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Prestigious award advances OHSU research on impact of drug use over generations – OHSU News

Jamie Lo, M.D., M.C.R.,associate professor of obstetrics and gynecology (perinatology and maternal-fetal medicine), OHSU School of Medicine, and Division of Reproductive & Developmental Sciences, Oregon National Primate Research Center at OHSU. (OHSU/Christine Torres Hicks)

A physician-scientist at Oregon Health & Science University is one of just six researchers across the country to receive an Avenir Award in Genetics and Epigenetics of Substance Abuse from the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.

Jamie Lo, M.D., M.C.R., will use the award to develop and execute creative and transformative research to explore how parents behavior and environment affects their offspring before birth in some cases, even before conception.

The award is expected to provide $1.5 million over five years. NIDAs DP1 Avenir Awards support early-career investigators proposing new areas of research for the genetics or epigenetics of addiction.

Lo is an associate professor of obstetrics and gynecology (maternal-fetal medicine) in the OHSU School of Medicine and the Division of Reproductive and Developmental Sciences at the Oregon National Primate Research Center (ONPRC) at OHSU.

Being a scientist at ONPRC has allowed for leading-edge scientific pursuits across scientific and clinical disciplines with researchers at OHSU and at other institutions, and has allowed me to leverage the translational strength of nonhuman primate models that drive scientific discovery, she said. Im grateful and really looking forward to new discoveries we can achieve next.

In her clinical practice, Lo focuses on caring for people with high-risk pregnancies. She frequently encounters patients asking about the safety of cannabis use and other substances while theyre trying to conceive, while pregnant and during breastfeeding..

Most recently, Lo published two widely publicized studies suggesting that chronic use of cannabis may greatly affect male fertilityand reproductive outcomes, and female reproductive health, including increased menstrual cycle length. The male fertility study, in nonhuman primates, used edible cannabis similar to human dosages and found significant decreases in male reproductive hormones, including testosterone, and greater than 50% shrinkage of the testicles.

In earning the elite Avenir Award, Lo credits the support shes received from her clinical and academic departments, along with collaborations forged with other scientists at OHSU, including those in the departments of urology and biomedical engineering, and researchers at other top academic institutions.

Lo plans to use the new funding to delve into how the active ingredient in cannabis, THC, affects the expression of genes in the brains of offspring. The research will set out to determine how a fathers or mothers consumption of cannabis may affect their offspring both in early childhood and later in life or even their childrens offspring.

Were going to look at whether or not those changes that happen to the sperm, egg, fetus or infant are then inherited and how they impact offspring development, she said.

Generally, due to the lack of safety data and the preliminary findings of her work, she advises expectant parents to refrain from cannabis use while pregnant and for those who cannot quit to limit use.

Lo said she feels privileged to be part of ONPRCs team of scientists making discoveries that she can bring back to patients in the clinic.

We do know that cannabis use seems likely to impact reproductive health and fertility in both males and females, and that prenatal cannabis exposure can adversely affect the placenta and fetus, Lo said. But its very hard to study cannabis in humans, especially in pregnancy, because people are often using other substances, affected by their socioeconomic conditions, limited by the inaccuracies of self-reporting, and the quantity and dose of THC used is often difficult to determine.

Using a nonhuman primate model, scientists can control background variables, including diet and exercise, that would not be possible to achieve in people. The award number is 1DP1DA056493-01, through the National Institute on Drug Abuse of the NIH.

OHSU IACUC

All research involving animal subjects at OHSU must be reviewed and approved by the universitysInstitutional Animal Care and Use Committee(IACUC). The IACUCs priority is to ensure the health and safety of animal research subjects. The IACUC also reviews procedures to ensure the health and safety of the people who work with the animals. The IACUC conducts a rigorous review of all animal research proposals to ensure they demonstrate scientific value and justify the use of live animals.

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Prestigious award advances OHSU research on impact of drug use over generations - OHSU News

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Breast Cancer Awareness Month: The importance of getting to know your lemons – Bothell-Kenmore Reporter

While looking towards the excitement of candy and costumes this Halloween, October is also a time to pull out the pink for Breast Cancer Awareness Month. While women who are 40 years old have the option to begin an annual breast cancer screening with mammograms, familiarizing oneself with their lemonsregardless of agecan assist with early detection if breast cancer occurs.

Breast cancer is fairly common. About 1 in 8 women are going to be diagnosed with breast cancer at some point in their lives, said Marianne Vivien, a genetic counselor at Overlake Clinics & Medical Center.

According to Vivien about 5-10% of cancer cases are due to genetic mutations or hereditary conditions, while over 90% of cancer cases are random, sporadic, and are usually due to age, and environmental and lifestyle factors.

We all have cancer genes and their job is to protect us from cancer generally, but if someone is born with a mutation or inherits that mutation from a parent, all that really means is theres a change in the DNA, said Vivien.

The change in the DNA causes the gene to no longer function properly, and when this happens to a cancer gene, tumors develop more easily and at earlier ages. BRCA 1 and BRCA 2 are the most common breast cancer genes that are also associated with ovarian cancer, pancreatic cancer, melanoma and prostate cancer, said Vivien.

The general population risk for female breast cancer over a lifetime is 12%, according to Vivien, which increases to greater than 60% with BRCA mutations.

Male breast cancer is pretty rare in the general population. I believe its roughly a half a percent chance over a lifetime for someone who was born male to develop breast cancer, said Vivien, who said that risk increases to about 7% over a lifetime with BRCA mutations.

Vivien expressed that if an individual has any breast tissue, regardless of gender, its important to screen for breast cancer.

We definitely have that conversation with our patients who are Trans[gender], said Vivien. Depending on what surgeries they may or may not have had already, we would discuss essentially what screening or management would be recommended based on the particular gene that were concerned with and what other cancers are associated with that gene.

A breakdown of breast cancer rates on the Eastside

The Washington State Cancer Registry collects incidence data for numerous types of cancer across the state, including female breast cancer. Incidence rates are per 100,000 and the registry data for female breast cancer from 2014-2018 include:

Further data from the National Cancer Institutes state cancer profiles shows that the age-adjusted incidence rate cases per 100,000 for females in King County who are under 50 years old is 50.7; the average annual count is 372 cases and that the recent trends of rates for this demographic are rising.

The lens of a genetic counselor

Part of Viviens work as a genetic counselor includes talking to patients who have received a cancer diagnosis from their primary care physician, or those who received a referral to see if genetic testing would be beneficial.

Im starting to see a lot younger peoplewomen in their twentiescoming in and having that conservation, said Vivien. It doesnt necessarily mean were doing testing right now or were starting screening right now, but were having a conversation so that we can determine when testing or when screening should start and what that might look like for them.

In addition to seeing younger women, Vivien has also been seeing patients who want to know their risks because they were adopted and have no information on their family history.

During the counseling sessions, Viven conducts a thorough family history and medical history to decide if genetic testing is appropriate and to assist with developing a personalized management care plan moving forward. Red flags with genetics include individuals diagnosed at 50 years of age or younger and multiple generations having been affected by breast and other types of cancer, said Vivien.

Ideally, if were getting this information ahead of time, or even if somebody is already diagnosed with breast cancer, were able to make better decisions in terms of treatment, surgical decisions and then management moving forward, said Vivien.

Vivien mentioned how genetic testing and breast cancer screenings are generally covered by health insurance if an individual meets specific criteria. If the criteria is not met and health insurance wont cover, the majority of labs offer genetic testing for approximately $250, said Vivien. For those who are uninsured or underinsured, Vivien feels like breast cancer screenings can be moreso a barrier when compared to genetic testing.

Testing can only get you so far. If youre not going to follow through with the management then testing is a little bit pointless, said Vivien.

You can call them lemons, or you can call them limes

While Vivien believes that Breast Cancer Awareness Month shouldnt be merely one month, she said a good way to celebrate the month is by learning how to conduct a self breast exam.

Know Your Lemons, a nonprofit organization focused on improving early detection of breast cancer through education, provides signs and symptoms of breast cancer, which include:

While theres never a bad time to conduct a self breast exam, Know Your Lemons suggests conducting the exam after ones period, which is when the breast is the least tender and swollen.

A self breast exam can be conducted while standing, sitting or lying down. One should flatten their breast by stretching their arm behind their head. Then, the individual should feel the area (using any pattern such as circles, side to side, and up-down/all around) from their armpit to their collarbone, and then to the bottom of their ribs where lymph nodes live. According to Know Your Lemons, sometimes the areas where lymph nodes are located swell when cancer is present.

Milk lobes and lymph nodes are normal lumps in breasts that feel like soft peas or beans. To be more specific, the soft feeling peas are milk lobes while the soft feeling beans are lymph nodes. Cancerous lumps feel hard like a lemon seed, are usually immovable and can be any shape or size. On the other hand, those hard feeling lemon seeds could potentially be cysts.

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Identification of hub genes and candidate herbal treatment in obesity through integrated bioinformatic analysis and reverse network pharmacology |…

Identification of DEGs after weight loss

After standardizing gene sets (Fig.1), 1011 DEGs (|logFC|>1, p<0.05) were screened out from GSE103766, GSE35411, GSE112307, GSE43471, and GSE35710 based on the above method. The results included 513 downregulated and 498 upregulated genes, as shown in the volcano plot (Fig.2 and Supplementary Table S1). The abscissa in the volcano plot is log2 (fold change) value, and the ordinate is log10 (p-value).

Box-plots of the expression profiles after consolidation and standardization. The x-axis label represents the sample symbol and the y-axis label represents gene expression values. The black line in the box-plot represents the median value of gene expression. (a) Standardization of GSE43471, (b) Standardization of GSE35411, (c) Standardization of GSE103766, (d) Standardization of GSE35710, (e) Standardization of GSE112307.

Volcano plot to identify differentially expressed genes (DEGs). (a) GSE43471, (b) GSE35710, (c) GSE35411, (d) GSE103766, (e) GSE112307. The x-axis label represents fold changes and the y-axis label represents the p-values. Red dots represent the 498 upregulated genes and green dots represent the 513 downregulated genes.

As shown in Supplementary Fig. S1, the PPI network of DEGs, based on the Search Tool for the Retrieval of Interacting Genes (STRING) database, includes 584 nodes and 1417 edges. Using the MCODE plugin in Cytoscape software, the most significant modules (score=6.667) were recognized from the PPI network as comprising 27 hub genes, including ACP5, CETP, COL1A1, COL1A2, CSF1, DNMT3B, EED, HIST1H2AI, HIST1H2BB, HIST1H2BD, HIST1H4B, HIST1H4H, HIST2H3C, HP, LCN2, LIPC, LPA, MMP2, MMP7, MMP9, MSR1, MUC1, PLA2G7, SPP1, THBS1, THBS2, and VLDLR (Table 1 and Fig.3).

Subnetwork of 27 hub genes from the proteinprotein interaction (PPI) network. Node size and temperature color reflect the degree of connectivity (bigger node represents a higher degree and smaller node represents a lower degree; red node represents a higher degree and yellow node represents a lower degree).

An enrichment analysis bubble chart was drawn under GO level 2 classifications using Omicshare tools (Fig.4 and Supplementary Table S2). As shown in the figure, hub genes were significantly enriched in regulating plasma lipoprotein particle levels, lipid transport, extracellular matrix (ECM) organization, response to reactive oxygen species, and the oxygen-containing compound for biological process (BP). The hub genes were significantly enriched for cell composition (CC) in lipoprotein particles, extracellular regions, ECM, extracellular exosomes, and secretory granules. For molecular function (MF), the hub genes were significantly elevated in lipoprotein particle binding, glycosaminoglycan binding, ECM structural constituents, and peptidase activity.

Biological functions based on Gene Ontology (GO) analysis of obesity-related hub genes. Advanced bubble chart shows significance in GO enrichment items of hub genes in three functional groups: biological process (BP), cell composition (CC), and molecular function (MF). The x-axis label represents the gene ratio (Rich Factor) and the y-axis label represents GO terms.

KEGG pathway enrichment analysis showed that the hub genes were primarily enriched in ECMreceptor interaction, cholesterol metabolism, PI3K-Akt, IL-17, and TNF signaling pathways, endocrine resistance, and leukocyte transendothelial migration (Fig.5 and Supplementary Table S3).

Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of hub genes. The x-axis label represents the gene ratio (Rich factor) and the y-axis label represents the pathway.

We converted 27 gene names of the hub genes into protein names that could be recognized through the TCMSP database using the Universal Protein Resource (Uniprot). Moreover, the hub genes can be input in the required format to identify potential herbs with anti-obesity effects from the TCMSP database. After excluding the genes that were not present in the databases or those that had no related ingredients, nine were screened for further research, namely, COL1A1, MMP2, MMP9, SPP1, DNMT3B, MMP7, CETP, COL1A2, and MUC1. These genes corresponded to 16 ingredients [(-)-epigallocatechin-3-gallate (EGCG), arachidonic acid, arctiin, baicalein, beta-carotene, capillarisin, deoxypodophyllotoxin, ellagic acid, fisetin, irisolidone, luteolin, matrine, nobiletin, quercetin, rutaecarpine, tanshinone IIa] showing adequate OB and DL values (OB30%, DL0.18) (Supplementary Table S4).

There were 254 herbs with active ingredients in the databases. The top 10 herbs were Aloe, Portulacae Herba, Mori Follum, Silybum Marianum, Phyllanthi Fructus, Pollen Typhae, Ginkgo Semen, Leonuri Herba, Eriobotryae Folium, and Litseae Fructus. These were associated with more DEGs (related genes=6) and were, therefore, selected as crucial herbs in our study and annotated using Chinese pharmaceutical properties (CMPs), including characters, tastes, and meridian tropisms (Table 2).

We screened the key ingredients in treating obesity using an Ingredients-Targets network containing 25 nodes and 27 edges (Fig.6). The nine orange nodes represent the target genes and 16 green nodes represent the active ingredients. As most genes could be linked (degree=4), quercetin and EGCG were considered the most critical components in the treatment of obesity.

Ingredients-Targets network. Nine orange nodes represent the target genes, whereas the 16 green nodes represent the active compounds. The edges represent the interaction between the compounds and targets.

As shown in Fig.7a, the Herbs-Ingredients-Targets network containing 24 nodes and 43 edges was constructed to demonstrate the relationship between them: the 10 green nodes represent the key herbs and the six yellow nodes represent the active ingredients in them; the eight blue nodes depict the target genes. By analyzing the network, Phyllanthi Fructus and Portulacae Herba were associated with the most ingredients (degree=4). Moreover, quercetin was the most frequent active ingredient (degree=23) found in all herbs. Regarding gene targets, MMP2 was targeted by most ingredients (degree=5) followed by MMP9 (degree=4). Other genes were only acted upon by one component (degree=1).

Herbs-Ingredients-Targets network (a) and Herbs-Taste-Meridian tropism (b) network. (a) Yellow nodes represent the active ingredients and the blue nodes represent the target genes. (b) Yellow nodes represent tastes and purple nodes represent meridian tropisms. In all networks, the light green nodes represent cold-cool herbs, medium green nodes represent calm herbs, and dark green nodes represent warm herbs.

We also established the Herbs-Taste-Meridian tropism network containing 24 nodes and 40 edges to clarify the distribution of CMPs (Fig.7b). Five yellow nodes represent tastes and eight purple nodes represent meridian tropisms. To indicate different characters, we presented 10 nodes of herbs having different greens (light green, medium green, and dark green). Regarding characters, cold-cool herbs like Mori Follum were the most frequent (nodes=7), followed by herbs having calm (nodes=2) and warm (nodes=1) characters. In terms of taste, herbs were mostly bitter (edges=6), followed by sweet (edges=4), acid (edges=2), symplectic (edges=2), and astringent (edges=2). Regarding meridian tropism, most herbs belonged to the liver meridian (edges=6), followed by the stomach and lung (edges=4), large intestine (edges=2), bladder (edges=2), kidney (edges=2), pericardium (edges=2), spleen (edges=1), and gallbladder (edges=1) meridians.

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Behind this Nobel prize is a very human story: theres a bit of Neanderthal in all of us – The Guardian

The Neanderthals have won a Nobel prize. Well, almost. Even if most people havent heard of Svante Pbo, the Swedish geneticist whose work on ancient genomes and human evolution has landed him with 2022s award for physiology or medicine, or the exact science behind palaeogenomics and ancient DNA, they certainly have heard of Neanderthals.

Honouring his contribution to building this incredibly vibrant field of palaeogenomics, the award is much deserved: you need vision, persistence and pioneering methods to recover and sequence immensely old, fragile genetic material. But its also a recognition of the astonishing revelations about our deep history that have come from palaeogenomics, which holds many untapped secrets about who we are today, including settling the long-debated question of whether Neanderthals and Homo sapiens ever encountered each other and, lets say, warmed up those icy tundra nights (the answer is yes, many times).

For research communities, the prize also feels like a recognition of the relevance of work on palaeogenomics, human origin and archaeology more broadly and its continuing importance. Research in the 21st century on our hominin relations, including Neanderthals, is an entirely interdisciplinary, collaborative endeavour. All kinds of material analyses take place, in all sorts of ways. We use photogrammetry or lasers to record entire caves in 3D; trace how stone tools were moved across the land; examine microlayers within ancient hearths; even pick out the starches preserved in grot between ancient teeth. And the advent of the ability to retrieve palaeogenomics from extraordinarily old contexts was nothing short of revolutionary. Today, DNA can be extracted not only from bones, but even from cave sediments: the dust of long vanished lives, waiting for millennia to be found. It has made it possible to assess individual Neanderthals genetic profiles, and has opened windows into previously invisible population histories and interactions.

More than a decade on from the first big findings, today there is a huge community of palaeogenomics researchers, in large part thanks to Pbo, with many having trained with him. Among the younger generations at the front end of the sampling, processing and analytical work who may be the first to make and recognise key new discoveries many are women. They include Mateja Hajdinjak of the Crick Institute whose work has identified complex patterns of interbreeding among Neanderthals and the earliest Homo sapiens in Europe, and Samantha Brown from the University of Tbingen, whose meticulous work on unidentifiable bone scraps found the only known first-generation hybrid, a girl whose mother was Neanderthal and father Denisovan (closely related hominins from eastern Eurasia). Alongside wielding scientific clout, they are overturning outdated ideas that the hard sciences of statistics and white coats (or, in palaeogenomics, full-body protection) are male domains.

As an incredibly fast-moving field, palaeogenomics has achieved an enormous amount in a relatively short space of time. Innovative approaches are constantly being developed, and it must be admitted, even for those of us working in human origins, that keeping up with new methods and jargon can be challenging. The rapidity of advances, especially in competitive academic contexts, has also led to a number of ethical issues. While many are being tackled, the direction of some research may soon force the field to lay out official standards and draw ethical red lines when, for example, reconstructing the brains of Neanderthals using genetic engineering.

Ultimately, while decoding ancient hominin genomes has allowed us to identify which inherited genes we have today hence the physiology or medicine element of the Nobel prize the recognition of Pbos work seems more about much deeper themes, resonating with something of a Neanderthal zeitgeist. Since the discovery of their fossils more than 165 years ago, science has been engaged in dethroning Homo sapiens, demoting us from special creations to something still marvellous but not entirely unique.

Palaeogenomics bolstered this vision of an Earth that hosted many sorts of human, at least five of which were still walking around just 40,000 years ago; translate that figure to a generational scale, and youd see a chain of just 2,000 people linking hands. Ancient DNA has confirmed that we are both embedded within a rich history of hominin diversity, and that we still embody that history ourselves. Alongside the genetic material we acquired sideways through interbreeding with Neanderthals and other species, a recent study found that less than 10% of our genome is distinctive to Homo sapiens, evolved uniquely in us.

Most strikingly, popular understanding has shifted too. While some still drag out Neanderthal as a slur, it now seems somewhat abstracted from general public views. The archaeological evidence for Neanderthals complex, sophisticated minds, with genetic revelations of how close we really are to them, has transformed opinion on who they were, and what that means for us. The knowledge that the very stuff of Neanderthals is still present today in each human heart, thumping with fear or joy has forged a new emotional connection not just to them, but to all our other hominin relations. It also underlines the fact that they, and we, have always been part of a planetary web of life.

The most profound legacy of Pbos establishment of palaeogenomics is, or should be, humility. Because it turns out that many of the earliest Homo sapiens populations entering Eurasia eventually shared the same fate as the Neanderthals they met and mingled with. Their lineages vanished, culturally but also genetically, leaving behind no descendants among living humans. Perhaps the greatest inheritance they left us is understanding that our story is not one of predestined, exceptional success, but a blend of serendipity and coincidence; and that being the last hominin standing is not necessarily something to be proud of.

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Behind this Nobel prize is a very human story: theres a bit of Neanderthal in all of us - The Guardian

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Column One: Why this UCLA professor is studying female animals to gain insights into women’s health – Los Angeles Times

Zainabu was in good health in the days before she gave birth to her fourth baby, despite the fact that her blood pressure was likely somewhere around 280/220.

For a human, such a reading would be catastrophic. Spiking blood pressure in a pregnant or recently postpartum woman is a sign of preeclampsia, a common but potentially fatal condition that can affect the heart, lungs, liver and kidneys.

Zainabu, fortunately, is a Masai giraffe at the Los Angeles Zoo. Giraffes have the highest known blood pressure in the animal kingdom, but this has no apparent effect on fetal or maternal health.

Zainabu, a Masai giraffe, with her fourth baby at the Los Angeles Zoo.

(Los Angeles Zoo)

For Dr. Barbara Natterson-Horowitz, a UCLA cardiologist with a long-standing interest in cross-species health, this raises some compelling questions.

What adaptations have evolved in female giraffes that protect their cardiovascular systems from the damage high blood pressure can cause?

And why dont we know enough about the physiology of human females to prevent a common complication like preeclampsia?

Natterson-Horowitzs side gig treating animals at the L.A. Zoo has led her to explore health connections across species. She and collaborator Kathryn Bowers wrote the 2012 bestseller Zoobiquity about the intersection of human medicine, veterinary medicine and evolutionary biology, followed by 2019s Wildhood, which examined adolescence across the animal kingdom.

Her latest focus is on cross-species similarities in female health, a field that has long been underfunded, understudied and misunderstood. Diseases that primarily affect women get a disproportionately small amount of research money relative to the years of healthy life they steal. (The reverse is true for diseases that primarily affect men.) In addition, women have historically been a minority of clinical trial participants, and for several years those of childbearing age were barred as research subjects in the U.S., a policy the National Institutes of Health reversed in 1986.

We cant go back in time, Natterson-Horowitz says. But we can fill some of the gaps by looking to the animal world.

Many of the species that share our planet are exposed to similar stressors and environmental contaminants. Some endure the same chronic diseases that humans do, while others appear to be naturally resistant. Solutions to some of medicines most vexing questions could be walking on four feet beside us.

Theres a pretty vast landscape of unexamined assumptions about human uniqueness, Natterson-Horowitz said. Failing to recognize our place in the animal kingdom, she added, can prevent us from recognizing connections that, were we to see and understand them, could allow us to better understand the cause of disease and to be better at innovating effective solutions.

Natterson-Horowitz grew up in Los Angeles as the daughter of two psychotherapists. She made occasional trips to the zoo as a child, with no inkling that some of the animals she was looking at would later become her patients.

She studied evolutionary biology at Harvard under famed biologists E.O. Wilson and Stephen Jay Gould. She returned to California for medical school at UC San Francisco and a residency and fellowship at UCLA.

Shed been on the faculty at UCLA for a decade when, in 2005, she got a call from the zoo asking for assistance with a transesophageal echocardiogram, a type of ultrasound exam she specialized in. This one would be for a chimpanzee, her first nonhuman patient.

It was a procedure shed performed countless times before. But probing the internal biology of a fellow primate, albeit one that wasnt human, was like that gleam of light you see when you crack open a door, she recalled: In this case, the door happened to be separating my world of modern human medicine and the natural worlds endless health insights.

Physicians tend to be human-centric in their approach. But veterinarians investigating perplexing problems often look to the medical histories of other species including Homo sapiens.

Natterson-Horowitz feeds a giraffe at the Los Angeles Zoo. Giraffes have the highest known blood pressure in the animal kingdom, but this has no apparent effect on fetal or maternal health.

(Robert Gauthier / Los Angeles Times)

Weve always done that, because we know that theres a lot more research that goes on in many of these diseases in humans, said Jane Sykes, a professor of small animal internal medicine at the UC Davis School of Veterinary Medicine. Were always looking for parallels. ... Is there anything in humans that can help this dog in front of us?

Now Natterson-Horowitz wanted to do the same thing, just in the other direction. The more she consulted with the L.A. Zoo, the more she came to admire that inclusive approach and to question its absence in human medicine.

Anthropocentrism is a blindfold, she said of humans fixation on our own species. If we can move beyond that, we could see connections that are meaningful and powerful.

One of the first patients to spark her interest in female health was a lioness with pericardial effusion, or fluid in the sac around her heart. The condition affects at least 20% of cancer patients, both feline and human, and breast cancer is common in lions. Those two facts made veterinarians worry the lioness had an advanced case of the disease.

Natterson-Horowitz started researching. She knew that breast cancers in some women were connected to BRCA1, a gene on the 17th chromosome. People born with certain versions of the gene are more likely to develop breast cancer when exposed to an environmental or hormonal trigger.

Natterson-Horowitz visits the flamingo enclosure at the zoo. Theres a pretty vast landscape of unexamined assumptions about human uniqueness, she said.

(Robert Gauthier / Los Angeles Times)

What she had not realized was how many non-primate species shared this vulnerability. English springer spaniels with certain BRCA1 variants were four times more likely to develop breast cancer than dogs with the most common version of the gene, Natterson-Horowitz noted in Zoobiquity. Another study found that zoo jaguars taking a particular type of hormonal birth control developed breast cancer in rates similar to human women with high-risk BRCA1 variants, and that the cancer was common in lions and other big cats.

Many factors influence breast cancer rates in females across the animal kingdom: age, genetics, the frequency and duration of lactation, environmental factors and hormonal changes.

Column One

A showcase for compelling storytelling from the Los Angeles Times.

Taken together, the range of mammals vulnerable to breast cancers could offer a trove of valuable comparative data, Natterson-Horowitz realized. But virtually no one was looking for it even for a disease that claims the lives of more than 42,000 women in the U.S. alone each year.

So she started researching these evolutionary links herself. As she dug in, she said she noticed something else: Not only is human medicine anthropocentric, its androcentric that is, focused on cisgender men.

Until the 1993 passage of the NIH Revitalization Act, women and people of color were not required to be part of research studies or clinical trials funded by the NIH, and as a result they usually werent. The same preference for males is even seen in research on mice. In 2016, NIH set a new policy requiring researchers to at least consider biological sex as a variable in the design of human cell and animal studies, though they can study one only sex if they can show strong justification for it.

The good news is that today, over half of the participants in NIH clinical trials are women, said Dr. Janine Austin Clayton, director of the NIH Office of Research on Womens Health. But, she noted, women are still underrepresented in studies of several major diseases, including cardiovascular disease, kidney disease, hepatitis and HIV/AIDS.

Until we have representation across every disease category that affects women and men, she said, we still have work to do.

A male-centered research approach manifests in many ways. It isnt just the dearth of funding for conditions primarily affecting women, like endometriosis and rheumatoid arthritis. Its that data on female bodies are often absent from medical research altogether, resulting in skewed results that can shortchange all genders.

The result is that researchers often havent even realized when their results apply only to men.

Take heart attacks. When the Physicians Health Study, whose sample consisted of 22,071 men and zero women, found in 1989 that a low regular dose of aspirin led to a 44% decrease in heart attacks, many physicians recommended the treatment to men and women alike.

But the 39,876 participants in the Womens Health Study allowed researchers to report in 2005 that for women younger than 65, aspirin didnt help at all. And for those 65 and older, aspirin prevented not only heart attacks but strokes a benefit that was not apparent in the all-male study and would have remained unseen without studying women.

Excluding women from research studies forces doctors to treat them as guinea pigs, generation after generation after generation, said Chloe Bird, a sociologist who heads the Center for Health Equity Research at Tufts Medical Center in Boston.

For the record:

1:22 p.m. Oct. 14, 2022An earlier version of this article reported that the Center for Health Equity Research was at Tufts University. It is based at Tufts Medical Center, which is not part of the university.

Bird has not been involved in Natterson-Horowitzs efforts to take a broader look at the female population of the animal kingdom, which she called fantastic, and so needed.

There is a tremendous opportunity to look across species, and begin to understand ... what happens with what systems and why, and how we could improve healthcare, Bird said.

Natterson-Horowitz is now leading a team of obstetrician/gynecologists, wildlife veterinarians and veterinary pathologists to study giraffe pregnancy to understand why animals like Zainabu who delivered a healthy, 172-pound calf in April are not vulnerable to the cardiovascular crises that strike pregnant humans. Shes also working with dairy veterinarians to better understand mastitis, a common but painful inflammation of breast tissue, to come up with improved treatments and design a better breast pump for women.

But Natterson-Horowitz knows unlocking the secrets of the animal world is not a one-person job. Since 2011 she has organized Zoobiquity conferences that have brought together thousands of physicians, veterinarians and evolutionary biologists to examine health issues from multispecies perspectives. The most recent, titled Female Health Across the Tree of Life, took place in July in Lisbon, Portugal.

She also teaches the relevance of the animal world to undergraduates and medical students at UCLA and Harvard, and is heartened to see the eagerness of a new generation of physicians to look across species for answers.

Climate change and urbanization have blurred the boundaries between the human and nonhuman animal worlds, Natterson-Horowitz pointed out. Zoonotic diseases like COVID-19 and influenza have shown us how closely were tied to fellow members of the animal kingdom.

When she first got into medicine, she pledged to do no harm. Today, she believes, If we can move from an androcentric, anthropocentric view to a sex-, gender-, and species-spanning perspective, then we can do good.

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Column One: Why this UCLA professor is studying female animals to gain insights into women's health - Los Angeles Times

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Books wrap: Simone Kaho on her new poetry collection and PTSD; a conversation with Richard Wolfe; and more – New Zealand Herald

Simone Kaho.

Tulia Thompson talks to Simone Kaho about writing, surviving PTSD and the silencing of survivors

When you study poetry at university you are told you can write a poem about anything as long as it is well-crafted, but then you also learn that poetry in Aotearoa actually means restrained, lyric poems about nature. There's an invisible forcefield around what "counts" as a good poem.

Poets like Hera Lindsay Bird and Chris Tse push past the forcefield. Tongan-Pkeh writer Simone Kaho's stunning collection of poetry, Heal!, about being attacked, fighting back and experiencing PTSD, is a vital challenge to the poetry canon.

Kaho is a documentary-maker who works as a reporter/director for Tagata Pasifika. In Heal! the sexual assault acts as a refracting prism for her interactions with men, who are revealed to be rape-complicit by expressing "common-sense" views that support rape. There's the British guy she swims naked with who says, "Perhaps it's because you are so beautiful." When she is stalked, there is a drunk boss: "You're a sexy beast / he said / you / should / expect / stalkers."

When she posts a poem about the stalker, a male in the poetry community says, "What if he'd committed suicide?" It is the ordinary, banal comments from men that convey to women that they see us as sexually available, able to be objectified, and given less empathy. It's a profoundly uncomfortable read, in part because these views are so familiar.

It reminds me a lot of Claudia Rankine's award-winning Citizen: An American Lyric, about white privilege, in which short prose poems about things white people said to her create a sustained, multilayered impression of racism. In both poetry collections, the repeated incidents reveal their force.

While not being strictly narrative, Heal! maintains narrative tension, and a sense of movement. Assault has given Kaho a different lens on past events. In one poem, set during her childhood, she remembers her Tongan dad taking a machete to the bus stop, trying to find a man who sexually assaulted her.

She writes, "The machete is evidence of love and she enjoys the moment quietly." Kaho asked me when we met if anything surprised me about the collection. I said, "No, nothing really surprised me." But it was a lie. What actually surprised me was that another girl had felt about her dad's machete the way I felt about my dad's machete that it was an ordinary, protective and appropriate weapon.

Tulia Thompson: It's a very brave book. What made you decide to tell this story?

Simone Kaho: Can I just ask you why you think it's brave?

TT: I think it's brave because it's explicitly talking about rape and PTSD. Within New Zealand poetry, it feels like you're discouraged from writing about experiences like this, not necessarily explicitly, but just through the atmosphere.

SK: Yeah, I haven't heard anybody say to me, "You shouldn't write about that." But it feels like there's just a vibe about it. Like it's sharp or the wrong colour or too pungent or visceral or too political. This is not something that fits in.

But I didn't think about that writing this. I'd done the South Seas Film and Television course in 2017, when a lot of my PTSD symptoms were really becoming noticeable. I was really struggling.

I tried to make an action film about a female vigilante. And there was pushback. Pushback can be quite subtle. I was discouraged from making a film about a female protagonist responding violently to male violence. When I was pitching it to industry professionals in front of the whole school, it was questioned whether it was morally right, what the protagonist wanted to do. The horror film pitched straight after me featured a guy eating his mother's face, and got the feedback, "That was a delicious moment!"

So the pushback I got led to an understanding that I was being hushed. And at some point, I just really was like "Nah, f*** this s***." I need to use the most powerful way I have to express myself, which is poetry.

TT: If you're a woman, you are used to men making excuses for male violence. It's just so pervasive.

SK: It's co-opted into politeness. Boys will be boys. That's a blind spot that we all have to agree on. If you respond aggressively or even just assertively to predatory male behaviour, you're being rude. You're the problem. That is definitely something I felt all the time. I was enraged all the time. It was so tiring. And because I'd been in that moment, physically fighting a man during the assault, when I knew there was nothing between us that could protect me, all of those "boys will be boys" behaviours happening afterwards triggered the same sort of horror I'd felt in that moment. Like the only difference between them and the attacker was that he'd made a decision to commit and deal with the consequences.

TT: There's a rigour to your poetry. Is that because of your time at the International Institute of Modern Letters?

SK: I became the poet I am at the IIML, because you're absorbed in it. I had Hinemoana Baker as my supervisor. She said, "Do you care about line breaks? I want you to have no punctuation." And this guttural voice appeared. It's not blaming, even, it's just like brutal truth.

TT: There are men in the book who say sorry that happened, but they don't change their own misogyny. It seems very difficult to create change without men taking more responsibility for talking about sexual violence. What do you think needs to happen?

SK: My concern is with people who've been through sexual violence. My first concern is around our ability to talk about it it's not a crime that we have done. I don't mean with no regard for context or incessantly but in the same way that if somebody robbed your house and beat you up [you'd talk about it]. It's been really hard, working and going back to life, and trying to find a safe place. It's a lot to navigate. I really want to smash the hushing and shaming that makes survivors of sexual violence have to be brave just to talk about it.

Heal! by Simone Kaho (Saufo'i Press, $30) is out now.

Aroha, by Dr Hinemoana Elder, was Aotearoa's biggest-selling non-fiction title of last year. The acclaimed psychiatrist is following up with Wawata: Moon Dreaming (Penguin, $30), a book of wisdom centred around the cycle of the moon which offers 30 lessons based on the 30 faces of Hina, the Maori moon goddess.

Black Ferns star Ruby Tui's new biography, Straight Up (Allen & Unwin, $37), lays it all out there. Her tough childhood, her drive to overcome personal tragedy, her love of rugby and her incredible rise to international fame.

The fifth short story collection from a master of the form, George Saunders, Liberation Day (Bloomsbury, $33) is out on Tuesday. Saunders won the Man Booker Prize for his only novel, Lincoln in the Bardo, in 2017 but is best known for his short stories and essays.

1. You deliver an ecological message in the guise of a coffee table book. Is the artwork a lure?

It was too good an opportunity to miss. Collectively our early painters and photographers produced a rich and unique record of a relatively pristine New Zealand, at the time when settlement from Europe was just beginning. For example, the book includes two paintings, from 1839 and 1840, by Charles Heaphy of the kauri forests on the Wairoa River, Kaipara.

Such images were used as propaganda by the New Zealand Company, to encourage immigration, with the result that vast areas of kauri were felled and destroyed in the process to provide timber for the new settlers' homes. Then there's Alfred Sharpe's 1876 subtly elevated panorama of the Waikato plains, which provides a stark contrast with a photograph of a similar view 140 years later, of the Taupiri interchange on the Waikato Expressway.

2. If a reader takes away one nugget from this book, what do you hope it will be?

My aim in compiling the book was to record the various changes that a thousand or so years of human settlement have inflicted on the New Zealand landscape. With those in mind, I hope it will encourage us to question where we go from here. As we become increasingly aware of the effects of climate change, we must wonder how, and to what extent, we can keep on modifying our natural environment. This is, of course, not just a New Zealand problem. It's worldwide, and at its heart is the ability of the Earth's resources to sustain a growing population in the manner to which it has grown accustomed. As for New Zealanders, this poses such challenges as the degree to which our towns and cities can continue to sprawl, destroying remaining areas of bush and gobbling up good agricultural land.

3. Do you have a favourite image in the book?

There are many "landmark" images, such as the well-known and starkly symbolic Frozen Flames, painted in 1931 by Christopher Perkins, which depicts the aftermath of a bush burn-off. Another of my favourites is Kennett Watkins' 1885 painting, The Haunt of the Moa: A Scene in a Puriri Forest, also in the collection of the Auckland Art Gallery Toi o Tmaki. Deep withIn a dark forest of nkaupalms and gnarled puriri trunks, a hapless moa emerges from behind a tree and is about to reveal itself to a pair of Mori stalkers. The big bird appears to be at the crossroads, for if the hunt is successful it might mark the extinction of the species.

4. You are that rare thing in New Zealand, a full-time writer. How do you make that work?

I had never planned to be a full-time writer. Back in 1997, along with two dozen other staff members, I was made redundant (as Curator of Display) at the Auckland War Memorial Museum. That unexpected change of direction gave me the opportunity to spend more time on what had previously been just an after-hours activity. A quarter of a century and some 40 books later, I'm still at it. I enjoy coming up with ideas for books, and am grateful to publishers who have given me opportunities to realise them. I also enjoy the challenge of dreaming up and researching articles for our leading art quarterly, Art New Zealand.

5. What book have you read this year that you are recommending to others?

I have recently read and enjoyed A Brief History of Everyone Who Ever Lived: The Stories in Our Genes, by English science writer and genetics expert Adam Rutherford (no relation to Sir Ernest). He divulges the startling fact that anyone of European extraction is descended from Charlemagne, the first emperor of the Holy Roman Empire, who lived from 747 to 814AD. The point is that the further we go back up our family trees, the more interconnected and related all of us are. Perhaps if humanity at large was more aware of this fact, the world would be a much happier place.

Footprints on the Land, by Richard Wolfe (Oratia Books, $45), is out now.

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Books wrap: Simone Kaho on her new poetry collection and PTSD; a conversation with Richard Wolfe; and more - New Zealand Herald

Recommendation and review posted by Bethany Smith

Masculinizing hormone therapy – Mayo Clinic

Overview

Masculinizing hormone therapy is used to induce the physical changes in your body caused by male hormones during puberty (secondary sex characteristics) to promote the matching of your gender identity and body (gender congruence). If masculinizing hormone therapy is started before the changes of female puberty begins, female secondary sex characteristics, such as the development of breasts, can be avoided. Masculinizing hormone therapy is also known as gender-affirming hormone therapy.

During masculinizing hormone therapy, you'll be given the male hormone testosterone, which suppresses your menstrual cycles and decreases the production of estrogen from your ovaries. Changes caused by these medications can be temporary or permanent. Masculinizing hormone therapy can be done alone or in combination with masculinizing surgery.

Masculinizing hormone therapy isn't for all transgender men, however. Masculinizing hormone therapy can affect your fertility and sexual function and cause other health problems. Your doctor can help you weigh the risks and benefits.

Masculinizing hormone therapy is used to alter your hormone levels to match your gender identity.

Typically, people who seek masculinizing hormone therapy experience discomfort or distress because their gender identity differs from their sex assigned at birth or from their sex-related physical characteristics (gender dysphoria). To avoid excess risk, the goal is to maintain hormone levels in the reference range for the target gender.

Masculinizing hormone therapy can:

Research suggests that masculinizing hormone therapy can be safe and effective.

If used in an adolescent, hormone therapy typically begins at age 16. Ideally, treatment starts before the development of secondary sex characteristics so that teens can go through puberty astheir identified gender. Gender affirming hormone therapy is not typically used in children.

Masculinizing hormone therapy isn't for everyone, however. Your doctor might discourage masculinizing hormone therapy if you:

Talk to your doctor about the changes in your body and any concerns you might have. Complications of masculinizing hormone therapy include:

Evidence suggests that transgender men have no increased risk of breast cancer or cardiovascular disease when compared to women whose gender identity and expression matches the stereotypical societal characteristics related to their sex assigned at birth (cisgender women).

Conclusions cant be drawn about whether masculinizing hormone therapy increases the risk of ovarian and uterine cancer. Further research is needed.

Because masculinizing hormone therapy might reduce your fertility, you'll need to make decisions about your fertility before starting treatment. The risk of permanent infertility increases with long-term use of hormones, especially when hormone therapy is initiated before puberty. Even after stopping hormone therapy, ovarian and uterine function might not recover well enough to ensure that you can become pregnant without reproductive technology assistance.

If you want to have biological children, talk to your doctor about egg freezing (mature oocyte cryopreservation) or embryo freezing (embryo cryopreservation). Another option involves having ovarian tissue surgically removed, frozen and later thawed and reimplanted (ovarian tissue cryopreservation). Keep in mind that egg freezing has multiple steps ovulation induction, egg retrieval and freezing. If you want to freeze embryos, you'll need to go through the additional step of having your eggs fertilized before they are frozen.

At the same time, while testosterone might limit your fertility, you're still at risk of pregnancy if you have your uterus and ovaries. If you want to avoid becoming pregnant, use an intrauterine device, a barrier form of contraception or a continuous progestin form of birth control.

Before starting masculinizing hormone therapy, your doctor will evaluate your health to rule out or address any medical conditions that might affect or contraindicate treatment. The evaluation might include:

You might also need a behavioral health evaluation by a provider with expertise in transgender health. The evaluation might assess:

Adolescents younger than age 18, accompanied by their custodial parents or guardians, also should see doctors and behavioral health providers with expertise in pediatric transgender health to discuss the risks of hormone therapy, as well as the impact and possible complications of gender transition in that age group.

You'll begin masculinizing hormone therapy by taking testosterone. Typically, your doctor will prescribe a low dose and slowly increase the dosage over a period of months. Testosterone is given either by injection or a gel applied to the skin. Other testosterone preparations can be used, such as a patch or pellets placed under the skin. In the U.S., testosterone also can be given as a long lasting injection or as twice daily pills (testosterone undecanoate). Oral methyltestosterone or synthetic male sex hormone (androgen) medication shouldn't be used because of potential harmful effects on your liver and lipids.

If you have persistent menstrual flow, your doctor might recommend taking progesterone to control it.

Masculinizing hormone therapy will begin producing changes in your body within weeks to months. Your timeline might look as follows:

While on masculinizing hormone therapy, you'll meet regularly with your doctor. He or she will:

You will also need routine preventive care if you havent had certain surgical interventions, including:

The rest is here:
Masculinizing hormone therapy - Mayo Clinic

Recommendation and review posted by Bethany Smith

Human Growth Hormone (hGH) – Cleveland Clinic

What is human growth hormone (hGH)?

Human growth hormone, also known as hGH and somatotropin, is a natural hormone your pituitary gland makes and releases that acts on many parts of the body to promote growth in children. Once the growth plates in your bones (epiphyses) have fused, hGH no longer increases height, but your body still needs hGH. After youve finished growing, hGH helps to maintain normal body structure and metabolism, including helping to keep your blood sugar (glucose) levels within a healthy range.

Hormones are chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, muscles and other tissues. These signals tell your body what to do and when to do it. Your body makes over 50 hormones, and many of them interact with each other, creating a complex web of processes.

Your pituitary gland is a small, pea-sized endocrine gland located at the base of your brain below your hypothalamus. Its made of two lobes: the anterior (front) lobe and posterior (back) lobe. Your anterior lobe makes hGH.

Your pituitary gland is connected to your hypothalamus through a stalk of blood vessels and nerves. This is called the pituitary stalk. Your hypothalamus is the part of your brain that controls functions like blood pressure, heart rate, body temperature and digestion. Through the stalk, your hypothalamus communicates with your pituitary gland and tells it to release certain hormones. In this case, your hypothalamus releases growth hormone-releasing hormone (GHRH), which stimulates your pituitary gland to release hGH, and somatostatin, which prevents (inhibits) that release.

Healthcare providers use a synthetic form of hGH (sometimes called recombinant hGH) to treat certain health conditions, including growth hormone deficiency. You should never take synthetic hGH without a prescription from your provider.

Your pituitary gland normally releases hGH in short bursts (pulses) throughout the day. The release of hGH is mainly controlled by two hormones your hypothalamus releases: growth hormone-releasing hormone (GHRH), which stimulates hGH release, and somatostatin, which prevents (inhibits) hGH release.

Several other endocrine hormones also regulate hGH, including insulin-like growth factor 1 (IGF-1). IGF-1 is a major suppressor of GH production, whereas thyroxine, glucocorticoids and ghrelin stimulate hGH release.

IGF-1 thats released by your liver is one of the best-characterized effects of hGH activity. IGF-1 plays a critical role in preventing (inhibiting) the release of the hGH through a negative feedback loop by stimulating somatostatin and inhibiting GHRH release. However, hGH and IGF-1 secretion are regulated by each other, where hGH triggers IGF-1 release and the IGF-1 inhibits hGH release in a feedback loop. In healthy people, hGH release is inhibited by hyperglycemia (high blood sugar) and stimulated by sleep, stress, exercise, hypoglycemia (low blood sugar) and amino acids.

Human growth hormone has two main functions: stimulating growth (mainly in children) and impacting metabolism (how your body turns the food you eat into energy).

Human growth hormone triggers growth in nearly every tissue and organ in your body. However, its most well-known for its growth-promoting effect on cartilage and bone, especially in the adolescent years during puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts receive signals from hGH to increase replication and thus allow for growth in size.

Once the growth plates in a childs bones have fused, hGH no longer increases height. Instead, hGH helps to maintain normal body structure throughout the rest of your life.

Metabolism consists of the chemical reactions in your body that change the food you eat into energy. All of the cells in your body need energy to function properly. Several different complex processes are involved in metabolism.

hGH impacts metabolism primarily by increasing the production of insulin-like growth factor-1 (IGF-1) and its effect on cells in your body. IGF-1 is a hormone similar in structure to insulin that manages the effects of hGH in your body. Insulin is an essential hormone your pancreas makes that helps regulate your blood sugar (glucose) levels by decreasing them. Like insulin, IGF-1 has glucose-lowering effects.

Your body normally carefully regulates your blood glucose levels. Blood glucose, or sugar, is the main sugar found in your blood. You get glucose from carbohydrates in the food you eat. This sugar is an important source of energy and provides nutrients to your body's organs, muscles and nervous system.

Insulin is the main hormone your pancreas makes to lower blood glucose levels when they get too high, and glucagon is the main hormone your pancreas makes to raise glucose levels when they get too low. Other hormones can counteract the effects of insulin, such as epinephrine (adrenaline) and cortisol.

While hGH normally increases blood glucose levels when they get too low, if you have excess amounts of hGH in your body, it can counteract the effects of insulin, causing elevated blood glucose levels.

Human growth hormone increases vertical growth in children. However, once your growth plates have fused, hGH cannot make you taller. Instead, after youve reached your final height, hGH helps maintain your bodys structure and has other important effects on your metabolism.

Your pituitary gland releases hGH in pulses. The size and duration of the pulses vary with time of day and your age and sex. Because of this, random hGH measurements are rarely useful to healthcare providers in confirming or ruling out a diagnosis. Instead, hGH measurement tests are most useful when measured as part of a stimulation or suppression test.

In general, the normal range for hGh levels include:

Normal value ranges may vary from lab to lab. Be sure to reference your labs normal range on your lab report when analyzing your results. If you have any questions about your results, talk to your healthcare provider.

Having lower-than-normal levels of hGH is called growth hormone deficiency. Its usually due to an issue with or damage to your pituitary gland that results in hypopituitarism when one, several or all of the hormones your pituitary gland makes are deficient. Human growth hormone could be one of the affected hormones.

Growth hormone deficiency affects adults and children differently.

When adults have a lack of hGH, it causes the following issues:

In adults, hypopituitarism that results in hGH deficiency may develop due to a benign pituitary adenoma (a noncancerous tumor) or damage to your pituitary gland or hypothalamus.

A lack of hGH in children results in poor growth. The main sign of hGH deficiency in children is slow height growth each year after a child's third birthday. This means they grow less than about 1.4 inches in height a year. A child with hGH deficiency may also have:

In children, hypopituitarism that results in hGH deficiency may be present from birth where the cause can be unknown (idiopathic), genetic or due to injury to their pituitary gland (during fetal development or at birth).

Children can also develop hypopituitarism due to damage to their pituitary gland or hypothalamus later in life.

The main condition associated with higher-than-normal hGH levels is a condition called acromegaly, though it affects adults and children differently. Its a rare condition.

Adults with acromegaly usually have enlarged or swollen hands and feet and altered facial features.

Adults with acromegaly can also have thickened bones and enlarged organs and are more likely to have conditions such as high blood pressure (hypertension), Type 2 diabetes and heart disease. Over 99% of acromegaly cases are due to pituitary adenomas, noncancerous (benign) tumors on your pituitary gland. These tumors can produce excess amounts of hGH. Acromegaly is more common after middle-age when growth is complete. Because of this, adults with acromegaly dont get any taller. Instead, their bones can become thicker.

Very rarely, children can experience elevated growth hormone levels before they reach their final height, which can lead to excessive growth of long bones and very tall height. This condition is called pediatric acromegaly, but its sometimes called gigantism. If left untreated, children with acromegaly usually grow to be seven feet tall or taller. Children with acromegaly may also have general weakness, delayed puberty and headaches.

Pituitary adenomas are usually the cause of pediatric acromegaly.

Your healthcare provider can order a series of blood tests to check your hGH levels if youre experiencing symptoms related to hGH issues.

Your pituitary gland normally releases hGH into your bloodstream in pulses throughout the day and night, with peaks that occur mostly during the night. Because of this, a single blood test to measure hGH measurement is difficult to interpret and is not usually medically useful.

Providers most often use procedures called growth hormone stimulation and suppression tests to diagnose conditions caused by hGH deficiency or excess.

They may also order a blood test that measures the amount of insulin-like growth factor 1 (IGF-1) in your blood.

The U.S. Food and Drug Administration (FDA) has approved the synthetic form of hGH for treatment for certain conditions. The synthetic form of hGH is available only by prescription and is injected.

In children, healthcare providers prescribe hGH to treat:

In adults, providers prescribe hGH to treat:

Its important to only take synthetic hGH if your provider has prescribed it for you.

The use of synthetic hGH for medical treatment can cause certain side effects including:

Researchers dont have enough information about the long-term effects of hGH treatment.

If you or your child are experiencing symptoms related to hGH deficiency or excess, contact your healthcare provider.

If youre receiving treatment for abnormal hGH levels, its important to see your provider regularly to make sure your treatment is working.

A note from Cleveland Clinic

Human growth hormone (hGH) is a powerful hormone thats necessary for several important bodily processes. Sometimes, your pituitary gland can make too much or too little of it. If you or your child are experiencing symptoms related to hGH deficiency or excess, its important to talk to your healthcare provider. Theyre there to help.

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Human Growth Hormone (hGH) - Cleveland Clinic

Recommendation and review posted by Bethany Smith

Chronic stress puts your health at risk – Mayo Clinic

Chronic stress puts your health at risk

Chronic stress can wreak havoc on your mind and body. Take steps to control your stress.

Your body is hard-wired to react to stress in ways meant to protect you against threats from predators and other aggressors. Such threats are rare today, but that doesn't mean that life is free of stress.

On the contrary, you likely face many demands each day, such as taking on a huge workload, paying the bills and taking care of your family. Your body treats these so-called minor hassles as threats. As a result, you may feel as if you're constantly under attack. But you can fight back. You don't have to let stress control your life.

When you encounter a perceived threat such as a large dog barking at you during your morning walk your hypothalamus, a tiny region at your brain's base, sets off an alarm system in your body. Through a combination of nerve and hormonal signals, this system prompts your adrenal glands, located atop your kidneys, to release a surge of hormones, including adrenaline and cortisol.

Adrenaline increases your heart rate, elevates your blood pressure and boosts energy supplies. Cortisol, the primary stress hormone, increases sugars (glucose) in the bloodstream, enhances your brain's use of glucose and increases the availability of substances that repair tissues.

Cortisol also curbs functions that would be nonessential or harmful in a fight-or-flight situation. It alters immune system responses and suppresses the digestive system, the reproductive system and growth processes. This complex natural alarm system also communicates with the brain regions that control mood, motivation and fear.

The body's stress response system is usually self-limiting. Once a perceived threat has passed, hormone levels return to normal. As adrenaline and cortisol levels drop, your heart rate and blood pressure return to baseline levels, and other systems resume their regular activities.

But when stressors are always present and you constantly feel under attack, that fight-or-flight reaction stays turned on.

The long-term activation of the stress response system and the overexposure to cortisol and other stress hormones that follows can disrupt almost all your body's processes. This puts you at increased risk of many health problems, including:

That's why it's so important to learn healthy ways to cope with your life stressors.

Your reaction to a potentially stressful event is different from anyone else's. How you react to your life stressors is affected by such factors as:

You may have some friends who seem relaxed about almost everything and others who react strongly to the slightest stress. Most people react to life stressors somewhere between those extremes.

Stressful events are facts of life. And you may not be able to change your current situation. But you can take steps to manage the impact these events have on you.

You can learn to identify what causes you stress and how to take care of yourself physically and emotionally in the face of stressful situations.

Stress management strategies include:

Avoid unhealthy ways of managing your stress, such as using alcohol, tobacco, drugs or excess food. If you're concerned that your use of these products has increased or changed due to stress, talk to your doctor.

The rewards for learning to manage stress can include peace of mind, less stress and anxiety, a better quality of life, improvement in conditions such as high blood pressure, better self-control and focus, and better relationships. And it might even lead to a longer, healthier life.

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Chronic stress puts your health at risk - Mayo Clinic

Recommendation and review posted by Bethany Smith

Menstrual Migraines (Hormone Headaches) – Cleveland Clinic

OverviewWhats a migraine? What does it feel like?

A migraine is more than a bad headache. Its a neurologic disease with a series of symptoms that might include debilitating pain on one side of your head that you may describe as pulsing or throbbing. Menstrual migraines, also known as hormone headaches, happen right before or during a womans period (up to two days before through three days during) and may get worse with movement, light, smells, or sound. Your symptoms may last for a few hours, but theyll likely last days.

Its estimated that 70% of people who experience migraines are women. Of these women, 60% to 70% report a connection between their menstruation (periods) and their migraine attacks. Women experience migraine attacks three times more frequently than men.

A menstrual migraine is one of several types of migraine headaches. Examples of other migraines include migraine with aura, migraine without aura and chronic migraine.

Hormones are often called your bodys chemical messengers. Theyre in your organs, tissues and bloodstream and theyre made by the endocrine glands. Examples of endocrine glands include your thyroid gland, adrenal glands and pituitary gland. If you have too little of a certain hormone, or too much, that can throw your entire system off balance.

Estrogen and progesterone are the two main sex hormones in women. Estrogen causes female physical features, sets off puberty and aids with reproduction. It also affects your cholesterol, controls your menstrual cycle, protects bone health and affects your heart, skin, bones, brain and other tissues. Its mostly produced by your ovaries.

Your levels of estrogen change. Theyre at the highest amount in the middle of your cycle and the lowest amount when youre on your period. When youre in menopause, they drop very low.

Headaches in women, especially migraines, are related to changes in the levels of estrogen. Levels of estrogen drop immediately before the start of your menstrual flow (menses).

Premenstrual migraines regularly occur during or after the time when the female hormones, estrogen and progesterone, drop to their lowest levels.

Migraine attacks usually improve during pregnancy. However, some women have reported that their migraines started during the first trimester of pregnancy, and then went away.

Menstrual migraines are triggered by a drop in estrogen. Other migraines may be triggered by stress, missing a meal, caffeine, or many other reasons.

About 12% of Americans experience migraines. The majority are women, at least 60% of those women have observed a correlation between their menstrual cycle and their migraines. In other words, theyve noticed that they get a migraine right before or during their period.

Menstrual migraines can start up to three days before your period.

While migraines can start when youre a child, menstrual migraines dont until your periods begin. Women who have periods are the ones who get menstrual migraines.

Changes in estrogen levels, which happen right before your period begins.

In addition to a drop in estrogen, birth control pills and hormone replacement therapy for menopause can change the frequency or severity of migraines. If you notice your migraine headache getting worse after starting one of these medications, it may be worthwhile to ask your healthcare provider for a medication that contains a lower dose of estrogen, or ask for a change from an interrupted dosing regimen to a continuous one.

The symptoms of a menstrual migraine are the same as the symptoms for other types of migraines:

Your healthcare provider will want to establish a history of your migraine-related symptoms, likely asking you to:

Your healthcare provider may also order blood tests and imaging tests (such as a CT scan or MRI) to make sure there are no other causes for your headache. An electroencephalogram (EEG) may be ordered to rule out seizures.

Its helpful to both you and your healthcare provider if you keep a migraine journal. Take note of what symptoms you get, how long your symptoms last, and what makes your menstrual migraine better or worse. You and your healthcare provider may be able to use that information to help you heal, and possibly prevent or anticipate your migraine.

A menstrual migraine is usually treated with nonsteroidal anti-inflammatory medications (NSAIDs). The NSAIDs most often used for menstrual migraine include:

Treatment with the NSAID should begin two to three days before your period starts, and continue through your menstrual flow. Because the medication is taken for a short time only, the risk of gastrointestinal side effects is limited.

Triptans selective serotonin receptor agonists are medicines used for acute migraines. They stop your menstrual migraine after it begins. In the United States there are seven triptan medications approved for use:

Other medications that might be prescribed include:

These drugs should also be started two to three days before your period starts. Continue taking them throughout your menstrual flow.

Because fluid retention (retaining water) often occurs at the same time as your menses, diuretics have been used to prevent menstrual migraines. Some healthcare providers may recommend that you follow a low-salt diet immediately before the start of your menses.

Leuprolide (Lupron) is a medication that affects your hormone levels. Its used only when all other treatment methods have been tried and havent worked.

Talk with your healthcare provider and pharmacist about the side effects of each medication prescribed. The most common side effects of medications prescribed to fight migraines include:

Ask your primary healthcare provider to refer you to a headache specialist.

If you need to continue estrogen supplements after menopause, you should start on the lowest dose of these agents, on an uninterrupted basis. Instead of seven days off the drug, you may be told to take it every day. By maintaining a steady dose of estrogen, the headaches may be prevented. An estrogen patch (such as Estraderm) may be effective in stabilizing the levels of estrogen.

Because most medications taken for migraines can affect your baby, you should avoid them. However, your healthcare provider may give you permission to take a mild pain reliever like acetaminophen. Talk to your healthcare provider before you take any medicine.

Do your best to figure out what makes your hormone headaches better or worse. For example, if light causes pain and you feel overheated, stay in a cool, dark room. Additional tips include:

Your healthcare provider may prescribe preventative medications that you take daily, then increase the dose when youre near your period. Possibilities include:

No type of migraine causes brain damage.

You may have menstrual migraines until youre in menopause.

Schedule a visit with your healthcare provider if:

Call 911 or go immediately to an Emergency Room if:

A note from Cleveland Clinic

A migraine is more than a bad headache. Not only can menstrual migraines get severe, but women have reported that they can be even worse than a migraine that occurs when theyre not on their period. Talk to your healthcare provider about your symptoms. There are preventative measures and treatment options. A menstrual migraine might not be something you just have to live with every month.

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Menstrual Migraines (Hormone Headaches) - Cleveland Clinic

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Acromegaly: What It Is, Causes, Symptoms & Treatment – Cleveland Clinic

OverviewWhat is acromegaly?

Acromegaly (pronounced a-krow-meh-guh-lee) is a rare but serious medical condition that happens when you have high levels of growth hormone (GH) in your body. Your pituitary gland normally produces GH, but tumors on your pituitary or in other parts of your body produce excess GH in acromegaly.

Your pituitary gland is a small, pea-sized endocrine gland located at the base of your brain below your hypothalamus. Your pituitary gland releases eight important hormones, including GH.

Growth hormone, also known as human growth hormone (hGH) and somatotropin, is a natural hormone that acts on many parts of the body to promote growth in children. Once the growth plates (epiphyses) in your bones have fused, GH no longer increases height, but your body still needs GH. After youve finished growing, GH helps to maintain normal bone, cartilage and organ structure and metabolism, including helping to keep your blood glucose (sugar) levels within a healthy range.

If you have too much GH in your body as an adult, it can result in irregularly-shaped bones, increased organ size, elevated blood sugar levels (hyperglycemia) and other symptoms.

Acromegaly and gigantism are both conditions that result from excess growth hormone (GH). The difference is in who the conditions affect adults develop acromegaly, whereas children develop gigantism.

In children, gigantism occurs when they experience excess GH before the growth plates in their bones fuse (before the end of puberty). This causes them to grow very tall. Gigantism is more rare than acromegaly. Some healthcare providers refer to gigantism as pediatric acromegaly.

Once your growth plates have fused, excess GH causes acromegaly. In this case, you dont grow in height, but the excess GH affects your bones shape and your organ size as well as other health factors.

Acromegaly can develop at any age after puberty, but healthcare providers most often diagnose it during the fourth and fifth decades of life (middle age).

Acromegaly is rare. Approximately 3 to 14 of every 100,000 people have been diagnosed with acromegaly.

In adults, acromegaly (excess growth hormone) causes bones, cartilage, body organs and other tissues to increase in size. Characteristic changes in appearance include larger hands, feet, ears, lips and nose and a more prominent jaw and forehead.

Growth hormone (GH) signals your liver to produce another hormone called insulin-like growth factor 1 (IGF-1). IGF-1 is the hormone that actually causes your bones and body tissue to grow and also affects how your body processes blood glucose (sugar) and lipids (fats). High levels of GH result in high levels of IFG-1, which can lead to Type 2 diabetes, high blood pressure (hypertension) and heart disease.

The most common cause of acromegaly is a tumor in your pituitary gland called a pituitary adenoma that causes your pituitary gland to release excess growth hormone (GH).

Pituitary adenomas (tumors) are almost always benign (noncancerous). Most adenomas that cause acromegaly grow slowly, and you may not notice symptoms of excess GH for many years.

Depending on its size and location, the adenoma may press against other pituitary tissue and affect other hormones your pituitary gland makes. If the adenoma is large, it may also press against nearby parts of your brain, causing headaches and vision problems.

In adults, acromegaly affects your bodys bones and tissues and causes them to grow in irregular ways.

Adults with acromegaly may experience the following symptoms:

Other symptoms include:

Acromegaly symptoms often start slowly and may be difficult to notice at first. Some people only notice their hands have grown in size when rings they regularly wear feel tight or their shoe size changes, especially the width.

If youre experiencing these symptoms, its important to talk to your healthcare provider.

Symptoms of acromegaly often show up very slowly over many years. This makes it hard to diagnose.

Your healthcare provider may recommend you see an endocrinologist, a healthcare provider who specializes in hormone-related conditions. They'll make a diagnosis based on your medical history, a thorough clinical evaluation and specialized tests like blood tests and imaging tests.

If youve been diagnosed with acromegaly, your provider may order additional tests to see if the condition has affected other parts of your body. These tests may include:

There are several treatment options for acromegaly. Your healthcare provider will consider your symptoms and circumstances before offering treatment options that are right for you.

The most common treatments for acromegaly are surgery, medication and radiation therapy.

In many cases, surgery greatly improves acromegaly symptoms or corrects the condition entirely. Surgeons most often use a type of surgery called transsphenoidal surgery, which involves going through your nose and sphenoid sinus, a hollow space in your skull behind the nasal passages and below your brain, to perform surgery.

The specifics of the surgery will depend on the size and location of the tumor. The goal of surgery is to remove all of a tumor that is causing excess growth hormone production. If your surgeon removes enough of the tumor, you may not need further treatment. If your surgeon can remove only a part of a tumor, you may need medication or radiation therapy to manage your symptoms and reduce the production of growth hormone.

Your healthcare provider may prescribe one medication or a combination of medications. Medications work in different ways to normalize your bodys growth hormone levels and improve your symptoms. In some cases, a person may take medication until the tumor has shrunk. This can allow a surgeon to then safely remove it. Other people may need to take medication long-term to effectively manage growth hormone levels and symptoms.

Acromegaly is curable in some situations but not all. The cure rate for surgical removal of a pituitary tumor thats causing acromegaly is about 85% for small tumors and 40% to 50% percent for large tumors.

Medication cant cure acromegaly but offers long-term, safe treatment.

Unfortunately, theres nothing you can do to prevent acromegaly. Scientists arent sure what causes pituitary tumors that cause acromegaly to develop, though they think certain genetic factors may play a role.

The prognosis (outlook) for acromegaly depends on how severe it is and how effectively therapies treat the symptoms. Many people with acromegaly see a significant improvement in symptoms after treatment.

If its not treated, acromegaly can significantly change your appearance and the shape of your bones. These symptoms can greatly affect your self-image and quality of life. Support groups help some people cope with the challenges they face because of acromegaly.

Health complications of acromegaly such as heart disease or Type 2 diabetes can also decrease quality of life and even shorten your lifespan. Because of this, its important to contact your healthcare provider if youre experiencing symptoms and to adhere to your treatment plan if youve been diagnosed.

If left untreated, acromegaly can cause the following complications:

Life expectancy for someone with acromegaly depends on the severity of the condition and if they have other health conditions, usually due to untreated acromegaly.

If your growth hormone levels arent properly managed and you have other conditions like heart disease and Type 2 diabetes, your life expectancy may reduce by approximately 10 years.

If you have acromegaly thats properly treated and have normal growth hormone and insulin-like growth factor 1 (IGF-1) levels, youll likely have a normal life expectancy.

If youre experiencing symptoms of acromegaly, its important to talk to your healthcare provider.

If youve been diagnosed with acromegaly, youll need to see your provider regularly to make sure your treatment is working well.

A note from Cleveland Clinic

Acromegaly is a rare but serious condition. The good news is that its treatable with surgery, medication and/or radiation therapy. If youve noticed an increase in size in your hands, feet and/or facial features, its important to talk to your healthcare provider. They can order some simple tests to see if your growth hormone levels are the cause of your symptoms.

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Acromegaly: What It Is, Causes, Symptoms & Treatment - Cleveland Clinic

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Hormone Therapy and Shoulder Pain During Menopause – Healthline

It is sometimes called frozen shoulder, even menopause shoulder.

Doctors say the condition, known as adhesive capsulitis, causes stiffness and pain in the shoulder joint. Little is definitively known about the cause.

The ailment more commonly occurs in women over the age of 40. Having diabetes, thyroid disease, heart disease, or Parkinsons disease can also put you at higher risk.

In a new study, researchers decided to hone in on the demographic most affected by adhesive capsulitis menopausal women.

The Duke University team conducted the first known study evaluating whether hormone therapy might reduce the risk of adhesive capsulitis in menopausal women.

The team evaluated medical records from a single institution for nearly 2,000 menopausal women ages 45 to 60. In the group, 152 of the women were receiving hormone replacement therapy (HRT).

While acknowledging the small sample size, the researchers concluded that those not receiving hormone replacement therapy had 99% greater odds of adhesive capsulitis compared to those receiving HRT.

The findings are being presented this week at the North American Menopause Society annual meeting in Atlanta, Georgia. The results have not been published yet in a peer-reviewed journal.

Dr. Anne Cunanan Ford, NCMP, an associate professor of obstetrics and gynecology at the Duke University Medical Center in North Carolina, is the studys lead author.

Our study draws attention to estrogens potential benefit apart from the FDA (Food and Drug Administration) approved indications vasomotor symptoms, bone protection, and vulvovaginal atrophy, she told Healthline.

We know that estrogen plays an important role in the musculoskeletal system, stimulating new bone formation, promoting muscle growth and repair, maintaining connective tissue integrity, and reducing inflammation Ford explained.

If borne out by future prospective studies, the use of systemic hormone therapy may be protective in minimizing adhesive capsulitis she added. Its a condition that causes significant pain, reduction in range of motion, and decreased quality of life in peri and post-menopausal women.

Experts who spoke to Healthline agreed that there needs to be more research.

This pilot study provides preliminary data that will guide future studies further investigating a potential link between menopause and hormone therapy use or non-use, and risk of adhesive capsulitis, said Dr. Stephanie Faubion, the director of the Mayo Clinics Center for Womens Health in Minnesota and Medical Director of the North American Menopause Society.

No conclusions can be made based on these data, she told Healthline.

Its a small study so something like this has to be looked at in bigger numbers, added Dr. G. Thomas Ruiz, the lead OB-GYN at MemorialCare Orange Coast Medical Center in California.

I think its an interesting study in that we know that estrogen receptors are found throughout a womans body, he told Healthline. So its not surprising that there would also be an interaction between joint function ligaments and tendons with estrogen.

So the menopausal state in the absence of estrogen is probably going to change he added. We know with bone, for example, in the absence of estrogen, women will start to lose calcium at a more rapid rate. That puts them at risk of osteoporosis and osteopenia, at an increased risk for hip fractures. So looking at this study I dont necessarily find it too surprising but its also too small a number to make a definitive statement.

Going forward, Ford said: Our data is preliminary and due to the small sample size, this association did not reach statistical significance. Larger prospective studies are needed to evaluate and confirm our findings.

Would hormone therapy work to treat adhesive capsulitis?

We have no idea. There is no data. Hormone therapy does appear to be associated with less joint pain. But the mechanism behind this effect is unknown Faubion said.

Hormone therapy is effective for management of hot flashes, night sweats, sleep disturbance associated with menopause, prevention of osteoporosis, fractures and the treatment of genitourinary syndrome of menopause she explained. It also appears to help with depressive symptoms in the menopause transition.

The benefits of hormone therapy typically outweigh the risks for symptomatic women who are under the age of 60 and within 10 years of the onset of menopause, she added.

Still, many women have questions about the safety of hormone treatment because of previous studies linking some forms of hormone treatment to an increased breast cancer risk.

The American Cancer Society states that estrogen-only HRT is not linked to a higher risk of breast cancer. The Womens Health Initiative studies also found no increase in breast cancer risk in women using systemic estrogen-only HRT.

But organization officials note that in women who have a uterus, using systemic estrogen-only HRT has been shown to increase the risk of endometrial cancer.

Other studies have found a link between systemic estrogen-only HRT and a higher risk of ovarian cancer.

Ruiz says theres an increase in the use of bioidentical hormones that replicate those your body produces and methods of delivering the hormones that bypass the liver.

Keep in mind the medications that were used Premarin and Provera were taken orally and metabolized through the liver, he said. Physiologically that causes a lot of activity in the breast tissue.

Bioidentical hormones are more like your ovaries made thats the definition he added. Then the estrogen can even be given in cream or patch thats absorbed directly So these medications are not metabolized in the liver to make them active.

Ruiz says hormone replacement doses are much lower now and that perhaps new studies need to be done.

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Hormone Therapy and Shoulder Pain During Menopause - Healthline

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Helping Reduce Your Risk of Breast Cancer ThedaCare – ThedaCare

October is recognized as Breast Cancer Awareness Month. During this time, health care systems and organizations aim to provide education, resources, support and prevention information regarding the disease.

The American Cancer Society (ACS), offers these statistics about breast cancer:

Early detection is important because there are more treatment options available and a better chance of survival when breast cancer is caught early, said Charissa Williams, APN, a ThedaCare Hematology & Oncology Specialist. Studies show theres a more than 90% survival rate, if the tumor is caught early.

Regular self-breast exams are one way to detect a cancerous tumor. A breast cancer screening is another way. Mammograms can spot tiny tumors, making it more likely to catch the disease at an earlier stage.

For most women, screening mammography is a safe and effective way to detect breast cancer early, Williams added.

Medical organizations vary on the best age to start screening mammograms (some say as early as age 40) and how often to repeat them. The Centers for Disease Control and Prevention (CDC) has a comparative chart, Breast Cancer Screening Guidelines for Women, to better sort out the timing and frequency of mammogram screening based on your particular situation.

It is important to discuss your individual screening guidelines with your primary care provider, said Williams. For example, those who have a strong family history or certain genetic mutations (BRCA1 or BRCA2) often have earlier screening guidelines than the general population.

Women might also help minimize their chances of developing the disease by modifying their lifestyle. However, Williams notes there are some risks factors that cannot be changed: your age, family history, genetics, race, and being a woman.

There are several modifiable factors that can increase your breast cancer risk, including obesity, poor diet, lack of physical activity, alcohol and tobacco use, and certain types of hormone replacement therapy, she said.

To reduce your risk of breast cancer, Williams suggests you form these habits:

There are more than 3.8 million breast cancer survivors in the United States.

For more information on breast cancer prevention tips, screenings and treatments, visit thedacare.org/breast-cancer.

About ThedaCare

For more than 110 years, ThedaCare has been committed to improving the health and well-being of the communities it serves in Northeast and Central Wisconsin. The organization delivers care to more than 600,000 residents in 17 counties and employs approximately 7,000 health care professionals. ThedaCare has 180 points of care, including eight hospitals. As an organization committed to being a leader in Population Health, team members are dedicated to empowering people to live their unique, best lives. ThedaCare also partners with communities to understand needs, finding solutions together, and encouraging health awareness and action. ThedaCare is the first in Wisconsin to be a Mayo Clinic Care Network Member, giving specialists the ability to consult with Mayo Clinic experts on a patients care. ThedaCare is a not-for-profit health system with a level II trauma center, comprehensive cancer treatment, stroke and cardiac programs, as well as primary care.

For more information, visit thedacare.org or follow ThedaCare on social media. Members of the media should call Cassandra Wallace, Public and Media Relations Consultant at 920.442.0328 or the ThedaCare Regional Medical Center-Neenah switchboard at 920.729.3100and ask for the marketing person on call.

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Helping Reduce Your Risk of Breast Cancer ThedaCare - ThedaCare

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CHOICES Reproductive Health clinic now open in Carbondale – WSIL TV

CARBONDALE (WSIL) -- A reproductive health clinic that will also provide abortion serves has opened in Carbondale.

TheCHOICES: Memphis Center for Reproductive Health announced they would open a clinic in southern Illinois after learning the Supreme Court would overrule Roe v. Wade. Tennessee has now banned abortion services.

The CHOICES clinic is located on Giant City Road and is now accepting appointments for medication abortions. They started seeing their first patients Tuesday.

The clinic will be the southernmost abortion clinic for most people across the southeast, according to a release.

Eventually, the clinic will also offer gender-affirming hormone therapy, procedural abortions, birth control, sexual wellness and more.

The Memphis location is still open, they just will no longer provide abortion services. They will still provide reproductive and sexual health care.

More coverage:

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CHOICES Reproductive Health clinic now open in Carbondale - WSIL TV

Recommendation and review posted by Bethany Smith

HIV patients abused and humiliated – News24

Its not all bad news for the province, however, as it received the fewest reports of stock-outs by public healthcare users. Photo: Reuters

NEWS

Every three months, Vuyo* has to travel for about four hours from Matatiele in the Eastern Cape to Durban in KwaZulu-Natal to get her antiretroviral (ARV) treatment.

She has been featured in the second edition of the Eastern Cape State of Health report by Ritshidze, a community-led monitoring system developed by organisations representing people living with HIV.

The organisations include the Treatment Action Campaign, the National Association of People Living with HIV, the Positive Action Campaign, the Positive Womens Network, and the SA Network of Religious Leaders Living with and affected by HIV/Aids.

The Ritshidze data, which was launched on Thursday, reveal improvements at Eastern Cape clinics, but patients still complained about poor treatment at healthcare facilities, which saw them missing their appointments and even stopping their clinic visits.

READ: Intimate partner violence impedes ARV treatment adherence among adolescents - study

Vuyo tested positive for HIV two years ago and was getting her treatment from Matatiele Community Clinic.

On this day, I was in pain and decided to go to the clinic. I told the nurse my problem and she started shouting that I was being careless with my life for not using a condom. She called other nurses and they started talking about me as if I was not there. That day was so embarrassing, and I was hating myself so much. I even thought of dying, and thats when I decided to quit the clinic, she said.

For some time after that incident, Vuyo defaulted on her medication because, when she went to other clinics, she was referred back to Matatiele.

She said:

I then decided to go and get my medication in Durban, as my sister works there. It is working better for me like that, and they give me medication for three months. I dont have problems with the medication and I dont default.

No privacy

Ritshidze data show that 55% of the people interviewed thought that clinic staff were always friendly and professional in the Eastern Cape. This is down from 63% last year.

This poor treatment is off-putting enough for people to miss appointments or even stop going to the clinic altogether. Some report being terrified at what awaits them, read the report.

Some people complained that clinic staff members disclose the status of patients living with HIV in waiting areas.

There were also reports of two or more patients consulted with or counselled in the same room, and people living with HIV separated from other chronic patients.

According to the report for key populations, clinic visits can be traumatic, and staff can be unfriendly and even openly hostile.

Many people we spoke to had given up on healthcare altogether, including 47% of gay and bisexual people, and men who have sex with men; 41% of people who use drugs; 39% of sex workers; and 47% of transgender people.

Despite commitments by Pepfar [The US Presidents Emergency Plan for Aids Relief] and the national health department to roll out a robust key population sensitisation toolkit as part of standard in-service training for all facility staff, disrespect, ill-treatment and dehumanisation of key populations remain a widespread challenge that should be urgently fixed, with consequences for clinic staff who commit privacy violations.

READ: Study finds SA street sex workers have a high chance of being infected with HIV

The report states that, for those key populations still getting healthcare, most go to public healthcare facilities, yet specific services remain extremely limited.

Lubricants were only available in 41% of sites during this reporting period. While, notably, PrEP [pre-exposure prophylaxis] was reported as available at all 45 facilities monitored, the number of facilities that reported offering PrEP to key populations was far lower. Drug dependence and overdose treatments are not available at our clinics, neither is hormone therapy, yet 36% of people who use drugs wanted access to methadone and 35% wanted access to naloxone, and 29% of transgender people wanted access to hormone treatments at their facilities, reads the report.

Slight improvement

Its not all bad news for the province, however, as it received the fewest reports of stock-outs by public healthcare users in the current reporting period, with only 7% of patients who had left, or knew someone who had left, a facility without the medication they needed.

The report said:

Of the sites that reported a stock-out, 15% were forced to send people away empty-handed. The issues outlined in the second edition of the state of health report identify reasons people do not want to go to the clinic to access HIV and tuberculosis prevention and treatment services, and why some people interrupt treatment or disengage from care altogether.

According to the report, understaffed clinics meant that healthcare workers were overburdened, which led to longer waiting times, limited time to attend to public healthcare users and bad attitudes.

These factors directly and negatively impact people living with HIV from starting and staying on treatment. By June next year, the Eastern Cape health department should fill 70% of vacancies in the province, including the 322 vacancies reported at Ritshidze sites, and fill the remaining 30% by the end of the 2023/24 financial year.

The provincial health department should produce annual reports on the number of healthcare workers employed in each district and the number of people and size of areas covered by these healthcare workers. These reports should also include year-on-year comparisons (from at least 2020) of the number of filled posts in all districts and the cost of these posts to the government, the report recommends.

*Not her real name

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HIV patients abused and humiliated - News24

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Diabetes and the gut: How a bacterial protein may impact insulin – Medical News Today

Diabetes is characterized by insufficient production of insulin due to the loss or dysfunction of pancreatic beta cells.

A new study published in Cell Metabolism shows that a protein called beta cell expansion factor A (BefA) secreted by gut bacteria could induce the replication of insulin-producing beta cells in neonatal mice.

Understanding the mechanisms underlying the actions of BefA protein could help develop therapies to stimulate beta cell proliferation in individuals with diabetes.

The study also provides a potential explanation of how the gut microbiome could play a role in the development of diabetes.

Study author Dr. Karen Guillemin, a professor at the University of Oregon in Eugene, told Medical News Today:

[Our findings imply] that the activities of gut bacteria in young animals including possibly humans can shape the development of the pancreas in early life. This is important because early life corresponding to about the first 2 years of life in a human is when insulin-producing beta cells are most proliferative, after which they become more quiescent. If this population of beta cells does not proliferate enough during early life, it means that the individual with a small beta cell pool is more vulnerable to developing type 1 diabetes if beta cells are depleted by autoimmune attack.

Dr. Martin Blaser, a professor in the Departments of Medicine and Pathology and Laboratory Medicine at Rutgers University, NJ, commented that this study is exciting because it represents a novel way that we might be able to regrow beta cells in situations with injury like type 1 diabetes.

This is a great example of how basic research on the microbiome of zebrafish can lead to new approaches to treating important human diseases, he added.

Individuals with type 1 diabetes are unable to regulate blood sugar levels due to the loss of insulin-producing beta cells in the pancreas. The loss of beta cells in type 1 diabetes is caused by an autoimmune response against these cells.

In contrast, in type 2 diabetes the body is initially able to produce insulin but the cells in the body do not respond to insulin. In response to the consequent increase in blood glucose levels, beta cells produce more insulin to compensate for the resistance of cells to the hormone. This leads to the exhaustion of beta cells and their dysfunction, resulting in lower insulin levels.

The replication rate of beta cells is high immediately after birth but rapidly declines thereafter. Thus, therapies that stimulate the replication or regeneration of beta cells in adults could help treat diabetes.

The studys authors had previously identified such a protein, called BefA, secreted by gut microbes that could stimulate the proliferation of beta cells in zebrafish.

Moreover, the authors had also identified a version of the BefA protein synthesized by gut bacteria in humans that could stimulate the proliferation of beta cells in zebrafish. In other words, the BefA proteins secreted by gut microbes in humans and zebrafish share a similar structure and function.

In the present study, the researchers further examined the mechanism through which BefA could facilitate the proliferation of pancreatic beta cells in young mice and zebrafish.

Previous studies have shown that the gut microbiome could potentially play a role in the development of diabetes. In their previous work, the study authors had shown that germ-free zebrafish larvae, which show a complete absence of gut microbes, show lower levels of pancreatic beta cell proliferation during development.

In addition, exposure to BefA prevented this decline in beta cell proliferation in germ-free zebrafish larvae.

In the current study, the researchers examined whether the BefA protein performed a similar function in mice. Specifically, they examined the impact of BefA in germ-free and specific pathogen-free (SPF) mice.

SPF mice are reared so that they are not exposed to disease-causing microorganisms that may interfere with the goals of the study.

Similar to germ-free zebrafish larvae, germ-free neonatal mice and SPF mice treated with antibodies at birth showed lower levels of beta cells than untreated SPF.

Notably, the BefA protein was able to rescue beta cell development in germ-free and antibody-treated SPF neonatal mice. Moreover, mice treated with BefA also showed lower blood glucose levels than untreated animals.

The researchers then examined whether the BefA protein could directly interact with beta cells to stimulate their expansion instead of exerting these effects by interacting with other tissues. They cultured pancreatic tissue dissected from germ-free zebrafish larvae and mice pups in the laboratory and exposed the cells to the BefA protein.

The researchers found that the BefA protein was able to directly interact with and stimulate the proliferation of pancreatic beta cells.

In subsequent studies using zebrafish larvae, the researchers examined how BefA protein synthesized by gut microbes could reach the beta cells in the pancreas. The BefA protein could be transmitted to the pancreas via the bloodstream or the hepatopancreatic duct, which connects the pancreas to the gut.

Using zebrafish models with a compromised hepatopancreatic duct or lacking blood vessels, the researchers found that pancreatic beta cell proliferation was reduced in both models.

These results show that BefA protein produced by intestinal microbiota could indeed travel from the intestine via the hepatopancreatic duct or blood vessels to reach the pancreas.

To better understand the function of the BefA protein, the researchers examined the structure of the protein. They found that BefA proteins derived from the bacterial species Klebsiella aerogenes in the human gut, and Aeromonas veronii in zebrafish showed considerable structural differences but shared an identical domain or region of the protein called SYLF.

The researchers found that the SYLF domain could rescue the loss of pancreatic beta cells in germ-free zebrafish larvae. These results suggest that this region could underlie the ability of the BefA protein to induce the proliferation of pancreatic cells.

Evidence from previous studies examining other proteins containing the SYLF domain from a wide range of organisms suggested that the ability of the BefA protein to stimulate beta cell proliferation may be mediated by its interaction with lipid membranes that surround cells.

Consistent with this, the researchers found that the BefA protein was able to permeabilize or disrupt synthetic membranes as well as membranes surrounding the cells of bacteria.

The secretion of BefA protein by certain gut bacteria could damage the cell membrane of other gut bacteria and confer a competitive advantage over these microbes. Moreover, this ability to disrupt cell membranes could also potentially explain the BefA proteins ability to enhance beta cell proliferation.

To test this hypothesis, the researchers exposed cultured pancreatic beta cells to a mutated form of BefA protein with a reduced ability to permeabilize membranes. The mutated BefA protein had a reduced ability to induce the proliferation of cultured pancreatic beta cells from neonatal mice.

These results suggest that the membrane permeabilizing activity of BefA was responsible for mediating its effects on beta cell proliferation. Proteins such as BefA may be secreted by gut microbes to gain a competitive advantage over other bacteria, but could also confer incidental benefits to the human host by facilitating normal pancreatic development.

However, Dr. Guillemin noted: We dont know yet whether BefA can stimulate proliferation of beta cells in older animals, in animals that have experienced beta cell autoimmune attack, or in people, but these are questions we are currently pursuing. We also dont know yet how membrane permeabilization stimulates beta cells to proliferate, but we are also pursuing this question.

In addition to the BefA protein synthesized by a subset of gut microbes, other proteins produced by human cells also possess membrane permeabilizing properties. This includes antimicrobial proteins that form pores in the membrane of bacterial cells and protect the body from harmful bacteria.

The researchers found that the Reg3 protein, a member of the antimicrobial protein family, was also able to increase the proliferation of mice and zebrafish pancreatic cells.

Proteins such as BefA that are produced during microbial competition are known to activate antimicrobial proteins. The study authors think that proteins secreted by gut microbes such as BefA and the antimicrobial proteins that are produced in response to these proteins could play an important role in the development of pancreatic beta cells.

These findings could facilitate the development of strategies for the prevention or treatment of diabetes. The diversification of the microbial communities in the gut occurs at the same time as the proliferation of beta cells after birth.

A lack of microbial diversity during early childhood, especially lower levels of microbes that secrete proteins such as BefA, could thus increase the risk of type 1 diabetes.

Dr. Guillemin explained:

There are several potential future therapeutic applications of our findings. One area is in prevention. It may be possible to perform microbiome profiling combined with other genetic and environmental data analysis to predict whether infants are at high risk for developing type 1 diabetes and if they may benefit from prophylactic administration of BefA-producing gut bacteria or BefA protein formulations to stimulate the development of their beta cell population in the first 2 years of life, which is when beta cells are most proliferative and when the lifelong pool of beta cells is established.

The second area is in the treatment of [type 1 diabetes], she added. It is possible that BefA will prove useful for stimulating the proliferation of beta cells in older individuals and in pancreases following the autoimmune destruction of beta cells, which is the process that causes [type 1 diabetes].

Even if BefA itself is not able to stimulate beta cell proliferation in these circumstances, our studies of the BefA mechanism may uncover new strategies to stimulate beta cell proliferation through membrane manipulations, said Dr. Guillemin.

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Diabetes and the gut: How a bacterial protein may impact insulin - Medical News Today

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Recommended Approaches to Treatment for Early-Stage HER2+ Breast Cancer – Targeted Oncology

During a Targeted Oncology case-based roundtable event, Jennifer M. Matro, MD, discussed the data supporting systemic therapies for treatment of early-stage HER2-positive breast cancer including trastuzumab and pertuzumab.

Targeted OncologyTM: What are the recommended approaches to treating early-stage HER2-positive breast cancer?

MATRO: [What I will discuss] is by no means meant to be a dogmatic approach, but more an adaptive algorithm for early-stage HER2-positive breast cancer. There are patients for whom neoadjuvant treatment is appropriate and patients for whom adjuvant treatment would be appropriate. Starting in the neoadjuvant population, which is now most of our patients: Generally, these are patients who have either positive lymph nodes or T2 tumors, and IV chemotherapy along with dual HER2-targeted therapies [is] appropriate.

After their up-front chemotherapy, they go to surgery. If they have a pCR, like our patient did here, then they proceed to HER2-directed therapy to complete 1 year. [When looking at] trastuzumab plus or minus pertuzumab there is some thought, extrapolating from the APHINITY trial [NCT01358877], that for patients who presented initially with a node-negative diseasemaybe they were T2N0and had a pCR, that you do not necessarily need the pertuzumab; but for patients who are node positive at presentation, include the pertuzumab.1,2

For patients who did not have a pCR, based on the KATHERINE trial [NCT01772472], we have the adjuvant T-DM1 [trastuzumab emtansine (Kadcyla)] for 14 cycles.3 Patients who do not have preoperative therapy and have surgery first are going to be patients who are mostly earlier stage with imaging, T1N0, or if there is a question of the extent of disease.

[In the patient in this case] there are 6 cm of nonmass enhancement and biopsy of the nonmass enhancement shows DCIS. It is unclear what the extent of disease is, and you go ahead with surgery first. If the patient comes out of surgery with negative lymph nodes and smaller tumors, then paclitaxel/trastuzumab for 12 weeks is recommended, as it has been shown in the APT trial [NCT00542451] and a subsequent larger study that the outcomes for those patients are excellent.4

For patients who have larger node-negative cancers, maybe 2 or 3 cm, or are younger and you are worried more about their risk, TCH [docetaxel, carboplatin, and trastuzumab] would also be appropriate. For node-positive patients, we are going to include the dual HER2 therapy. Neratinib [Nerlynx] in the ExteNET trial [NCT00878709] was shown to provide some benefit, particularly for patients with hormone receptorpositive disease and multiple positive lymph nodes.5 That is also part of the consideration in the algorithm for higher-risk patients.

I want to highlight that the trastuzumab biosimilars can be used interchangeably with the brand-name Herceptin, and the subcutaneous formulations of trastuzumab and trastuzumab/pertuzumab can also be used in place of the IV formulations.

Can you discuss APHINITY?

APHINITY is the study that led to the use of dual HER2 therapy in the adjuvant setting.1 The patients, who already had surgery, were randomized to chemotherapy with trastuzumab plus pertuzumab or placebo. The primary end point was invasive-diseasefree survival. They did not restrict the type of chemotherapy; it could be anthracycline or nonanthracycline based. Patients who had hormone-positive disease also got endocrine therapy.

[In the] updated analyses, with invasive-diseasefree survival by subgroup, in the intention-to-treat population, there was just under 3% improvement with the use of pertuzumab. It did not seem to matter whether they were hormone positive or hormone negative, but where the difference was really seen was in the patients who were node positive. The patients who were node positive were driving the benefit seen, and patients who were node negative did not see [much] difference with the addition of pertuzumab. So far, we do not have any overall survival benefit, but it is early and we are waiting for those results.

What is the role of the subcutaneous formulation of trastuzumab and pertuzumab?

The combination of trastuzumab, pertuzumab, and hyaluronidase [Phesgo] for subcutaneous injection has an FDA-approved indication for both early-stage and metastatic disease.6 It can be used in the neoadjuvant or adjuvant setting in combination with chemotherapy, and in the metastatic setting in combination with taxane therapy, predominantly in the first line. I believe it is preconcentrated. I know with the loading dose it is a slightly higher volumeI think it is 15 mL as opposed to 10 mLbut it is [like] a fixed dose.

The FeDeriCa study [NCT03493854] showed that the pharmacokinetics are essentially the same between the subcutaneous formulation and the IV formulation.7 In other studies that have used combination trastuzumab and pertuzumab in those settings, the thought is that the fixed-dose combination can be used for those indications as well.

FeDeriCa was a phase 3 study that was looking primarily at the pharmacokinetics. Patients who were getting preoperative chemotherapy, which was predominantly anthracycline based, were randomly assigned to IV formulation or subcutaneous formulation, and then they had surgery, and then afterward they were continued either on the IV formulation or the subcutaneous formulation. The primary end point was noninferiority of the cycle 7 trough concentration of the pertuzumab, with the fixed dose compared with the IV formulation.

One of the advantages of doing neoadjuvant studies is that we have an immediate end point of response rate. The rate of pCR was the same for both [Figure7]. It was well tolerated; no major differences in risks associated with the IV vs the subcutaneous formulation. A few more patients had a little bit of irritation at the injection site vs infusion reactions.

If you want to discontinue pertuzumab in a low-risk patient as adjuvant therapy, do you have to change back to IV?

There is a trastuzumab-[plus hyaluronidase] subcutaneous injection. The brand name is Hylecta. So, it is the same idea: If you can get access to Phesgo or the dual HER2 injection, you should be able to get access to the trastuzumab-based injection. The trastuzumab-based injection also has extensive pharmacokinetics studies showing that it is similar in efficacy to IV trastuzumab.8,9

Can you discuss the difference in timing between IV and subcutaneous administration?

With standard IV, in the first loading dose, the pertuzumab is supposed to be given over [30 to 60] minutes, and the trastuzumab is given over 30 to 90 minutes, and you have this observation period in between [of 30 to 60 minutes]. It can take hours.

Once you are on and tolerating the trastuzumab and pertuzumab IV, they can be given over 30 minutes each. There is a much shorter observation window, but nonetheless it is going to be at least 1 hour, potentially up to 2 hours. Whereas with the fixed-dose subcutaneous administration, the injection itself takes a couple of minutes. You watch them for another 15 to 30 minutes, so the total time is generally 20 to 40 minutes, so it takes at least half the time. This opens chair time for other patients who need IV infusions, and saves patients from having an IV placed, and it allows them to potentially get their port removed earlier. Generally, it can provide benefits to patients and providers. One thing that remains to be seen is whether this is something that eventually could be given at home.

I was working in Philadelphia at the beginning of the [COVID-19] pandemic, and the University of Pennsylvania at that time took most of the patients who were on leuprolide [Lupron] for ovarian suppression and transitioned them to home nursing. All of those patients were getting injections at home with their leuprolide. They did not have to come in. If you have skilled nursing in the community, is this something that patients may even be able to get at their home or their office? I think that is something that has potential for opening that up as an option, which would be even better for patients.

What is known about which option patients prefer?

We see, based on the PHranceSCa study [NCT03674112], that patients do prefer the subcutaneous formulation.10 PHranceSCa looked at patient preference. Patients who had completed their chemotherapy and surgery and were going to be completing a year of HER2-directed therapy were randomized. Half of the patients got the IV formulation, half got subcutaneous administration for the first 3 cycles, and then they crossed over and switched to whichever one they had not received before, and then they were allowed to choose which one they wanted to finish the rest of the year of HER2 therapy with. The primary objective was patient preference.

What we saw was that 85% of patients preferred the subcutaneous formulation over the IV and 87% chose to use that subcutaneous formulation to finish their treatment after experiencing it. The main reasons were less time in clinic and administration being more comfortable.

REFERENCES

1. Piccart M, Procter M, Fumagalli D, et al; APHINITY Steering Committee and Investigators. Adjuvant pertuzumab and trastuzumab in early HER2-positive breast cancer in the APHINITY trial: 6 years follow-up. J Clin Oncol. 2021;39(13):1448-1457. doi:10.1200/JCO.20.01204

2. von Minckwitz G, Procter M, de Azambuja E, et al; APHINITY Steering Committee and Investigators. Adjuvant pertuzumab and trastuzumab in early HER2-positive breast cancer. N Engl J Med. 2017;377(2):122-131. Published correction in N Engl J Med. 2017;377(7):702

3. von Minckwitz G, Huang CS, Mano MS, et al; KATHERINE Investigators. Trastuzumab emtansine for residual invasive HER2-positive breast cancer. N Engl J Med. 2019;380(7):617-628. doi:10.1056/NEJMoa1814017

4. Tolaney SM, Barry WT, Dang CT, et al. Adjuvant paclitaxel and trastuzumab for node-negative, HER2-positive breast cancer. N Engl J Med. 2015;372(2):134-141. doi:10.1056/NEJMoa1406281

5. Chan A, Delaloge S, Holmes FA, et al; ExteNET Study Group. Neratinib after trastuzumab-based adjuvant therapy in patients with HER2-positive breast cancer (ExteNET): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol. 2016;17(3):367-377. doi:10.1016/S1470-2045(15)00551-3

6. Phesgo. Prescribing information. Genentech; 2020. Accessed May 5, 2022. https:// bit.ly/3RFnCsv

7. Tan AR, Im SA, Mattar A, et al; FeDeriCa study group. Fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection plus chemotherapy in HER2-positive early breast cancer (FeDeriCa): a randomised, open-label, multicentre, non-inferiority, phase 3 study. Lancet Oncol. 2021;22(1):85-97. Published correction in Lancet Oncol. 2021;22(2):e42

8. Pivot X, Verma S, Fallowfield L, et al. Efficacy and safety of subcutaneous trastuzumab and intravenous trastuzumab as part of adjuvant therapy for HER2-positive early breast cancer: Final analysis of the randomised, two-cohort PrefHer study. Eur J Cancer. 2017;86:82-90. doi:10.1016/j.ejca.2017.08.019

9. Jackisch C, Stroyakovskiy D, Pivot X, et al. Subcutaneous vs intravenous trastuzumab for patients with ERBB2-positive early breast cancer: final analysis of the HannaH phase 3 randomized clinical trial. JAMA Oncol. 2019;5(5):e190339. doi:10.1001/ jamaoncol.2019.0339

10. OShaughnessy J, Sousa S, Cruz J, et al; PHranceSCa study group. Preference for the fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection in patients with HER2-positive early breast cancer (PHranceSCa): a randomised, open-label phase II study. Eur J Cancer. 2021;152:223-232. doi:10.1016/j.ejca.2021.03.047

Originally posted here:
Recommended Approaches to Treatment for Early-Stage HER2+ Breast Cancer - Targeted Oncology

Recommendation and review posted by Bethany Smith

TUCKER CARLSON: The Democratic Party is replacing parents with itself – Fox News

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In your head, you always imagine the revolution when it starts. It'll start with tanks and gunfire with chaos and soldiers in the street. You'll know when it comes, but it never does. Instead, the really big changes to American life, the profound ones that affect all of us forever, those changes almost always begin quietly with gentle pleas for tolerance. We'd like to do things a little differently, they tell you. We'd like to make a change to some custom or belief that people have been attached to for the last few thousand years, but don't be alarmed. It's not a big deal. You don't even need to participate. All we ask is that you let us live the way we want to live.

That's always the pitch and of course, you always agree to it. Why wouldn't you? Who could say no to that? Some guy down the street wants to wear a dress? OK, fine, have a party. It doesn't affect you. You don't have to wear a dress, so go ahead. Live and let live, but it turns out that's never actually the deal. The guy down the street wears his dress, but after a while, that's not enough for him. He's still angry and for some reason, he's angry with you. And that doesn't make sense because you're the person who had no problem with him wearing a dress in the first place. What did you do wrong?

Well, the problem is you're not wearing a dress and neither are your kids. Your normal-person clothes, the ones you've always worn, are suddenly immoral. You've got to change immediately.

Now, wait a second, you say, that's not what we agreed to. You do your thing and I'll do mine. Remember? They don't remember. They don't care. That's not how it works. You don't get to do your thing anymore. The dress guy's in charge now. Everybody's got to do his thing, the dress thing or face punishment. That's how it goes. "Be tolerant" becomes "show some respect" which evolves very quickly into "bow down before us and lick our feet or else will hurt you." That's the final stage. That's where we are now.

For example, a Democratic lawmaker in Virginia called Elizabeth Guzman is introducing a bill that will charge parents with a felony, strip them of their employment and imprison them if they don't wholeheartedly endorse their minor children's sex changes. So, your 12-year-old daughter says she wants a mastectomy. If you object to that in any way, if you raise questions, Elizabeth Guzman will send you to jail for real. Here's a local news report.:

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REPORTER: Her bill would expand the state's definition of child abuse and neglect to include parents who do not affirm their child's gender identity or sexual orientation.

ELIZABETH GUZMAN: There is an investigation also in place that is not only, you know, from a social worker, but there's also a police investigation before we make that decision that there is going to be a CPS charge.

REPORTER: What could the penalties be if the investigation concludes and it's concluded that a parent is not affirming of their LGBTQ child? What could the consequences be?

ELIZABETH GUZMAN: Well, we first have to have an investigation. You know, it could be a felony. It could be a misdemeanor, but we know a CPS charge could harm, you know, your employment, could harm your education.

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Who is this Elizabeth Guzman? Well, Elizabeth Guzman came to this country not so long ago from Peru as a single mother. Now, rather than wait a while, maybe spend a few generations here before telling you how to raise your children in America, she's decided to get right to it and completely change child-rearing in this country in a way that would never be tolerated for a second in the country from which she comes. Try that in the Andes, honey, and see how that works. Yeah.

But in this country, according to Elizabeth Guzman, you have to affirm your child's sex change or else you're going to prison and the state will raise your kids.

Now you got to think maybe they've wanted this for a while. What would this mean? Well, it would mean fewer intact families. It would mean people like Elizabeth Guzman make the decisions, the meaningful decisions within your house. It means less resistance from you. It means more powerful them. What it doesn't mean is that Elizabeth Guzman will be protecting your kids. She doesn't even claim this law will protect your kids. Instead, she acknowledges the whole point is to "educate parents." Right.

Like the COVID vaccine, this is a pretty easy way to figure out who's on which side. Are you for this? OK, you're on our team. You're willing to surrender control of your own children to Elizabeth Guzman, who, again, just got here. But if you're not for it, then we know you're not on our team. We know who you are. We can silence you. We can punish you because you refuse to be educated.

So, it's a signaling mechanism and you know that because the ideology that underlies it, gender ideology, is completely incoherent. It doesn't make any sense at all. It is not rooted in science. It's a form of religion that's so crazy it dares you to say something about it. What? You can't even say that. If you do, they know you're on the other side.

And it's not just lunatics and ideologues like Elizabeth Guzman from Peru. It's doctors, it's medical professionals.

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Here's a video from Boston Children's Hospital, one of the most famous hospitals in the world, which like many hospitals in the United States at this point under the Joe Biden administration cut the breasts off of minor girls for no medically justifiable reason. Watch a practicing psychologist, now attending psychologist, at Boston Children's Hospital explain how early children can become trans.

DR KERRY MCGREGOR, BOSTON CHILDRENS HOSPITAL: So, most of the patients that we have in the clinic actually know their gender, usually around the age of puberty, but a good portion of children do know as early as seemingly from the womb, and they will usually express their gender identity as very young children, some as soon as they can talk. They might say phrases such as "I'm a girl" or "I'm a boy" or "I'm going to be a woman" or I'm going to be a mom." Kids know very, very early. So, in the Gems Clinic, we see a variety of young children all the way down to ages two and three and usually up to the ages of 9.

That's Kerry McGregor. She's a psychologist. She works at Harvard. I wonder how many children Kerry McGregor has. Has she raised a lot of kids? Has she watched kids carefully? Does she know anything about kids? Because she's telling you if you're a little kid says, "Oh I may be on the other sex," that means your kid is the other sex. Well, that's insane, because almost 100% of kids at one point or another, at a certain point in development, say things like, "I think I'm a boy. I think I'm a girl" and you smile indulgently, "Get back to me in 15 years."

But no, says Kerry McGregor, in the womb you can know.

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Think about what they're telling you. They're telling you that developing child in the womb is just a part of the mother. Therefore, you can abort that child at any time. It's like an appendectomy, but at the same time, that same cluster of cells, that fetus, can also be woke and ascribe to left liberal gender ideology and you need to honor that.

No sane person could believe any of this voluntarily. It doesn't even make sense on its face. Again, it's a religion and if you resist it, they resort immediately to force. No questions allowed. Again, this is science and the essence of science is relentless questioning about what you think you know is true. That is the scientific method. That's science itself, but it's no longer allowed.

The American Medical Association, which hasutterly beclowned itself, along with the American Academy of Pediatrics and the Children's Hospital Association, just sent a letter to the attorney general of the United States demanding that the Biden administration, and we're quoting, "take swift action to investigate and prosecute high profile users on social media" who have engaged in "disinformation."

You hate to always invoke the German government of 80 years ago, but what else is that? That's totalitarian. They're saying if you disagree with what we're doing, people with guns should come and take you away. Now you'd think someone in the media would point out, "Wow, you know, we can't have that in the United States where people are free to believe what they want and to talk about it in public and to ask questions." In fact, they should be encouraged to, but the media don't say anything like that. They're joining with the Children's Hospital Association, the AMA, to call for more censorship at gun point. Watch.

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MEDHI HASAN:Obviously the question becomes then when misinformation, disinformation is being spread, when hate and threats are being spread, where are the social media companies? What's YouTube doing? What's Twitter doing? And of course, then you have the reaction to that "Oh, this is big tech silencing people." It always becomes a debate about free speech, doesn't it?

BRANDY ZADROZNY: Yeah, it does. You know, last week, Twitter suspended Libs of TikTok specifically for the policy against the promotion of threats, violence and harassment. So, great job, right? But it's been seven days and Libs of TikTok is back now and they're tweeting right this very minute. This is violence, this is harassment. It's clear what these accounts are doing.

It's so funny. Back to the point at the open, when the revolution comes, there won't be tanks and soldiers won't be stormtroopers in all uniforms and symbols. It'll be some unmarried 30-year-old woman talking in a singsong voice inflection at the end. Right. Right. Special glasses or complex glasses that don't actually improve her vision. She'll have all kinds of pointless humanities degrees and she'll be on cable news and say its violence. What she's really saying is "shut up and obey or will hurt you." She's delivering the same message any stormtrooper delivers, but she's doing it in a singsong way. This is disinformation.

Call us literal, but this is the opposite of disinformation, isn't disinformation. This is literally what they're seeing. Boston Children's Hospitals, which we showed you on tape, is telling you what they're doing. They perform double mastectomies on miners for no medical reason whatsoever. That's insane. It ought to be a crime. In a civilized country it would be and they know that because when they were caught, they tried to erase the evidence and they're not alone.

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UCSF, U.W. Health in Wisconsin, Golisano Children's Hospital in New York, Vanderbilt Health, Children's Minnesota, all of these hospitals have deleted the evidence of their gender-affirming procedures, their grotesque mutilation of children after they were publicized. Their own words were publicized online. No one's twisting it. People are just putting up their words and not all the videos have been deleted.

Planned Parenthood is big into this now because it's lucrative. Here's Planned Parenthood in 2021 telling children that so-called puberty blockers are harmless. Oh, right. That's a lie and by the way, there's no such thing as a puberty blocker. These drugs are hormone agonists and they're FDA approved for things like cancer treatment. You get prostate cancer and they lower your testosterone, for example, to prevent the cancer from growing quickly. They are not approved for so-called "puberty blocking." They're unapproved and the long-term effects are not known, but it's pretty obvious they're grim, but Planned Parenthood won't tell you that. Here's their video.

PLANNED PARENTHOOD VIDEO: You're transgender or non-binary. You may find that your puberty experiences don't line up with your gender identity or how you see yourself. That feeling can be uncomfortable, scary and stressful. If that sounds like you, know that you're not alone. There are medicines you can take to delay puberty for a while. They're called puberty blockers, and they work like a stop sign by halting the hormones, testosterone and estrogen that cause puberty changes like facial hair growth and periods. Puberty blockers are safe and can give you more time to figure out what feels right for you, your body and your gender identity.

Everything about that is dark and horrifying and there should be an uprising against that. That's aimed at your childrennot at adults who can make rational decisionsbut children who are people too young to drive or drink alcohol or smoke cigarettes or serve in the military or vote, people who are not (we have agreed as a group) capable of making rational adult decisions and that's aimed at them. It's propaganda aimed at them and it's a lie. Puberty blockers are safe. They are absolutely not safe. You can't delay puberty without damaging severely the bodies of young children. The FDA just identified several "clinically serious cases" of side effects after these drugs were recklessly administered to children by lunatic ideologues.

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FILE- In this June 4, 2019, file photo, a Planned Parenthood clinic is photographed in St. Louis. (AP Photo/Jeff Roberson, File) (AP Photo/Jeff Roberson, File)

The FDA found a "plausible association" between the use of puberty blockers and something called intracranial hypertension. Do you want that for your 13-year-old?

According to the Mayo Clinic, that condition can cause brain swelling, double vision, severe headaches, permanent vision loss. In other words, brain damage. Brain damage! Oh, great. OK.

On top of that, the European Journal of Endocrinology, among many other publications, has found that so-called puberty blockers often cause, "decreased bone density, which is associated with a high risk of osteoporosis" and there are other permanent side effects as well. We don't even know the scope of them because this has never been tested longitudinally ever, but the effects are very obvious and if you poke around on the internet for about 4 minutes, you will see them. One teenage girl just uploaded a video showing the effects of five years of puberty blockers on her. Watch this.

VIDEO: When I talk about being too far gone, I don't really know what else to call it, this is what I mean. This is how deep my voice is. It's gotten deeper over time and it's settled. This is what I mean by hair loss and it just keeps getting worse. It keeps thinning. It keeps receding backwards. You know and I'm not exactly sure that's coming back. Those are the main things when I talk about being androgenized to a point of no return. This is what happens when you give a women testosterone for five years. This is what happens.

Yeah. That's what happens. That and a lot of other things. That's what they're telling you is "gender-affirming." No, it's mutilation. It's grotesque. It's destroying people's lives, children's lives. We made a documentary on this for "Tucker Carlson Originals." We spoke to a lot of people who had endured similar torture.

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HELENA: The testosterone kind of had this effect on me, where with every step that I took, it would feel good for a short amount of time, but then eventually it's like those same feelings come back up.

WALT: There's the initial euphoria that you go through. I changed my gender and everything's going to be wonderful.

KATHY: It was euphoric. I was like, the feeling I had when I started living as a man was I was free. I was finally who I should have been all along.

TUCKER NARRATION: But that euphoria was short-lived.

KATHY: My mental health just got worse. My ability to socialize just got worse. I felt so disconnected from myself. I started using, like drugs and alcohol as a crutch, and I was just a total disaster and the effects of the testosterone on my mental health specifically just made everything 10 million times worse.

WALT: I had bought into the lie and almost took my life.

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It's just awful and every person who is participating in this in their moments of clarity knows that ten years from now, there will be thousands of vocal victims of this moment of true craziness and hysteria that has gripped our country. People's lives are being destroyed right before us. Most adults are too cowardly to say a word about it and the Democratic Party is actively doing all it can to promote this to protect hospitals that are mutilating and destroying the lives of children.

in the state of California Always a bellwether a legislator called ScottWienerhas just sponsored legislation to make California a so-called sanctuary state for kids who want to mutilate their own bodies to castrate themselves. Scott Wiener, really? Is he a good father? Would you trust this guy within 500 yards of a child? Probably not.

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Democrat Gov. Gavin Newsom of California (Tom Williams/CQ-Roll Call, Inc via Getty Images)

Gavin Newsom just signed the bill, of course. So, what's the point here? It's not to protect children. It's not protecting them. Any parent will tell you if you want to protect children, you tell them, take a deep breath and reach adulthood and then make rational decisions about how to live their lives.

You would definitely not let them make a decision, an irreversible decision like this, for themselves. You're their parent. That's the whole point. But the Democratic Party doesn't like parents. The Democratic Party is replacing parents with itself. We're in charge now. It's the most recognizable possible move for any totalitarian movement. Break up the family. Replace parents with politicians. The state is in charge. The party is in charge, obviously, and it's happening all over the country.

Tucker Carlson currently serves as the host of FOX News Channels (FNC) Tucker Carlson Tonight (weekdays 8PM/ET). He joined the network in 2009 as a contributor.

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TUCKER CARLSON: The Democratic Party is replacing parents with itself - Fox News

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‘You will get your heart broken. Not might, will.’: Foster mom shares heartwarming adoption after infertility, heartbreak – Love What Matters

Disclaimer: This story contains details of miscarriage which may be upsetting for some.

March 21st, 2022 was the best day of our lives. We adopted our middle daughter and our family was complete. But what got us there? Its easy to see all the highs of adoption, but few know all that goes into getting to that point.

Our story starts back in 2012, when Jared and I (Taylor) met at a softball game. Jared and I went to the same small high school in rural Indiana but did not know each other well as Jared was a few years older than me. After high school, I went to a softball game with a friend to watch her boyfriend play. I was then introduced to Jared and we became friends.

We started dating in the beginning of 2013, and we were engaged just before Christmas that year. We bought a house in May, adopted a couple dogs, and married July 26, 2014.

It was a quick engagement but we were both so confident in our decision and commitment to one another. Early on in our relationship we knew we wanted to have kids. We always envisioned having three or four kids and had always tossed around the idea of foster care and adoption, but were really enjoying just being married.

Two years after getting married, I found out I was pregnant! We were so excited and couldnt wait to begin our lives as parents. I had a relatively easy pregnancy and our daughter, Claire Kristine, was born December 6th, 2016. She was a perfect 9-pound baby, and we ooohed and ahhed over her for days. We quickly settled into our roles as parents and tried our best every day to raise Claire with love and kindness.

The sleepless nights were rough and the exhaustion was catching up with us, but nothing could wipe that new parent glow off our faces. Around Claires first birthday, we bought some land in our hometown and decided to build a home so we could raise Claire (and our future children we were dreaming of having) in the same small-town we grew up in.

We dreamt of farm animals, land to run on, unobstructed sunsets, and perfectly clear starry nights. We lived with my parents during the (longer than expected) building process and were beyond grateful for that opportunity, but were anxious to get back into our own house. We closed on our newly built home on Valentines Day 2019!

At this point in time, Claire was two years old and we had started getting the dreaded questions: Are you going to have more kids? Claire needs a brother or sister! Is she going to be an only child forever? We knew we wanted more kids and now that we were finally in our new house, we felt comfortable adding to our family.

After months of negative pregnancy tests, we were referred to a fertility clinic just to check on everything. The questions from well-meaning people started to hurt and I started to feel like there was something wrong with me. Maybe we would just have one child.

Lots of tests and blood work was done and I had a procedure scheduled. A week before the procedure I found out I was pregnant! I told Jared right away and we were beyond thrilled. I giddily called the fertility clinic and they asked me to come in so they could draw labs and check hormone levels. A couple days later I confidently walked into the clinic to have my blood drawn and was told my due date, June 14th 2020.

Not long after that, the bleeding started and my hormone levels dropped. I was having a very early miscarriage. My world shattered. What? A miscarriage? How is this fair? Didnt that baby know how loved they already were? Did God know how much we wanted this? We were doing everything right; this shouldnt be happening. But it was. Our very wanted child was gone and I was broken.

Thankfully, we were still working with the fertility clinic, had wonderfully supportive family and friends, and clung to our faith. All together they were helping us navigate how to move forward. I remember listening to the song Even If by MercyMe on repeat day after day, just trying to remind myself it would all be okay.

Several doctors appointments and trips to Chicago later, I was told my fallopian tubes were blocked and it was very unlikely I would have more children naturally. The doctor recommended IVF. The state of Indiana does not require health insurance companies to cover fertility treatment, so very few do. The cost, as so many families know, is extreme and it wasnt something we were ready to look into yet. After much prayer and discussion, we decided foster care was the right path for us.

Foster care wasnt a new subject for us. I grew up with an aunt and uncle who fostered children and ended up adopting 2 boys. I have cousins adopted from other countries. We had friends who fostered and we had talked about becoming foster parents in the past. Both of our families are extremely supportive and we knew we would have endless help on this journey.

Shortly after our miscarriage, we contacted our local DCS agency and started the literal mountain of paperwork. The paperwork is long and intense. The questions get personal and it took months to finish.

After we submitted our paperwork, a caseworker came over and studied our home. You talk about fire plans, how to properly store cleaning supplies, and they look into every part of your home and life. We took classes, were re-certified in CPR, had forms filled out and physicals done by our doctors, and asked for references to fill out forms for DCS. Once all of that was said and done, we each sat down separately with our caseworker and had a five-hour interview. Yes, you read that correctly, five hours.

In this interview they dove into our childhood, our past, our traumas, and the highs and lows of our life. They asked hypothetical questions, and attempted to learn every part of our life. Though it seemed daunting and excessive, I understand it now. If my child had to be placed in a strangers home (even if the reason for removal was my own doing) I would want to know they were staying with a family who could appropriately love and care for them.

I remember during one point of my interview, the very nice lady who was interviewing me asked why we wanted to foster and what we were hoping to gain from becoming foster parents. I explained our past fertility issues, the miscarriage, our desire to grow our family, and wanting to share the love we had to give with other children, even if it would only be for a short period of time.

The woman looked at me, gently placed her hand on mine, and said, I need you to know, you will get your heart broken. Not might, will. In this journey, your heart will shatter into a million pieces, things wont always go how you think they will, and your heart will break. Please reach out for help and get support to help you through those inevitable times. She wasnt saying that to scare me but rather to prepare me, and I often thought back to her words during our foster care time.

We became officially licensed foster parents in March of 2020, right at the beginning of the Covid-19 pandemic. Life went on and we didnt receive any phone calls for placements. We had specified we wanted to only foster children younger than our daughter for the time being; we felt that would be best for our family. DCS was more than happy to accommodate our wishes, but did let us know we might not get a call right away.

One month after becoming licensed, I found out I was pregnant again! Joy and fear filled our souls as we anxiously fumbled through the first trimester. Our fear began to subside as bloodwork showed rising hormone levels and we got to see our sweet babe on the ultrasound.

June 14th, 2021 came and it was a hard day. It was our miscarried babys due date and although I was pregnant again, I longed to have that baby in my arms. It was a Sunday and after church Claire and I went to watch Jareds weekly softball game. The game had barely started and my phone rang it was DCS.

I answered and they explained to me they were looking for a placement for a three-day old baby girl. Without even talking to Jared, I said yes. DCS told me to head to the hospital with a car seat for the baby and to have Jared go to the house to meet the social worker and go over everything for the placement. I pulled Jared out of the game and excitedly told him what was happening. He was completely on board and we all headed home to prepare.

As soon as I got home, I grabbed the infant car seat, gave Claire and Jared a hug and a kiss, then headed for the hospital while they stayed behind to wait for the social worker and prepare things for the baby. Upon arrival at the hospital, I was put in a room and told to wait.

A few minutes went by and the nurse wheeled in this tiny, precious 6-pound baby girl. I held her, rocked her, and told her how much I loved her while the nurse went over all the basic discharge information. During this process it hit me: I am in the hospital, holding a newborn baby, on my miscarried babys due date.

God knew what I needed and He provided, like He always does. After lots of paperwork, I carefully drove home and introduced Jared to our foster daughter and Claire to her foster sister, Addisyn.

Addie was such an easy baby and the love we felt for her was no different than the love we felt for our biological child. Our family fell in love with her just as quickly and they were all so helpful as we adjusted to life with a newborn again. Addie had visits with her biological mother on a regular basis as well as several court hearings. It was hard to get used to the ever-changing schedule of visits, court, and caseworkers stopping by but we managed.

Time was flying by and Addie was growing so quickly. Before we knew it, summer turned to fall and Thanksgiving was approaching. During various court hearings and conversations with our caseworker, talks of adoption began to happen. We tried not to get our hopes up, but we couldnt help it. The thought of adopting Addie made our hearts soar. We carried on and were so excited for the holiday season with Addie and the upcoming due date of our baby.

The day before Thanksgiving 2020, Claire and I were in the kitchen baking pies while Addie napped when my phone rang. It was our case worker telling me they needed a home for Addies older brother immediately. We were the only option and he would be at our house in a few hours.

We couldnt turn down a child in need of a home but we were in no way prepared for a 2-year-old boy! I frantically called my husband, my parents, family members, and a few friends, and cried to them as I tried to figure out what to do. (Eight-month pregnant Taylor was very overwhelmed at this point).

Jared came home from work, rearranged Addies room, and put together the extra bed we had in our basement. My dad went to the store to purchase a mattress and bedding. My mom and sister helped me pick up the house and get everything ready. My aunt and grandparents dropped off diapers, clothes, sippy cups, and toys (because this girl mom didnt have anything for a little boy!).

My boss and her husband dropped off more diapers, clothes, and shoes in a variety of sizes. My two best friends came over and made dinner, folded laundry, and reassured me everything would be okay. Our friends and family rallied together and made so much happen in such a short period of time. Ill never be able to appropriately express my gratitude toward them.

The sweetest little boy came to our home that night, scared and confused, but thanks to our amazing people, we had everything we needed to help make him feel comfortable and loved. The next few weeks were an absolute whirlwind. We often werent sure what was happening from one day to the next; we were just trying our best to make the world a little calmer for our kids.

We moved on with the busy holiday season, making it special for everyone in our home. We went Christmas shopping, cut down our Christmas tree, sent out Christmas cards, looked at the lights, and tried to soak up the magic of the holiday season.

A couple weeks into December, shortly after Claires 4th birthday, our caseworker called to tell us Addie and her brothers grandparents were going to be taking both kids. Our hearts sank, we couldnt speak. We knew these children might not be permanent members of our home, but that didnt ease the heartache.

We packed up all of the childrens belongings the best we could and spent every last second showering them with love. Addies brother left first as he already had a relationship with his grandparents. Addies grandparents graciously let us have a few extra days with her.

Over those days we finished packing up Addies whole life into Rubbermaid totes, taking her to see family and friends so they could say goodbye, and soaking up every last second with this perfect 6-month-old baby girl. We were fortunate enough to be able to meet Addies grandparents and actually drop her off at their house. While it didnt make saying goodbye any easier, it was nice to get to know the people who would be caring for her. They even agreed to exchange phone numbers so they could text us pictures and updates.

Claire, Jared, and I all gave Addie one last hug and kiss, as we sobbed getting back into the minivan we had purchased that summer to fit all of the kids. The heartbreak DCS warned us about was happening and it was awful.

Jared and I tried to get back to normal as quickly as possible in order to make things easier for Claire. She had been through a lot over the last six months and we didnt want her to be any more sad or confused than she already was.

The three of us enjoyed a nice Christmas, prepared for the arrival of our second biological baby, and thought about Addie every single day. We were able to stay in touch with her grandparents on a semi-regular basis but we missed her like no other.

We decided to be listed as on hold with DCS as we grieved our last placement, and to give us time to adjust when our baby arrived. January 15, 2022, I gave birth to another beautiful baby girl, Piper Kate. She was the sweetest baby and she healed our hearts.

Claire was loving being a big sister again, but often asked if we would always get to keep this baby. Jared and I reassured her Piper was here to stay, forever. We carried on as a family of four, getting into a routine, and enjoying every moment (except maybe not the ones when Piper was screaming nonstop).

In April, when Piper was four months old, Addies grandparents reached out to us. They asked if we would be willing to take Addie back into our home and family. Due to some unforeseen circumstances, they felt it was best if we raised her, but they would still like to be a part of her life. We said we would absolutely love to foster her again and they would 100% be involved as grandparents.

We talked to and arranged everything with DCS, and a few weeks later Addie moved back in. Our home was so full of joy! Life was hard but so incredibly full. It took time and a lot of support from our family and friends. We slowly settled into our roles as parents of three girls.

In the following months we had lots of court dates, caseworker visits, and Addie had visits with her biological family just like before but things were a bit different this time. Addies permanency plan was changed to adoption. We were cautiously hopeful.

That winter our caseworker advised us to hire an attorney and start getting paperwork ready to adopt Addisyn. We found an amazing attorney to represent us and she began drawing up everything we would need for adoption.

During this time we began to develop a relationship with Addies birth mom. I sent her pictures and updates periodically and she mailed us letters to give to Addie when she is older. She expressed her gratitude to us for caring for sweet Addie and we did our best to express our gratitude to her for blessing us with such an amazing little girl, though theres no way to every thank her for that beautiful gift.

March 21st, 2022, we gathered in a courtroom to officially make Addisyn our daughter. The room was filled with people we love: parents, grandparents, siblings, friends, caseworkers, and even Addies biological grandparents. We hired a photographer to capture every moment of this special day so we would never forget.

We promised to love, care for, and provide for Addisyn, just as we would Claire and Piper, for her entire life. There were tears, smiles, fist bumps, and cheers because Addisyn was officially an Emmons! Addisyn Kay Jean Emmons, forever.

Our days are chaotic but full of love. Claire is 5, Addie is 2, and Piper is 1.5. They wear Jared and I out every single day, but we wouldnt have it any other way. Never in our wildest dreams did we think we would have daughters just seven months apart in age, but God had other plans for our family!

Our foster care license is temporarily suspended so we can focus on our three young children and not losing our sanity. Im not sure what the future looks like for us as foster parents, but we love to help any way we can. There is a great need for loving people in the foster care system and even if you cant foster, you can still help. Adopt, foster, donate, or volunteer. Everybody can do something to make the world a little brighter for our future.

This article was submitted to Love What Matters by Taylor Emmons of Rolling Prairie, IN. You can follow her on Instagram. Join the Love What Matters family and subscribe to our newsletter.

Read more stories like this:

They chose us. Theyre coming in two hours!: Couple shares unexpected sibling adoption from foster care

We got a call for an 8-month-old boy. There were no details. If were going to do it, we might as well just do it!: Woman details journey becoming foster parents

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'You will get your heart broken. Not might, will.': Foster mom shares heartwarming adoption after infertility, heartbreak - Love What Matters

Recommendation and review posted by Bethany Smith

31 days of horror movies: Orphan: First Kill is a reminder to have fun with movies – 1428 Elm

Orphan: First Kill, directed by William Brent Bell (The Boy, Brahms: The Boy II), was released in 2022 and is a prequel to the 2009 flick, Orphan. Like its predecessor, First Kill follows the exploits of the murderous Leena (Isabelle Fuhrman), a 31-year-old woman with a hormonal disorder called hypopituitarism that gives her the appearance of a 10-year-old child. Leena uses this to her advantage, scheming her way into different families who have a first date with their Maker once the gloves (or in this case, the teeth) come off and Leena reveals her true intentions. While the story is loosely based on a case in real life, the campy set-up suggests a film that doesnt take itself too seriously and audiences shouldnt either. Note: I will be discussing spoilers from Orphan and Orphan: Kill, so consider this your official spoiler warning.

Isabelle Fuhrman as Esther in Orphan: First Kill from Paramount Players, eOne, and Dark Castle Entertainment. Photo Credit: Steve Ackerman/Paramount Pictures

Orphan: First Kill has the benefit of leaning into all the campy elements in the first film, which had to play them off as slightly more serious and presented Leena as a straightforward villain. I think the first film is well-made, definitely thrilling, and pretty shocking with some of the material it presents, and not just with Leenas twist. However, First Kill is where the fun begins and it centers the attention directly on Leena rather than the family shes infiltrating.

First Kill opens with Lena staging her escape from the Saarne Institute by seducing one of the guards and killing the institutes art therapist Anna. Because audiences are already familiar with the twist, First Kill wastes no time in presenting Leena as a homicidal, but calculated maniac. Leena researches missing American children with whom she bears a resemblance, choosing to pass herself off as Esther.

Within no time and hardly any investigation later, Esther is the in the states with her family the Albrights: mother Tricia (Julia Stiles), father Allen (Rossif Sutherland), and their son Gunnar (Matthew Finlan). Julia Stiles steals the spotlight as the matriarch of the Albright clan, and while Vera Farmigas character in Orphan was beaten down and broken by tragedy, Stiles Tricia is the opposite: calculated, cruel, manipulative, and straight-up evil.

You see, the twist of First Kill is that Julia was responsible for killing her own daughter Esther and staging her kidnapping to protect the reputation of her equally as awful son Gunnar. Leenas arrival as Esther presents Julia with an unexpected opportunity, to save her marriage with her unaware husband and position her family back to the top of the social ladder. Julia wastes no time in letting Leena know shes on to her, suddenly forcing the audience to take Leenas side as she faces off against someone whos just as manipulative and cruel.

First Kill takes the psychological elements present in Orphan and turns them on their head for a ridiculous slasher film that allows itself to have fun with its premise. Sure the film might have some plot holes and other elements worth critiquing, but at the end of the day, its an entertaining outing with Esther, who I would love to see in more films. A certain suspension of disbelief is required when tuning in to films like Orphan: First Kill.

Sometimes its okay to have fun with a movie and relax the expectation that each new film will break the mold or be the next huge thing. To be honest, I was grinning the entire movie because its just what I like in a horror flick, unapologetic fun, and off-the-rails insanity.

Orphan: First Kill is currently streaming on Paramount+.

Do you think Orphan: First Kill deserves a spot on your October watch list? Tell us why or why not in the comments section.

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31 days of horror movies: Orphan: First Kill is a reminder to have fun with movies - 1428 Elm

Recommendation and review posted by Bethany Smith

The 2016 WHO Classification of Tumours of the Urinary System and Male …

The fourth edition of the World Health Organization (WHO) classification of urogenital tumours (WHO "blue book"), published in 2016, contains significant revisions. These revisions were performed after consideration by a large international group of pathologists with special expertise in this area. A subgroup of these persons met at the WHO Consensus Conference in Zurich, Switzerland, in 2015 to finalize the revisions. This review summarizes the most significant differences between the newly published classification and the prior version for renal, penile, and testicular tumours. Newly recognized epithelial renal tumours are hereditary leiomyomatosis and renal cell carcinoma (RCC) syndrome-associated RCC, succinate dehydrogenase-deficient RCC, tubulocystic RCC, acquired cystic disease-associated RCC, and clear cell papillary RCC. The WHO/International Society of Urological Pathology renal tumour grading system was recommended, and the definition of renal papillary adenoma was modified. The new WHO classification of penile squamous cell carcinomas is based on the presence of human papillomavirus and defines histologic subtypes accordingly. Germ cell neoplasia in situ (GCNIS) of the testis is the WHO-recommended term for precursor lesions of invasive germ cell tumours, and testicular germ cell tumours are now separated into two fundamentally different groups: those derived from GCNIS and those unrelated to GCNIS. Spermatocytic seminoma has been designated as a spermatocytic tumour and placed within the group of non-GCNIS-related tumours in the 2016 WHO classification.

Patient summary: The 2016 World Health Organization (WHO) classification contains new renal tumour entities. The classification of penile squamous cell carcinomas is based on the presence of human papillomavirus. Germ cell neoplasia in situ of the testis is the WHO-recommended term for precursor lesions of invasive germ cell tumours.

Keywords: Male genital organs; Urogenital tract; WHO classification.

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The 2016 WHO Classification of Tumours of the Urinary System and Male ...

Recommendation and review posted by Bethany Smith

How to Tell If a Squirrel Is Male or Female | Sciencing

Most species of squirrels -- rodents that inhabit various regions across the globe -- can be grouped as tree or ground squirrels. Information about each groups behaviors and physical traits provides insight needed to determine whether the squirrel of that group is male or female. The sex of a squirrel is difficult to determine if attempting to go by obvious physical characteristics, because male and female squirrels are usually of the same size, shape and color.

Both male and female squirrels are communal, interacting with other squirrels within their immediate living area. However, the nesting habits of male and female tree squirrels differ. Males can be observed nesting together during winter months. It is uncommon for some female tree squirrels, such as fox squirrels, to nest together. An adult squirrel observed interacting with a litter is likely to be the mother of the litter. Male squirrels of any kind do not participate in the rearing process.

Female ground squirrels emerge from hibernation later than their male counterparts. For this reason, ground squirrels observed the soonest after a hibernation period are more likely to be male. Juvenile ground squirrel males exhibit much more movement, exploration and boldness compared to juvenile females. In accordance with this increased movement and exploration, all male juvenile ground squirrels leave the area in which they are born by the time they are one year old. Female ground squirrels stay near the burrows they were born in and form communes with other related females.

The squirrel mating ritual involves a single male or multiple males chasing a female. The males also compete with each other by chasing each other. The most dominant male is the one who typically mates with the female first. The female will sometimes mate with additional suitors afterwards. For some species of tree squirrels, the mating window is so short that the female only remains in estrus, the period of time when pregnancy is possible, for a few hours.

Certain telltale traits of male and female squirrels emerge during the mating season. The scrotum of male squirrels becomes visible because it enlarges and descends. During non-mating periods, the testes are withdrawn into the body. The nipples of adult female squirrels become more prominent during the mating season. The location of the genitals differs between male and female squirrels. The male reproductive organs are located closer to the navel, while the females' are located closer to the anus.

To prevent injury to themselves or the rodents, people should avoid attempting to handle wild squirrels. Feeding squirrels with human food or even a squirrel feeder is discouraged for several reasons. These reasons include accidentally providing food for invasive species, diminishing squirrels' protective fear of humans or providing unhealthy food to the squirrels.

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How to Tell If a Squirrel Is Male or Female | Sciencing

Recommendation and review posted by Bethany Smith

The Genetic Drivers Of Longevity In Mice, Humans And Worms – Science 2.0

Since the dawn of civilization, people have searched for the secret to long life. Famously, Gianni Pes, Michel Poulain and Dan Buettner proposed that diet drives a persons longevity. Other researchers have favored a genetics based explanation for longevity. Recently, a study published in Science found that a mouses genes determine its lifespan, and that there are human orthologs, or analogous genes. The study also found that female and male mice have different genes controlling their lifespans, which is interesting considering that female mice have longer lifespans. The study firmly lands on the side of those who have argued that genes directly determine lifespan. This means that reducing the risk of disease alone is not enough to increase longevity.

While the idea of aging is universal, in scientific terms, it does not have a precise measure. Much as Socrates asked us to investigate the real meaning of widely discussed concepts, scientists have had to work out ways to measure aging, and, this implies, asking what aging really is. Broadly, as the authors of the study note, it is a progressive decline in physical, mental and reproductive capacities, in which a person accumulates morbidities and the risk of dying increases. However, it is not known what the exact interplay is between genes, sex and environment, in determing lifespan.

Researchers have measured aging through a number of traits, such as lifespan, and age-related disease onset. Researchers believe that if they can figure out what the genetic and nongenetic drivers of longevity are, they can develop treatments to improve not just quality of life, but longevity.

A team of scientists led by Robert Williams, looked at the determinants of longevity in 3276 UM-HET3 mice, a type of, or genetically diverse mice that the National Institute on Agings (NIA) Interventions Testing Program (ITP) had been studying. The NIAs TIP had collected this data in 2003, when they were trying to see if dietary interventions would affect the longevity of mice. The mice were raised in closely controlled, homogeneous conditions, and the program collected tissue from them, so they could isolate the impact of genes on the lifespan of mice. The diversity of mice was a result of the need to mirror the diversity in the human genepool. Typically, mice do tend to inbreed, and this warps studies on longevity.

The NIAs TIP did not study the genetic drivers of longevity, and that is the point at which Robert WIlliams and his team began their study. The team were charged with figuring out whether the genetic drivers of longevity are related to sex and age, and whether the nongenetic drivers, such as litter size, or having a good diet from early in life, was important to longevity. In studying these drivers, they were able to classify the changes in liver gene expression of mice in the same genetic cross, according to whether they were driven by age or genotype. The last step in the study was to bring those results together with the orthogonal or itnesecting datasets, to undertake quantitative trait locus mapping, associating phenotypes with genotypes. This would allow the team to figure out which genes are associated with increased longevity.

The team was able to determine genetic loci important for longevity. Sevel of these loci were found in female mice, but, at first, no genetic loci linked specifically to longevity in male mice, were found. When the scientists removed the data for male mice who died at the beginning of the study, they then found genetic loci associated specifically with longevity in male mice. They also found that the factors such as body weight and litter size also impact longevity. For instance, mice with larger body weights and who grew up in smaller litters, died earlier. Consequently, genes linked to body weight and litter size could arguably be linked to longevity. Longevity could be indirectly impacted by the effect of these genes on those factors. However, it is important to note that not all longevity genes are correlated with those factors, opening up the door to the possibility that there are other genes influencing longevity.

The goal of this study was to say something meaningful about longevity in humans, so the study then went to human genome biobanks, and the researchers found sequences that mirrored those in mice. In addition, there was a similar relationship between early development and longevity. They then looked at genes in worms, to see if a similar relationship existed, and if broader conclusions could be drawn about the association of these genes and longevity. Ultimately, they concluded that genes are the primary determinants of longevity.

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The Genetic Drivers Of Longevity In Mice, Humans And Worms - Science 2.0

Recommendation and review posted by Bethany Smith

A Guide To The Best Fertility Supplements And Vitamins For Men – Forbes

When youre trying to conceive or dealing with fertility issues, it may be tempting to reach for one of the many supplements marketed to boost male fertility. However, research on the safety and efficacy of these supplements is limited.

Since supplements arent regulated by the U.S. Food and Drug Administration (FDA) the way medications are, it can be challenging to know if a supplement contains what it says it does, and what effect it will have on the body, explains Philip Cheng, M.D., a male infertility doctor and urologist with Reproductive Medicine Associates of New Jersey. In order to get the nutrients you need to support healthy sperm production, he recommends focusing on a healthy diet.

Research suggests the following supplements may improve sperm quality, especially if you arent getting enough of the nutrients they provide through your dietbut remember, its always a good idea to check with your physician before adding new supplements to your regimen to avoid interactions with any medications you are taking.

Research notes Coenzyme Q10, also known as ubiquinol, is one of the most studied and promising supplements for improving male fertility. Coenzyme Q10 is an antioxidant naturally produced in your body and stored in your mitochondria (the energy factories in your cells). Its antioxidant properties may help protect sperm from damaging free radicals.

One review found that men who supplemented with CoQ10 experienced significant increases in sperm concentration and sperm motility compared to those who took a placebo.

Russell Hayden, M.D., a Harvard-trained urologist with a sub-specialty in male infertility and microsurgery, recommends 300 milligrams to 400 milligrams of a generic coenzyme Q10 supplement daily to his male infertility patients.

When it comes to supplements for male fertility, DHA omega-3 fatty acid supplementation appears to have some of the strongest data supporting its use, says Lauren Manaker, a registered dietitian and author of Fueling Male Fertility.

Fatty acids like docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are important components of sperm cell membranes, and omega-3 fatty acid intake directly correlates to sperm qualityso the more you consume, you may have higher quality of sperm.

A recent review on the effects of the omega-3 fatty acids EPA and DHA on male infertility found that men who took omega-3 treatments had significantly increased sperm motility compared with men who took a placebo.

If your intake of omega-3s from foods like fatty fish, walnuts, chia and flax seeds is low, you might benefit from taking a supplement.

Women who are trying to conceive are routinely advised to take a prenatal vitamin, but mens prenatals are starting to become popular as well, notes licensed dietitian Becca Romero, a functional nutritionist specializing in fertility. She recommends mens prenatal multivitamins WeNatal For Him and Needed to her patients.

WeNatal For Him is a prenatal supplement for men that is formulated to support overall sperm health. It contains a range of vitamins and minerals along with other ingredients and antioxidants that are marketed to boost male fertility, like maca, CoQ10 and acetyl L-carnitine.

Needed Mens Multi is recommended for men before conceiving and in the years that follow. It contains a wide range of vitamins and minerals, as well as an organic antioxidant blend of foods like grape, cranberry, pomegranate, blueberry, apple, mangosteen, bilberry, chokeberry and goji berry.

A male prenatal multivitamin can fill any nutrition gaps in your diet and help you avoid deficiencies that could impact your sperm quality. When choosing a mens prenatal supplement, steer clear of formulations that contain unstudied ingredients or excessive amounts of vitamins and minerals.

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A Guide To The Best Fertility Supplements And Vitamins For Men - Forbes

Recommendation and review posted by Bethany Smith

Why Not All ‘House of the Dragon’ Mixed Race Targaryens Are Blonde – Newsweek

House of the Dragon fans were left scratching their heads last week when the children of a Targaryen and Velaryon union had dark hair.

Viewers saw how the children of Princess Rhaenyra Targaryen (Emma D'Arcy) and Laenor Velaryon (John Macmillan) were fair skinned, brunette ladsthe complete antithesis of their platinum haired parents.

Laenor also happens to be black, adding further mystery to the children's appearance.

House of the Dragon quickly explains the anomaly, revealing the boys were the result of Rhaenyra's affair with Ser Harwin Strong.

In George R. R. Martin's book upon which House of the Dragon and its predecessor Game of Thrones are based, the Targaryens are described as having silver-gold hair with purple eyes that was so distinct it almost looked white thanks to their Valyrian heritage.

Even knowing the boys' true lineage, their brunette coloring still does not entirely explain why their mother's half-siblingsAegon II (Ty Tennant), Helaena (Evie Allen) and Aemond (Leo Ashton)sport the trademark Targaryen blondeness.

They are also the products of a mixed-race union, that of King Viserys Targaryen (Paddy Considine) and Alicent Hightower (Olivia Cooke), a very brunette queen.

In fact, another famous Targaryen from the original Game of Thrones series, Jon Snow (Kit Harrington), was well known for his luscious locks of dark curly hair.

Born as Aegon Targaryen, Snow was the son of Lyanna Stark and Rhaegar Targaryen, a fact only revealed towards the final episodes of the HBO series.

Plenty of fans have theorized over the years as to why some of the most important Targaryens are not blonde at all.

Using 'real world' genetics they analyzed how it would be possible for some mixed race Targaryens are born fair-haired while others do not.

The fans used genome knowledge of dominant and recessive genes to make their conclusions. A dominant gene "refers to the relationship between two versions of a gene," according to the National Genome Research Institute.

Individuals receive two versions of each gene from each of their parents and if the genes differ, the dominant gene will present in their offspring, whether it be in hair color, susceptibility to disease, or other markers.

Fans concluded the Targaryen genes were recessive, but when it came to children of a Targaryen male and non-Valyrian mother their first would be born with darker features, while subsequent offspring were blonde.

"Targaryen males somehow transfer Targaryen traits to their wives and lovers, so second child of the couple inherits Targaryen traits from both mother and father and has Valyrian look. Targaryen genes are somehow "infectious," wrote one fan on a Game of Thornes forum.

This theory works well to explain Snow's dark hair, but is not conclusive because the law of recessive and dominant genes do not seem to be applied consistently across Westeros.

Game of Thrones blogger, Lady Knits A Lot, pointed out that in the original books, three of the five children of Ned and Catelyn Stark were born with the "'Tully look' of red hair and blue eyes, and both of these traits are recessive traits."

"[But] Ned's parents, grandparents and damn near the entire North are described as dark haired and grey eyed," they added.

"So maybe recessive traits are a furphy that we should ignore in Westeros?"

This point was reinforced by Robert Oliver, co-host of The Longest Night podcast dedicated to talking all things Game of Thrones and House of the Dragon.

Oliver told Newsweek the inconsistencies across the shows come down to the fact that how these characters look is key to a plot point.

Rhaenyra's children prove she had an affair, and Jon's very dark hair helped hide the fact he was a Targaryen until the final season.

"It's just storytelling, it needs to be done to move a plot forward," he told Newsweek.

In the case of the House of the Dragon, Rhaenyra's children portrayed as brunette are critical to the conflict which is about to ensue within the dynasty.

"For the purposes of the show, I think what it's doing is it's helpful for Alicent who is trying to implore and impress upon everybody that surrounds her that Rhynaera is not worthy and her children aren't worthy," she said.

"And that it's her children [Alicent's] who should rule after Viserys."

Oliver's assertion comes after Martin himself admitted things don't always add up in the books or series, because it's a fictional world.

"What the fans have to keep in mind... but we're making this s**t up," he told the History of Westeros YouTube channel.

See original here:
Why Not All 'House of the Dragon' Mixed Race Targaryens Are Blonde - Newsweek

Recommendation and review posted by Bethany Smith


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