: This potent flavonoid boasts antioxidant and anti-inflammatory prowess, making it a valuable ally in UTI combat. Its antibacterial action, particularly against E. coli, coupled with biofilm inhibition, enhances efficacy in UTI management. Vitamin C: Beyond bolstering the immune system, vitamin C wields antibacterial effects, bolstering the body's defense against UTIs. 2’-Fucosyllactose: Derived from human milk, 2’-Fucosyllactose acts as a decoy for pathogens, thwarting their colonization and adhesion to epithelial cells in the gut—a pivotal aspect of UTI prevention. The Proof in Research: Pilot studies featuring women with UTIs showcase significant symptom and quality of life enhancements with D-mannose supplementation. Combining D-mannose and cranberry with antibiotics elevates cure rates by a remarkable 53%, underscoring the ingredients' synergistic effects. Comparative investigations between D-mannose and antibiotics for recurrent UTI prevention highlight D-mannose's superiority, offering renewed hope to recurrent infection sufferers. In Conclusion: Despite the daunting prevalence of UTIs, natural remedies offer a beacon of hope. By harnessing the potency of nature's arsenal, UTI management transcends conventional limitations. Bid adieu to UTI discomfort and embrace a journey toward wellness with nature's nurturing touch—a journey powered by D-mannose, cranberry, quercetin, vitamin C, and 2’-Fucosyllactose. References:
 by Bianca Garilli, ND
For women, the pre- and post-menopausal years represent a time of major change in many aspects of life including spiritual, emotional, and physical. From a physical perspective, shifting levels of sex hormones such as dehydroepiandrosterone (DHEA), testosterone, and estrogen play critical roles in the transition in and through menopause. It’s during this chapter of a woman’s life that the number of ovarian follicles begin to decline. Their eventual depletion cause the ovaries to no longer respond to FSH and LH from the pituitary, resulting in cessation of estrogen and progesterone production from the ovaries.1 Declining estrogen levels typically begin several years before the final menstrual period (FMP)- which is defined as the cessation of the menstrual period for at least 1 year- and stabilize around two years after the FMP.2 In a similar fashion, testosterone levels change in women during the menopausal timeframe, although this sex hormone does not seem to experience as dramatic of a decline as estrogen. Frequently this results in a higher ratio of testosterone to estrogen in the post-menopausal timeframe.3 This higher testosterone level as compared to estrogen level has been associated with higher risk factors for cardiovascular disease (CVD) in women, although the impact on incident events of CVD, coronary heart disease (CHD), and heart failure (HF) in response to this sex hormone ratio is less clear.4 A study published in the Journal of the American College of Cardiology studied 2,834 post-menopausal women from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, with a mean age of 64.9 years and without CVD at baseline.4 Levels of testosterone, estradiol, DHEA, and sex hormone-binding globulin (SHBG) were assessed at the beginning of the study; participants were followed for an average of 12.1 years.4 Levels of sex hormones were evaluated for association with incident CVD, CHD, and HF. Adjustments were made for relevant variables including demographics, CVD risk factors, and hormone therapy use.4 The study found no associations between DHEA nor SHBG levels with incident CVD, CHD, and HF outcomes.4 However, an elevated risk for incident CVD, CHD, and HF events was found to be associated with a higher testosterone/estradiol ratio, with higher testosterone levels associated with higher CVD and CHD.4 Conversely, higher estradiol levels were associated with a lower CHD risk, leading the authors of this study to conclude that “sex hormone levels after menopause are associated with women’s increased CVD risk later in life”.4 Why is this Clinically Relevant?
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 Exploring key factors associated with sleep disturbances during perimenopause by Bianca Garilli, ND
The demarcations of a woman’s physiological stages of life are often delineated by the various, unique phases and cycles associated with fertility, reproduction, and the hormones at work behind the scenes. These stages include:1
For many women, after many years of sleep deprivation during the child-bearing and rearing years, a good night’s rest is welcomed. Unfortunately, perimenopause, which typically begins sometime in a woman’s mid-to-late 40s and can last anywhere from 2-10 years, may create a whole new set of sleep challenges.2,3 Prevalence of sleep problems during perimenopause Compared to men, sleep complaints are approximately twice as prevalent in women of all ages, with a prevalence during perimenopause ranging from 39-47%, underscoring the importance of investigating sleep problems in a female-centric way.3 To this end, sleep duration and quality of a nationally representative sample of women 40-59 years of age were studied by the CDC and broken down categorically by menstrual cycle/menopausal phase; sleep data during the perimenopausal phase revealed that:4
Hormones are at play Sex hormones So what is happening during perimenopause that so dramatically and negatively impacts sleep patterns? For starters, the decline in levels of sex hormones (in particular estrogen, progesterone, and testosterone) during the perimenopausal years lead to an array of symptoms, most of which can adversely affect sleep habits. These include: hot flashes, migraines, sleep apnea, circadian rhythm abnormalities, restless legs syndrome, lifestyle factors, as well as mood disturbances such as anxiety.2,4,5 Interestingly, in an analysis reviewing sleep concerns in various stages of menses/menopause, it was found that vasomotor symptoms (hot flashes) and sleep disturbances may work bidirectionally.6 In other words, hot flashes may increase difficulties obtaining appropriate duration and quality of sleep, while sleep problems may worsen vasomotor symptoms,6 a circuitous “what came first?- chicken or egg,” kind of hormonal dance. The types of sleep disturbances most often noted by perimenopausal women include difficulties with initiating and/or maintaining sleep, as well as frequent nocturnal and/or early morning awakenings.5 It’s well known that during perimenopause, estrogen levels drop sharply, corresponding to many of the symptoms associated with this transition period. However, less well known is another hormone whose levels decline and no doubt, play a key role in sleep dysfunction. That hormone is melatonin, which decreases during perimenopause, although the decline in melatonin is more gradual than that of estrogen.7 Melatonin Melatonin secretion from the pineal gland drops as individuals hit their mid-life years, coinciding with the perimenopausal phase in women.7 An article published in the Journal of Sleep Disorders and Therapy indicates that exogenous use of melatonin may improve some of these sleep challenges, including the nocturnal awakenings observed during perimenopause.5 Further research indicates that the use of slow-release melatonin preparations increase total sleep time and sleep efficiency, as well as reducing sleep latency in patients with insomnia.5 Interestingly, melatonin may also play a role in the modulation of many symptoms and conditions associated with menopause, including reduction in bone density, mood disorders, fibromyalgia, and potentially even neurodegenerative diseases.7 Assuredly, much more research is needed in the area of sleep disorders, perimenopause, and related hormonal fluctuations. Sociodemographic factors Sociodemographic variables can also contribute to perimenopausal sleep disturbances:
Women who are experiencing sleep concerns should work with a healthcare practitioner trained to 1) take a deep dive into the various aspects of lifestyle that may be affecting sleep health and 2) identify and address any deleterious health consequences from inadequate sleep. These areas should encompass the full spectrum of her individual health and wellness, from a focused cardiovascular and metabolic exam, to an in-depth look into the social and emotional aspects of her life. Each of these areas is important to consider and address to effectively and safely treat sleep challenges during the perimenopausal years and beyond. Citations
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