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Estrogen

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Posted on November 9th 2023 (over 1 year)

Dr. Rhonda Patrick explores cheese's health impact, ergothioneine's longevity properties, sleep and joint supplements, and red light therapy in her latest Q&A.

Posted on June 13th 2023 (almost 2 years)

Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.

Posted on June 21st 2020 (almost 5 years)

In this clip, Dr. Rhonda Patrick describes the effect of sex hormones on immune function.

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News & Publications

  • Growth hormone improves bone density and reduces the risk of fractures in women with osteoporosis, according to a 2015 study. Women who received growth hormone were half as likely to experience a fracture over a 10-year period than women who did not.

    The study involved 80 women (50 to 70 years old) who had osteoporosis and were taking estrogen-based hormone replacement therapy. Researchers randomly assigned the women to receive daily injections of either a low or high dose of growth hormone for three years or a placebo for 18 months. All the women took daily vitamin D and calcium supplements for the study’s duration. The researchers measured the women’s body composition and bone mass at regular intervals.

    They found that women who received growth hormone injections showed marked improvements in their bone mineral density and bone mineral content compared to those who received the placebo. Over the 10-year period, the number of fractures among the women who received growth hormone dropped from 56 percent to 28 percent, whereas fractures among those who received the placebo increased from 8 percent to 32 percent.

    Growth hormone, a peptide hormone produced in the pineal gland, promotes growth in childhood and adolescence. During middle age, growth hormone production decreases. Some evidence suggests that because growth hormone is secreted at night (during sleep), not getting enough sleep may hinder growth hormone release, exacerbating age-related bone loss. Learn how body temperature can influence how well you sleep at night in this clip featuring Dr. Matthew Walker.

  • Estrogen mitigates the association between visceral fat on cognitive decline.

    Estradiol, a form of estrogen, is the primary female sex hormone. It participates in menstrual cycle regulation and drives the development of female secondary sex characteristics, such as breasts, a wider pelvis, and gynoid fat – fat that forms around the hips, thighs, and breasts. Evidence suggests that estradiol exerts both cardioprotective and neuroprotective effects. Findings from a 2020 study demonstrate that estradiol mitigates the association between visceral fat on cognitive decline.

    Cognitive decline is characterized by altered brain structural networks and accelerated degeneration with aging. Scientists don’t fully understand the biological mechanisms that drive cognitive decline, but evidence indicates that visceral fat – a type of fat that accumulates in the abdominal cavity – may play a role. Visceral fat is metabolically active and is associated with increased markers of inflammation and oxidative stress, and decreased levels of anti-inflammatory proteins, such as adiponectin

    The cross-sectional study involved 974 cognitively healthy females and males (average age, ~50 years). Using magnetic resonance imaging, the investigators measured the participants' gray matter volume, cerebral cortex area, intracranial blood vessels, and visceral fat. They also measured estradiol concentrations in a subset (390) of the females. All the participants completed neuropsychological testing to assess memory performance.

    The investigators found that visceral fat exacerbated the harmful effects of aging on the brain’s structural networks in both females and males. However, estradiol mitigated some of these effects in the females, but not the males. Females between the ages of 35 and 55 years (the period surrounding menopause) who had lower estradiol concentrations were more likely to exhibit greater structural network impairments and worse memory performance.

    These findings suggest that estradiol mitigates some of the harmful effects of visceral fat on the brain’s structural networks and cognitive health. Interestingly, the fasting-mimicking diet preferentially depletes visceral fat. Learn more in this clip featuring Dr. Valter Longo.

  • Obesity and metabolic disease are associated with reduced fertility and alterations in several markers of reproductive health, including plasma concentrations of sex hormone-binding globulin. Low levels of sex hormone-binding globulin are common in those with obesity and are predictive of cardiovascular disease and type 2 diabetes risk, although it is unclear how glucose and insulin regulation affect sex hormone-binding globulin levels. A group of investigators recently performed a series of experiments with the aim of identifying mechanisms of sugar metabolism and sex hormone-binding globulin production.

    Sex hormone-binding globulin, which is produced by liver, transports sex hormones in the blood and regulates their uptake by sensitive tissues. Hepatocyte nuclear factor-4α, also produced by the liver, stimulates sex hormone-binding globulin production and increases serum testosterone by decreasing its half-life. De novo lipogenesis, the process by which the liver converts excess sugar into fatty acids, suppresses hepatocyte nuclear factor-4α activation and sex hormone-binding globulin production.

    In the first experiment, the researchers used transgenic mice whose genomes had been altered to express the human sex hormone-binding globulin gene. They fed these mice a diet high in either sucrose, glucose, or fructose (three types of simple sugars) for one week and measured blood levels of sex hormone-binding globulin. In a second experiment, the researchers exposed human liver cells to varying amounts of insulin and to high concentrations of either glucose or fructose and measured gene expression. Finally, they exposed the same type of liver cells to varying concentrations of glucose and fructose and to the fatty acid palmitate and measured gene expression.

    After five days a high fructose diet reduced sex hormone-binding globulin levels in the mice by fructose 80 percent. Sex hormone-binding globulin levels decreased by 40 percent on a high glucose diet and 50 percent on a high sucrose diet. Insulin exposure did not affect sex hormone-binding globulin production in mice. In liver cells, glucose and fructose exposure over five days reduced sex hormone-binding globulin accumulation by 50 percent. This change corresponded to a three- to fourfold reduction in the expression of hepatocyte nuclear factor-4α. Additionally, glucose or fructose exposure over five days resulted in a two- to threefold increase in palmitate production (due to de novo lipogenesis), which corresponded to reductions in sex hormone-binding globulin. Finally, exposure to varying amounts of palmitate over five days reduced hepatocyte nuclear factor-4α expression and sex hormone-binding globulin production.

    The authors of this comprehensive study concluded that excess sugar intake resulted in increased de novo lipogenesis, which led to a suppression of hepatic HNF-4α activity, which in turn attenuated sex hormone-binding globulin expression. This work provides a detailed explanation of why sex hormone-binding globulin is a sensitive biomarker of metabolic syndrome and why simple sugars, especially fructose, decrease fertility.