Parkinsons disease is a neurological disorder with symptoms that become more severe over time. It affects about 1% of people ages 60 years and older in industrialized nations. The exact cause of the disease isnt known, but experts believe that both genetic and environmental factors play a role.

Parkinsons disease causes neurons to die in certain parts of your brain, leading to a decrease of dopamine. Dopamine is a neurotransmitter. Cells in your brain release dopamine as a way of sending signals to other nearby cells.

When you have Parkinsons, a decrease in dopamine activity can lead to such symptoms as:

Theres no cure for Parkinsons disease. But over the past few decades, researchers have been studying stem cell therapy to provide better treatment options.

Read on to learn more about current and future developments in using stem cell therapy to treat Parkinsons disease.

Stem cells are special because theyre undifferentiated, meaning they have the potential to become many types of specialized cells.

You might think of stem cells as natural resources for your body. When your body needs a specific type of cell from bone cells to brain cells an undifferentiated stem cell can transform to fit the need.

There are three main types of stem cells:

Stem cell therapy is the use of stem cells usually from a donor, but sometimes from your own body to treat a disorder.

Because Parkinsons disease leads to the death of brain cells, researchers are trying to use stem cells to replace brain cells in the affected areas. This could help treat the symptoms of Parkinsons disease.

Researchers are exploring various approaches to use stem cells to treat Parkinsons disease.

The current idea is to introduce stem cells directly into the affected areas of your brain where they can transform into brain cells. These new brain cells could then help regulate dopamine levels, which should improve the symptoms of the disease.

Its important to note that experts believe this would only be a treatment for Parkinsons disease and not a cure.

While stem cell therapy has the potential to replace the brain cells destroyed by Parkinsons disease, the disease would still be present. Parkinsons disease would likely destroy the implanted stem cells eventually.

Its unclear right now whether stem cell therapy could be used multiple times to continue to reduce symptoms of Parkinsons disease or if the effect would be the same after multiple procedures.

Until the discovery of the process of creating iPSCs, the only stem cell therapies for Parkinsons disease required the use of embryonic stem cells. This came with ethical and practical challenges, making research more difficult.

After iPSCs became available, stem cells have been used in clinical trials for many conditions involving neural damage with overall mixed results.

The first clinical trial using iPSCs to treat Parkinsons disease was in 2018 in Japan. It was a very small trial with only seven participants. Other trials have been completed using animal models.

So far, trials have shown improvement to symptoms affecting movement as well as nonmotor symptoms such as bladder control.

Some challenges do arise from the source of the stem cells.

Stem cell therapy can be thought of as being similar to an organ transplant. If the iPSCs are derived from a donor, you may need to use immunosuppressant drugs to prevent your body from rejecting the cells.

If the iPSCs are derived from your own cells, your body might be less likely to reject them. But experts believe that this will delay stem cell therapy while the iPSCs are made in a lab. This will probably be more costly than using an established line of tested iPSCs from a donor.

There are many symptoms of Parkinsons disease. Theyre often rated using the Unified Parkinsons Disease Rating Scale (UPDRS) or the Movement Disorder Societys updated revision of that scale, the MDS-UPDRS.

Clinical trials today are generally looking to significantly improve UPDRS or MDS-UPDRS scores for people with Parkinsons disease.

Some trials are testing new delivery methods, such as intravenous infusion or topical applications. Others are looking to determine the safest number of effective doses. And other trials are measuring overall safety while using new medical devices in stem cell therapy.

This is an active area of research. Future trials will help narrow down the most safe and effective approach to stem cell therapy for Parkinsons disease.

Clinical trials are usually conducted in three phases. Each phase adds more participants, with the first phase usually limited to a few dozen people and several thousand in the third phase. The purpose is to test the treatments safety and effectiveness.

Clinical trials testing stem cell therapy for Parkinsons disease are still in the early phases. If the current trials are successful, it will likely still be 4 to 8 years before this treatment is widely available.

The goal of stem cell therapy for Parkinsons disease is to replace destroyed brain cells with healthy, undifferentiated stem cells. These stem cells can then transform into brain cells and help regulate your dopamine levels. Experts believe this can relieve many of the symptoms of Parkinsons disease.

This therapy is still in the early stages of clinical testing. Many trials are either proposed, currently recruiting, or already active. The results of these trials will determine how soon stem cell therapy might become widely available as a treatment for Parkinsons disease.

At the moment, its not believed that stem cell therapy will cure Parkinsons disease. But it might be an alternative to existing treatments such as drug therapies and deep brain stimulation.

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Stem Cell Therapy for Parkinson's: Current Developments - Healthline

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Heart failure is a life-threatening disorder worldwide and many papers reported about myocardial regeneration through surgical method induced by LVAD, cellular cardiomyoplasty (cell injection), tissue cardiomyoplasty (bioengineered cardiac graft implantation), in situ engineering (scaffold implantation), and LV restrictive devices. Some of these innovated technologies have been introduced to clinical settings. Especially, cell sheet technology has been developed and has already been introduced to clinical situation. As the first step in development of cell sheet, neonatal cardiomyocyte sheets were established and these sheets showed electrical and histological homogeneous heart-like tissue with contractile ability in vitro and worked as functional heart muscle which has electrical communication with recipient myocardium in small animal heart failure model. Next, as a preclinical study, noncontractile myoblast sheets have been established and these sheets have proved to secrete multiple cytokines such as HGF or VEGF in vitro study. Moreover, in vivo studies using large and small animal heart failure model have been done and myoblast sheets could improve diastolic and systolic performance by cytokine paracrine effect such as angiogenesis, antifibrosis, and stem cell migration. Recently evidenced by these preclinical results, clinical trials using autologous myoblast sheets have been started in ICM and DCM patients and some patients showed LV reverse remodelling, improved symptoms, and exercise tolerance. Recent works demonstrated that iPS cell-derived cardiomyocyte sheet were developed and showed electrical and microstructural homogeneity of heart tissue in vitro, leading to the establishment of proof of concept in small and large animal heart failure model.

Therapeutic treatments using cells or cell-based tissues have been developed to regenerate the damaged myocardium associated with ischemic heart disease. This technique has already been evaluated in the clinical setting, using myoblasts [1] or bone marrow mononuclear cells (BM-MNCs) [2]. Although these studies demonstrated the feasibility and safety of this approach, the efficacy associated with this technology was generally insufficient to repair severe myocardial damage. Thus, a second generation of myocardial regenerative therapy, tissue-engineered cardiomyoplasty, is currently being developed. A large number of achievements concerning basic, preclinical, and clinical works about cell sheet technology have been done and this review summarizes recent advances in myocardial regeneration emerging from the development of cell sheet technology.

Cell-sheet techniques have been applied to several diseased organs, such as the heart [3], eye [4], and kidney [5], in the laboratory and the clinic. Cell sheets can be prepared on special dishes that are coated with a temperature-responsive polymer, poly(N-isopropylacrylamide) (PIPAAm), that changes from being hydrophobic to hydrophilic when the temperature is lowered. This change allows cells to be removed without EDTA or enzymatic treatment and without destroying the cell-cell or cell-extracellular matrix (ECM) interactions within the cell sheet.

Shimizu et al. used such temperature-sensitive culture dishes to develop a contractile chick cardiomyocyte sheet that exhibited a recognizable heart tissue-like structure and showed electrical pulsatile amplitude [6]. Next, they layered single-cell sheets to generate bilayer-cell sheets, forming an electrically communicative three-dimensional cardiac construct, which exhibited spontaneous and synchronous pulsation with electrical communication between the cell sheets, mediated by connexin 43. Furthermore, the cell sheets adhered together rapidly, as indicated by the presence of desmosomes and intercalated disks between them [7]. When the pulsatile cardiac tissue was implanted subcutaneously, it was found to assume a heart tissue-like structure and exhibited neovascularization and spontaneous beating for up to one year. The size, conduction velocity, and contractile force of the engrafted sheets increased in proportion to the host growth [8, 9].

Miyagawa et al. demonstrated that a neonatal cardiomyocyte sheet could communicate electrically with the host myocardium, as indicated by the presence of connexin 43, and changes in the QRS wave and action potential amplitude, leading to improved cardiac performance in a rat model of ischemic heart disease [3]. This study clearly showed electrical and morphological coupling between the cell sheet and host myocardium and that the cell sheet could contract synchronously with the beating of the host heart and improve the regional systolic function.

A detailed analysis of the vascularization process following cell sheet implantation was undertaken by Sekiya et al. These authors reported that the cardiomyocyte sheet expresses angiogenesis-associated genes and forms an endothelial cell network. Evidence was also presented suggesting that the vessels arising in the engrafted sheet migrate to connect with the host vasculature [10].

Myocardial tissue grafts engineered with cell sheet technology represent a promising therapy for repairing the damaged myocardium, but there may be some inherent limitations. For example, cellular treatment for heart failure may be not suitable for emergency situations. Another issue is that wide therapeutic use will require improvement in the uniformity in the quality of the cultured cells.

Recently, new medications that imitate the paracrine effects of cytokines in cell sheets have been reported, and the addition of such medications could improve the regenerative treatment for heart failure. It was reported that the direct introduction of a prostacyclin agonist into the damaged myocardium induced significant functional recovery in a canine model of dilated cardiomyopathy, via the upregulation of multiple cytokines, including HGF, VEGF, and SDF-1 [11]. Similarly, the implantation of an atelocollagen sheet containing a prostacyclin analogue induced improved cardiac function and a prolonged survival rate in a mouse model of acute myocardial infarction, accompanied by an enhanced expression of SDF-1 [12]. Recent work has also revealed that prostacyclin may be upregulated in the implanted myoblast sheet in the early phases after implantation in response to ischemic conditions and may in turn stimulate endothelial or smooth muscle cells to secrete multiple cytokines including HGF, VEGF, and SDF-1 (data not shown).

In the clinical setting, cellular cardiomyoplasty is reported to have potential regenerative capability, and a method using skeletal myoblasts has been evaluated in clinical trials and found to be relatively feasible and safe [13]. For tissue cardiomyoplasty, skeletal myoblasts are the cell source closest to being ready for clinical application at this time. Memon et al. demonstrated that the nonligature implantation of a skeletal myoblast sheet into a rat cardiac ligation model regenerated the damaged myocardium and improved global cardiac function, by attenuating cardiac remodeling via hematopoietic stem-cell recruitment and growth-factor release, with better restoration of the implanted cells than that obtained using needle injection [14]. In another study, the application of a skeletal myoblast sheet into a 27-week dilated cardiomyopathy hamster model resulted in the attenuated deterioration of cardiac performance accompanied by the preservation of alpha-sarcoglycan and beta-sarcoglycan expression in the host myocytes, and an inhibition of fibrosis, leading to prolonged survival rates [15]. In addition, the grafting of skeletal myoblast sheets attenuated cardiac remodeling and improved cardiac performance in a pacing-induced canine heart failure model [16]. Studies from our group have shown that myoblast sheets may improve cardiac performance via cytokines such as HGF or VEGF (XX).

The mechanism of recovery in the damaged myocardium has not been completely elucidated and may be very complicated. As mentioned above, cytokine release and hematopoietic stem-cell recruitment are possible mechanisms of regeneration; however, other regenerative mechanisms are likely to be involved as well. Skeletal myoblasts cannot beat synchronously with the host myocardium in vitro [17] or in vivo [18], and, thus, they do not appear to be functionally integrated. However, data from our human and porcine studies suggested that after myoblast sheet implantation, the diastolic dysfunction in the distressed region of the myocardium was significantly recovered compared with controls, leading to improved systolic function in the same region, without contraction of the implanted myoblasts (data not shown). Massive angiogenesis in the implanted region was detected histologically and appeared to be a critical feature associated with the improvement. Thus, we speculate that angiogenesis and the recovery of diastolic function are both major components of the regenerative mechanism in myoblast sheet implantation [19].

On the other hand, immunohistochemical analysis has indicated that the myoblast sheet may only survive for a few months after implantation. We speculate that in the early phases after implantation of the myoblast sheet, the ischemic conditions induce the upregulated expression of several cytokines by the myoblasts that promote their own survival. These cytokines then in turn enhance angiogenesis and the recruitment of stem cells, leading to improved blood perfusion to reactivate the damaged myocardium. The system may continue to be effective in spite of the short-lived myoblast sheet, due to long-term maintenance of the newly developed vasculature.

We recently initiated a clinical evaluation of autologous myoblast sheet implantation. We tested the technology in four patients who were using left ventricular assist devises (LVADs); three of the four patients showed functional recovery, and in two of the patients, the treatment provided a bridge to recovery [20]. Six years later, these two patients have no symptoms of heart failure. We have also implanted myoblast sheets into eight patients with ischemic cardiomyopathy and seven with dilated cardiomyopathy (who were not using LVADs). In that study, some of the patients exhibited left ventricle reverse remodeling and improvements in exercise tolerance and symptoms, with no major adverse cardiac events (MACEs) (data not shown). This clinical research program is ongoing, as we continue to evaluate patients with dilated cardiomyopathy and ischemic cardiomyopathy with and without the use of LVADs.

In addition to cardiomyocytes and myoblasts, other types of cell sheets have been used effectively to improve cardiac performance. The transplantation of a mesenchymal stem cell (MSC) sheet onto the infarcted myocardium of rats resulted in increased anterior wall thickness and new vessel formation, accompanied by a low incidence of differentiation of the implanted cells to cardiomyocytes [21]. While the small number of differentiated cardiomyocytes may not have contributed to the observed improvement in systolic function in this study, the cell sheet exhibited self-propagating properties that promoted the generation of a thick-layered sheet. Although the MSC sheet exhibited a maximum thickness of approximately 600m, which would not be strong enough to correct human end-stage heart failure [22], this method of self-propagation is a potential strategy for creating a thick-layered sheet in vivo, with the potential for cardiac tissue regeneration.

A further development in cell sheet technology is the creation of a cell sheet composed of two types of cocultured cells; this type of cell sheet was developed to enhance angiogenesis [23, 24]. The cocultured cell sheet, which combined fibroblasts and endothelial progenitor cells, enhanced blood vessel formation and led to functional improvement in a rat myocardial infarction model [24]. Cocultured cell sheets combining fibroblasts and human smooth muscle cells were found to accelerate the secretion of angiogenic factors in vitro and to increase blood perfusion in vivo by the formation of new vessels [25]. This enhanced effectiveness attained by coculturing two cell types is supported by another study in which the coimplantation of BMCs and myoblasts showed improved results compared to the transplantation of a single cell type in a canine model of ischemic cardiomyopathy [26].

Cell sheets composed of stem cell antigen-1- (sca-1-) positive, or kit-positive cells may represent additional promising approaches. Matsuura et al. demonstrated that sca-1-positive cell sheets could differentiate into cardiomyocytes in vivo and produce VCAM-1, leading to improved cardiac performance in a mouse model of myocardial infarction [27]. The administration of c-kit-positive stem cells has shown efficacy in animal models of cardiac dysfunction, and this approach is currently being tested in clinical trials in combination with coronary artery bypass grafting, with encouraging preliminary results [28]. In another study, a c-kit-positive cell sheet combined with endothelial progenitor cell injection was found to induce better functional recovery of endocardial scar tissue than that induced by the cell sheet alone, despite the poor transdifferentiation ability of the c-kit-positive cells into cardiomyocytes [29].

Many of the cell sources mentioned above demonstrate regenerative ability based on the paracrine effect of secreted cytokines; however, newly differentiated cardiomyocytes may be the best candidate cells to regenerate the damaged myocardium. In 2006, Takahashi and Yamanaka reported the development of induced pluripotent stem (iPS) cells that can differentiate into various types of cells, such as cardiomyocytes, cartilage, and nerve cells [30]. Since then, there have been many reports showing that cardiomyocytes derived from iPS cells demonstrate electrophysiological, functional, and microstructural similarities to native cardiomyocytes [31]. Cardiomyocyte sheets derived from human or mouse iPS cells that contract synchronously in vitro have been developed, and studies indicate that these cardiomyocyte sheets can contract in vivo as analyzed by X-ray diffraction with synchrotron radiation. The transplantation of these sheets leads to functional recovery with upregulated electrical potential in the scarred areas in large [32] and small animal myocardial infarction models [33].

Although preclinical studies appear promising, the safety of these artificially generated cells must be evaluated thoroughly before they can be used in the clinic. In addition, a potential limitation of iPS cell-derived cardiomyocytes may be the loss of cardiomyocytes due to ischemia after implantation. Recent studies have proposed supplemental strategies to avoid ischemia. In one study, the combination of an iPS-derived cardiomyocyte sheet with omentum, which has a rich vasculature network, resulted in retention of the implanted cardiomyocytes and enhanced functional recovery compared with the cardiomyocyte sheet alone [34]. In another study, the transplantation of a cardiomyocyte sheet containing iPS cell-derived endothelial cells led to enhanced functional recovery in a rat myocardial infarction model and increased survival of the implanted cardiomyocytes [35]. Thus, to successfully treat the severely damaged myocardium using iPS cell-derived cardiomyocyte sheets, additional strategies to increase angiogenesis and reduce ischemia may be required.

Studies on the original myoblast cell therapy, in which cells were directly injected into the myocardium, indicated that the proportion of injected cells surviving to engraft the infarcted myocardium was too low to be effective. This low level of engraftment may have been caused by the injected cells leaking out of the injected region and being carried to other organs, or due to mechanical stress resulting in cellular loss of function. The resulting rapid cell loss [14] limited the usefulness of the original myoblast cell therapy.

To overcome the problems associated with the intramyocardial injection of cells, many investigators have combined cell transplantation with protein or gene therapy [36], or with tissue-engineered techniques [3]. We have also developed a new cell delivery system that uses tissue-engineered myoblast grafts grown as cell sheets and have utilized animal studies to guide clinical trials. These studies showed that the viability of the transplanted cells was higher than that of injected cells, and that the transplanted myoblasts survived for at least 3 months in the cardiac tissue of a porcine model of heart failure treated with autologous myoblast sheets. Using tissue-engineered temperature responsive techniques, we found that the implanted cells could be applied in larger numbers, were viable during transplantation, and were not lost from the applied region. Furthermore, we showed that cell sheets could be engrafted onto the failed myocardium and contribute to the attenuation of cardiac dysfunction and remodeling [14].

In cell therapy for cardiac disease, life-threatening adverse events involving arrhythmogenicity are a potential risk in both animal models and human clinical trials [37]; however, life-threatening arrhythmias have not been observed during the clinical course of patients who have received autologous cell sheet transplants. In any case, arrhythmias can occur during the natural clinical course of severe heart failure, so their cause may not be easily determined. Procedures using needle injection may cause scars in the myocardium that could in turn induce arrhythmias. Our cell delivery techniques using cell sheets prepared on temperature-responsive culture dishes may carry less risk for the induction of arrhythmias. Myoblasts have a weak electrical potential, and it may be possible for these cells to induce arrhythmia if they survive in the myocardium. However, cell sheets may not be able to induce arrhythmia, since they are attached to the epicardium.

Another potential problem is the limited blood perfusion to the implanted cell sheets. Although the survival of implanted cells using the cell sheet technique has already been shown to exceed the cell survival using other delivery routes, the survival rate was still found to be relatively low when the cells were implanted on the epicardium with this technique [38]. Although we have reported that improved cardiac performance depends on the dose of implanted myoblast sheets, the use of too many cell sheets results in a reduced blood supply. Thus, additional strategies, such as combining myoblasts with angiogenic factors [36] or other types of cells [23] to establish a vasculature network, may be needed to solve this problem. One strategy discussed above, is the combination of a myoblast sheet with omentum tissue that has a rich vasculature network. One report recently demonstrated the effectiveness of this approach for retention of the implanted cell sheets [39]. This report also suggested that the implanted myoblast sheet might induce vasculature connections between arteries of the transplanted omentum and the native coronary arteries, suggesting the possibility of biocoronary artery bypass grafting. This method may also be used in conjunction with iPS cell-derived cardiomyocytes to generate an artificial thick cardiac structure with increased vascular connections.

In this review, we surveyed many exciting topics in the area of cell sheet technology for cardiac repair. Owing to these studies, some techniques have already been tested in clinical applications, but the mechanisms by which they improve cardiac function are only partially understood, and much of the technology is still in the early stages of development, both experimentally and in the clinic. Nevertheless, the field of clinical myocardial regenerative therapy holds much promise, and we expect to witness more progress in this innovative technology in the near future.

The authors declare that there is no conflict of interests regarding the publication of this paper.

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Present and Future Perspectives on Cell Sheet-Based ... - Hindawi

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Your Health and Hormones Close

We are here to help you understand how hormones work and use that knowledge to manage your health.

We empower high-quality, equitable healthcare for people with hormone health conditions, including diabetes and obesity, infertility, thyroid conditions, osteoporosis, and hormone-related cancers. Together, we promote an environment that helps people of all backgrounds and ethnicities access the medical care they need.

Through our multi-lingual educational materials, and EndoCares program, the Endocrine Society provides opportunities for you to connect with endocrinologists across the globe. For more than two decades, our 18,000 members have leveraged their medical and scientific expertise to provide trusted information to the public.

Endocrinology is the study of medicine that relates to the endocrine system, which is the system that controls hormones. Hormones regulate:

Hormones are produced by glands and sent into the bloodstream to the various tissues in the body. They send signals to those tissues to tell them what they are supposed to do. When the glands do not produce the right amount of hormones, diseases develop that can affect many aspects of life.

Endocrinologists are specially trained physicians, who treat those that suffer from hormonal imbalances. They have thoroughly studied hormonal conditions and know the best treatments and therapies. options. Most general practitioners have the skills necessary to diagnose and treat basic hormonal conditions, but sometimes the help of a specialist is needed.

The Patient Engagement Committee is comprised of Endocrine Society members, clinicians, researchers, educators, with expertise in endocrinology's major therapeutic areas. The committees role is to identify the educational needs of endocrine science for patients and the public, oversee the impact and outcomes of our program, and provide translational knowledge on specific hormone-related conditions.

Are you an Endocrine Society member interested in creating or reviewing content? Let us know you are interested, by filling out the volunteer form here.

DISCLAIMER:WE DO NOT PROVIDE MEDICAL ADVICE -The information, including but not limited to, text, graphics, images and other material contained on this website are for informational and educational purposes only. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

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Patient Engagement | Endocrine Society

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Anemia: Abnormally low levels of red blood cells in the bloodstream. Most cases are caused by iron deficiency (lack of iron).

Cervix: The lower, narrow end of the uterus at the top of the vagina.

Cesarean Birth: Birth of a fetus from the uterus through an incision made in the womans abdomen.

Computed Tomography (CT): A type of X-ray that shows internal organs and structures in cross section.

Estrogen: A female hormone produced in the ovaries.

Fetus: The stage of human development beyond 8 completed weeks after fertilization.

Fallopian Tubes: Tubes through which an egg travels from the ovary to the uterus.

Gonadotropin-releasing Hormone (GnRH): A hormone made in the brain that tells the pituitary gland when to produce follicle-stimulating hormone (FSH) and luteinizing hormone.

Hysterectomy: Surgery to remove the uterus.

Hysterosalpingography: A special X-ray procedure in which a small amount of fluid is placed in the uterus and fallopian tubes to find abnormal changes or see if the tubes are blocked.

Hysteroscopy: A procedure in which a lighted telescope is inserted into the uterus through the cervix to view the inside of the uterus or perform surgery.

Intrauterine Device (IUD): A small device that is inserted and left inside the uterus to prevent pregnancy.

Laparoscopy: A surgical procedure in which a thin, lighted telescope called a laparoscope is inserted through a small incision (cut) in the abdomen. The laparoscope is used to view the pelvic organs. Other instruments can be used with it to perform surgery.

Laparotomy: A surgical procedure in which an incision is made in the abdomen.

Magnetic Resonance Imaging (MRI): A test to view internal organs and structures by using a strong magnetic field and sound waves.

Menopause: The time when a woman's menstrual periods stop permanently. Menopause is confirmed after 1 year of no periods.

Menstruation: The monthly shedding of blood and tissue from the uterus that happens when a woman is not pregnant.

Osteoporosis: A condition of thin bones that could allow them to break more easily.

Pelvic Exam: A physical examination of a womans pelvic organs.

Progesterone: A female hormone that is made in the ovaries and prepares the lining of the uterus for pregnancy.

Progestin: A synthetic form of progesterone that is similar to the hormone made naturally by the body.

Resectoscope: A slender telescope with an electrical wire loop or roller-ball tip used to remove or destroy tissue.

Sonohysterography: A procedure in which sterile fluid is injected into the uterus through the cervix while ultrasound images are taken of the inside of the uterus.

Tranexamic Acid: A drug to treat or prevent heavy bleeding.

Ultrasound Exam: A test in which sound waves are used to examine inner parts of the body. During pregnancy, ultrasound can be used to check the fetus.

Uterus: A muscular organ in the female pelvis. During pregnancy, this organ holds and nourishes the fetus. Also called the womb.

Uterine Artery Embolization: A procedure to block the blood vessels to the uterus. This procedure is used to stop bleeding after delivery. It is also used to stop other causes of bleeding from the uterus.

Vagina: A tube-like structure surrounded by muscles. The vagina leads from the uterus to the outside of the body.

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New Illinois Laws in 2023 That Focus on the Health, Wellness of State Residents  NBC Chicago

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New Illinois Laws in 2023 That Focus on the Health, Wellness of State Residents - NBC Chicago

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Topiramate Weight Loss Reviews: Top 4 Over The Counter Alternative To Topamax For Weight Loss  Outlook India

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Topiramate Weight Loss Reviews: Top 4 Over The Counter Alternative To Topamax For Weight Loss - Outlook India

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Milanova next to her award-winning microscopy image named "Making Waves: Delivery for Ageless Skin" ... [+] which was on display in 2017 at the Koch Institute Gallery celebrating extraordinary visuals at MIT

In my previous articles, I covered the wonderful female medical doctors working in longevity medicine, female reproductive longevity and inequality, skincare, and other areas. Here, we continue on this journey and look at the stellar scientist and entrepreneur, Dr. Denitsa Milanova. I heard about Dr. Milanova a few years back when she just joined Harvard, and met her for the first time in person in May 2022 when she told me about her new exciting venture - Marble Therapeutics and her quest to use genetic engineering to target aging.

Denitsa Milanova, PhD, founder and CEO of Marble Therapeutics

Denitsa was born in Bulgaria to a family of engineers. As a child, she excelled at analytical disciplines, and especially in math and physics. She learned at a young age that exceptional results can be achieved with hard work and perseverance. In school, she participated in science competitions routinely winning top places. For college, she moved to Florida, and then continued her graduate studies at Stanford University where she earned her masters and doctorate degrees in mechanical engineering and completed a business degree. Her studies were focused on microfluidics and she pursued research in single-cell sequencing using microfluidic technologies with prominent scientists including Michael Snyder. For her postdoctoral training, she moved to Harvard Medical School and Wyss Institute to work with George Church and soon focused on aging research.

Professor George Church of Harvard Medical School in Boston, MA on November 30, 2012. Church, a ... [+] professor of Genetics with the MAGE Device Multiplex automated Genome Engineering. (Photo by Rick Friedman/rickfriedman.com/Corbis via Getty Images)

Milanova tells me that this is simply the perfect time to build a rejuvenation company with new tools and large amounts of human data. We are doing great things in molecular biology, she says. But from her perspective, scientists are too focused on accumulating experimental evidence - hugely important - but when a field is starting to mature, we need to ask larger questions beyond what is there? but more how can we manipulate it? We need to shift from knowledge-based to inquiry-based frameworks, focusing on the complexities and stabilities of aging systems, and how they evolved to be a certain way.

Milanova and her team spend a lot of time on the why questions. This is the data but why does it look like that? We want to think from first principles, she explains. Drug development is expensive and betting on the wrong targets can be detrimental to companies. Identifying the right drivers amidst a sea of passengers, and spurious events is very hard. We are building algorithms that probe tipping points, thresholds and breakpoints, regime shifts. Going after those genetic perturbations that lead to the largest changes of aging states, she continues.

While Marble is still more or less in stealth mode without a public website, word had gotten around over the last year through top biotechnology and longevity investors that George Churchs lab was cooking up a secretive rejuvenation startup. Now known as Marble, led by his engineer-biotechnologist protg Dr. Milanova, the effort has garnered considerable inbound attention. Denitsa says that her team is developing methods to drive rejuvenation of skin cells with gene therapy and is working on a product that could reverse wrinkles like a genetic Botox.

The magic words in longevity biotech nowadays are platform and pipeline, where the company develops a platform for drug discovery and is using this platform to discover and develop its own therapeutic programs. And Marble is building target discovery and delivery platforms to drive its first pipeline program in the skin. To search for such powerful genes, they use computational methods taken from the study of non-linear dynamics and complex systems. The sort of things which can infer causality in other fields like ecology and finance. And they are attempting to predict the effects of changes in gene expression over time and thereby identifying key driving events and genes of aging.

The Marble team is taking an unbiased approach, agnostic to biological mechanism, and instead search the entire genome for those genes and proteins responsible for large, global shifts in the biology of cells as they transition from young to old. The aging field has leaned too heavily on hypothesis-driven approaches which insist that specific pathways must be involved in longevity and age-associated molecular mechanisms. These things do not necessarily tell us how a cell becomes old, or how to make it young, Milanova points out. The precise details of Marbles approach are being kept a secret, but Milanova has assembled an all-star team led by chairman Matt Rabinowitz (the man behind Natera) and an acclaimed scientific board that includes George Church, Michael Snyder, Carl June, Bob Langer, George Sugihara, Yoav Freund. Rabinowitz says, Aging is the king of all maladies. It remains to be seen how much we can massage our natural mortality, but usually when people place limits on science - and biotech in particular - they are wrong. The approaches Marble is working on to better understand dynamic gene signaling networks and drive those networks with gene therapy are important, would have broad application and are guided by a strong team of scientists.

NEW YORK, NY - MARCH 07: Tony Robbins attends Build series to discuss "UNSHAKEABLE: Your Financial ... [+] Freedom Playbook" at Build Studio on March 7, 2017 in New York City. (Photo by Chance Yeh/FilmMagic)

While building Marble, Milanova sought the advice of a man who would become one of her early backers, Tony Robbins. Robbins, who has coached presidents, elite athletes, and business leaders on the psychology and mechanics of building organizations, became a mentor and advised her on building the most effective team. I met Denitsa when she had just assembled an impressive team of experts prior to any funding into the company. People had signed solely based on the science and mission. What stood out to me was her ability to influence, in a very raw, authentic way. To sell the dream equally well to scientists, and business people, Robbins says. This quality is crucially important and at the core of exceptional leadership. It is truly amazing to see how much Marble has grown in a short period of time and I am excited to be part of it.

As one example of how the company is building competitive advantage, Milanova points to the future collection of proprietary human multi-omics data to fuel rejuvenation target discovery. And the company is well positioned to execute on this goal. Not only are two of its founders Church and Snyder pioneers in multi-omic technologies, they have also worked for decades to develop primary human data collection initiatives. As Church explains, Despite 20 million-fold improvement in the cost of reading human genomes, and trillion dollars per year avoidable by testing, the word is spreading slowly - in part because people feel that they are in the lucky 98% (similar to past denialism for cigarettes and seat belts.) He continues, We need to know our genome but for most of us, it is not actionable. It is different with aging and epigenetics (broadly defined as all -omes). We all age and likely care about aspects of aging (at least most of us).

Dr. Denitsa Milanova at Abundance360 with early supporter and visionary entrepreneur scientist, Dr. ... [+] Peter Diamandis.

This focus on human data is at the core of Marble. Our vision is that aging research will become more human data focused. That is, discovery will start with human data first, not hypotheses based on comparative longevity or mechanistic studies between species. We expect that targets best-suited for rejuvenation of specific cells and tissues may not be one-size-fits-all. And its hard to identify such targets if we are focused solely on highly conserved master regulators, explains Milanova.

Dr. Denitsa Milanova, founder and CEO of Marble Therapeutics

Marble is starting with skin rejuvenation, but they arent trying to be just a skin company. Think of deep-omic profiling of skin, blood, muscle, even reproductive cells with a time stamp on it, Milanova says. Our vision is to have high-quality cross-sectional and longitudinal datasets and all discoveries being data-driven rather than hypothesis-driven, she continues. If you think about those tissues, there are some unique and untapped markets to break into, if you had the right technology, says Milanova. And importantly, they may not have to follow human subjects over years to collect the right data. The cross-sectional data capability is really where our data analytics could shine. We could potentially cut through the noise of human-to-human variation to find deterministic signals, and likely with hundreds of donors. Not like with GWAS where you need tens of thousands.

Longevity Dinner in Boston, 2022. Right to left: Denitsa Milanova, PhD, Marble Therapeutics; Joe ... [+] Betts-LaCroix and Anastasia Shindyapina, PhD, Retro Biosciences; Alex Zhavoronkov, PhD, Insilico Medicine; Vadim Gladyshev, PhD, Brigham and Women's Hospital, Harvard Medical School.

Alex: Denitsa, you have a very impressive resum with multiple graduate degrees from Stanford, postdoctoral training at one of the top labs at Harvard and consulting engagements with a variety of companies. When did you decide to go into aging research?

Denitsa: Thank you, Alex. Id say about five years ago when I started working with George Church. Being new to the field helps with bringing in a fresh perspective. George took a chance on me when I had no background in aging research and taught me how to take risks and pursue groundbreaking science. And this is the best way to tackle big problems, starting with the basic science but also being comfortable for things to take time and even failing before succeeding.

From the beginning I had a vision to do gene therapy for skin rejuvenation, and at the time, everyone thought that was a totally crazy idea. The cost of gene therapy then was as high as $2.8 million, but we have seen huge reductions in the cost of similar modalities like mRNA to as low as $2 per dose, largely driven by the market size. Clinical products in the skin have an enormous market (Botox alone is larger than all of cell and gene therapy combined), and true rejuvenation therapies could reach markets larger even than COVID vaccines.

Alex: This is your first venture. Did you think you would be able to raise funding? Do you have any notable investors in your seed round?

Denitsa: I am a big optimist and even a little bit of a dreamer by nature, but I do get anxious about fundraising. I think some fear of failure and a certain level of anxiety actually helps me, it motivates me to deliver. Yes, we were fortunate to attract prominent investors, and even more so to have them mentor and advise. Success leaves clues and learning from experience saves years. I force myself to maintain a no limitations mindset, both in science and business. What keeps me highly motivated is the certainty that rejuvenation is fundamentally possible, that we have the tools, and is worth doing it is one of the biggest problems of our time.

Alex: When are you planning to get to the preclinical proof of concept (POC) in animals and start IND-enabling studies? And if all goes well, when do you think we will be able to see Marbles products in the clinic? I understand how speculative this is but what is your vision?

Denitsa: It is early to say, we are at the preclinical stage right now. Skin is a very interesting organ clinically and an attractive entry point for newer therapies both in terms of targets and modality. You can test human organ skin grafts in mice to validate function in live human tissue physiology. Clinical trials and endpoints are more defined too because you can have multiple treatment and control locations across the skin, and the accessibility of the skin lets you assess aging phenotypes visually and mechanically to prove effectiveness of your therapy and approach in general.

Alex: What is your long-term vision for the company and for longevity biotechnology in general?

Denitsa: Over the long term we have no shortage of ambition. Skin is the start, because thats where we could get the right data. But I want all tissues. All ages made functionally young. We are starting with single-gene perturbations, but changes in complex cell states are typically polygenic processes. So we have a plan for moving into multi-gene targets using concepts analogous to those which have powered engineering and evolution of antibodies, enzymes, and protein-based drugs, but applied to whole-cell states. That is where I think the future is. We should be evolving cells in the lab to just be very good at being young. Thats not how our cells have evolved naturally, but it is how we can select them to be. Screening, genetic libraries and evolutionary approaches are central to the world of George Churchs lab, and that mindset has definitely rubbed off on me. We will need to intelligently explore genetic space to really ratchet up young-like cell behaviors.

Alex: And another very personal question. You do not need to answer it if it is too sensitive. I know what it takes to run a startup in the longevity space. It does not get intense from time to time - it is a life at full throttle when there is no time to stop and take a breath. How are you planning to maintain the work-life balance?

I have no idea what that [work-life balance] is, she smiles. But really, this isnt work to me. Its not some necessary evil to be balanced. Its a mission, its my life and I love what we are doing, she continued. Of course, I do things to keep sane. I love cryotherapy, another smile.

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This Harvard Female Scientist Wants To Use Genetics To Reverse The Age ...

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Aspect of human growth

Human height or stature is the distance from the bottom of the feet to the top of the head in a human body, standing erect. It is measured using a stadiometer,[1] in centimetres when using the metric system or SI system,[2][3] or feet and inches when using United States customary units or the imperial system.[4][5]

In the early phase of anthropometric research history, questions about height techniques for measuring nutritional status often concerned genetic differences.[6]

Height is also important because it is closely correlated with other health components, such as life expectancy.[6] Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the "longevity gene" FOXO3 that reduces the effects of aging is more commonly found in individuals of small body size.[7] Short stature decreases the risk of venous insufficiency.[8]

When populations share genetic backgrounds and environmental factors, average height is frequently characteristic within the group. Exceptional height variation (around 20% deviation from average) within such a population is sometimes due to gigantism or dwarfism, which are medical conditions caused by specific genes or endocrine abnormalities.[9]

The development of human height can serve as an indicator of two key welfare components, namely nutritional quality and health.[10] In regions of poverty or warfare, environmental factors like chronic malnutrition during childhood or adolescence may result in delayed growth and/or marked reductions in adult stature even without the presence of any of these medical conditions.

A study of 20th-century British natality trends indicated that while tall men tended to reproduce more than short men, women of below-average height had more children than taller women.[11]

The study of height is known as auxology.[12] Growth has long been recognized as a measure of the health of individuals, hence part of the reasoning for the use of growth charts. For individuals, as indicators of health problems, growth trends are tracked for significant deviations, and growth is also monitored for significant deficiency from genetic expectations. Genetics is a major factor in determining the height of individuals, though it is far less influential regarding differences among populations. Average height is relevant to the measurement of the health and wellness (standard of living and quality of life) of populations.[13]

Attributed as a significant reason for the trend of increasing height in parts of Europe are the egalitarian populations where proper medical care and adequate nutrition are relatively equally distributed.[14] The uneven distribution of nutritional resources makes it more plausible for individuals with better access to resources to grow taller, while the other population group who does not have so much of a nutritious food availability height growth is not as promising.[15] Average height in a nation is correlated with protein quality. Nations that consume more protein in the form of meat, dairy, eggs, and fish tend to be taller, while those that obtain more protein from cereals tend to be shorter.[citation needed] Therefore, populations with high cattle per capita and high consumption of dairy live longer and are taller. Historically, this can be seen in the cases of the United States, Argentina, New Zealand and Australia in the beginning of the 19th century.[16] Moreover, when the production and consumption of milk and beef is taken to consideration, it can be seen why the Germanic people who lived outside of the imperium Romanum were taller than those who lived at the heart of the Empire.[17]

Changes in diet (nutrition) and a general rise in quality of health care and standard of living are the cited factors in the Asian populations. Malnutrition including chronic undernutrition and acute malnutrition is known to have caused stunted growth in various populations.[18] This has been seen in North Korea, parts of Africa, certain historical Europe, and other populations.[19] Developing countries such as Guatemala have rates of stunting in children under 5 living as high as 82.2% in Totonicapn, and 49.8% nationwide.[20]

Height measurements are by nature subject to statistical sampling errors even for a single individual. In a clinical situation, height measurements are seldom taken more often than once per office visit, which may mean sampling taking place a week to several months apart. The smooth 50th percentile male and female growth curves illustrated above are aggregate values from thousands of individuals sampled at ages from birth to age 20. In reality, a single individual's growth curve shows large upward and downward spikes, partly due to actual differences in growth velocity, and partly due to small measurement errors.

For example, a typical measurement error of plus or minus 0.5cm (0.20in) may completely nullify 0.5 cm of actual growth resulting in either a "negative" 0.5 cm growth (due to overestimation in the previous visit combined with underestimation in the latter), up to a 1.5cm (0.6in) growth (the first visit underestimating and the second visit overestimating) in the same elapsed period between measurements. Note there is a discontinuity in the growth curves at age 2, which reflects the difference in recumbent length (with the child on his or her back), used in measuring infants and toddlers, and standing height typically measured from age 2 onwards.

Height, like other phenotypic traits, is determined by a combination of genetics and environmental factors. A child's height based on parental heights is subject to regression toward the mean, therefore extremely tall or short parents will likely have correspondingly taller or shorter offspring, but their offspring will also likely be closer to average height than the parents themselves. Genetic potential and several hormones, minus illness, is a basic determinant for height. Other factors include the genetic response to external factors such as diet, exercise, environment, and life circumstances.

Humans grow fastest (other than in the womb) as infants and toddlers, rapidly declining from a maximum at birth to roughly age 2, tapering to a slowly declining rate, and then, during the pubertal growth spurt (with an average girl starting her puberty and pubertal growth spurt at 10 years[21] and an average boy starting his puberty and pubertal growth spurt at 12 years[22][23]), a rapid rise to a second maximum (at around 1112 years for an average female, and 1314 years for an average male), followed by a steady decline to zero. The average female growth speed trails off to zero at about 15 or 16 years, whereas the average male curve continues for approximately 3 more years, going to zero at about 1819. These are also critical periods where stressors such as malnutrition (or even severe child neglect) have the greatest effect.

Moreover, the health of a mother throughout her life, especially during her critical period and pregnancy, has a role. A healthier child and adult develops a body that is better able to provide optimal prenatal conditions.[19] The pregnant mother's health is essential for herself but also the fetus as gestation is itself a critical period for an embryo/fetus, though some problems affecting height during this period are resolved by catch-up growth assuming childhood conditions are good. Thus, there is a cumulative generation effect such that nutrition and health over generations influence the height of descendants to vary degrees.

The age of the mother also has some influence on her child's height. Studies in modern times have observed a gradual increase in height with maternal age, though these early studies suggest that trend is due to various socio-economic situations that select certain demographics as being more likely to have a first birth early in the mother's life.[24][25][26] These same studies show that children born to a young mother are more likely to have below-average educational and behavioural development, again suggesting an ultimate cause of resources and family status rather than a purely biological explanation.[25][26]

It has been observed that first-born males are shorter than later-born males.[27]However, more recently the reverse observation was made.[28] The study authors suggest that the cause may be socio-economic in nature.

The precise relationship between genetics and environment is complex and uncertain. Differences in human height is 6080% heritable, according to several twin studies[29] and has been considered polygenic since the Mendelian-biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height.[30] The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.[31] In a separate study of body proportion using sitting-height ratio, it reports that these 697 variants can be partitioned into 3 specific classes, (1) variants that primarily determine leg length, (2) variants that primarily determine spine and head length, or (3) variants that affect overall body size. This gives insights into the biological mechanisms underlying how these 697 genetic variants affect overall height.[32] These loci do not only determine height, but other features or characteristics. As an example, 4 of the 7 loci identified for intracranial volume had previously been discovered for human height.[33]

The effect of environment on height is illustrated by studies performed by anthropologist Barry Bogin and coworkers of Guatemala Mayan children living in the United States. In the early 1970s, when Bogin first visited Guatemala, he observed that Mayan Indian men averaged 157.5 centimetres (5ft 2in) in height and the women averaged 142.2 centimetres (4ft 8in). Bogin took another series of measurements after the Guatemalan Civil War, during which up to a million Guatemalans fled to the United States. He discovered that Maya refugees, who ranged from six to twelve years old, were significantly taller than their Guatemalan counterparts.[34] By 2000, the American Maya were 10.24cm (4.03in) taller than the Guatemalan Maya of the same age, largely due to better nutrition and health care.[35] Bogin also noted that American Maya children had relatively longer legs, averaging 7.02cm (2.76in) longer than the Guatemalan Maya (a significantly lower sitting height ratio).[35][36]

The Nilotic peoples of Sudan such as the Shilluk and Dinka have been described as some of the tallest in the world. Dinka Ruweng males investigated by Roberts in 195354 were on average 181.3 centimetres (5ft 11+12in) tall, and Shilluk males averaged 182.6 centimetres (6ft 0in).[37] The Nilotic people are characterized as having long legs, narrow bodies and short trunks, an adaptation to hot weather.[38] However, male Dinka and Shilluk refugees measured in 1995 in Southwestern Ethiopia were on average only 176.4cm (5ft 9+12in) and 172.6cm (5ft 8in) tall, respectively. As the study points out, Nilotic people "may attain greater height if privileged with favourable environmental conditions during early childhood and adolescence, allowing full expression of the genetic material."[39] Before fleeing, these refugees were subject to privation as a consequence of the succession of civil wars in their country from 1955 to the present.

The tallest living married couple are ex-basketball players Yao Ming and Ye Li (both of China) who measure 228.6cm (7ft 6in) and 190.5cm (6ft 3in) respectively, giving a combined height of 419.1cm (13ft 9in). They married in Shanghai, China, on 6 August 2007.[40]

In Tibet, the Khampas are known for their great height. Khampa males are on average 180cm (5ft 11in).[41][42]

Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the longevity gene FOXO3 that reduces the effects of aging is more commonly found in individuals of a small body size.[7] Short stature decreases the risk of venous insufficiency.[8] Certain studies have shown that height is a factor in overall health while some suggest tallness is associated with better cardiovascular health and shortness with longevity.[43] Cancer risk has also been found to grow with height.[44] Moreover, scientists have also observed a protective effect of height on risk for Alzheimer's disease, although this fact could be a result of the genetic overlap between height and intracraneal volume and there are also genetic variants influencing height that could affect biological mechanisms involved in Alzheimer's disease etiology, such as Insulin-like growth factor 1 (IGF-1).[45]

Nonetheless, modern westernized interpretations of the relationship between height and health fail to account for the observed height variations worldwide.[46] Cavalli-Sforza and Cavalli-Sforza note that variations in height worldwide can be partly attributed to evolutionary pressures resulting from differing environments. These evolutionary pressures result in height-related health implications. While tallness is an adaptive benefit in colder climates such as those found in Europe, shortness helps dissipate body heat in warmer climatic regions.[46] Consequently, the relationships between health and height cannot be easily generalized since tallness and shortness can both provide health benefits in different environmental settings.

In the end, being excessively tall can cause various medical problems, including cardiovascular problems, because of the increased load on the heart to supply the body with blood, and problems resulting from the increased time it takes the brain to communicate with the extremities. For example, Robert Wadlow, the tallest man known to verifiable history, developed trouble walking as his height increased throughout his life. In many of the pictures of the latter portion of his life, Wadlow can be seen gripping something for support. Late in his life, although he died at age 22, he had to wear braces on his legs and walk with a cane; and he died after developing an infection in his legs because he was unable to feel the irritation and cutting caused by his leg braces.

Sources are in disagreement about the overall relationship between height and longevity. Samaras and Elrick, in the Western Journal of Medicine, demonstrate an inverse correlation between height and longevity in several mammals including humans.[43]

Women whose height is under 150cm (4ft 11in) may have a small pelvis, resulting in such complications during childbirth as shoulder dystocia.[47]

A study done in Sweden in 2005 has shown that there is a strong inverse correlation between height and suicide among Swedish men.[48]

A large body of human and animal evidence indicates that shorter, smaller bodies age more slowly, and have fewer chronic diseases and greater longevity. For example, a study found eight areas of support for the "smaller lives longer" thesis. These areas of evidence include studies involving longevity, life expectancy, centenarians, male vs. female longevity differences, mortality advantages of shorter people, survival findings, smaller body size due to calorie restriction, and within-species body size differences. They all support the conclusion that smaller individuals live longer in healthy environments and with good nutrition. However, the difference in longevity is modest. Several human studies have found a loss of 0.5 years/centimeter of increased height (1.2 yr/inch). But these findings do not mean that all tall people die young. Many live to advanced ages and some become centenarians.[49][dubious discuss]

In medicine, height is measured to monitor child development, this is a better indicator of growth than weight in the long term.[50]For older people, excessive height loss is a symptom of osteoporosis.[51] Height is also used to compute indicators like body surface area or body mass index.

There is a large body of research in psychology, economics, and human biology that has assessed the relationship between several physical features (e.g., body height) and occupational success.[52] The correlation between height and success was explored decades ago.[53][54] Shorter people are considered to have an advantage in certain sports (e.g., gymnastics, race car driving, etc.), whereas in many other sports taller people have a major advantage. In most occupational fields, body height is not relevant to how well people are able to perform; nonetheless several studies found that success was positively correlated with body height, although there may be other factors such as gender or socioeconomic status that are correlated with height which may account for the difference in success.[52][53][55][56]

A demonstration of the height-success association can be found in the realm of politics. In the United States presidential elections, the taller candidate won 22 out of 25 times in the 20th century.[57] Nevertheless, Ignatius Loyola, founder of the Jesuits, was 150cm (4ft 11in) and several prominent world leaders of the 20th century, such as Vladimir Lenin, Benito Mussolini, Nicolae Ceauescu and Joseph Stalin were of below-average height. These examples, however, were all before modern forms of multi-media, i.e., television, which may further height discrimination in modern society. Further, growing evidence suggests that height may be a proxy for confidence, which is likewise strongly correlated with occupational success.[58]

In the 150 years since the mid-nineteenth century, the average human height in industrialised countries has increased by up to 10 centimetres (3.9in).[59] However, these increases appear to have largely levelled off.[59][60] Before the mid-nineteenth century, there were cycles in height, with periods of increase and decrease;[61] however, apart from the decline associated with the transition to agriculture, examinations of skeletons show no significant differences in height from the neolithic revolution through the early-1800s.[62][63]

In general, there were no significant differences in regional height levels throughout the nineteenth century.[64] The only exceptions of this rather uniform height distribution were people in the Anglo-Saxon settlement regions who were taller than the average and people from Southeast Asia with below-average heights. However, at the end of the nineteenth century and in the middle of the first globalization period, heights between rich and poor countries began to diverge.[65] These differences did not disappear in the deglobalization period of the two World wars. Baten and Blum (2014) [66] find that in the nineteenth century, important determinants of height were the local availability of cattle, meat and milk as well as the local disease environment. In the late twentieth century, however, technologies and trade became more important, decreasing the impact of local availability of agricultural products.

In the eighteenth and nineteenth centuries, people of European descent in North America were far taller than those in Europe and were the tallest in the world.[14] The original indigenous population of Plains Native Americans was also among the tallest populations of the world at the time.[67]

Some studies also suggest that there existed the correlation between the height and the real wage, moreover, the correlation was higher among the less developed countries. The difference in height between children from different social classes was already observed by age two.[68]

In the late nineteenth century, the Netherlands was a land renowned for its short population, but today Dutch people are among the world's tallest with young men averaging 183.8cm (6ft 0.4in) tall.[69]

According to a study by economist John Komlos and Francesco Cinnirella, in the first half of the eighteenth century, the average height of an English male was 165cm (5ft 5in), and the average height of an Irish male was 168cm (5ft 6in). The estimated mean height of English, German, and Scottish soldiers was 163.6cm (5ft 4+12in) 165.9cm (5ft 5+12in) for the period as a whole, while that of Irish was 167.9cm (5ft 6in). The average height of male slaves and convicts in North America was 171cm (5ft 7+12in).[70]

The average height of Americans and Europeans decreased during periods of rapid industrialization, possibly due to rapid population growth and broad decreases in economic status.[71] This has become known as the early-industrial growth puzzle in the U.S. context the Antebellum Puzzle. In England during the early nineteenth century, the difference between the average height of English upper-class youth (students of Sandhurst Military Academy) and English working-class youth (Marine Society boys) reached 22cm (8+12in), the highest that has been observed.[72]

Data derived from burials show that before 1850, the mean stature of males and females in Leiden, The Netherlands was respectively 167.7cm (5ft 6in) and 156.7cm (5ft 1+12in). The average height of 19-year-old Dutch orphans in 1865 was 160cm (5ft 3in).[73]

According to a study by J.W. Drukker and Vincent Tassenaar, the average height of a Dutch person decreased from 1830 to 1857, even while Dutch real GNP per capita was growing at an average rate of more than 0.5% per year. The worst decline was in urban areas that in 1847, the urban height penalty was 2.5cm (0.98in). Urban mortality was also much higher than in rural regions. In 1829, the average urban and rural Dutchman was 164cm (5ft 4+12in). By 1856, the average rural Dutchman was 162cm (5ft 4in) and urban Dutchman was 158.5cm (5ft 2+12in).[74]

A 2004 report citing a 2003 UNICEF study on the effects of malnutrition in North Korea, due to "successive famines," found young adult males to be significantly shorter.[specify] In contrast South Koreans "feasting on an increasingly Western-influenced diet," without famine, were growing taller. The height difference is minimal for Koreans over forty years old, who grew up at a time when economic conditions in the North were roughly comparable to those in the South, while height disparities are most acute for Koreans who grew up in the mid-1990s a demographic in which South Koreans are about 12cm (4.7in) taller than their North Korean counterparts as this was a period during which the North was affected by a harsh famine where hundreds of thousands, if not millions, died of hunger.[75] A study by South Korean anthropologists of North Korean children who had defected to China found that eighteen-year-old males were 13 centimetres (5in) shorter than South Koreans their age due to malnutrition.[76]

The tallest living man is Sultan Ksen of Turkey, at 251cm (8ft 3in). The tallest man in modern history was Robert Pershing Wadlow (19181940), from Illinois, United States, who was 272cm (8ft 11in) at the time of his death. The tallest woman in medical history was Trijntje Keever of Edam, Netherlands, who stood 254cm (8ft 4in) when she died at the age of seventeen. The shortest adult human on record was Chandra Bahadur Dangi of Nepal at 54.6cm (1ft 9+12in).

An anecdotal article titled "Ancient American Giants" from the 14 August 1880 edition of Scientific American notes a case from Brushcreek Township, Ohio, when Dr. J. F. Everhart supervised a team that discovered ancient clay coffins within a mound which were reported to contain skeletons of the following length: 8ft 0in (2.44m) woman with a child 3.5ft 0in (1.07m), a second coffin with a 9ft 0in (2.74m) man and 8ft 0in (2.44m) woman, a third coffin with a 9ft 4in (2.84m) man and 8ft 0in (2.44m) woman, and seven other independent skeletons measuring between 8ft 0in (2.44m) and 10ft 0in (3.05m). An image and stone tablet were found with the giants.[77]

Adult height between populations often differs significantly. For example, the average height of women from the Czech Republic is greater than that of men from Malawi. This may be caused by genetic differences, childhood lifestyle differences (nutrition, sleep patterns, physical labor), or both.

Depending on sex, genetic and environmental factors, shrinkage of stature may begin in middle age in some individuals but tends to be universal in the extremely aged. This decrease in height is due to such factors as decreased height of inter-vertebral discs because of desiccation, atrophy of soft tissues, and postural changes secondary to degenerative disease.

Working on data of Indonesia, the study by Baten, Stegl and van der Eng suggests a positive relationship of economic development and average height. In Indonesia, human height has decreased coincidentally with natural or political shocks.[78]

As with any statistical data, the accuracy of such data may be questionable for various reasons:

Crown-rump length is the measurement of the length of human embryos and fetuses from the top of the head (crown) to the bottom of the buttocks (rump). It is typically determined from ultrasound imagery and can be used to estimate gestational age.

Until two years old, recumbent length is used to measure infants.[92] Length measures the same dimension as height, but height is measured standing up while the length is measured lying down. In developed nations, the average total body length of a newborn is about 50cm (20in), although premature newborns may be much smaller.

Standing height is used to measure children over two years old[93] and adults who can stand without assistance. Measure is done with a stadiometer. In general, standing height is about 0.7cm (0.28in) less than recumbent length.[94]

Surrogate height measurements are used when standing height and recumbent length are impractical. For sample Chumlea equation use knee height as indicator of stature.[95] Other techniques include: arm span, sitting height, ulna length, etc.

Original post:
Human height - Wikipedia

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Medical condition

Pattern hair loss (also known as androgenetic alopecia (AGA)[1]) is a hair loss condition that primarily affects the top and front of the scalp.[2][3] In male-pattern hair loss (MPHL), the hair loss typically presents itself as either a receding front hairline, loss of hair on the crown (vertex) of the scalp, or a combination of both. Female-pattern hair loss (FPHL) typically presents as a diffuse thinning of the hair across the entire scalp.[3]

Male pattern hair loss seems to be due to a combination of oxidative stress,[4] the microbiome of the scalp,[5][6] genetics, and circulating androgens; particularly dihydrotestosterone (DHT).[3] Men with early onset androgenic alopecia (before the age of 35) have been deemed as the male phenotypic equivalent for polycystic ovary syndrome (PCOS).[7][8][9][10] As an early clinical expression of insulin resistance and metabolic syndrome, AGA is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders,[11] type 2 diabetes,[12][13] and enlargement of the prostate.[14]

The cause in female pattern hair loss remains unclear,[3] androgenetic alopecia for women is associated with an increased risk of polycystic ovary syndrome (PCOS).[15][16][17]

Management may include simply accepting the condition[3] or shaving one's head to improve the aesthetic aspect of the condition.[18] Otherwise, common medical treatments include minoxidil, finasteride, dutasteride, or hair transplant surgery.[3] Use of finasteride and dutasteride in women is not well-studied and may result in birth defects if taken during pregnancy.[3]

Pattern hair loss by the age of 50 affects about half of males and a quarter of females.[3] It is the most common cause of hair loss. Both males aged 4091 [19] and younger male patients of early onset AGA (before the age of 35), had a higher likelihood of metabolic syndrome (MetS) [20][21][22][23] and insulin resistance.[24] With younger males, studies found metabolic syndrome to be at approximately a 4x increased frequency which is clinically deemed as significant.[25][26] Abdominal obesity, hypertension and lowered high density lipoprotein were also significantly higher for younger groups.[27]

Pattern hair loss is classified as a form of non-scarring hair loss.

Male-pattern hair loss begins above the temples and at the vertex (calvaria) of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a "Hippocratic wreath", and rarely progresses to complete baldness.[28]

Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss.[29] The Ludwig scale grades severity of female-pattern hair loss. These include Grades 1, 2, 3 of balding in women based on their scalp showing in the front due to thinning of hair.[citation needed]

In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides.[30][citation needed]

KRT37 is the only keratin that is regulated by androgens.[31] This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et al. found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body, but decrease it on the scalp, this lack of scalp KRT37 may help explain the paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long.[citation needed]

The initial programming of pilosebaceous units of hair follicles begins in utero.[32] The physiology is primarily androgenic, with dihydrotestosterone (DHT) being the major contributor at the dermal papillae. Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared to men without pattern hair loss.[10] Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitor cells from which the follicles arose.[33][34][non-primary source needed]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (IGF) at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on the face, but can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[35]

Men with androgenic alopecia typically have higher 5-reductase, higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.[36] 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate gland. DHT is most commonly formed at the tissue level by 5-reduction of testosterone.[37] The genetic corollary that codes for this enzyme has been discovered.[38] Prolactin has also been suggested to have different effects on the hair follicle across gender.[39]

Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway that leads to hair loss. At the level of the somatic stem cell, androgens promote differentiation of facial hair dermal papillae, but inhibit it at the scalp.[35] Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive.[40]

These observations have led to study at the level of the mesenchymal dermal papillae.[41] Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[42] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[35] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but can also stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[35] Hair follicles in anaphase express four different caspases. Significant levels of inflammatory infiltrate have been found in transitional hair follicles.[43] Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss.[44]

The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains a mystery, but possible explanations are higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress.[45] The mechanism by which the androgen receptor triggers dermal papilla permanent senescence is not known, but may involve IL6, TGFB-1 and oxidative stress. Senescence of the dermal papilla is measured by lack of mobility, different size and shape, lower replication and altered output of molecules and different expression of markers. The dermal papilla is the primary location of androgen action and its migration towards the hair bulge and subsequent signaling and size increase are required to maintain the hair follicle so senescence via the androgen receptor explains much of the physiology.[citation needed]

Male pattern baldness is a complex genetic condition with a "particularly strong signals on the X chromosome".[46]

Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome,[47][48] with low HDL being the component of metabolic syndrome with highest association.[49] Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors.[50] Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome.[51] Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.[52] With early-onset AGA having an increased risk of metabolic syndrome, poorer metabolic profiles are noticed in those with AGA, including metrics for body mass index, waist circumference, fasting glucose, blood lipids, and blood pressure.[53]

In support of the association, finasteride improves glucose metabolism and decreases glycated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[54] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[55] and for which it still is used as an assay for pediatric diabetes mellitus.[56]

Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing the relationship, SHBG is downregulated by insulin in vitro, although SHBG levels do not appear to affect insulin production.[57] In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men.[58] The relationship between SHBG and insulin resistance has been known for some time; decades prior, ratios of SHBG and adiponectin were used before glucose to predict insulin resistance.[59] Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.[60]

Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II.[10] Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen.[61] SHBG association with fasting blood glucose is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison.[62]

Female patients with mineralocorticoid resistance present with androgenic alopecia.[63]

IGF levels have been found lower in those with metabolic syndrome.[64] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[65] Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids such as arginine and leucine. Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone.[66]

A number of hormonal changes occur with aging:

This decrease in androgens and androgen receptors, and the increase in SHBG are opposite the increase in androgenic alopecia with aging. This is not intuitive, as testosterone and its peripheral metabolite, DHT, accelerate hair loss, and SHBG is thought to be protective. The ratio of T/SHBG, DHT/SHBG decreases by as much as 80% by age 80, in numeric parallel to hair loss, and approximates the pharmacology of antiandrogens such as finasteride.[69]

Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. About 30% of normal male testosterone level, the approximate level in females, is not enough to induce alopecia; 60%, closer to the amount found in elderly men, is sufficient.[70] The testicular secretion of testosterone perhaps "sets the stage" for androgenic alopecia as a multifactorial diathesis stress model, related to hormonal predisposition, environment, and age. Supplementing eunuchs with testosterone during their second decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within a month.[71]

An example of premature age effect is Werner's syndrome, a condition of accelerated aging from low-fidelity copying of mRNA. Affected children display premature androgenic alopecia.[72]

Permanent hair-loss is a result of reduction of the number of living hair matrixes. Long-term of insufficiency of nutrition is an important cause for the death of hair matrixes. Misrepair-accumulation aging theory [73][74] suggests that dermal fibrosis is associated with the progressive hair-loss and hair-whitening in old people.[75] With age, the dermal layer of the skin has progressive deposition of collagen fibers, and this is a result of accumulation of Misrepairs of derma. Fibrosis makes the derma stiff and makes the tissue have increased resistance to the walls of blood vessels. The tissue resistance to arteries will lead to the reduction of blood supply to the local tissue including the papillas. Dermal fibrosis is progressive; thus the insufficiency of nutrition to papillas is permanent. Senile hair-loss and hair-whitening are partially a consequence of the fibrosis of the skin.

The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia.[76] Trichoscopy can be used for further evaluation.[77] Biopsy may be needed to exclude other causes of hair loss,[78] and histology would demonstrate perifollicular fibrosis.[79][80] The HamiltonNorwood scale has been developed to grade androgenic alopecia in males by severity.

Finasteride is a medication of the 5-reductase inhibitors (5-ARIs) class.[81] By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp.[81][82] Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use.[82] Treatment with finasteride more effectively treats male-pattern hair loss at the crown than male-pattern hair loss at the front of the head and temples.[82]

Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase.[82] Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States.[82] However, it is commonly used off-label to treat male-pattern hair loss.[82]

Minoxidil dilates small blood vessels; it is not clear how this causes hair to grow.[83] Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling (Collagen induction therapy), spironolactone,[84] alfatradiol, topilutamide (fluridil),[81] topical melatonin,[85][86][87] and intradermal and intramuscular botulinum toxin injections to the scalp.[88]

There is evidence supporting the use of minoxidil as a safe and effective treatment for female pattern hair loss, and there is no significant difference in efficiency between 2% and 5% formulations.[89] Finasteride was shown to be no more effective than placebo based on low-quality studies.[89] The effectiveness of laser-based therapies is unclear.[89] Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss.[90][4][91]

More advanced cases may be resistant or unresponsive to medical therapy and require hair transplantation. Naturally occurring units of one to four hairs, called follicular units, are excised and moved to areas of hair restoration.[84] These follicular units are surgically implanted in the scalp in close proximity and in large numbers. The grafts are obtained from either follicular unit transplantation (FUT) or follicular unit extraction (FUE). In the former, a strip of skin with follicular units is extracted and dissected into individual follicular unit grafts, and in the latter individual hairs are extracted manually or robotically. The surgeon then implants the grafts into small incisions, called recipient sites.[92][93] Cosmetic scalp tattoos can also mimic the appearance of a short, buzzed haircut.

Many people use unproven treatments.[94] Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements.[95] As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss.[96] The same applies to special lights.[95] Dietary supplements are not typically recommended.[96] A 2015 review found a growing number of papers in which plant extracts were studied but only one randomized controlled clinical trial, namely a study in 10 people of saw palmetto extract.[97][98]

Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[99] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[100]

Although baldness is not as common in women as in men, the psychological effects of hair loss tend to be much greater. Typically, the frontal hairline is preserved, but the density of hair is decreased on all areas of the scalp. Previously, it was believed to be caused by testosterone just as in male baldness, but most women who lose hair have normal testosterone levels.[101]

Female androgenic alopecia has become a growing problem that, according to the American Academy of Dermatology, affects around 30million women in the United States. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, it is now occurring at earlier ages with reported cases in women as young as 15 or 16.[102]

For male androgenic alopecia, by the age of 50 30-50% of men have it, hereditarily there is an 80% predisposition.[103] Notably, the link between androgenetic alopecia and metabolic syndrome is strongest in non-obese men.[104]

Studies have been inconsistent across cultures regarding how balding men rate on the attraction scale. While a 2001 South Korean study showed that most people rated balding men as less attractive,[105] a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable.[106] One of the proposed social theories for male pattern hair loss is that men who embraced complete baldness by shaving their heads subsequently signaled dominance, high social status, and/or longevity.[18]

Biologists have hypothesized the larger sunlight-exposed area would allow more vitamin D to be synthesized, which might have been a "finely tuned mechanism to prevent prostate cancer" as the malignancy itself is also associated with higher levels of DHT.[107]

Many myths exist regarding the possible causes of baldness and its relationship with one's virility, intelligence, ethnicity, job, social class, wealth, and many other characteristics.

Because it increases testosterone levels, many Internet forums[which?] have put forward the idea that weight training and other forms of exercise increase hair loss in predisposed individuals. Although scientific studies do support a correlation between exercise and testosterone, no direct study has found a link between exercise and baldness. However, a few have found a relationship between a sedentary life and baldness, suggesting exercise is causally relevant. The type or quantity of exercise may influence hair loss.[108][109]Testosterone levels are not a good marker of baldness, and many studies actually show paradoxical low testosterone in balding persons, although research on the implications is limited.[citation needed]

Emotional stress has been shown to accelerate baldness in genetically susceptible individuals.[110]Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG.[111] Thus, stress due to sleep deprivation in fit males is unlikely to elevate DHT, which is one cause of male pattern baldness. Whether sleep deprivation can cause hair loss by some other mechanism is not clear.

Levels of free testosterone are strongly linked to libido and DHT levels, but unless free testosterone is virtually nonexistent, levels have not been shown to affect virility. Men with androgenic alopecia are more likely to have a higher baseline of free androgens. However, sexual activity is multifactoral, and androgenic profile is not the only determining factor in baldness. Additionally, because hair loss is progressive and free testosterone declines with age, a male's hairline may be more indicative of his past than his present disposition.[112][113]

Many misconceptions exist about what can help prevent hair loss, one of these being that lack of sexual activity will automatically prevent hair loss. While a proven direct correlation exists between increased frequency of ejaculation and increased levels of DHT, as shown in a recent study by Harvard Medical School, the study suggests that ejaculation frequency may be a sign, rather than a cause, of higher DHT levels.[114] Another study shows that although sexual arousal and masturbation-induced orgasm increase testosterone concentration around orgasm, they reduce testosterone concentration on average, and because about 5% of testosterone is converted to DHT, ejaculation does not elevate DHT levels.[115]

The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1,390 subjects) and found no correlation, although persons with only vertex androgenetic alopecia had fewer female sexual partners than those of other androgenetic alopecia categories (such as frontal or both frontal and vertex). One study may not be enough, especially in baldness, where there is a complex with age.[116]

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[117] chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[118][119]

Baldness is not a trait unique to human beings. One possible case study is about a maneless male lion in the Tsavo area. The Tsavo lion prides are unique in that they frequently have only a single male lion with usually seven or eight adult females, as opposed to four females in other lion prides. Male lions may have heightened levels of testosterone, which could explain their reputation for aggression and dominance, indicating that lack of mane may at one time have had an alpha correlation.[120]

Although primates do not go bald, their hairlines do undergo recession. In infancy the hairline starts at the top of the supraorbital ridge, but slowly recedes after puberty to create the appearance of a small forehead.[citation needed]

Diseases of the skin and appendages by morphology

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Pattern hair loss - Wikipedia

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Figure 4.. Terminal differentiation of T EFF cells is dependent upon Pofut1 and associated with

(A) Differentially expressed genes in sgPofut1- compared to sgNTC-transduced P14 cells at day 7.5 post-infection (p.i.). Upregulated (orange) or downregulated (blue) transcripts [false discovery rate (FDR) < 0.05] are highlighted. Selective MP- and TE-associated genes are labelled. (B) Enrichment plots of cell cycle-related signatures. NES, normalized enrichment score. (C) Flow cytometry (left) and quantification (right) of BrdU incorporation. (D) UMAP plot of published scRNA-seq dataset of P14 cells at day 8 p.i. (Chen et al., 2019). Each dot corresponds to an individual cell. The number and frequency of cells in each of the color-coded clusters (clusters 13) are indi cated. (E) Violin plots of Klrg1, Cxcr3 or Il7r expression in clusters 13 from (D). (F) Gating str ategy (left) and quantification (right) of the proportions of TE (KLRG1hiCXCR3loCD127lo), MP (KLRG1loCXCR3hiCD127hi) and TINT (CXCR3hiCD127lo) cells among WT P14 cells. (G) PCA plot of TE, MP and TINT cells [gating strategy in (F)] at day 7.5 p.i., with the percentage of variance shown. (H) Quantification of the relative frequency of BrdU+ cells in MP and TINT cells compared to TE cells. (I) Diagram of the in vivo differentiation assay (left), flow cytometry of KLRG1 versus CXCR3 expression (middle), and quantification of TINT, TE and CXCR3hiCD127hi cells (right). Only representative plots of KLRG1 versus CXCR3 are shown (TE population is largely defined by KLRG1hiCXCR3lo cells, which constitute ~ 95% of TE cells). (J) Quantification of TE, MP and TINT cells in the indicated P14 cells. (K) UMAP plot of Pofut1-dependent signature [downregulated genes as identified in (A)] in published scRNA-seq dataset from (D) (Chen et al., 2019). (L) UMAP plot of scRNA-seq data from sgNTC- (in black, left) and sgPofut1- (in red, right) transduced P14 cells (from dual-color transfer system) at day 7 p.i. Gray shadow indicates location of all cells; the number of analyzed cells in each group is indicated. (M) UMAP plot of the expression of Klrg1 (left), Cxcr3 (middle) and Il7r (right) in scRNA-seq data described in (L). (N) Flow cytometry of KLRG1 versus CXCR3 expression (left) and quantification (right) of TE cells in the in vivo differentiation assay similar as (I), except for the use of both wild-type and Pofut1-null TINT groups as the pretransfer cells. Data are from one (A, B, D, E, G, and KM), representative of two (C, H, and N), or compiled from at least two (I, J, and N) independent experiments, with 4 (A, C, G, H, and I), 17 (F), 11 (J), or 3 (L and N) biological replicates per group. *P < 0.05, **P < 0.01, and ***P < 0.001; NS, not significant; two-tailed paired Students t-test (C), two-tailed unpaired Students t-test (I, J, and N), or one-way analysis of variance (ANOVA) (F and H). Data are presented as mean s.e.m. See also Figures S4S6 and Tables S3S6.

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In vivo CRISPR screening reveals nutrient signaling processes ... - PubMed

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A risk factor is anything that affects your chance of getting a disease, such as breast cancer.

But having a risk factor, or even many, does not mean that you are sure to get the disease. Some men with one or more breast cancer risk factors never develop the disease, while most men with breast cancer have no apparent risk factors.

We don't yet completely understand the causes of breast cancer in men, but researchers have found several factors that may increase the risk of getting it. As with female breast cancer, many of these factors are related to your body's sex hormone levels.

Aging is an important risk factor for the development of breast cancer in men. The risk of breast cancer goes up as a man ages. On average, men with breast cancer are about 72 years old when they are diagnosed.

Breast cancer risk is increased if other members of the family (blood relatives) have had breast cancer. About 1 out of 5 men with breast cancer have a close relative, male or female, with the disease.

Men with a mutation (defect) in the BRCA2 gene have an increased risk of breast cancer, with a lifetime risk of about 6 in 100. BRCA1 mutations can also cause breast cancer in men, but the risk is lower, about 1 in 100.

Although mutations in these genes most often are found in members of families with many cases of breast and/or ovarian cancer, they have also been found in men with breast cancer who did not have a strong family history.

Mutations in CHEK2, PTEN and PALB2 genesmight also be responsible for some breast cancers in men.

Klinefelter syndrome is a congenital (present at birth) condition that affects about 1 in 1,000 men. Normally the cells in men's bodies have a single X chromosome along with a Y chromosome, while women's cells have two X chromosomes. Men with Klinefelter syndrome have cells with a Y chromosome plus at least two X chromosomes (but sometimes more).

Men with Klinefelter syndrome also have small testicles and are often infertile because they are unable to produce functioning sperm cells. Compared with other men, they have lower levels of androgens (male hormones) and more estrogens (female hormones). For this reason, they often develop gynecomastia (benign male breast growth).

Men with Klinefelter syndrome are more likely to get breast cancer than other men. Having this condition can increase the risk anywhere between 20 - 60 times the risk of a man in the general population.

A man whose chest area has been treated with radiation (such as for the treatment of a cancer in the chest, like lymphoma) has an increased risk of developing breast cancer.

Heavy drinking (of alcoholic beverages) increases the risk of breast cancer in men. This may be because of its effects on the liver (see next paragraph).

The liver plays an important role in balancing the levels of sex hormones. In cases of severe liver disease, such as cirrhosis, the liver is not working well and the hormone levels are uneven, causinglower levels of androgens and higher levels of estrogen. Men with liver disease can also have a higher chance of developing benign male breast growth (gynecomastia) and also have an higher risk of developing breast cancer.

Estrogen-related drugs were once used in hormonal therapy for men with prostate cancer. This treatment may slightly increase breast cancer risk.

There is concern that transgender/transsexual individuals who take high doses of estrogens as part of sex reassignment could also have a higher breast cancer risk. Still, there havent been any studies of breast cancer risk in transgendered individuals, so it isnt clear what their breast cancer risk is.

Studies have shown that women's breast cancer risk is increased by obesity (being extremely overweight) after menopause. Obesity is also a risk factor for male breast cancer as well. The reason is that fat cells in the body convert male hormones (androgens) into female hormones (estrogens). This means that obese men have higher levels of estrogens in their body.

Certain conditions, such as having an undescended testicle, having mumps as an adult, or having one or both testicles surgically removed (orchiectomy) may increase male breast cancer risk.

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Risk Factors for Breast Cancer in Men - American Cancer Society

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A

Adenine

Allele

Amino Acid

Aneuploidy

Animal Model

Anticodon

Antisense

Autism

Autosomal Dominant Disorder

Autosomal Recessive Disorder

Autosome

Base Pair

Bioinformatics

Birth Defect

BRCA1/BRCA2

Cancer

Cancer-Susceptibility Gene

Candidate Gene

Carcinogen

Carrier

Carrier Screening

Copy DNA (cDNA)

Cell-Free DNA Testing

Centimorgan (cM)

Central Dogma

Centromere

Chromatid

Chromatin

Chromosome

Cloning

Codominance

Codon

Complex Disease

Congenital

Contig

Copy Number Variation (CNV)

CRISPR

Crossing Over

Cystic Fibrosis (CF)

Cytogenetics

Cytosine

Data Science

Deletion

Deoxyribonucleic Acid (DNA)

Diploid

DNA Fingerprinting

DNA Replication

DNA Sequencing

Dominant Traits and Alleles

Double Helix

Down Syndrome (Trisomy 21)

Duplication

Electrophoresis

Environmental Factors

Epigenetics

Epistasis

Eugenics

Evolution

Exome

Exon

Family History

Fibroblast

First-Degree Relative

Fluorescence In Situ Hybridization (FISH)

Founder Effect

Fragile X Syndrome

Frameshift Mutation

Fraternal Twins

Gamete

Gender

Gene

Gene Amplification

Gene Expression

Gene Mapping

Gene Pool

Gene Regulation

Gene Therapy

GeneEnvironment Interaction

Genetic Ancestry

Genetic Code

Genetic Counseling

Genetic Discrimination

Genetic Drift

Genetic Engineering

Genetic Epidemiology

Genetic Imprinting

Genetic Information Nondiscrimination Act (GINA)

Genetic Map

Genetic Testing

Genetics

Genome

Genome-Wide Association Study (GWAS)

Genomic Medicine

Genomic Variation

Genomics

Genotype

Germ Line

Gigabase (Gb)

GMO (Genetically Modified Organism)

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Talking Glossary of Genetic Terms | NHGRI - Genome

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We have the killers DNA, we just need a name: Genetic game changer offers hope for near-unsolvable Ontario cold cases  Toronto Star

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We have the killers DNA, we just need a name: Genetic game changer offers hope for near-unsolvable Ontario cold cases - Toronto Star

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US leukemia patient becomes 1st woman & 3rd person in the world to be cured of HIV  Republic World

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US leukemia patient becomes 1st woman & 3rd person in the world to be cured of HIV - Republic World

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Woman, 41, With Bubbles In Her Urine Dismissed By Doctors. Turns Out To Have The Blood Cancer Multiple Myeloma.  SurvivorNet

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Woman, 41, With Bubbles In Her Urine Dismissed By Doctors. Turns Out To Have The Blood Cancer Multiple Myeloma. - SurvivorNet

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Given that death is one of the things people fear more than anything, its not surprising that weve been thinking for awhile about how we can thwart it.

Cryonics, which is the attempt to freeze the bodies of the recently deceased in the hope that they can be revived and cured later on, has a long and honestly pretty grim history.

An article published in 1992 detailed some of the more gruesome mistakes, probably in the hopes that future scientists would be able to learn from previous miscalculations.

One of the biggest issues is the freezing process itselfthe ice crystals that for in your cells will eventually destroy them beyond repair.

Basically, you remain a popsicle forever, because no one can revive you if you have no working cells.

Cryonics company Alcor defrosted three corpses in 1984 with the intention of checking what damage had been sustained. First, the bodies were converted to neuropreservation, which means their heads were preserved (ew), and then scientists dug in.

From the outside, the damage didnt look all that bad, resembling the type of cracking observed in deteriorating coatings, such as is seen in paint peeling away from a wall. The skin adjoining the fracture fissure was somewhat raised from the underlying fat and gave the appearance of having peeled away slightly.

Again, ew.

Deeper fractures were discovered, however, as the bodies thawed, and there was also plenty of organ damage to go around.

Examination of the internal organs of patient three revealed fractures present in almost every organ. The spinal cord, aorta, thoracic inferior vena cava, pulmonary artery, myocardium, right lung, liver, pericardium, stomach, ileum, colon, mesentery, spleen, skeletal muscle, and pancreas, were all seriously fractured.

Also? The spinal cord had been snapped in three places.

The team believed that all of the damage could be put down to the thawing process.

As cooling proceeds below the glass transition phase of water (TG), different organs and tissues within the patients body will begin to contract at different rates. However, because the system is now in a solid state, these materials, bonded to each other by ice/cryoprotective agent mixtures, will be unable to contract independently.

And this is what happens when everything goesright during the freezing process.

What happens if, for some reasons, bodies are not kept at the optimal temperature in their chambers?

Unsurprisingly, nothing pretty.

We know that because at least one company, started by Robert Nelson, saw too many storage, venue, and payment issues that resulted in him just eventually allowing the bodies in his care to thaw.

The stench near the crypt is disarming, strips away all defenses, spins the stomach into a thousand dizzying somersaults.

Nelson defended himself, though he likely realized they had not realized the best possible outcome.

I havent done anything criminal, anything wrong other than a lot of bad decisions. It didnt work. It failed. There was no money. Who can guarantee that youre going to be suspended for 10 or 15 years.

When malfunctions happen, families usually opt to bury their loved ones traditionally, though the reality of being the mortician in these cases is less than pleasant.

One detailed that they used a breathing apparatus when the capsule on its side had to be entered to remove the remains which had fallen to the bottom and frozen in place in a plug of body fluids.

Ew. Right?

Now that cryonics has garnered more financial backing and interest from those who are invested in its future, proponents are sure all of those hurdles will be overcome.

Only time will tell.

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The Gross And Horrifying Early Days Of Cryonics TwistedSifter

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Slowing or stopping of life without death

Suspended animation is the temporary (short- or long-term) slowing or stopping of biological function so that physiological capabilities are preserved. It may be either hypometabolic or ametabolic in nature. It may be induced by either endogenous, natural or artificial biological, chemical or physical means. In its natural form it may be spontaneously reversible as in the case of species demonstrating hypometabolic states of hibernation or require technologically mediated revival when applied with therapeutic intent in the medical setting as in the case of deep hypothermic circulatory arrest (DHCA).[1][2]

Suspended animation is understood as the pausing of life processes by exogenous or endogenous means without terminating life itself.[3] Breathing, heartbeat and other involuntary functions may still occur, but they can only be detected by artificial means.[4] For this reason, this procedure has been associated with a lethargic state in nature when animals or plants appear, over a period, to be dead but then can wake up or prevail without suffering any harm. This has been termed in different contexts hibernation, dormancy or anabiosis (this last in some aquatic invertebrates and plants in scarcity conditions).

In July 2020, marine biologists reported that aerobic microorganisms (mainly), in "quasi-suspended animation", were found in organically-poor sediments, up to 101.5 million years old, 68.9 metres (226 feet) below the seafloor in the South Pacific Gyre (SPG) ("the deadest spot in the ocean"), and could be the longest-living life forms ever found.[5][6]

This condition of apparent death or interruption of vital signs may be similar to a medical interpretation of suspended animation. It is only possible to recover signs of life if the brain and other vital organs suffer no cell deterioration, necrosis or molecular death principally caused by oxygen deprivation or excess temperature (especially high temperature).[7]

Some examples of people that have returned from this apparent interruption of life lasting over half an hour, two hours, eight hours or more while adhering to these specific conditions for oxygen and temperature have been reported and analysed in depth, but these cases are not considered scientifically valid. The brain begins to die after five minutes without oxygen; nervous tissues die intermediately when a "somatic death" occurs while muscles die over one to two hours following this last condition.[8]

It has been possible to obtain a successful resuscitation and recover life in some instances, including after anaesthesia, heat stroke, electrocution, narcotic poisoning, heart attack or cardiac arrest, shock, newborn infants, cerebral concussion, or cholera.

Supposedly, in suspended animation, a person technically would not die, as long as he or she were able to preserve the minimum conditions in an environment extremely close to death and return to a normal living state. An example of such a case is Anna Bgenholm, a Swedish radiologist who allegedly survived 80 minutes under ice in a frozen lake in a state of cardiac arrest with no brain damage in 1999.[9] [10]

Other cases of hypothermia where people survived without damage are:

It has been suggested that bone lesions provide evidence of hibernation among the early human population whose remains have been retrieved at the Archaeological site of Atapuerca. In a paper published in the journal LAnthropologie, researchers Juan-Luis Arsuaga and Antonis Bartsiokas point out that primitive mammals and primates like bush babies and lorises hibernate, which suggests that the genetic basis and physiology for such a hypometabolism could be preserved in many mammalian species, including humans.[15]

Since the 1970s, induced hypothermia has been performed for some open-heart surgeries as an alternative to heart-lung machines. Hypothermia, however, provides only a limited amount of time in which to operate and there is a risk of tissue and brain damage for prolonged periods.

There are many research projects currently investigating how to achieve "induced hibernation" in humans.[16][17] This ability to hibernate humans would be useful for a number of reasons, such as saving the lives of seriously ill or injured people by temporarily putting them in a state of hibernation until treatment can be given.

The primary focus of research for human hibernation is to reach a state of torpor, defined as a gradual physiological inhibition to reduce oxygen demand and obtain energy conservation by hypometabolic behaviors altering biochemical processes. In previous studies, it was demonstrated that physiological and biochemical events could inhibit endogenous thermoregulation before the onset of hypothermia in a challenging process known as "estivation". This is indispensable to survive harsh environmental conditions, as seen in some amphibians and reptiles.[18]

Lowering the temperature of a substance reduces chemical activity by the Arrhenius equation. This includes life processes such as metabolism. If cryonics are ever perfected, it would then be a form of long-term suspended animation.[19]

Emergency Preservation and Resuscitation (EPR) is a way to slow the bodily processes that would lead to death in cases of severe injury.[20] This involves lowering the body's temperature below 34C (93F), which is the current standard for therapeutic hypothermia.[20]

In June 2005, scientists at the University of Pittsburgh's Safar Center for Resuscitation Research announced they had managed to place dogs in suspended animation and bring them back to life, most of them without brain damage, by draining the blood out of the dogs' bodies and injecting a low temperature solution into their circulatory systems, which in turn keeps the bodies alive in stasis. After three hours of being clinically dead, the dogs' blood was returned to their circulatory systems, and the animals were revived by delivering an electric shock to their hearts. The heart started pumping the blood around the body, and the dogs were brought back to life.[21]

On 20 January 2006, doctors from the Massachusetts General Hospital in Boston announced they had placed pigs in suspended animation with a similar technique. The pigs were anaesthetized and major blood loss was induced, along with simulated - via scalpel - severe injuries (e.g. a punctured aorta as might happen in a car accident or shooting). After the pigs lost about half their blood the remaining blood was replaced with a chilled saline solution. As the body temperature reached 10C (50F) the damaged blood vessels were repaired and the blood was returned.[22] The method was tested 200 times with a 90% success rate.[23]

The laboratory of Mark Roth at the Fred Hutchinson Cancer Research Center and institutes such as Suspended Animation, Inc are trying to implement suspended animation as a medical procedure which involves the therapeutic induction to a complete and temporary systemic ischemia, directed to obtain a state of tolerance for the protection-preservation of the entire organism, this during a circulatory collapse "only by a limited period of one hour". The purpose is to avoid a serious injury, risk of brain damage or death, until the patient reaches specialized attention.[24]

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Suspended animation - Wikipedia

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Women are using menstrual blood for skincare here's why I think beauty has gone too far this time  VOGUE India

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Women are using menstrual blood for skincare here's why I think beauty has gone too far this time - VOGUE India

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Mesenchymal Stem Cells: Stem cells are the basic building blocks of tissues and organs in the body. It is important to note that there is no single stem cell that gives rise to them, but in fact, a variety of them coming from different locations in the body and formed at different time periods.

One of the most common type of stem cells is the mesenchymal stem cells (aka MSCs). But what exactly is it? Lets take a closer look.

By definition, mesenchymal stem cells are multipotent cells that can differentiate and mature into different types of cells. Mesenchymal cells are characterized by having long and thin bodies and a very prominent nucleus.

In terms of size, they are relatively smaller than fibrocytes and are quite difficult to observe in histological sections. And overall morphologically speaking, they appear to have no difference from fibroblasts.

A group of mesenchymal stem cells is called a mesenchyme and together, they form the undifferentiated filling of the embryo. Mesenchymal stem cells (or tissue) have a wide distribution in the body.

Like most stem cells, mesenchymal stem cells are capable of self-renewal and differentiation.

Despite its size, the mesenchymal stem cell plays a lot of significant roles within an organism. The following are just some of them.Functions of Mesenchymal Stem Cells (Image Source: frontiersin.org)

1.Suppression of immune cells activation

Aside from being the progenitor of most cells in the body, mesenchymal cells also control the activities of immune cells (i.e. T-lymphocytes, B-lymphocytes, macrophages, mast cells, and neutrophils) during an organ transplant. This is important because it prevents further inflammation and eventual rejection of the transplanted organ.

2. Increase the number of nerve cells

3. Reduction of Cell Death

4. Secretion of neurotrophic and angiogenic factors

Mesenchymal stem cells secrete both neurotrophic and angiogenic factors which are responsible for stabilizing the extracellular matrix (ECM).

5. Increase synaptic connections

When transplanted into the brain, mesenchymal stem cells promote the reduction of free radical levels and enhance the synaptic connections of damaged neurons. In addition to that, they also increase the number of astrocytes (star-shaped cells associated with the formation of functional synapses). As a result, impulses (messages) are being passed on at a faster speed, hence, reactions are also immediate.

6. Increase the myelination of axons

Myelin sheath is the insulating layer that covers the axons of nerve cells. By further enhancing the myelination of axons, mesenchymal cells (similar with above) further increase the speed at which impulses are passed along.

7. Increase the number of blood vessels and astrocytes in the brain

According to a recent study published in the World Journal of Stem Cells, mesenchymal cells are also able to replace and repair any damaged blood vessel in the cerebrum part of the brain. Hence, mesenchymal cells are being viewed as potential therapeutic remedy for stroke patients.

Mesenchymal cells undergo mesengenic process in order to transform into different cell types such as osteocytes (bone cells), chondrocytes (cartilage cells), muscle cells, and others.The Differentiation of Mesenchymal Stem Cells into different types of cells (Image Source: frontiersin.org)

Present-day studies are now paving the way for the further applications of mesenchymal stem cells into numerous clinical measures and techniques. In addition to the natural functions of mesenchymal cells mentioned above, several commercialized products from these cells have already been approved.

Despite their promising effect on overall organism health, the knowledge about mesenchymal stem cells is still incomplete. Hence, further research is still needed to ensure the safety of patients and improve quality control.

Key References

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Mesenchymal Stem Cells | Properties, Process, Functions, & Therapies

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Expulsion of a fetus from the pregnant mother's uterus

Medical condition

Childbirth, also known as labour and delivery, is the ending of pregnancy where one or more babies exits the internal environment of the mother via vaginal delivery or caesarean section.[7] In 2019, there were about 140.11 million births globally.[9] In the developed countries, most deliveries occur in hospitals,[10][11] while in the developing countries most are home births.[12]

The most common childbirth method worldwide is vaginal delivery.[6] It involves four stages of labour: the shortening and opening of the cervix during the first stage, descent and birth of the baby during the second, the delivery of the placenta during the third, and the recovery of the mother and infant during the fourth stage, which is referred to as the postpartum. The first stage is characterized by abdominal cramping or back pain that typically lasts half a minute and occurs every 10 to 30 minutes.[13] Contractions gradually becomes stronger and closer together.[14] Since the pain of childbirth correlates with contractions, the pain becomes more frequent and strong as the labour progresses. The second stage ends when the infant is fully expelled. The third stage is the delivery of the placenta.[15] The fourth stage of labour involves the recovery of the mother, delayed clamping of the umbilical cord, and monitoring of the neonate.[16] As of 2014,[update] all major health organizations advise that immediately following a live birth, regardless of the delivery method, that the infant be placed on the mother's chest (termed skin-to-skin contact), and to delay neonate procedures for at least one to two hours or until the baby has had its first breastfeeding.[17][18][19]

A vaginal delivery is recommended over a cesarean section due to increased risk for complications of a cesarean section and natural benefits of a vaginal delivery in both mother and baby. Various methods may help with pain, such as relaxation techniques, opioids, and spinal blocks.[14] It is best practice to limit the amount of interventions that occur during labour and delivery such as an elective cesarean section, however in some cases a scheduled cesarean section must be planned for a successful delivery and recovery of the mother. An emergency cesarean section may be recommended if unexpected complications occur or little to no progression through the birthing canal is observed in a vaginal delivery.

Each year, complications from pregnancy and childbirth result in about 500,000 birthing deaths, seven million women have serious long-term problems, and 50 million women giving birth have negative health outcomes following delivery, most of which occur in the developing world.[5] Complications in the mother include obstructed labour, postpartum bleeding, eclampsia, and postpartum infection.[5] Complications in the baby include lack of oxygen at birth, birth trauma, and prematurity.[4][20]

The most prominent sign of labour is strong repetitive uterine contractions. Pain in contractions has been described as feeling similar to very strong menstrual cramps. Women giving birth are often encouraged to refrain from screaming.[citation needed] However, moaning and grunting may be encouraged to help lessen pain. Crowning may be experienced as an intense stretching and burning.

Back labour is a term for specific pain occurring in the lower back, just above the tailbone, during childbirth.[21]

Another prominent sign of labour is the rupture of membranes, commonly known as "water breaking". This is the leaking of fluid from the amniotic sac that surrounds a fetus in the uterus and helps provide cushion and thermoregulation. However, it is common for water to break long before contractions begin and in which case it is not a sign of immediate labour and hospitalization is generally required for monitoring the fetus and prevention of preterm birth.

During the later stages of gestation there is an increase in abundance of oxytocin, a hormone that is known to evoke feelings of contentment, reductions in anxiety, and feelings of calmness and security around the mate.[22] Oxytocin is further released during labour when the fetus stimulates the cervix and vagina, and it is believed that it plays a major role in the bonding of a mother to her infant and in the establishment of maternal behavior. The act of nursing a child also causes a release of oxytocin to help the baby get milk more easily from the nipple.[23]

Station refers to the relationship of the fetal presenting part to the level of the ischial spines. When the presenting part is at the ischial spines the station is 0 (synonymous with engagement). If the presenting fetal part is above the spines, the distance is measured and described as minus stations, which range from 1 to 4cm. If the presenting part is below the ischial spines, the distance is stated as plus stations ( +1 to +4cm). At +3 and +4 the presenting part is at the perineum and can be seen.[24]

The fetal head may temporarily change shape (becoming more elongated or cone shaped) as it moves through the birth canal. This change in the shape of the fetal head is called molding and is much more prominent in women having their first vaginal delivery.[25]

Cervical ripening is the physical and chemical changes in the cervix to prepare it for the stretching that will take place as the fetus moves out of the uterus and into the birth canal. A scoring system called a Bishop score can be used to judge the degree of cervical ripening in order to predict the timing of labour and delivery of the infant or for women at risk for preterm labour. It is also used to judge when a woman will respond to induction of labour for a postdate pregnancy or other medical reasons. There are several methods of inducing cervical ripening which will allow the uterine contractions to effectively dilate the cervix.[26]

Vaginal delivery involves four stages of labour: the shortening and opening of the cervix during the first stage, descent and birth of the baby during the second, the delivery of the placenta during the third, and the 4th stage of recovery which lasts until two hours after the delivery. The first stage is characterized by abdominal cramping or back pain that typically lasts around half a minute and occurs every 10 to 30 minutes.[13] The contractions (and pain) gradually becomes stronger and closer together.[14] The second stage ends when the infant is fully expelled. In the third stage, the delivery of the placenta.[15] The fourth stage of labour involves recovery, the uterus beginning to contract to pre-pregnancy state, delayed clamping of the umbilical cord, and monitoring of the neonatal tone and vitals.[16] As of 2014,[update] all major health organizations advise that immediately following a live birth, regardless of the delivery method, that the infant be placed on the mother's chest, termed skin-to-skin contact, and delaying routine procedures for at least one to two hours or until the baby has had its first breastfeeding.[17][18][19]

Definitions of the onset of labour include:

Many women are known to experience what has been termed the "nesting instinct". Women report a spurt of energy shortly before going into labour.[30] Common signs that labour is about to begin may include what is known as lightening, which is the process of the baby moving down from the rib cage with the head of the baby engaging deep in the pelvis. The pregnant woman may then find breathing easier, since her lungs have more room for expansion, but pressure on her bladder may cause more frequent need to void (urinate). Lightening may occur a few weeks or a few hours before labour begins, or even not until labour has begun.[30] Some women also experience an increase in vaginal discharge several days before labour begins when the "mucus plug", a thick plug of mucus that blocks the opening to the uterus, is pushed out into the vagina. The mucus plug may become dislodged days before labour begins or not until the start of labour.[30]

While inside the uterus the baby is enclosed in a fluid-filled membrane called the amniotic sac. Shortly before, at the beginning of, or during labour the sac ruptures. Once the sac ruptures, termed "the water breaks", the baby is at risk for infection and the mother's medical team will assess the need to induce labour if it has not started within the time they believe to be safe for the infant.[30]

The first stage of labour is divided into latent and active phases, where the latent phase is sometimes included in the definition of labour,[31] and sometimes not.[32]

The latent phase is generally defined as beginning at the point at which the woman perceives regular uterine contractions.[33] In contrast, Braxton Hicks contractions, which are contractions that may start around 26 weeks gestation and are sometimes called "false labour", are infrequent, irregular, and involve only mild cramping.[34]

Cervical effacement, which is the thinning and stretching of the cervix, and cervical dilation occur during the closing weeks of pregnancy. Effacement is usually complete or near-complete and dilation is about 5cm by the end of the latent phase.[35] The degree of cervical effacement and dilation may be felt during a vaginal examination.

The active phase of labour has geographically differing definitions. The World Health Organization describes the active first stage as "a period of time characterized by regular painful uterine contractions, a substantial degree of cervical effacement and more rapid cervical dilatation from 5 cm until full dilatation for first and subsequent labours.[36] In the US, the definition of active labour was changed from 3 to 4cm, to 5cm of cervical dilation for multiparous women, mothers who had given birth previously, and at 6cm for nulliparous women, those who had not given birth before.[37] This was done in an effort to increase the rates of vaginal delivery.[38]

Health care providers may assess the mother's progress in labour by performing a cervical exam to evaluate the cervical dilation, effacement, and station. These factors form the Bishop score. The Bishop score can also be used as a means to predict the success of an induction of labour.

During effacement, the cervix becomes incorporated into the lower segment of the uterus. During a contraction, uterine muscles contract causing shortening of the upper segment and drawing upwards of the lower segment, in a gradual expulsive motion.[39] The presenting fetal part then is permitted to descend. Full dilation is reached when the cervix has widened enough to allow passage of the baby's head, around 10cm dilation for a term baby.

A standard duration of the latent first stage has not been established and can vary widely from one woman to another. However, the duration of active first stage (from 5 cm until full cervical dilatation) usually does not extend beyond 12 hours in the first labour("primiparae"), and usually does not extend beyond 10 hours in subsequent labours ("multiparae").[40]

Dystocia of labour, also called "dysfunctional labour" or "failure to progress", is difficult labour or abnormally slow progress of labour, involving progressive cervical dilatation or lack of descent of the fetus. Friedman's Curve, developed in 1955, was for many years used to determine labour dystocia. However, more recent medical research suggests that the Friedman curve may not be currently[when?] applicable.[41][42]

The expulsion stage begins when the cervix is fully dilated, and ends when the baby is born. As pressure on the cervix increases, a sensation of pelvic pressure is experienced, and, with it, an urge to begin pushing. At the beginning of the normal second stage, the head is fully engaged in the pelvis; the widest diameter of the head has passed below the level of the pelvic inlet. The fetal head then continues descent into the pelvis, below the pubic arch and out through the vaginal opening. This is assisted by the additional maternal efforts of pushing, or bearing down, similar to defecation. The appearance of the fetal head at the vaginal opening is termed crowning. At this point, the mother will feel an intense burning or stinging sensation.

When the amniotic sac has not ruptured during labour or pushing, the infant can be born with the membranes intact. This is referred to as "delivery en caul".

Complete expulsion of the baby signals the successful completion of the second stage of labour. Some babies, especially preterm infants, are born covered with a waxy or cheese-like white substance called vernix. It is thought to have some protective roles during fetal development and for a few hours after birth.

The second stage varies from one woman to another. In first labours, birth is usually completed within three hours whereas in subsequentlabours, birth is usually completed within two hours.[43] Second-stage labours longer than three hours are associated with declining rates of spontaneous vaginal delivery and increasing rates of infection, perineal tears, and obstetric haemorrhage, as well as the need for intensive care of the neonate.[44]

The period from just after the fetus is expelled until just after the placenta is expelled is called the third stage of labour or the involution stage. Placental expulsion begins as a physiological separation from the wall of the uterus. The average time from delivery of the baby until complete expulsion of the placenta is estimated to be 1012 minutes dependent on whether active or expectant management is employed.[45] In as many as 3% of all vaginal deliveries, the duration of the third stage is longer than 30 minutes and raises concern for retained placenta.[46]

Placental expulsion can be managed actively or it can be managed expectantly, allowing the placenta to be expelled without medical assistance. Active management is the administration of a uterotonic drug within one minute of fetal delivery, controlled traction of the umbilical cord and fundal massage after delivery of the placenta, followed by performance of uterine massage every 15 minutes for two hours.[47] In a joint statement, World Health Organization, the International Federation of Gynaecology and Obstetrics and the International Confederation of Midwives recommend active management of the third stage of labour in all vaginal deliveries to help to prevent postpartum haemorrhage.[48][49][50]

Delaying the clamping of the umbilical cord for at least one minute or until it ceases to pulsate, which may take several minutes, improves outcomes as long as there is the ability to treat jaundice if it occurs. For many years it was believed that late cord cutting led to a mother's risk of experiencing significant bleeding after giving birth, called postpartum bleeding. However a recent review found that delayed cord cutting in healthy full-term infants resulted in early haemoglobin concentration and higher birthweight and increased iron reserves up to six months after birth with no change in the rate of postpartum bleeding.[51][52]

The fourth stage of labour is the period beginning immediately after childbirth, and extends for about six weeks. The terms postpartum and postnatal are often used for this period.[53] The woman's body, including hormone levels and uterus size, return to a non-pregnant state and the newborn adjusts to life outside the mother's body. The World Health Organization (WHO) describes the postnatal period as the most critical and yet the most neglected phase in the lives of mothers and babies; most deaths occur during the postnatal period.[54]

Following the birth, if the mother had an episiotomy or a tearing of the perineum, it is stitched. This is also an optimal time for uptake of long-acting reversible contraception (LARC), such as the contraceptive implant or intrauterine device (IUD), both of which can be inserted immediately after delivery while the woman is still in the delivery room.[55][56] The mother has regular assessments for uterine contraction and fundal height,[57] vaginal bleeding, heart rate and blood pressure, and temperature, for the first 24 hours after birth. Some women may experience an uncontrolled episode of shivering or postpartum chills following the birth. The first passing of urine should be documented within six hours.[54] Afterpains (pains similar to menstrual cramps), contractions of the uterus to prevent excessive blood flow, continue for several days. Vaginal discharge, termed "lochia", can be expected to continue for several weeks; initially bright red, it gradually becomes pink, changing to brown, and finally to yellow or white.[58]

At one time babies born in hospitals were removed from their mothers shortly after birth and brought to the mother only at feeding times.[59] Mothers were told that their newborn would be safer in the nursery and that the separation would offer the mother more time to rest. As attitudes began to change, some hospitals offered a "rooming in" option wherein after a period of routine hospital procedures and observation, the infant could be allowed to share the mother's room. As of 2020, rooming in has increasingly become standard practice in maternity wards.[60]

Humans are bipedal with an erect stance. The erect posture causes the weight of the abdominal contents to thrust on the pelvic floor, a complex structure which must not only support this weight but allow, in women, three channels to pass through it: the urethra, the vagina and the rectum. The infant's head and shoulders must go through a specific sequence of maneuvers in order to pass through the ring of the mother's pelvis. Range of motion and ambulation are typically unaffected during labour and it is encouraged that the mother move to help facilitate progression of labour. The vagina is called a 'birth canal' when the baby enters this passage. Six phases of a typical vertex or cephalic (head-first presentation) delivery:

Failure to complete the cardinal movements of birth in the correct order may result in complications of labour and birth injuries.

Skin-to-skin contact (SSC), sometimes also called kangaroo care, is a technique of newborn care where babies are kept chest-to-chest and skin-to-skin with a parent, typically their mother, though more recently (2022) their father as well. This means without the shirt or undergarments on the chest of both the baby and parent. A 2011 medical review found that early skin-to-skin contact resulted in a decrease in infant crying, improved cardio-respiratory stability and blood glucose levels, and improved breastfeeding duration.[61][62] A 2016 Cochrane review also found that SSC at birth promotes the likelihood and effectiveness of breastfeeding.[63]

As of 2014, early postpartum SSC is endorsed by all major organizations that are responsible for the well-being of infants, including the American Academy of Pediatrics.[17] The World Health Organization (WHO) states that "the process ofchildbirth is not finished until the baby has safely transferred from placental to mammary nutrition." It is advised that the newborn be placed skin-to-skin with the mother following vaginal birth, or as soon as the mother is alert and responsive after a Caesarean section, postponing any routine procedures for at least one to two hours. The baby's father or other support person may also choose to hold the baby SSC until the mother recovers from the anesthetic.[64]

The WHO suggests that any initial observations of the infant can be done while the infant remains close to the mother, saying that even a brief separation before the baby has had its first feed can disturb the bonding process. They further advise frequent skin-to-skin contact as much as possible during the first days after delivery, especially if it was interrupted for some reason after the delivery.[18][19]

La Leche League advises women to have a delivery team which includes a support person who will advocate to assure that:

It has long been known that a mother's level of the hormone oxytocin elevates in a mother when she interacts with her infant. In 2019, a large review of the effects of oxytocin found that the oxytocin level in fathers that engage in SSC is increased as well. Two studies found that "when the infant is clothed only in a diaper and placed in between the mother or father's breasts, chest-to-chest [elevated paternal oxytocin levels were] shown to reduce stress and anxiety in parents after interaction."[66]

For births that occur in hospitals the WHO recommends a hospital stay of at least 24 hours following an uncomplicated vaginal delivery and 96 hours for a Cesarean section. Looking at length of stay (in 2016) for an uncomplicated delivery around the world shows an average of less that 1 day in Egypt to 6 days in (pre-war) Ukraine. Averages for Australia are 2.8 days and 1.5 days in the UK.[67] While this number is low, two-thirds of women in the UK have midwife-assisted births and in some cases the mother may choose a hospital setting for birth to be closer to the wide range of assistance available for an emergency situation. However, women with midwife care may leave the hospital shortly after birth and her midwife will continue her care at her home.[68]In the U.S. the average length of stay has gradually dropped from 4.1 days in 1970 to a current stay of 2 days. The CDC attributed the drop to the rise in health care costs, saying people could not afford to stay in the hospital any longer. To keep it from dropping any lower, in 1996 congress passed the Newborns' and Mothers' Health Protection Act that requires insurers to cover at least 48 hours for uncomplicated delivery.[67]

In many cases and with increasing frequency, childbirth is achieved through labour induction or caesarean section. Labour induction is the process or treatment that stimulates childbirth and delivery. Inducing labour can be accomplished with pharmaceutical or non-pharmaceutical methods. Inductions are most often performed either with prostaglandin drug treatment alone, or with a combination of prostaglandin and intravenous oxytocin treatment.[69]Caesarean section is the removal of the neonate through a surgical incision in the abdomen, rather than through vaginal birth.[70] Childbirth by C-sections increased 50% in the US from 1996 to 2006. In 2012, about 23 million deliveries occurred by Caesarean section.[71][14] Induced births and elective cesarean before 39 weeks can be harmful to the neonate as well as harmful or without benefit to the mother. Therefore, many guidelines recommend against non-medically required induced births and elective cesarean before 39 weeks.[72] The 2012 rate of labour induction in the United States was 23.3 per cent, and had more than doubled from 1990 to 2010.[73][74]The American Congress of Obstetricians and Gynecologists (ACOG) guidelines recommend a full evaluation of the maternal-fetal status, the status of the cervix, and at least a 39 completed weeks (full term) of gestation for optimal health of the newborn when considering elective induction of labour. Per these guidelines, indications for induction may include:

Induction is also considered for logistical reasons, such as the distance from hospital or psychosocial conditions, but in these instances gestational age confirmation must be done, and the maturity of the fetal lung must be confirmed by testing. The ACOG also note that contraindications for induced labour are the same as for spontaneous vaginal delivery, including vasa previa, complete placenta praevia, umbilical cord prolapse or active genital herpes simplex infection.[75]

A Caesarean section, also called a C section, can be the safest option for delivery in some pregnancies. During a C section, the patient is usually numbed with an epidural or a spinal block, but general anesthesia can be used as well. A cut is made in the patients abdomen and then in the uterus to remove the baby. A C section may be the best option when the small size or shape of the mother's pelvis makes delivery of the baby impossible, or the lie or presentation of the baby as it prepares to enter the birth canal is dangerous. Other medical reasons for C section are placenta previa (the placenta blocks the babys path to the birth canal), uterine rupture, or fetal distress, like due to endangerment of the babys oxygen supply.[76] Before the 1970s, once a patient delivered one baby via C section, it was recommended that all of her future babies be delivered by C section, but that recommendation has changed. Unless there is some other indication, mothers can attempt a trial of labour and most are able to have a vaginal birth after C section (VBAC).[77]

Like any procedure, a C section is not without risks. Having a C section puts the mother at greater risk for uterine rupture and abnormal attachment of the placenta to the uterus in future pregnancies (placenta accreta spectrum).[78] The rate of deliveries occurring via C section instead of vaginal deliveries has been increasing since the 1970s. The WHO recommends a C section rate of between 10 to 15 percent because C sections rates higher than 10 percent are not associated with a decrease in morbidity and mortality.[79]

Obstetric care frequently subjects women to institutional routines, which may have adverse effects on the progress of labour. Supportive care during labour may involve emotional support, comfort measures, and information and advocacy which may promote the physical process of labour as well as women's feelings of control and competence, thus reducing the need for obstetric intervention. The continuous support may be provided either by hospital staff such as nurses or midwives, doulas, or by companions of the woman's choice from her social network.There is increasing evidence to show that the participation of the child's father in the birth leads to a better birth and also post-birth outcomes, providing the father does not exhibit excessive anxiety.[81]

Continuous labour support may help women to give birth spontaneously, that is, without caesarean or vacuum or forceps, with slightly shorter labours, and to have more positive feelings regarding their experience of giving birth. Continuous labour support may also reduce women's use of pain medication during labour and reduce the risk of babies having low five-minute Agpar scores.[82]

Eating or drinking during labour is an area of ongoing debate. While some have argued that eating in labour has no harmful effects on outcomes,[83] others continue to have concern regarding the increased possibility of an aspiration event (choking on recently eaten foods) in the event of an emergency delivery due to the increased relaxation of the oesophagus in pregnancy, upward pressure of the uterus on the stomach, and the possibility of general anaesthetic in the event of an emergency cesarean.[84] A 2013 Cochrane review found that with good obstetrical anaesthesia there is no change in harms from allowing eating and drinking during labour in those who are unlikely to need surgery. They additionally acknowledge that not eating does not mean there is an empty stomach or that its contents are not as acidic. They therefore conclude that "women should be free to eat and drink in labour, or not, as they wish."[85]

At one time shaving of the area around the vagina, was common practice due to the belief that hair removal reduced the risk of infection, made an episiotomy (a surgical cut to enlarge the vaginal entrance) easier, and helped with instrumental deliveries. It is currently less common, though it is still a routine procedure in some countries even though a systematic review found no evidence to recommend shaving.[86] Side effects appear later, including irritation, redness, and multiple superficial scratches from the razor. Another effort to prevent infection has been the use of the antiseptic chlorhexidine or providone-iodine solution in the vagina. Evidence of benefit with chlorhexidine is lacking.[87] A decreased risk is found with providone-iodine when a cesarean section is to be performed.[88]

An assisted delivery is used in about 1 in 8 births, and may be needed if either mother or infant appears to be at risk during a vaginal delivery. The methods used are termed obstetrical forceps extraction and vacuum extraction, also called ventouse extraction. Done properly, they are both safe with some preference for forceps rather than vacuum, and both are seen as preferable to an unexpected C-section. While considered safe, some risks for the mother include vaginal tearing, including a higher chance of having a more major vaginal tear that involves the muscle or wall of the anus or rectum. For women undergoing operative vaginal delivery with vacuum extraction or forceps, there is strong evidence that prophylactic antibiotics help to reduce the risk of infection.[89] There is a higher risk of blood clots forming in the legs or pelvis anti-clot stockings or medication may be ordered to avoid clots. Urinary incontinence is not unusual after childbirth but it is more common after an instrument delivery. Certain exercises and physiotherapy will help the condition to improve.[90]

Some women prefer to avoid analgesic medication during childbirth. Psychological preparation may be beneficial. Relaxation techniques, immersion in water, massage, and acupuncture may provide pain relief. Acupuncture and relaxation were found to decrease the number of caesarean sections required.[91] Immersion in water has been found to relieve pain during the first stage of labour and to reduce the need for anaesthesia and shorten the duration of labour, however the safety and efficacy of immersion during birth, water birth, has not been established or associated with maternal or fetal benefit.[92]

Most women like to have someone to support them during labour and birth; such as a midwife, nurse, or doula; or a lay person such as the father of the baby, a family member, or a close friend. Studies have found that continuous support during labour and delivery reduce the need for medication and a caesarean or operative vaginal delivery, and result in an improved Apgar score for the infant.[93][94]

Different measures for pain control have varying degrees of success and side effects to the woman and her baby. In some countries of Europe, doctors commonly prescribe inhaled nitrous oxide gas for pain control, especially as 53% nitrous oxide, 47% oxygen, known as Entonox; in the UK, midwives may use this gas without a doctor's prescription.[95] Opioids such as fentanyl may be used, but if given too close to birth there is a risk of respiratory depression in the infant.[needs update][96]

Popular medical pain control in hospitals include the regional anaesthetics epidurals (EDA), and spinal anaesthesia. Epidural analgesia is a generally safe and effective method of relieving pain in labour, but has been associated with longer labour, more operative intervention (particularly instrument delivery), and increases in cost.[97] However, a more recent (2017) Cochrane review suggests that the new epidural techniques have no effect on labour time and the use of instruments or the need for C-section deliveries.[98] Generally, pain and stress hormones rise throughout labour for women without epidurals, while pain, fear, and stress hormones decrease upon administration of epidural analgesia, but rise again later.[99]Medicine administered via epidural can cross the placenta and enter the bloodstream of the fetus.[100] Epidural analgesia has no statistically significant impact on the risk of caesarean section, and does not appear to have an immediate effect on neonatal status as determined by Apgar scores.[98]

Augmentation is the process of stimulating the uterus to increase the intensity and duration of contractions after labour has begun. Several methods of augmentation are commonly been used to treat slow progress of labour (dystocia) when uterine contractions are assessed to be too weak. Oxytocin is the most common method used to increase the rate of vaginal delivery.[101] The World Health Organization recommends its use either alone or with amniotomy (rupture of the amniotic membrane) but advises that it must be used only after it has been correctly confirmed that labour is not proceeding properly if harm is to be avoided. The WHO does not recommend the use of antispasmodic agents for prevention of delay in labour.[102]

For years an episiotomy was thought to help prevent more extensive vaginal tears and heal better than a natural tear. Perineal tears can occur at the vaginal opening as the baby's head passes through, especially if the baby descends quickly. Tears can involve the perineal skin or extend to the muscles and the anal sphincter and anus. Once common, they are now recognised as generally not needed.[14] When needed, the midwife or obstetrician makes a surgical cut in the perineum to prevent severe tears that can be difficult to repair. A 2017 Cochrane review compared episiotomy as needed (restrictive) with routine episiotomy to determine the possible benefits and harms for mother and baby. The review found that restrictive episiotomy policies appeared to give a number of benefits compared with using routine episiotomy. Women experienced less severe perineal trauma, less posterior perineal trauma, less suturing and fewer healing complications at seven days with no difference in occurrence of pain, urinary incontinence, painful sex or severe vaginal/perineal trauma after birth.[103]

In cases of a head first-presenting first twin, twins can often be delivered vaginally. In some cases twin delivery is done in a larger delivery room or in an operating theatre, in the event of complication e.g.

For external monitoring of the fetus during childbirth, a simple pinard stethoscope or doppler fetal monitor ("doptone") can be used.A method of external (noninvasive) fetal monitoring (EFM) during childbirth is cardiotocography (CTG), using a cardiotocograph that consists of two sensors: The heart (cardio) sensor is an ultrasonic sensor, similar to a Doppler fetal monitor, that continuously emits ultrasound and detects motion of the fetal heart by the characteristic of the reflected sound. The pressure-sensitive contraction transducer, called a tocodynamometer (toco) has a flat area that is fixated to the skin by a band around the belly. The pressure required to flatten a section of the wall correlates with the internal pressure, thereby providing an estimate of contraction.[104]Monitoring with a cardiotocograph can either be intermittent or continuous.[105] The World Health Organization (WHO) advises that for healthy women undergoing spontaneous labour continuous cardiotocography is not recommended for assessment of fetal well-being. The WHO states: "In countries and settings where continuous CTG is used defensively to protect against litigation, all stakeholders should be made aware that this practice is not evidence-based and does not improve birth outcomes."[106]

A mother's water has to break before internal (invasive) monitoring can be used. More invasive monitoring can involve a fetal scalp electrode to give an additional measure of fetal heart activity, and/or intrauterine pressure catheter (IUPC). It can also involve fetal scalp pH testing.[medical citation needed]

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Per figures retrieved in 2015, since 1990 there has been a 44 per cent decline in the maternal death rate. However, according to 2015 figures 830 women die every day from causes related to pregnancy or childbirth and for every woman who dies, 20 or 30 encounter injuries, infections or disabilities. Most of these deaths and injuries are preventable.[108][109]

In 2008, noting that each year more than 100,000 women die of complications of pregnancy and childbirth and at least seven million experience serious health problems while 50 million more have adverse health consequences after childbirth, the World Health Organization (WHO) has urged midwife training to strengthen maternal and newborn health services. To support the upgrading of midwifery skills the WHO established a midwife training program, Action for Safe Motherhood.[5]

The rising maternal death rate in the US is of concern. In 1990 the US ranked 12th of the 14 developed countries that were analysed. However, since that time the rates of every country have steadily continued to improve while the US rate has spiked dramatically. While every other developed nation of the 14 analysed in 1990 shows a 2017 death rate of less than 10 deaths per every 100,000 live births, the US rate has risen to 26.4. By comparison, the United Kingdom ranks second highest at 9.2 and Finland is the safest at 3.8.[110] Furthermore, for every one of the 700 to 900 US woman who die each year during pregnancy or childbirth, 70 experience significant complications such as haemorrhage and organ failure, totalling more than one per cent of all births.[111]

Compared to other developed nations, the United States also has high infant mortality rates. The Trust for America's Health reports that as of 2011, about one-third of American births have some complications; many are directly related to the mother's health including increasing rates of obesity, type 2 diabetes, and physical inactivity. The U.S. Centers for Disease Control and Prevention (CDC) has led an initiative to improve woman's health previous to conception in an effort to improve both neonatal and maternal death rates.[112]

The second stage of labour may be delayed or lengthy due to poor or uncoordinated uterine action, an abnormal uterine position such as breech or shoulder dystocia, and cephalopelvic disproportion (a small pelvis or large infant). Prolonged labour may result in maternal exhaustion, fetal distress, and other complications including obstetric fistula.[113]

Eclampsia is the onset of seizures (convulsions) in a woman with pre-eclampsia. Pre-eclampsia is a disorder of pregnancy in which there is high blood pressure and either large amounts of protein in the urine or other organ dysfunction. Pre-eclampsia is routinely screened for during prenatal care. Onset may be before, during, or rarely, after delivery. Around one per cent of women with eclampsia die.[medical citation needed]

A puerperal disorder or postpartum disorder is a complication which presents primarily during the puerperium, or postpartum period. The postpartum period can be divided into three distinct stages; the initial or acute phase, six to 12 hours after childbirth; subacute postpartum period, which lasts two to six weeks, and the delayed postpartum period, which can last up to six months. In the subacute postpartum period, 87% to 94% of women report at least one health problem.[114][115] Long-term health problems (persisting after the delayed postpartum period) are reported by 31 per cent of women.[116]

According to the WHO, hemorrhage is the leading cause of maternal death worldwide accounting for approximately 27.1% of maternal deaths.[117] Within maternal deaths due to hemorrhage, two-thirds are caused by postpartum hemorrhage.[117] The causes of postpartum hemorrhage can be separated into four main categories: Tone, Trauma, Tissue, and Thrombin. Tone represents uterine atony, the failure of the uterus to contract adequately following delivery. Trauma includes lacerations or uterine rupture. Tissue includes conditions that can lead to a retained placenta. Thrombin, which is a molecule used in the human bodys blood clotting system, represents all coagulopathies.[118]

Postpartum infections, also historically known as childbed fever and medically as puerperal fever, are any bacterial infections of the reproductive tract following childbirth or miscarriage. Signs and symptoms usually include a fever greater than 38.0C (100.4F), chills, lower abdominal pain, and possibly bad-smelling vaginal discharge. The infection usually occurs after the first 24 hours and within the first ten days following delivery. Infection remains a major cause of maternal deaths and morbidity in the developing world. The work of Ignaz Semmelweis was seminal in the pathophysiology and treatment of childbed fever and his work saved many lives.[119]

Childbirth can be an intense event and strong emotions, both positive and negative, can be brought to the surface. Abnormal and persistent fear of childbirth is known as tokophobia. The prevalence of fear of childbirth around the world ranges between 425%, with 37% of pregnant women having clinical fear of childbirth.[120][121]

Most new mothers may experience mild feelings of unhappiness and worry after giving birth. Babies require a lot of care, so it is normal for mothers to be worried about, or tired from, providing that care. The feelings, often termed the "baby blues", affect up to 80 per cent of mothers. They are somewhat mild, last a week or two, and usually go away on their own.[122]

Postpartum depression is different from the "baby blues". With postpartum depression, feelings of sadness and anxiety can be extreme and might interfere with a woman's ability to care for herself or her family. Because of the severity of the symptoms, postpartum depression usually requires treatment. The condition, which occurs in nearly 15 percent of births, may begin shortly before or any time after childbirth, but commonly begins between a week and a month after delivery.[122]

Childbirth-related posttraumatic stress disorder is a psychological disorder that can develop in women who have recently given birth.[123][124][125] Causes include issues such as an emergency C-section, preterm labour, inadequate care during labour,lack of social support following childbirth, and others. Examples of symptoms include intrusive symptoms, flashbacks and nightmares, as well as symptoms of avoidance (including amnesia for the whole or parts of the event), problems in developing a mother-child attachment, and others similar to those commonly experienced in posttraumatic stress disorder (PTSD). Many women who are experiencing symptoms of PTSD after childbirth are misdiagnosed with postpartum depression or adjustment disorders. These diagnoses can lead to inadequate treatment.[126]

More:
Childbirth - Wikipedia

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Overview

Hair loss (alopecia) can affect just your scalp or your entire body, and it can be temporary or permanent. It can be the result of heredity, hormonal changes, medical conditions or a normal part of aging. Anyone can lose hair on their head, but it's more common in men.

Baldness typically refers to excessive hair loss from your scalp. Hereditary hair loss with age is the most common cause of baldness. Some people prefer to let their hair loss run its course untreated and unhidden. Others may cover it up with hairstyles, makeup, hats or scarves. And still others choose one of the treatments available to prevent further hair loss or restore growth.

Before pursuing hair loss treatment, talk with your doctor about the cause of your hair loss and treatment options.

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Male-pattern baldness typically appears first at the hairline or top of the head. It can progress to partial or complete baldness.

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Female-pattern baldness typically starts with scalp hairs becoming progressively less dense. Many women first experience hair thinning and hair loss where they part their hair and on the top-central portion of the head.

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In the type of patchy hair loss known as alopecia areata, hair loss occurs suddenly and usually starts with one or more circular bald patches that may overlap.

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Hair loss can occur if you wear pigtails, braids or cornrows, or use tight hair rollers. This is called traction alopecia.

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Early treatment of a receding hairline (frontal fibrosing alopecia) might help avoid significant permanent baldness. The cause of this condition is unknown, but it primarily affects older women.

Hair loss can appear in many different ways, depending on what's causing it. It can come on suddenly or gradually and affect just your scalp or your whole body.

Signs and symptoms of hair loss may include:

See your doctor if you are distressed by persistent hair loss in you or your child and want to pursue treatment. For women who are experiencing a receding hairline (frontal fibrosing alopecia), talk with your doctor about early treatment to avoid significant permanent baldness.

Also talk to your doctor if you notice sudden or patchy hair loss or more than usual hair loss when combing or washing your or your child's hair. Sudden hair loss can signal an underlying medical condition that requires treatment.

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People typically lose 50 to 100 hairs a day. This usually isn't noticeable because new hair is growing in at the same time. Hair loss occurs when new hair doesn't replace the hair that has fallen out.

Hair loss is typically related to one or more of the following factors:

A number of factors can increase your risk of hair loss, including:

Most baldness is caused by genetics (male-pattern baldness and female-pattern baldness). This type of hair loss is not preventable.

These tips may help you avoid preventable types of hair loss:

See the original post:
Hair loss - Symptoms and causes - Mayo Clinic

Recommendation and review posted by Bethany Smith

Some cells are visible to the unaided eye

The smallest objects that the unaided human eye can see are about 0.1 mm long. That means that under the right conditions, you might be able to see an amoeba proteus, a human egg, and a paramecium without using magnification. A magnifying glass can help you to see them more clearly, but they will still look tiny.

Smaller cells are easily visible under a light microscope. It's even possible to make out structures within the cell, such as the nucleus, mitochondria and chloroplasts. Light microscopes use a system of lenses to magnify an image. The power of a light microscope is limited by the wavelength of visible light, which is about 500 nm. The most powerful light microscopes can resolve bacteria but not viruses.

To see anything smaller than 500 nm, you will need an electron microscope. Electron microscopes shoot a high-voltage beam of electrons onto or through an object, which deflects and absorbs some of the electrons. Resolution is still limited by the wavelength of the electron beam, but this wavelength is much smaller than that of visible light. The most powerful electron microscopes can resolve molecules and even individual atoms.

The label on the nucleotide is not quite accurate. Adenine refers to a portion of the molecule, thenitrogenous base. It would be more accurate to label the nucleotide deoxyadenosine monophosphate, as itincludes the sugar deoxyribose and a phosphate group in addition to the nitrogenous base. However, the morefamiliar "adenine" label makes it easier for people to recognize it as one of the building blocks of DNA.

No, this isn't a mistake. First, there's less DNA in a sperm cell than there is in a non-reproductive cellsuch as a skin cell. Second, the DNA in a sperm cell is super-condensed and compacted into a highly dense form. Third, the head of a sperm cell is almost all nucleus. Most of the cytoplasm has been squeezed out in order to make the sperm an efficient torpedo-like swimming machine.

The X chromosome is shown here in a condensed state, as it would appear in a cell that's going through mitosis. It has also been duplicated, so there are actually two identical copies stuck together at their middles. A human sperm cell contains just one copy each of 23 chromosomes.

A chromosome is made up of genetic material (one long piece of DNA) wrapped around structural support proteins (histones). Histones organize the DNA and keep it from getting tangled, much like thread wrapped around a spool. But they also add a lot of bulk. In a sperm cell, a specialized set of tiny support proteins (protamines) pack the DNA down to about one-sixth the volume of a mitotic chromosome.

The size of the carbon atom is based on its van der Waals radius.

Original post:
Cell Size and Scale - University of Utah

Recommendation and review posted by Bethany Smith

SCOTTSDALE, Ariz., Oct 12 (Reuters) - Time and death are "on pause" for some people in Scottsdale, Arizona.

Inside tanks filled with liquid nitrogen are the bodies and heads of 199 humans who opted to be cryopreserved in hopes of being revived in the future when science has advanced beyond what it is capable of today. Many of the "patients," as Alcor Life Extension Foundation calls them, were terminally ill with cancer, ALS or other diseases with no present-day cure.

Matheryn Naovaratpong, a Thai girl with brain cancer, is the youngest person to be cryopreserved, at the age of 2 in 2015.

"Both her parents were doctors and she had multiple brain surgeries and nothing worked, unfortunately. So they contacted us," said Max More, chief executive of Alcor, a nonprofit which claims to be the world leader in cryonics.

Bitcoin pioneer Hal Finney, another Alcor patient, had his body cryopreserved after death from ALS in 2014.

The cryopreservation process begins after a person is declared legally dead. Blood and other fluids are removed from the patient's body and replaced with chemicals designed to prevent the formation of damaging ice crystals. Vitrified at extremely cold temperatures, Alcor patients are then placed in tanks at the Arizona facility "for as long as it takes for technology to catch up," More said.

The minimum cost is $200,000 for a body and $80,000 for the brain alone. Most of Alcor's almost 1,400 living "members" pay by making the company the beneficiary of life insurance policies equal to the cost, More said.

More's wife Natasha Vita-More likens the process to taking a trip to the future.

"The disease or injury cured or fixed, and the person has a new body cloned or a whole body prosthetic or their body reanimated and (can) meet up with their friends again," she said.

Many medical professionals disagree, said Arthur Caplan, who heads the medical ethics division at New York University's Grossman School of Medicine.

"This notion of freezing ourselves into the future is pretty science fiction and it's naive," he said. "The only group... getting excited about the possibility are people who specialize in studying the distant future or people who have a stake in wanting you to pay the money to do it."

Reporting by Liliana Salgado; Editing by Richard Chang

Our Standards: The Thomson Reuters Trust Principles.

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Arizona cryonics facility preserves bodies to revive later

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American baseball player (19182002)

Baseball player

Williams in 1949

As manager

Theodore Samuel Williams (August 30, 1918 July 5, 2002) was an American professional baseball player and manager. He played his entire 19-year Major League Baseball (MLB) career, primarily as a left fielder, for the Boston Red Sox from 1939 to 1960; his career was interrupted by military service during World War II and the Korean War. Nicknamed "Teddy Ballgame", "the Kid", "the Splendid Splinter", and "The Thumper", Williams is regarded as one of the greatest hitters in baseball history and to date is the last player to hit over .400 in a season.

Williams was a nineteen-time All-Star,[1] a two-time recipient of the American League (AL) Most Valuable Player Award, a six-time AL batting champion, and a two-time Triple Crown winner. He finished his playing career with a .344 batting average, 521 home runs, and a .482 on-base percentage, the highest of all time. His career batting average is the highest of any MLB player whose career was played primarily in the live-ball era, and ranks tied for 7th all-time (with Billy Hamilton).

Born and raised in San Diego, Williams played baseball throughout his youth. After joining the Red Sox in 1939, he immediately emerged as one of the sport's best hitters. In 1941, Williams posted a .406 batting average; he is the last MLB player to bat over .400 in a season. He followed this up by winning his first Triple Crown in 1942. Williams was required to interrupt his baseball career in 1943 to serve three years in the United States Navy and Marine Corps during World War II. Upon returning to MLB in 1946, Williams won his first AL MVP Award and played in his only World Series. In 1947, he won his second Triple Crown. Williams was returned to active military duty for portions of the 1952 and 1953 seasons to serve as a Marine combat aviator in the Korean War. In 1957 and 1958 at the ages of 39 and 40, respectively, he was the AL batting champion for the fifth and sixth time.

Williams retired from playing in 1960. He was inducted into the Baseball Hall of Fame in 1966, in his first year of eligibility.[2] Williams managed the Washington Senators/Texas Rangers franchise from 1969 to 1972. An avid sport fisherman, he hosted a television program about fishing, and was inducted into the IGFA Fishing Hall of Fame.[3] Williams's involvement in the Jimmy Fund helped raise millions in dollars for cancer care and research. In 1991, President George H. W. Bush presented Williams with the Presidential Medal of Freedom, the highest civilian award bestowed by the United States government. He was selected for the Major League Baseball All-Time Team in 1997 and the Major League Baseball All-Century Team in 1999.

Williams was born in San Diego on August 30, 1918,[4] and named Theodore Samuel Williams after former president Theodore Roosevelt as well as his father, Samuel Stuart Williams.[5] He later amended his birth certificate, removing his middle name,[5] which he claimed originated from a maternal uncle (whose actual name was Daniel Venzor), who had been killed in World War I.[6] His father was a soldier, sheriff, and photographer from Ardsley, New York,[7] while his mother, May Venzor, a Spanish-Mexican-American from El Paso, Texas, was an evangelist and lifelong soldier in the Salvation Army.[5] Williams resented his mother's long hours working in the Salvation Army,[8] and Williams and his brother cringed when she took them to the Army's street-corner revivals.[9]

Williams's paternal ancestors were a mix of Welsh, English, and Irish. The maternal, Spanish-Mexican side of Williams's family was quite diverse, having Spanish (Basque), Russian, and American Indian roots.[10] Of his Mexican ancestry he said that "If I had my mother's name, there is no doubt I would have run into problems in those days, [considering] the prejudices people had in Southern California."[11]

Williams lived in San Diego's North Park neighborhood (4121 Utah Street).[12] At the age of eight, he was taught how to throw a baseball by his uncle, Saul Venzor. Saul was one of his mother's four brothers, as well as a former semi-professional baseball player who had pitched against Babe Ruth, Lou Gehrig, and Joe Gordon in an exhibition game.[13][14] As a child, Williams's heroes were Pepper Martin of the St. Louis Cardinals and Bill Terry of the New York Giants.[15] Williams graduated from Herbert Hoover High School in San Diego, where he played baseball as a pitcher and was the star of the team.[16] During this time, he also played American Legion Baseball, later being named the 1960 American Legion Baseball Graduate of the Year.[17]

Though he had offers from the St. Louis Cardinals and the New York Yankees while he was still in high school,[18] his mother thought he was too young to leave home, so he signed up with the local minor league club, the San Diego Padres.[19]

Throughout his career, Williams stated his goal was to have people point to him and remark, "There goes Ted Williams, the greatest hitter who ever lived."[20]

Williams played back-up behind Vince DiMaggio and Ivey Shiver on the (then) Pacific Coast League's San Diego Padres. While in the Pacific Coast League in 1936, Williams met future teammates and friends Dom DiMaggio and Bobby Doerr, who were on the Pacific Coast League's San Francisco Seals.[21] When Shiver announced he was quitting to become a high school football coach in Savannah, Georgia, the job, by default, was open for Williams.[22] Williams posted a .271 batting average on 107 at bats in 42 games for the Padres in 1936.[22] Unknown to Williams, he had caught the eye of the Boston Red Sox's general manager, Eddie Collins, while Collins was scouting Bobby Doerr and the shortstop George Myatt in August 1936.[22][23] Collins later explained, "It wasn't hard to find Ted Williams. He stood out like a brown cow in a field of white cows."[22] In the 1937 season, after graduating from Hoover High in the winter, Williams finally broke into the line-up on June 22, when he hit an inside-the-park home run to help the Padres win 32. The Padres ended up winning the PCL title, while Williams ended up hitting .291 with 23 home runs.[22] Meanwhile, Collins kept in touch with Padres general manager Bill Lane, calling him two times throughout the season. In December 1937, during the winter meetings, the deal was made between Lane and Collins, sending Williams to the Boston Red Sox and giving Lane $35,000 and two major leaguers, Dom D'Allessandro and Al Niemiec, and two other minor leaguers.[24][25]

In 1938, the 19-year-old Williams was 10 days late to spring training camp in Sarasota, Florida, because of a flood in California that blocked the railroads. Williams had to borrow $200 from a bank to make the trip from San Diego to Sarasota.[26] Also during spring training Williams was nicknamed "the Kid" by Red Sox equipment manager Johnny Orlando, who after Williams arrived to Sarasota for the first time, said, "'The Kid' has arrived". Orlando still called Williams "the Kid" 20 years later,[26] and the nickname stuck with Williams the rest of his life.[27] Williams remained in major league spring training for about a week.[26] Williams was then sent to the Double-A-league Minneapolis Millers.[28] While in the Millers training camp for the springtime, Williams met Rogers Hornsby, who had hit over .400 three times, including a .424 average in 1924.[29] Hornsby, who was a coach for the Millers that spring,[29] gave Williams useful advice, including how to "get a good pitch to hit".[28] Talking with the game's greats would become a pattern for Williams, who also talked with Hugh Duffy, who hit .438 in 1894, Bill Terry who hit .401 in 1930, and Ty Cobb with whom he would argue that a batter should hit up on the ball, opposed to Cobb's view that a batter should hit down on the ball.[30]

While in Minnesota, Williams quickly became the team's star.[31] He collected his first hit in the Millers' first game of the season, as well as his first and second home runs during his third game. Both were inside-the-park home runs, with the second traveling an estimated 500 feet (150m) on the fly to a 512-foot (156m) center field fence.[31] Williams later had a 22 game hitting streak that lasted from Memorial Day through mid-June.[31] While the Millers ended up sixth place in an eight-team race,[31] Williams ended up hitting .366 with 46 home runs and 142 RBIs. He received the American Association's Triple Crown and finished second in the voting for Most Valuable Player.[32]

Williams came to spring training three days late in 1939, thanks to Williams driving from California to Florida, as well as respiratory problems, the latter of which would plague Williams for the rest of his career.[33] In the winter, the Red Sox traded right fielder Ben Chapman to the Cleveland Indians to make room for Williams on the roster, even though Chapman had hit .340 in the previous season.[34][35] This led Boston Globe sports journalist Gerry Moore to quip, "Not since Joe DiMaggio broke in with the Yankees by "five for five" in St. Petersburg in 1936 has any baseball rookie received the nationwide publicity that has been accorded this spring to Theodore Francis [sic] Williams".[33] Williams inherited Chapman's number 9 on his uniform as opposed to Williams's number 5 in the previous spring training. He made his major league debut against the New York Yankees on April 20,[36] going 1-for-4 against Yankee pitcher Red Ruffing. This was the only game which featured both Williams and Lou Gehrig playing against one another.[37] In his first series at Fenway Park, Williams hit a double, a home run, and a triple, the first two against Cotton Pippen, who gave Williams his first strikeout as a professional while Williams had been in San Diego.[38] By July, Williams was hitting just .280, but leading the league in RBIs.[38] Johnny Orlando, now Williams's friend, then gave Williams a quick pep talk, telling Williams that he should hit .335 with 35 home runs and he would drive in 150 runs. Williams said he would buy Orlando a Cadillac if this all came true.[39] Williams ended up hitting .327 with 31 home runs and 145 RBIs,[36] leading the league in the latter category, the first rookie to lead the league in RBIs[40] and finishing fourth in MVP voting.[41] He also led the AL in walks, with 107, a rookie record. Even though there was not a Rookie of the Year award yet in 1939, Babe Ruth declared Williams to be the Rookie of the Year, which Williams later said was "good enough for me".[42]

Williams's pay doubled in 1940, going from $5,000 to $10,000.[43] With the addition of a new bullpen in right field of Fenway Park, which reduced the distance from home plate from 400 feet to 380 feet, the bullpen was nicknamed "Williamsburg", because the new addition was "obviously designed for Williams".[44] Williams was then switched from right field to left field, as there would be less sun in his eyes, and it would give Dom DiMaggio a chance to play. Finally, Williams was flip-flopped in the order with the great slugger Jimmie Foxx, with the idea that Williams would get more pitches to hit.[44] Pitchers, though, were not afraid to walk him to get to the 33-year-old Foxx, and after that the 34-year-old Joe Cronin, the player-manager.[45] Williams also made his first of 16 All-Star Game appearances[46] in 1940, going 0-for-2.[47] Although Williams hit .344, his power and runs batted in were down from the previous season, with 23 home runs and 113 RBIs.[36] Williams also caused a controversy in mid-August when he called his salary "peanuts", along with saying he hated the city of Boston and reporters, leading reporters to lash back at him, saying that he should be traded.[48] Williams said that the "only real fun" he had in 1940 was being able to pitch once on August 24, when he pitched the last two innings in a 121 loss to the Detroit Tigers, allowing one earned run on three hits, while striking out one batter, Rudy York.[49][50]

In the second week of spring training in 1941, Williams broke a bone in his right ankle, limiting him to pinch hitting for the first two weeks of the season.[51] Bobby Doerr later claimed that the injury would be the foundation of Williams's season, as it forced him to put less pressure on his right foot for the rest of the season.[52] Against the Chicago White Sox on May 7, in extra innings, Williams told the Red Sox pitcher, Charlie Wagner, to hold the White Sox, since he was going to hit a home run. In the 11th inning, Williams's prediction came true, as he hit a big blast to help the Red Sox win. The home run is still considered to be the longest home run ever hit in the old Comiskey Park, some saying that it went 600 feet (180m).[53] Williams's average slowly climbed in the first half of May, and on May 15, he started a 22-game hitting streak. From May 17 to June 1, Williams batted .536, with his season average going above .400 on May 25 and then continuing up to .430.[54] By the All-Star break, Williams was hitting .406 with 62 RBIs and 16 home runs.[55]

In the 1941 All-Star Game, Williams batted fourth behind Joe DiMaggio, who was in the midst of his record-breaking hitting streak, having hit safely in 48 consecutive games.[56] In the fourth inning Williams doubled to drive in a run.[57] With the National League (NL) leading 52 in the eighth inning, Williams struck out in the middle of an American League (AL) rally.[56] In the ninth inning the AL still trailed 53; Ken Keltner and Joe Gordon singled, and Cecil Travis walked to load the bases.[57] DiMaggio grounded to the infield and Billy Herman, attempting to complete a double play, threw wide of first base, allowing Keltner to score.[57] With the score 54 and runners on first and third, Williams homered with his eyes closed to secure a 75 AL win.[57][58] Williams later said that that game-winning home run "remains to this day the most thrilling hit of my life".[59]

In late August, Williams was hitting .402.[59] Williams said that "just about everybody was rooting for me" to hit .400 in the season, including Yankee fans, who gave pitcher Lefty Gomez a "hell of a boo" after walking Williams with the bases loaded after Williams had gotten three straight hits one game in September.[60] In mid-September, Williams was hitting .413, but dropped a point a game from then on.[59] Before the final two games on September 28, a doubleheader against the Philadelphia Athletics, he was batting .39955, which would have been officially rounded up to .400.[59] Red Sox manager Joe Cronin offered him the chance to sit out the final day, but he declined. "If I'm going to be a .400 hitter", he said at the time, "I want more than my toenails on the line."[61] Williams went 6-for-8 on the day, finishing the season at .406.[62] (Sacrifice flies were counted as at-bats in 1941; under today's rules, Williams would have hit between .411 and .419, based on contemporaneous game accounts.[61]) Philadelphia fans ran out on the field to surround Williams after the game, forcing him to protect his hat from being stolen; he was helped into the clubhouse by his teammates.[63] Along with his .406 average, Williams also hit 37 home runs and batted in 120 runs, missing the triple crown by five RBI.[36][61]

Williams's 1941 season is often considered to be the best offensive season of all time, though the MVP award would go to DiMaggio. The .406 batting averagehis first of six batting championshipsis still the highest single-season average in Red Sox history and the highest batting average in the major leagues since 1924, and the last time any major league player has hit over .400 for a season after averaging at least 3.1 plate appearances per game. ("If I had known hitting .400 was going to be such a big deal", he quipped in 1991, "I would have done it again."[61]) Williams's on-base percentage of .553 and slugging percentage of .735 that season are both also the highest single-season averages in Red Sox history. The .553 OBP stood as a major league record until it was broken by Barry Bonds in 2002 and his .735 slugging percentage was the highest mark in the major leagues between 1932 and 1994. His OPS of 1.287 that year, a Red Sox record, was the highest in the major leagues between 1923 and 2001. Despite playing in only 143 games that year, Williams led the league with 135 runs scored and 37 home runs, and he finished third with 335 total bases, the most home runs, runs scored, and total bases by a Red Sox player since Jimmie Foxx's in 1938.[64] Williams placed second in MVP voting; DiMaggio won, 291 votes to 254,[65] on the strength of his record-breaking 56-game hitting streak and league-leading 125 RBI.[62]

In January 1942, just over 2 years after World War II began,[66][67] Williams was drafted into the military, being put into Class 1-A. A friend of Williams suggested that Williams see the advisor of the governor's Selective Service Appeal Agent, since Williams was the sole support of his mother, arguing that Williams should not have been placed in Class 1-A, and said Williams should be reclassified to Class 3-A.[66] Williams was reclassified to 3-A ten days later.[68] Afterwards, the public reaction was extremely negative,[69] even though the baseball book Season of '42 states only four All-Stars and one first-line pitcher entered military service during the 1942 season. (Many more MLB players would enter service during the 1943 season.)[70]

Quaker Oats stopped sponsoring Williams, and Williams, who previously had eaten Quaker products "all the time", never "[ate] one since" the company stopped sponsoring him.[68]

Despite the trouble with the draft board, Williams had a new salary of $30,000 in 1942.[68] In the season, Williams won the Triple Crown,[62] with a .356 batting average, 36 home runs, and 137 RBIs.[36] On May 21, Williams also hit his 100th career home run.[71] He was the third Red Sox player to hit 100 home runs with the team, following his teammates Jimmie Foxx and Joe Cronin.[citation needed] Despite winning the Triple Crown, Williams came in second in the MVP voting, losing to Joe Gordon of the Yankees. Williams felt that he should have gotten a "little more consideration" because of winning the Triple Crown, and he thought that "the reason I didn't get more consideration was because of the trouble I had with the draft [boards]".[62]

Williams joined the Navy Reserve on May 22, 1942, went on active duty in 1943, and was commissioned a second lieutenant in the United States Marine Corps as a Naval Aviator on May 2, 1944. Williams also played on the baseball team in Chapel Hill, North Carolina, along with his Red Sox teammate Johnny Pesky in pre-flight training, after eight weeks in Amherst, Massachusetts, and the Civilian Pilot Training Course.[72] While on the baseball team, Williams was sent back to Fenway Park on July 12, 1943, to play on an All-Star team managed by Babe Ruth. The newspapers reported that Babe Ruth said when finally meeting Williams, "Hiya, kid. You remind me a lot of myself. I love to hit. You're one of the most natural ballplayers I've ever seen. And if my record is broken, I hope you're the one to do it".[73] Williams later said he was "flabbergasted" by the incident, as "after all, it was Babe Ruth".[73] In the game, Williams hit a 425-foot home run to help give the American League All-Stars a 98 win.[74]

On September 2, 1945, when the war ended, Lt. Williams was in Pearl Harbor, Hawaii awaiting orders as a replacement pilot. While in Pearl Harbor, Williams played baseball in the Navy League. Also in that eight-team league were Joe DiMaggio, Joe Gordon, and Stan Musial. The Service World Series with the Army versus the Navy attracted crowds of 40,000 for each game. The players said it was even better than the actual World Series being played between the Detroit Tigers and Chicago Cubs that year.[75]

Williams was discharged by the Marine Corps on January 28, 1946, in time to begin preparations for the upcoming pro baseball season.[76][77] He joined the Red Sox again in 1946, signing a $37,500 contract.[78] On July 14, after Williams hit three home runs and eight RBIs in the first game of a doubleheader, Lou Boudreau, inspired by Williams's consistent pull hitting to right field, created what would later be known as the Boudreau shift (also Williams shift) against Williams, having only one player on the left side of second base (the left fielder). Ignoring the shift, Williams walked twice, doubled, and grounded out to the shortstop, who was positioned in between first and second base.[79][80] Also during 1946, the All-Star Game was held in Fenway Park. In the game, Williams homered in the fourth inning against Kirby Higbe, singled in a run in the fifth inning, singled in the seventh inning, and hit a three-run home run against Rip Sewell's "eephus pitch" in the eighth inning[81] to help the American League win 120.[82]

For the 1946 season, Williams hit .342 with 38 home runs and 123 RBIs,[36] helping the Red Sox win the pennant on September 13. During the season, Williams hit the only inside-the-park home run in his Major League career in a September 10 win at Cleveland,[83][84] and in June hit what is considered the longest home run in Fenway Park history, at 502 feet (153m) and subsequently marked with a lone red seat in the Fenway bleachers.[85] Williams ran away as the winner in the MVP voting.[86] During an exhibition game in Fenway Park against an All-Star team during early October, Williams was hit on the elbow by a curveball by the Washington Senators' pitcher Mickey Haefner. Williams was immediately taken out of the game, and X-rays of his arm showed no damage, but his arm was "swelled up like a boiled egg", according to Williams.[87] Williams could not swing a bat again until four days later, one day before the World Series, when he reported the arm as "sore".[87] During the series, Williams batted .200, going 5-for-25 with no home runs and just one RBI. The Red Sox lost in seven games,[88] with Williams going 0-for-4 in the last game.[89] Fifty years later when asked what one thing he would have done different in his life, Williams replied, "I'd have done better in the '46 World Series. God, I would".[87] The 1946 World Series was the only World Series Williams ever appeared in.[90]

Williams signed a $70,000 contract in 1947.[91] Williams was also almost traded for Joe DiMaggio in 1947. In late April, Red Sox owner Tom Yawkey and Yankees owner Dan Topping agreed to swap the players, but a day later canceled the deal when Yawkey requested that Yogi Berra come with DiMaggio.[92] In May, Williams was hitting .337.[93] Williams won the Triple Crown in 1947, but lost the MVP award to Joe DiMaggio, 202 points to 201 points. One writer left Williams off his ballot. Williams thought it was Mel Webb, whom Williams called a "grouchy old guy",[94] although it now appears it was not Webb.[95]

Through 2011, Williams was one of seven major league players to have had at least four 30-home run and 100-RBI seasons in their first five years, along with Chuck Klein, Joe DiMaggio, Ralph Kiner, Mark Teixeira, Albert Pujols, and Ryan Braun.[96]

In 1948, under their new manager, Joe McCarthy,[97] Williams hit a league-leading .369 with 25 home runs and 127 RBIs,[36] and was third in MVP voting.[98] On April 29, Williams hit his 200th career home run. He became just the second player to hit 200 home runs in a Red Sox uniform, joining his former teammate Jimmie Foxx.[64] On October 2, against the Yankees, Williams hit his 222nd career home run, tying Foxx for the Red Sox all-time record.[99] In the Red Sox' final two games of the regular schedule, they beat the Yankees (to force a one-game playoff against the Cleveland Indians) and Williams got on base eight times out of ten plate appearances.[97] In the playoff, Williams went 1-for-4,[100] with the Red Sox losing 83.

In 1949, Williams received a new salary of $100,000 ($1,139,000 in current dollar terms).[101] He hit .343 (losing the AL batting title by just .0002 to the Tigers' George Kell, thus missing the Triple Crown that year), hitting 43 home runs, his career high, and driving in 159 runs, tied for highest in the league, and at one point, he got on base in 84 straight games, an MLB record that still stands today, helping him win the MVP trophy.[36][102] On April 28, Williams hit his 223rd career home run, breaking the record for most home runs in a Red Sox uniform, passing Jimmie Foxx.[103] Williams is still the Red Sox career home run leader.[64] However, despite being ahead of the Yankees by one game just beforea 2-game series against them (last regular-season games for both teams),[97] the Red Sox lost both of those games.[104] The Yankees won the first of what would be five straight World Series titles in 1949.[105] For the rest of Williams's career, the Yankees won nine pennants and six World Series titles, while the Red Sox never finished better than third place.[105]

In 1950, Williams was playing in his eighth All-Star Game. In the first inning, Williams caught a line drive by Ralph Kiner, slamming into the Comiskey Park scoreboard and breaking his left arm.[46] Williams played the rest of the game, and he even singled in a run to give the American League the lead in the fifth inning, but by that time Williams's arm was a "balloon" and he was in great pain, so he left the game.[106] Both of the doctors who X-rayed Williams held little hope for a full recovery. The doctors operated on Williams for two hours.[107] When Williams took his cast off, he could only extend the arm to within four inches of his right arm.[108] Williams only played 89 games in 1950.[36] After the baseball season, Williams's elbow hurt so much he considered retirement, since he thought he would never be able to hit again. Tom Yawkey, the Red Sox owner, then sent Jack Fadden to Williams's Florida home to talk to Williams. Williams later thanked Fadden for saving his career.[109]

In 1951, Williams "struggled" to hit .318, with his elbow still hurting.[110] Williams also played in 148 games, 60 more than Williams had played the previous season, 30 home runs, two more than he had hit in 1950, and 126 RBIs, twenty-nine more than 1950.[36][110] Despite his lower-than-usual production at bat, Williams made the All-Star team.[47] On May 15, 1951, Williams became the 11th player in major league history to hit 300 career home runs. On May 21, Williams passed Chuck Klein for 10th place, on May 25 Williams passed Hornsby for ninth place, and on July 5 Williams passed Al Simmons for eighth place all-time in career home runs.[111] After the season, manager Steve O'Neill was fired, with Lou Boudreau replacing him. Boudreau's first announcement as manager was that all Red Sox players were "expendable", including Williams.[110]

Williams's name was called from a list of inactive reserves to serve on active duty in the Korean War on January 9, 1952. Williams, who was livid at his recalling, had a physical scheduled for April 2.[112] Williams passed his physical and in May, after only playing in six major league games, began refresher flight training and qualification prior to service in Korea. Right before he left for Korea, the Red Sox had a "Ted Williams Day" in Fenway Park. Friends of Williams gave him a Cadillac, and the Red Sox gave Williams a memory book that was signed by 400,000 fans. The governor of Massachusetts and mayor of Boston were there, along with a Korean War veteran named Frederick Wolf who used a wheelchair for mobility.[113] At the end of the ceremony, everyone in the park held hands and sang "Auld Lang Syne" to Williams, a moment which he later said "moved me quite a bit."[114] Private Wolf (an injured Korean veteran from Brooklyn) presented gifts from wounded veterans to Ted Williams. Ted choked and was only able to say,"... ok kid...".[115] The Red Sox went on to win the game 53, thanks to a two-run home run by Williams in the seventh inning.[114]

In August 1953, Williams practiced with the Red Sox for ten days before playing in his first game, garnering a large ovation from the crowd and hitting a home run in the eighth inning.[116] In the season, Williams ended up hitting .407 with 13 home runs and 34 RBIs in 37 games and 110 at bats (not nearly enough plate appearances to qualify for that season's batting title).[36] On September 6, Williams hit his 332nd career home run, passing Hank Greenberg for seventh all-time.[117]

On the first day of spring training in 1954, Williams broke his collarbone running after a line drive.[116] Williams was out for six weeks, and in April he wrote an article with Joe Reichler of the Saturday Evening Post saying that he intended to retire at the end of the season.[118] Williams returned to the Red Sox lineup on May 7, and he hit .345 with 386 at bats in 117 games, although Bobby vila, who had hit .341, won the batting championship. This was because it was required then that a batter needed 400 at bats, despite Lou Boudreau's attempt to bat Williams second in the lineup to get more at-bats. Williams led the league in base on balls with 136 which kept him from qualifying under the rules at the time. By today's standards (plate appearances) he would have been the champion. The rule was changed shortly thereafter to keep this from happening again.[36][119] On August 25, Williams passed Johnny Mize for sixth place, and on September 3, Williams passed Joe DiMaggio for fifth all-time in career home runs with his 362nd career home run. He finished the season with 366 career home runs.[120] On September 26, Williams "retired" after the Red Sox's final game of the season.[121]

During the off-season of 1954, Williams was offered the chance to be manager of the Red Sox. Williams declined, and he suggested that Pinky Higgins, who had previously played on the 1946 Red Sox team as the third baseman, become the manager of the team. Higgins later was hired as the Red Sox manager in 1955.[122] Williams sat out the first month of the 1955 season due to a divorce settlement with his wife, Doris. When Williams returned, he signed a $98,000 contract on May 13. Williams batted .356 in 320 at bats on the season, lacking enough at bats to win the batting title over Al Kaline, who batted .340.[123] Williams hit 28 home runs and drove in 83 runs[36] while being named the "Comeback Player of the Year."[124]

On July 17, 1956, Williams became the fifth player to hit 400 home runs, following Mel Ott in 1941, Jimmie Foxx in 1938, Lou Gehrig in 1936, and Babe Ruth in 1927.[125][126] Three weeks later at home against the Yankees on August7, after Williams was booed for dropping a fly ball from Mickey Mantle, he spat at one of the fans who was taunting him on the top of the dugout;[127] Williams was fined $5,000 for the incident.[128][129] The following night against Baltimore, Williams was greeted by a large ovation, and received an even larger one when he hit a home run in the sixth inning to break a 22 tie. In The Boston Globe, the publishers ran a "What Globe Readers Say About Ted" section made out of letters about Williams, which were either the sportswriters or the "loud mouths" in the stands. Williams explained years later, "From '56 on, I realized that people were for me. The writers had written that the fans should show me they didn't want me, and I got the biggest ovation yet".[130] Williams lost the batting title to Mickey Mantle in 1956, batting .345 to Mantle's .353, with Mantle on his way to winning the Triple Crown.[131]

In 1957, Williams batted .388 to lead the majors, then signed a contract in February 1958 for a record high $125,000 (or $135,000).[132][133] At age forty that season, he again led the American League with a .328 batting average.[134]

When Pumpsie Green became the first black player on the Red Soxthe last major league team to integratein 1959, Williams openly welcomed Green.[135]

Williams ended his career with a home run in his last at-bat on September 28, 1960. He refused to salute the fans as he returned the dugout after he crossed home plate or after he was replaced in left field by Carroll Hardy. An essay written by John Updike the following month for The New Yorker, "Hub Fans Bid Kid Adieu", chronicles this event.[136]

Williams is one of only 29 players in baseball history to date to have appeared in Major League games in four decades.[137]

Williams was an obsessive student of hitting. He famously used a lighter bat than most sluggers, because it generated a faster swing.[138] In 1970, he wrote a book on the subject, The Science of Hitting (revised 1986), which is still read by many baseball players.[138] The book describes his theory of swinging only at pitches that came into ideal areas of his strike zone, a strategy Williams credited with his success as a hitter. Pitchers apparently feared Williams; his bases-on-balls-to-plate-appearances ratio (.2065) is still the highest of any player in the Hall of Fame.

Williams nearly always took the first pitch.[139]

He helped pass his expertise of playing left-field in front of the Green Monster to his successor on the Red Sox, Carl Yastrzemski.[140]

Williams was on uncomfortable terms with the Boston newspapers for nearly twenty years, as he felt they liked to discuss his personal life as much as his baseball performance. He maintained a career-long feud with Sport due to a 1948 feature article in which the reporter included a quote from Williams's mother. Insecure about his upbringing, and stubborn because of immense confidence in his own talent, Williams made up his mind that the "knights of the keyboard", as he derisively labeled the press, were against him. After having hit for the league's Triple Crown in 1947, Williams narrowly lost the MVP award in a vote where one Midwestern newspaper writer left Williams entirely off his ten-player ballot.

During his career, some sportswriters also criticized aspects of Williams's baseball performance, including what they viewed as his lackadaisical fielding and lack of clutch hitting. Williams pushed back, saying: "They're always saying that I don't hit in the clutches. Well, there are a lot [of games] when I do."[141] He also asserted that it made no sense crashing into an outfield wall to try to make a difficult catch because of the risk of injury or being out of position to make the play after missing the ball.[142]

Williams treated most of the press accordingly, as he described in his 1969 memoir My Turn at Bat. Williams also had an uneasy relationship with the Boston fans, though he could be very cordial one-to-one. He felt at times a good deal of gratitude for their passion and their knowledge of the game. On the other hand, Williams was temperamental, high-strung, and at times tactless. In his biography, Ronald Reis relates how Williams committed two fielding miscues in a doubleheader in 1950 and was roundly booed by Boston fans. He bowed three times to various sections of Fenway Park and made an obscene gesture. When he came to bat he spat in the direction of fans near the dugout. The incident caused an avalanche of negative media reaction, and inspired sportswriter Austen Lake's famous comment that when Williams's name was announced the sound was like "autumn wind moaning through an apple orchard."

Another incident occurred in 1958 in a game against the Washington Senators. Williams struck out, and as he stepped from the batter's box swung his bat violently in anger. The bat slipped from his hands, was launched into the stands and struck a 60-year-old woman who turned out to be the housekeeper of the Red Sox general manager Joe Cronin. While the incident was an accident and Williams apologized to the woman personally, to all appearances it seemed at the time that Williams had hurled the bat in a fit of temper.

Williams gave generously to those in need. He was especially linked with the Jimmy Fund of the DanaFarber Cancer Institute, which provides support for children's cancer research and treatment. Williams used his celebrity to virtually launch the fund, which raised more than $750million between 1948 and 2010. Throughout his career, Williams made countless bedside visits to children being treated for cancer, which Williams insisted go unreported. Often parents of sick children would learn at check-out time that "Mr. Williams has taken care of your bill".[143] The Fund recently stated that "Williams would travel everywhere and anywhere, no strings or paychecks attached, to support the cause... His name is synonymous with our battle against all forms of cancer."[143]

Williams demanded loyalty from those around him. He could not forgive the fickle nature of the fansbooing a player for booting a ground ball, and then turning around and roaring approval of the same player for hitting a home run. Despite the cheers and adulation of most of his fans, the occasional boos directed at him in Fenway Park led Williams to stop tipping his cap in acknowledgment after a home run.

Williams maintained this policy up to and including his swan song in 1960. After hitting a home run at Fenway Park, which would be his last career at-bat, Williams characteristically refused either to tip his cap as he circled the bases or to respond to prolonged cheers of "We want Ted!" from the crowd by making an appearance from the dugout. The Boston manager Pinky Higgins sent Williams to his fielding position in left field to start the ninth inning, but then immediately recalled him for his back-up Carroll Hardy, thus allowing Williams to receive one last ovation as he jogged onto then off the field, and he did so without reacting to the crowd. Williams's aloof attitude led the writer John Updike to observe wryly that "Gods do not answer letters."[136]

Williams's final home run did not take place during the final game of the 1960 season, but rather in the Red Sox's last home game that year. The Red Sox played three more games, but they were on the road in New York City and Williams did not appear in any of them, as it became clear that Williams's final home at-bat would be the last one of his career.

In 1991, on Ted Williams Day at Fenway Park, Williams pulled a Red Sox cap from out of his jacket and tipped it to the crowd. This was the first time that he had done so since his earliest days as a player.

A Red Smith profile from 1956 describes one Boston writer trying to convince Ted Williams that first cheering and then booing a ballplayer was no different from a moviegoer applauding a "western" movie actor one day and saying the next "He stinks! Whatever gave me the idea he could act?" Williams rejected this; when he liked a western actor like Hoot Gibson, he liked him in every picture, and would not think of booing him.

Williams once had a friendship with Ty Cobb, with whom he often had discussions about baseball. He often touted Rogers Hornsby as being the greatest right-handed hitter of all time. This assertion actually led to a split in the relationship between Ty Cobb and Ted Williams. Once during one of their yearly debate sessions on the greatest hitters of all time, Williams asserted that Hornsby was one of the greatest of all time. Cobb apparently had strong feelings about Hornsby and he threw a fit, expelling Williams from his hotel room. Their friendship effectively terminated after this altercation.[144] This story was later refuted by Ted Williams himself.[145]

Williams served as a Naval Aviator during World War II and the Korean War. Unlike many other major league players, he did not spend all of his war-time playing on service teams.[146] Williams had been classified 3-A by Selective Service prior to the war, a dependency deferment because he was his mother's sole means of financial support. When his classification was changed to 1-A following the American entry into World War II, Williams appealed to his local draft board. The draft board ruled that his draft status should not have been changed. He made a public statement that once he had built up his mother's trust fund, he intended to enlist. Even so, criticism in the media, including withdrawal of an endorsement contract by Quaker Oats, resulted in his enlistment in the U.S. Naval Reserve on May 22, 1942.

Williams did not opt for an easy assignment playing baseball for the Navy, but rather joined the V-5 program to become a Naval aviator. Williams was first sent to the Navy's Preliminary Ground School at Amherst College for six months of academic instruction in various subjects including math and navigation, where he achieved a 3.85 grade point average.

Williams was talented as a pilot, and so enjoyed it that he had to be ordered by the Navy to leave training to personally accept his American League 1942 Major League Baseball Triple Crown.[146] Williams's Red Sox teammate, Johnny Pesky, who went into the same aviation training program, said this about Williams: "He mastered intricate problems in fifteen minutes which took the average cadet an hour, and half of the other cadets there were college grads." Pesky again described Williams's acumen in the advance training, for which Pesky personally did not qualify: "I heard Ted literally tore the sleeve target to shreds with his angle dives. He'd shoot from wingovers, zooms, and barrel rolls, and after a few passes the sleeve was ribbons. At any rate, I know he broke the all-time record for hits." Ted went to Jacksonville for a course in aerial gunnery, the combat pilot's payoff test, and broke all the records in reflexes, coordination, and visual-reaction time. "From what I heard. Ted could make a plane and its six 'pianos' (machine guns) play like a symphony orchestra", Pesky says. "From what they said, his reflexes, coordination, and visual reaction made him a built-in part of the machine."[147]

Williams completed pre-flight training in Athens, Georgia, his primary training at NAS Bunker Hill, Indiana, and his advanced flight training at NAS Pensacola. He received his gold Naval Aviator wings and his commission as a second lieutenant in the U.S. Marine Corps on May 2, 1944.

Williams served as a flight instructor at NAS Pensacola teaching young pilots to fly the complicated F4U Corsair fighter plane. Williams was in Pearl Harbor awaiting orders to join the Fleet in the Western Pacific when the War in the Pacific ended. He finished the war in Hawaii, and then he was released from active duty on January 12, 1946, but he did remain in the Marine Corps Reserve.[77]

On May 1, 1952, 14 months after his promotion to captain in the Marine Corps Reserve, Williams was recalled to active duty for service in the Korean War.[148] He had not flown any aircraft for eight years but he turned down all offers to sit out the war in comfort as a member of a service baseball team. Nevertheless, Williams was resentful of being called up, which he admitted years later, particularly regarding the Navy's policy of calling up Inactive Reservists rather than members of the Active Reserve.

Williams reported for duty on May 2, 1952. After eight weeks of refresher flight training and qualification in the F9F Panther jet fighter with VMF-223 at the Marine Corps Air Station Cherry Point, North Carolina, Williams was assigned to VMF-311, Marine Aircraft Group 33 (MAG-33), based at the K-3 airfield in Pohang, South Korea.[77]

On February 16, 1953, Williams, flying as the wingman for John Glenn (later an astronaut, then U.S. Senator), was part of a 35-plane raid against a tank and infantry training school just south of Pyongyang, North Korea. As the aircraft from VMF-115 and VMF-311 dove on the target, Williams's plane was hit by anti-aircraft fire, a piece of flak knocked out his hydraulics and electrical systems, causing Williams to have to "limp" his plane back to K-3 air base where he made a belly landing. For his actions of this day, he was awarded the Air Medal.[149]

Williams flew 39 combat missions in Korea, earning the Air Medal with two Gold Stars representing second and third awards, before being withdrawn from flight status in June 1953 after a hospitalization for pneumonia. This resulted in the discovery of an inner ear infection that disqualified him from flight status.[150] John Glenn described Williams as one of the best pilots he knew,[146] while his wife Annie described him as the most profane man she ever met.[151] In the last half of his missions, Williams was flying as Glenn's wingman.[152]

Williams likely would have exceeded 600 career home runs if he had not served in the military, and might even have approached Babe Ruth's then record of 714. He might have set the record for career RBIs as well, exceeding Hank Aaron's total.[146] While the absences in the Marine Corps took almost five years out of his baseball career, he never publicly complained about the time devoted to service in the Marine Corps. His biographer, Leigh Montville, argued that Williams was not happy about being pressed into service in South Korea, but he did what he thought was his patriotic duty.

Following his return to the United States in August 1953, he resigned his Reserve commission to resume his baseball career.[148]

After retirement from play, Williams helped Boston's new left fielder, Carl Yastrzemski, in hitting, and was a regular visitor to the Red Sox' spring training camps from 1961 to 1966, where he worked as a special batting instructor. He served as executive assistant to Tom Yawkey (196165), then was named a team vice president (196568) upon his election to the Hall of Fame. He resumed his spring training instruction role with the club in 1978.

Beginning in 1961, he would spend summers at the Ted Williams Baseball Camp in Lakeville, Massachusetts, which he had established in 1958 with his friend Al Cassidy and two other business partners. For eight summers and parts of others after that, he would give hitting clinics and talk baseball at the camp.[5] It was not uncommon to find Williams fishing in the pond at the camp. The area now is owned by the town and a few of the buildings still stand. In the main lodge one can still see memorabilia from Williams's playing days.

Williams served as manager of the Washington Senators, from 19691971, then continued with the team when they became the Texas Rangers after the 1971 season. Williams's best season as a manager was 1969 when he led the expansion Senators to an 8676 record in the team's only winning season in Washington. He was chosen "Manager of the Year" after that season. Like many great players, Williams became impatient with ordinary athletes' abilities and attitudes, particularly those of pitchers, whom he admitted he never respected. Fellow manager Alvin Dark thought Williams "was a smart, fearless manager" who helped his hitters perform better. Williams's issue with Washington/Texas, according to Dark, was when the ownership traded away his third baseman and shortstop, making it difficult for the club to be as competitive.[153]

On the subject of pitchers, in Ted's autobiography written with John Underwood, Ted opines regarding Bob Lemon (a sinker-ball specialist) pitching for the Cleveland Indians around 1951: "I have to rate Lemon as one of the very best pitchers I ever faced. His ball was always moving, hard, sinking, fast-breaking. You could never really uhmmmph with Lemon."

Williams was much more successful in fishing. An avid and expert fly fisherman and deep-sea fisherman, he spent many summers after baseball fishing the Miramichi River, in Miramichi, New Brunswick. Williams was named to the International Game Fish Association Hall of Fame in 2000. Williams, Jim Brown, Cumberland Posey, and Cal Hubbard are the only athletes to be inducted into the Halls of Fame of more than one professional sport. Williams was also known as an accomplished hunter; he was fond of pigeon-shooting for sport in Fenway Park during his career, on one occasion drawing the ire of the Massachusetts Society for the Prevention of Cruelty to Animals.[154]

Williams reached an extensive deal with Sears, lending his name and talent toward marketing, developing, and endorsing a line of in-house sports equipmentsuch as the "Ted Williams" edition Gamefisher aluminum boat and 7.5hp "Ted Williams" edition motor, as well as fishing, hunting, and baseball equipment. Williams continued his involvement in the Jimmy Fund, later losing a brother to leukemia, and spending much of his spare time, effort, and money in support of the cancer organization.

In his later years Williams became a fixture at autograph shows and card shows after his son (by his third wife), John Henry Williams, took control of his career, becoming his de facto manager. The younger Williams provided structure to his father's business affairs, exposed forgeries that were flooding the memorabilia market, and rationed his father's public appearances and memorabilia signings to maximize their earnings.

One of Ted Williams's final, and most memorable, public appearances was at the 1999 All-Star Game in Boston. Able to walk only a short distance, Williams was brought to the pitcher's mound in a golf cart. He proudly waved his cap to the crowda gesture he had never done as a player. Fans responded with a standing ovation that lasted several minutes. At the pitcher's mound he was surrounded by players from both teams, including fellow Red Sox player Nomar Garciaparra, and was assisted by Tony Gwynn in throwing out the first pitch of that year's All-Star Game. Later in the year, he was among the members of the Major League Baseball All-Century Team introduced to the crowd at Turner Field in Atlanta prior to Game Two of the World Series.

On May 4, 1944, Williams married Doris Soule, the daughter of his hunting guide. Their daughter, Barbara Joyce ("Bobbi Jo"), was born on January 28, 1948, while Williams was fishing in Florida.[155] They divorced in 1954. Williams married the socialite model Lee Howard on September 10, 1961, and they were divorced in 1967.

Williams married Dolores Wettach, a former Miss Vermont and Vogue model, in 1968. Their son John-Henry was born on August 27, 1968, followed by daughter Claudia, on October 8, 1971. They were divorced in 1972.[156]

Williams lived with Louise Kaufman for twenty years until her death in 1993. In his book, Cramer called her the love of Williams's life.[157] After his death, her sons filed suit to recover her furniture from Williams's condominium as well as a half-interest in the condominium they claimed he gave her.[158]

Williams had a strong respect for General Douglas MacArthur, referring to him as his "idol".[159] For Williams's 40th birthday, MacArthur sent him an oil painting of himself with the inscription "To Ted Williamsnot only America's greatest baseball player, but a great American who served his country. Your friend, Douglas MacArthur. General U.S. Army."[160]

Politically, Williams was a Republican,[161] and was described by one biographer as, "to the right of Attila the Hun" except when it came to Civil Rights.[162] Another writer similarly noted that while in the 1960s he had a liberal attitude on civil rights, he was pretty far right on other cultural issues of the time, calling him ultraconservative in the tradition of Barry Goldwater and John Wayne.[161]

Williams campaigned for Richard Nixon in the 1960 United States Presidential Election, and after Nixon lost to John F. Kennedy, refused several invitations from President Kennedy to gather together in Cape Cod. He supported Nixon again in 1968, and as manager of the Senators, kept a picture of him on his desk, meeting with the President several times while managing the team. In 1972 he called Nixon, the greatest president of my lifetime.[161] In the following years, Williams endorsed several other candidates in Republican Party presidential primaries, including George H. W. Bush in 1988 (whom he also campaigned for in New Hampshire),[163] Bob Dole in 1996, and George W. Bush in 2000.[164]

According to friends, Williams was an atheist[165] and this influenced his decision to be cryogenically frozen. His daughter Claudia stated "It was like a religion, something we could have faith in... no different from holding the belief that you might be reunited with your loved ones in heaven".[166]

Williams's brother Danny and his son John-Henry both died of leukemia.[167]

In his last years, Williams suffered from cardiomyopathy. He had a pacemaker implanted in November 2000 and he underwent open-heart surgery in January 2001. After suffering a series of strokes and congestive heart failure, he died of cardiac arrest at the age of 83 on July 5, 2002, at Citrus Memorial Hospital, Inverness, Florida, near his home in Citrus Hills, Florida.[168]

Though his will stated his desire to be cremated and his ashes scattered in the Florida Keys, Williams's son John-Henry and younger daughter Claudia chose to have his remains frozen cryonically.

Ted's elder daughter, Bobby-Jo Ferrell, brought a suit to have her father's wishes recognized. John-Henry's lawyer then produced an informal "family pact" signed by Ted, Claudia, and John-Henry, in which they agreed "to be put into biostasis after we die" to "be able to be together in the future, even if it is only a chance."[169] Bobby-Jo and her attorney, Spike Fitzpatrick (former attorney of Ted Williams), contended that the family pact, which was scribbled on an ink-stained napkin, was forged by John-Henry and/or Claudia.[170] Fitzpatrick and Ferrell believed that the signature was not obtained legally.[171] Laboratory analysis proved that the signature was genuine.[171] John-Henry said that his father was a believer in science and was willing to try cryonics if it held the possibility of reuniting the family.[172]

Though the family pact upset some friends, family and fans, a public plea for financial support of the lawsuit by Ferrell produced little result.[172] Citing financial difficulties, Ferrell dropped her lawsuit on the condition that a $645,000 trust fund left by Williams would immediately pay the sum out equally to the three children.[172] Inquiries to cryonics organizations increased after the publicity from the case.[170]

In Ted Williams: The Biography of an American Hero, author Leigh Montville claims that the family cryonics pact was a practice Ted Williams autograph on a plain piece of paper, around which the agreement had later been hand written. The pact document was signed "Ted Williams", the same as his autographs, whereas he would always sign his legal documents "Theodore Williams", according to Montville. However, Claudia testified to the authenticity of the document in an affidavit.[173]

Williams body was subsequently decapitated for the neuropreservation option from Alcor.[174] Following John-Henry's unexpected illness and death from acute myeloid leukemia on March 6, 2004, John-Henry's body was also transported to Alcor, in fulfillment of the family agreement.[175]

In 1954, Williams was inducted by the San Diego Hall of Champions into the Breitbard Hall of Fame honoring San Diego's finest athletes both on and off the playing surface.[176]

Williams was inducted into the Baseball Hall of Fame on July 25, 1966.[177] In his induction speech, Williams included a statement calling for the recognition of the great Negro leagues players: "I've been a very lucky guy to have worn a baseball uniform, and I hope some day the names of Satchel Paige and Josh Gibson in some way can be added as a symbol of the great Negro players who are not here only because they weren't given a chance."[178] Williams was referring to two of the most famous names in the Negro leagues, who were not given the opportunity to play in the Major Leagues before Jackie Robinson broke the color barrier in 1947. Gibson died early in 1947 and thus never played in the majors; and Paige's brief major league stint came long past his prime as a player. This powerful and unprecedented statement from the Hall of Fame podium was "a first crack in the door that ultimately would open and include Paige and Gibson and other Negro league stars in the shrine."[178] Paige was the first inducted in 1971. Gibson and others followed, starting in 1972 and continued on and off into the 21st century.

On November 18, 1991, President George H. W. Bush presented Williams with the Presidential Medal of Freedom, the highest civilian award in the US.[179]

The Ted Williams Tunnel in Boston, Massachusetts, carrying 1.6 miles (2.6km) of the final 2.3 miles (3.7km) of Interstate 90 under Boston Harbor, opened in December 1995, and Ted Williams Parkway (California State Route 56) in San Diego County, California, opened in 1992, were named in his honor while he was still alive. In 2016, the major league San Diego Padres inducted Williams into their hall of fame for his contributions to baseball in San Diego.[180]

The Tampa Bay Rays home field, Tropicana Field, installed the Ted Williams Museum (formerly in Hernando, Florida, 19942006) behind the left field fence. From the Tampa Bay Rays website: "The Ted Williams Museum and Hitters Hall of Fame brings a special element to the Tropicana Field. Fans can view an array of different artifacts and pictures of the 'Greatest hitter that ever lived.' These memorable displays range from Ted Williams's days in the military through his professional playing career. This museum is dedicated to some of the greatest players to ever 'lace 'em up,' including Willie Mays, Joe DiMaggio, Mickey Mantle, Roger Maris."

In 2013, the Bob Feller Act of Valor Award honored Williams as one of 37 Baseball Hall of Fame members for his service in the United States Marine Corps during World War II.[181]

At the time of his retirement, Williams ranked third all-time in home runs (behind Babe Ruth and Jimmie Foxx), seventh in RBIs (after Ruth, Cap Anson, Lou Gehrig, Ty Cobb, Foxx, and Mel Ott), and seventh in batting average (behind Cobb, Rogers Hornsby, Shoeless Joe Jackson, Lefty O'Doul, Ed Delahanty and Tris Speaker). His career batting average of .3444 is the highest of any player who played his entire career in the live-ball era following 1920.

Most modern statistical analyses[which?] place Williams, along with Ruth and Barry Bonds, among the three most potent hitters to have played the game. Williams's baseball season of 1941 is often considered favorably with the greatest seasons of Ruth and Bonds in terms of various offensive statistical measures such as slugging, on-base and "offensive winning percentage." As a further indication, of the ten best seasons for OPS, short for On-Base Plus Slugging Percentage, a popular modern measure of offensive productivity, four each were achieved by Ruth and Bonds, and two by Williams.

In 1999, Williams was ranked as number eight on The Sporting News' list of the 100 Greatest Baseball Players, where he was the highest-ranking left fielder.[182]

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Ted Williams - Wikipedia

Recommendation and review posted by Bethany Smith

Some men develop depression,loss of sex drive, erectile dysfunction, and other physical and emotional symptomswhen they reach their late 40s to early 50s.

Other symptoms common in men this ageare:

These symptoms can interfere with everyday life and happiness, so it's important tofind the underlying cause and work out what can be done to resolve it.

The "male menopause" (sometimes called the andropause) is an unhelpful term sometimes used in the media.

This label ismisleading because it suggests the symptoms are the result of a suddendrop in testosterone in middle age, similar to what occurs in the female menopause. This is not true.

Although testosterone levels fall as men age, the decline is steady at about 1% a year from around the age of 30 to 40,and this is unlikely to cause any problems in itself.

A testosterone deficiency that develops later in life, also known as late-onset hypogonadism, can sometimesbe responsible for these symptoms, but in many cases the symptoms are nothing to do withhormones.

Lifestyle factors or psychological problems can also be responsible for many of these symptoms.

For example,erectile dysfunction,low sex driveandmood swingsmay bethe result of:

There are alsophysical causes of erectile dysfunction, such as smoking or heart problems, which may happen alongside any psychological cause.

Psychological problems are typically brought on by workor relationship issues,money problems or worrying about ageing parents.

A "midlife crisis" can also be responsible. Thiscan happen when men think they have reached life's halfway stage.

Anxieties over what they have accomplished so far, either in their job or personal life, can lead to a period of depression.

Other possible causes of the "male menopause" include:

In some cases, where lifestyle or psychological problems do not seem to be responsible, the symptoms of the "male menopause" may bethe result ofhypogonadism, wherethe testes produce few or no hormones.

Hypogonadism issometimes present from birth,which can cause symptoms like delayed puberty and small testes.

Hypogonadism can also occasionallydevelop later in life, particularly in men who are obese or have type 2 diabetes.

This is known aslate-onset hypogonadism and can cause the "male menopause" symptoms.

But this is an uncommon and specific medical condition that's not a normal part of ageing.

A diagnosis oflate-onset hypogonadism can usually be made based on your symptoms and the results of blood testsused tomeasure your testosterone levels.

If you're experiencing any of these symptoms, see your GP. They'll ask about your work and personal life to see if your symptoms may be caused by a mental health issue, such as stress or anxiety.

If stress or anxiety are affecting you, you may benefit from medication or a talking therapy, such as cognitive behavioural therapy (CBT).

Exercise and relaxation can also help.

Read about:

Your GP may also order ablood test to measure your testosterone levels.

If the results suggest you have a testosterone deficiency, you may be referred to an endocrinologist, a specialist in hormone problems.

If the specialist confirms this diagnosis,youmay be offered testosterone replacementto correct the hormone deficiency, which should relieve your symptoms.

This treatment may be given as an injection or a gel.

Page last reviewed: 13 October 2022Next review due: 13 October 2025

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The 'male menopause' - NHS

Recommendation and review posted by Bethany Smith