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Archive for the ‘Population Health Management’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

The trillions of microbes in the human gut are known to aid the body in synthesizing key vitamins and other nutrients. But this new study suggests that things can sometimes be more adversarial.

 

Choline is a key nutrient in a range of metabolic processes, as well as the production of cell membranes. Researchers identified a strain of choline-metabolizing E. coli that, when transplanted into the guts of germ-free mice, consumed enough of the nutrient to create a choline deficiency in them, even when the animals consumed a choline-rich diet.

 

This new study indicate that choline-utilizing bacteria compete with the host for this nutrient, significantly impacting plasma and hepatic levels of methyl-donor metabolites and recapitulating biochemical signatures of choline deficiency. Mice harboring high levels of choline-consuming bacteria showed increased susceptibility to metabolic disease in the context of a high-fat diet.

 

DNA methylation is essential for normal development and has been linked to everything from aging to carcinogenesis. This study showed changes in DNA methylation across multiple tissues, not just in adult mice with a choline-consuming gut microbiota, but also in the pups of those animals while they developed in utero.

 

Bacterially induced reduction of methyl-donor availability influenced global DNA methylation patterns in both adult mice and their offspring and engendered behavioral alterations. This study reveal an underappreciated effect of bacterial choline metabolism on host metabolism, epigenetics, and behavior.

 

The choline-deficient mice with choline-consuming gut microbes also showed much higher rates of infanticide, and exhibited signs of anxiety, with some mice over-grooming themselves and their cage-mates, sometimes to the point of baldness.

 

Tests have also shown as many as 65 percent of healthy individuals carry genes that encode for the enzyme that metabolizes choline in their gut microbiomes. This work suggests that interpersonal differences in microbial metabolism should be considered when determining optimal nutrient intake requirements.

 

References:

 

https://news.harvard.edu/gazette/story/2017/11/harvard-research-suggests-microbial-menace/

 

http://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30304-9

 

https://www.ncbi.nlm.nih.gov/pubmed/23151509

 

https://www.ncbi.nlm.nih.gov/pubmed/25677519

 

http://mbio.asm.org/content/6/2/e02481-14

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

During menopause a woman’s ovaries stop working—leading to hot flashes, sleep problems, weight gain, and worse, bone deterioration. Now scientists are exploring whether transplanting lab-made ovaries might stop those symptoms. In one of the first efforts to explore the potential of such a technique, researchers say they used tissue engineering to construct artificial rat ovaries able to supply female hormones like estrogen and progesterone. A research carried out at Wake Forest Baptist Medical Center, suggests a potential alternative to the synthetic hormones millions of women take after reaching middle age. A paper describing the findings was published in Nature Communications.

 

Women going through menopause, as well as those who have undergone cancer treatment or had their ovaries removed for medical purposes, lose the ability to produce important hormones, including estrogen and progesterone. Lower levels of these hormones can affect a number of different body functions. To counteract unpleasant symptoms, many women turn to combinations of hormone replacement medications—synthetic estrogen and progestin. Pharmacologic hormone replacement therapy (pHRT) with estrogen alone or estrogen and progestogens is known to effectively ameliorate the unpleasant symptoms. But hormone replacement carries an increased risk of heart disease and breast cancer, so it’s not recommended for long-term use. In these circumstances artificial ovaries could be safer and more effective.

 

Regenerative medicine approaches that use cell-based hormone replacement therapy (cHRT) offer a potential solution to temporal control of hormone delivery and the ability to restore the HPO (Hypothalamo-Pituitary-Ovarian) axis in a way not possible with pHRT. Scientists have previously described an approach to achieve microencapsulation of ovarian cells that results in bioengineered constructs that replicate key structure-function relationships of ovarian follicles as an approach to cHRT. In the present study the scientists have adapted an isogeneic cell-based construct to provide a proof-of-concept for the potential benefits of cHRT.

 

Tissue or cell encapsulation may offer effective strategies to fabricate ovarian constructs for the purpose of fertility and/or hormone replacement. Approaches using segmental ovarian tissue or whole-follicle implantation (typically with a focus on cryopreservation of the tissue for reproductive purposes) have resulted in detectable hormone levels in the blood after transplantation. Previous studies have also shown that autotransplantation of frozen-thawed ovarian tissue can lead to hormone secretion for over 5 years in humans.

 

Although these approaches can be used to achieve the dual purpose of fertility and hormone replacement in premenopausal women undergoing premature ovarian failure, they would have limited application in postmenopausal women who only need hormone replacement to manage menopausal symptoms and in whom fertility is not desirable. In full development, the technology described in this research is focused on hormone replacement, would meet the needs of the latter group of women that is the postmenopausal women.

 

The cell-based system of hormone replacement described in this report offers an attractive alternative to traditional pharmacological approaches and is consistent with current guidelines in the U.S. and Europe recommending the lowest possible doses of hormone for replacement therapy. In the present research sustained stable hormone release over the course of 90 days of study was demonstrated. The study also demonstrated the effective end-organ outcomes in body fat composition, uterine health, and bone health. However, additional studies will be required to determine the sustainability of the hormone secretion of the constructs by measuring hormone levels from implanted constructs for periods longer than 3 months in the rat model.

 

This study highlights the potential utility of cHRT for the treatment and study of conditions associated with functional loss of the ovaries. Although longer-term studies would be of future interest, the 90-day duration of this rodent model study is consistent with others investigating osteoporosis in an ovariectomy model. However, this study provides a proof-of-concept for cHRT, it suffers the limitation that it is only an isogeneic-based construct implantation. Scientists think that further studies in either allogeneic or xenogeneic settings would be required with the construct design described in this report in the path towards clinical translation given that patients who would receive this type of treatment are unlikely to have sufficient autologous ovarian cells for transplantation.

 

References:

 

https://www.technologyreview.com/the-download/609677/will-artificial-ovaries-mean-no-more-menopause/

 

https://www.nature.com/articles/s41467-017-01851-3

 

https://www.ncbi.nlm.nih.gov/pubmed/23274068

 

https://www.ncbi.nlm.nih.gov/pubmed/26210678

 

https://www.ncbi.nlm.nih.gov/pubmed/21954279

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

A mutated gene called RAS gives rise to a signalling protein Ral which is involved in tumour growth in the bladder. Many researchers tried and failed to target and stop this wayward gene. Signalling proteins such as Ral usually shift between active and inactive states.

 

So, researchers next tried to stop Ral to get into active state. In inacvtive state Ral exposes a pocket which gets closed when active. After five years, the researchers found a small molecule dubbed BQU57 that can wedge itself into the pocket to prevent Ral from closing and becoming active. Now, BQU57 has been licensed for further development.

 

Researchers have a growing genetic data on bladder cancer, some of which threaten to overturn the supposed causes of bladder cancer. Genetics has also allowed bladder cancer to be reclassified from two categories into five distinct subtypes, each with different characteristics and weak spots. All these advances bode well for drug development and for improved diagnosis and prognosis.

 

Among the groups studying the genetics of bladder cancer are two large international teams: Uromol (named for urology and molecular biology), which is based at Aarhus University Hospital in Denmark, and The Cancer Genome Atlas (TCGA), based at institutions in Texas and Boston. Each team tackled a different type of cancer, based on the traditional classification of whether or not a tumour has grown into the muscle wall of the bladder. Uromol worked on the more common, earlier form, non-muscle-invasive bladder cancer, whereas TCGA is looking at muscle-invasive bladder cancer, which has a lower survival rate.

 

The Uromol team sought to identify people whose non-invasive tumours might return after treatment, becoming invasive or even metastatic. Bladder cancer has a high risk of recurrence, so people whose non-invasive cancer has been treated need to be monitored for many years, undergoing cystoscopy every few months. They looked for predictive genetic footprints in the transcriptome of the cancer, which contains all of a cell’s RNA and can tell researchers which genes are turned on or off.

 

They found three subgroups with distinct basal and luminal features, as proposed by other groups, each with different clinical outcomes in early-stage bladder cancer. These features sort bladder cancer into genetic categories that can help predict whether the cancer will return. The researchers also identified mutations that are linked to tumour progression. Mutations in the so-called APOBEC genes, which code for enzymes that modify RNA or DNA molecules. This effect could lead to cancer and cause it to be aggressive.

 

The second major research group, TCGA, led by the National Cancer Institute and the National Human Genome Research Institute, that involves thousands of researchers across USA. The project has already mapped genomic changes in 33 cancer types, including breast, skin and lung cancers. The TCGA researchers, who study muscle-invasive bladder cancer, have looked at tumours that were already identified as fast-growing and invasive.

 

The work by Uromol, TCGA and other labs has provided a clearer view of the genetic landscape of early- and late-stage bladder cancer. There are five subtypes for the muscle-invasive form: luminal, luminal–papillary, luminal–infiltrated, basal–squamous, and neuronal, each of which is genetically distinct and might require different therapeutic approaches.

 

Bladder cancer has the third-highest mutation rate of any cancer, behind only lung cancer and melanoma. The TCGA team has confirmed Uromol research showing that most bladder-cancer mutations occur in the APOBEC genes. It is not yet clear why APOBEC mutations are so common in bladder cancer, but studies of the mutations have yielded one startling implication. The APOBEC enzyme causes mutations early during the development of bladder cancer, and independent of cigarette smoke or other known exposures.

 

The TCGA researchers found a subset of bladder-cancer patients, those with the greatest number of APOBEC mutations, had an extremely high five-year survival rate of about 75%. Other patients with fewer APOBEC mutations fared less well which is pretty surprising.

 

This detailed knowledge of bladder-cancer genetics may help to pinpoint the specific vulnerabilities of cancer cells in different people. Over the past decade, Broad Institute researchers have identified more than 760 genes that cancer needs to grow and survive. Their genetic map might take another ten years to finish, but it will list every genetic vulnerability that can be exploited. The goal of cancer precision medicine is to take the patient’s tumour and decode the genetics, so the clinician can make a decision based on that information.

 

References:

 

https://www.ncbi.nlm.nih.gov/pubmed/29117162

 

https://www.ncbi.nlm.nih.gov/pubmed/27321955

 

https://www.ncbi.nlm.nih.gov/pubmed/28583312

 

https://www.ncbi.nlm.nih.gov/pubmed/24476821

 

https://www.ncbi.nlm.nih.gov/pubmed/28988769

 

https://www.ncbi.nlm.nih.gov/pubmed/28753430

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Anti-Müllerian Hormone (AMH), is secreted by growing follicles that contains the egg or ovum. According to regular practice low AMH and high Follicle Stimulating Hormone (FSH) are generally considered as indicators of diminished egg quantity in a female. But, there are several cases the female conceived absolutely normally without any support even after low AMH was reported.

 

Therefore, a new research published in the Journal of the American Medical Association declares that AMH doesn’t dictate a woman’s reproductive potential. Although AMH testing is one of the most common ways that doctors assess a woman’s fertility. Present research says that all it takes is one egg each cycle and AMH is not a marker of whether a female can or cannot become pregnant. So, for women who haven’t yet tried to get pregnant and who are wondering whether they are fertile, an AMH value isn’t going to be helpful in that context. In addition, AMH is not necessarily a good marker to predict that whether one has to cryopreserve her eggs. So, practically doctors don’t yet have a way to definitively predict egg quality or a woman’s long-term ability to conceive, but age is obviously one of the most important factors.

 

The above mentioned study followed 750 women between the ages of 30 and 44 who had been trying to conceive for three months or less. During the 12-month observation period, those with low AMH values of less than 0.7 were not less likely to conceive than those who had normal AMH values. The study had various limitations, however, that are worth noting. The researchers only included women who did not have a history of infertility. Women who sought fertility treatments (about 6 percent) were withdrawn. And only 12 percent of the women were in the 38-to-44 age range. In addition, the number of live births was unavailable.

 

Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility. These findings do not support the use of urinary or blood FSH tests or AMH levels to assess natural fertility for women with these characteristics. The researchers’ next want to see whether low AMH is associated with a higher risk of miscarriage among the women who conceived.

 

Although AMH testing isn’t designed to be an overall gauge of a woman’s fertility, it can still provide valuable information, especially for women who are infertile and seeking treatment. It can assist in diagnosing polycystic ovarian syndrome, and identify when a woman is getting closer to menopause. Previous research also showed that AMH is good predictor of a woman’s response to ovarian stimulation for in vitro fertilization and therefore it can predict the probability of conceiving via in vitro fertilization (I.V.F.).

 

References:

 

https://jamanetwork.com/journals/jama/article-abstract/2656811?JamaNetworkReader=True

 

https://www.nytimes.com/2017/10/16/health/fertility-test-ovarian-reserve.html

 

https://academic.oup.com/humrep/article/26/11/2925/656065

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339896/

 

https://www.ncbi.nlm.nih.gov/pubmed/27179263

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Scientists at the Stanford University School of Medicine have completed the first-ever characterization of the meticulously timed immune system changes in women that occur during pregnancy. The findings were published in Science Immunology revealed that there is an immune clock of pregnancy and suggest it may help doctors predict preterm birth.

 

The timing of immune system changes follows a precise and predictable pattern in normal pregnancy. Although physicians have long known that the expectant mother’s immune system adjusts to prevent her body from rejecting the fetus, no one had investigated the full scope of these changes, nor asked if their timing was tightly controlled.

 

Nearly 10 percent of U.S. infants are born prematurely, arriving three or more weeks early, but physicians lack a reliable way to predict premature deliveries. Previous research at Stanford and other places suggested that inflammatory immune responses may help in triggering early labor. It suggested that if scientists identify an immune signature of impending preterm birth, they should be able to design a blood test to detect it.

 

The researchers used mass cytometry, a technique developed at Stanford, to simultaneously measure up to 50 properties of each immune cell in the blood samples. They counted the types of immune cells, assessed what signaling pathways were most active in each cell, and determined how the cells reacted to being stimulated with compounds that mimic infection with viruses and bacteria.

 

The researchers developed an algorithm that captures the immunological timeline during pregnancy that both validates previous findings and sheds new light on immune cell interaction during gestation. By defining this immunological chronology during normal term pregnancy, they can now begin to determine which alterations associate with pregnancy-related pathologies.

 

With an advanced statistical modeling technique, introduced for the first time in this study, the scientists then described in detail how the immune system changes throughout pregnancy. Instead of grouping the women’s blood samples by trimester for analysis, the model treated gestational age as a continuous variable, allowing the researchers to account for the exact time during pregnancy at which each sample was taken. The mathematical model also incorporated knowledge from the existing scientific literature of how immune cells behave in nonpregnant individuals to help determine which findings were most likely to be important.

 

The study confirmed immune features of pregnancy that were already known. Such as the scientists saw that natural killer cells and neutrophils have enhanced action during pregnancy. The researchers also uncovered several previously unappreciated features of how the immune system changes, such as the finding that activity of the STAT5 signaling pathway in CD4+T cells progressively increases throughout pregnancy on a precise schedule, ultimately reaching levels much higher than in nonpregnant individuals. The STAT5 pathway is involved in helping another group of immune cells, regulatory T cells, to differentiate. Interestingly, prior research in animals has indicated that regulatory T cells are important for maintaining pregnancy.

 

The next step will be to conduct similar research using blood samples from women who deliver their babies prematurely to see where their trajectories of immune function differ from normal.

 

This study revealed a precisely timed chronology of immune adaptations in peripheral blood over the course of a term pregnancy. This finding was enabled by high-content, single-cell mass cytometry coupled with a csEN algorithm accounting for the modular structure of the immune system and previous knowledge. The study provided the conceptual backbone and the analytical framework to examine whether disruption of this chronology is a diagnostically useful characteristic of preterm birth and other pregnancy-related pathologies.

 

References:

 

http://immunology.sciencemag.org/content/2/15/eaan2946.full

 

http://med.stanford.edu/news/all-news/2017/09/immune-system-changes-during-pregnancy-are-precisely-timed.html

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078586/

 

http://www.nature.com/nm/journal/v19/n5/full/nm.3160.html?foxtrotcallback=true

 

https://www.ncbi.nlm.nih.gov/pubmed/14758358

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Decline in Sperm Count – Epigenetics, Well-being and the Significance for Population Evolution and Demography

 

Dr. Marc Feldman, Expert Opinion on the significance of Sperm Count Decline on the Future of Population Evolution and Demography

Dr. Sudipta Saha, Effects of Sperm Quality and Quantity on Human Reproduction

Dr. Aviva Lev-Ari, Psycho-Social Effects of Poverty, Unemployment and Epigenetics on Male Well-being, Physiological Conditions affecting Sperm Quality and Quantity

 

UPDATED on 2/3/2018

Nobody Really Knows What Is Causing the Overdose Epidemic, But Here Are A Few Theories

https://www.buzzfeed.com/danvergano/whats-causing-the-opioid-crisis?utm_term=.kbJPMgaQo4&utm_source=BrandeisNOW%2BWeekly&utm_campaign=58ada49a84-EMAIL_CAMPAIGN_2018_01_29&utm_medium=email#.uugW6mx1dG

 

Recent studies concluded via rigorous and comprehensive analysis found that Sperm Count (SC) declined 52.4% between 1973 and 2011 among unselected men from western countries, with no evidence of a ‘leveling off’ in recent years. Declining mean SC implies that an increasing proportion of men have sperm counts below any given threshold for sub-fertility or infertility. The high proportion of men from western countries with concentration below 40 million/ml is particularly concerning given the evidence that SC below this threshold is associated with a decreased monthly probability of conception.

1.Temporal trends in sperm count: a systematic review and meta-regression analysis 

Hagai Levine, Niels Jørgensen, Anderson Martino‐Andrade, Jaime Mendiola, Dan Weksler-Derri, Irina Mindlis, Rachel Pinotti, Shanna H SwanHuman Reproduction Update, July 25, 2017, doi:10.1093/humupd/dmx022.

Link: https://academic.oup.com/humupd/article-lookup/doi/10.1093/humupd/dmx022.

2. Sperm Counts Are Declining Among Western Men – Interview with Dr. Hagai Levine

https://news.afhu.org/news/sperm-counts-are-declining-among-western-men?utm_source=Master+List&utm_campaign=dca529d919-EMAIL_CAMPAIGN_2017_07_27&utm_medium=email&utm_term=0_343e19a421-dca529d919-92801633

3. Trends in Sperm Count – Biological Reproduction Observations

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

4. Long, mysterious strips of RNA contribute to low sperm count – Long non-coding RNAs can be added to the group of possible non-structural effects, possibly epigenetic, that might regulate sperm counts.

http://casemed.case.edu/cwrumed360/news-releases/release.cfm?news_id=689

https://scienmag.com/long-mysterious-strips-of-rna-contribute-to-low-sperm-count/

Dynamic expression of long non-coding RNAs reveals their potential roles in spermatogenesis and fertility

Published: 29 July 2017
Thus, we postulated that some lncRNAs may also impact mammalian spermatogenesis and fertility. In this study, we identified a dynamic expression pattern of lncRNAs during murine spermatogenesis. Importantly, we identified a subset of lncRNAs and very few mRNAs that appear to escape meiotic sex chromosome inactivation (MSCI), an epigenetic process that leads to the silencing of the X- and Y-chromosomes at the pachytene stage of meiosis. Further, some of these lncRNAs and mRNAs show strong testis expression pattern suggesting that they may play key roles in spermatogenesis. Lastly, we generated a mouse knock out of one X-linked lncRNA, Tslrn1 (testis-specific long non-coding RNA 1), and found that males carrying a Tslrn1 deletion displayed normal fertility but a significant reduction in spermatozoa. Our findings demonstrate that dysregulation of specific mammalian lncRNAs is a novel mechanism of low sperm count or infertility, thus potentially providing new biomarkers and therapeutic strategies.

This article presents two perspectives on the potential effects of Sperm Count decline.

One Perspective identifies Epigenetics and male well-being conditions

  1. as a potential explanation to the Sperm Count decline, and
  2. as evidence for decline in White male longevity in certain geographies in the US since the mid 80s.

The other Perspective, evaluates if Sperm Count Decline would have or would not have a significant long term effects on Population Evolution and Demography.

The Voice of Prof. Marc Feldman, Stanford University – Long term significance of Sperm Count Decline on Population Evolution and Demography

Poor sperm count appears to be associated with such demographic statistics as life expectancy (1), infertility (2), and morbidity (3,4). The meta-analysis by Levine et al. (5) focuses on the change in sperm count of men from North America, Europe, Australia, and New Zealand, and shows a more than 50% decline between 1973 and 2011. Although there is no analysis of potential environmental or lifestyle factors that could contribute to the estimated decline in sperm count, Levine et al. speculate that this decline could be a signal for other negative changes in men’s health.

Because this study focuses mainly on Western men, this remarkable decline in sperm count is difficult to associate with any change in actual fertility, that is, number of children born per woman. The total fertility rate in Europe, especially Italy, Spain, and Germany, has slowly declined, but age at first marriage has increased at the same time, and this increase may be more due to economic factors than physiological changes.

Included in Levine et al.’s analysis was a set of data from “Other” countries from South America, Asia, and Africa. Sperm count in men from these countries did not show significant trends, which is interesting because there have been strong fertility declines in Asia and Africa over the same period, with corresponding increases in life expectancy (once HIV is accounted for).

What can we say about the evolutionary consequences for humans of this decrease? The answer depends on the minimal number of sperm/ml/year that would be required to maintain fertility (per woman) at replacement level, say 2.1 children, over a woman’s lifetime. Given the smaller number of ova produced per woman, a change in the ovulation statistics of women would be likely to play a larger role in the total fertility rate than the number of sperm/ejaculate/man. In other words, sperm count alone, absent other effects on mortality during male reproductive years, is unlikely to tell us much about human evolution.

Further, the major declines in fertility over the 38-year period covered by Levine et al. occurred in China, India, and Japan. Chinese fertility has declined to less than 1.5 children per woman, and in Japan it has also been well below 1.5 for some time. These declines have been due to national policies and economic changes, and are therefore unlikely to signal genetic changes that would have evolutionary ramifications. It is more likely that cultural changes will continue to be the main drivers of fertility change.

The fastest growing human populations are in the Muslim world, where fertility control is not nearly as widely practiced as in the West or Asia. If this pattern were to continue for a few more generations, the cultural evolutionary impact would swamp any effects of potentially declining sperm count.

On the other hand, if the decline in sperm count were to be discovered to be associated with genetic and/or epigenetic phenotypic effects on fetuses, newborns, or pre-reproductive humans, for example, due to stress or obesity, then there would be cause to worry about long-term evolutionary problems. As Levine et al. remark, “decline in sperm count might be considered as a ‘canary in the coal mine’ for male health across the lifespan”. But to date, there is little evidence that the evolutionary trajectory of humans constitutes such a “coal mine”.

References

  1. Jensen TK, Jacobsen R, Christensen K, Nielsen NC, Bostofte E. 2009. Good semen quality and life expectancy: a cohort study of 43,277 men. Am J Epidemiol 170: 559-565.
  2. Eisenberg ML, Li S, Behr B, Cullen MR, Galusha D, Lamb DJ, Lipshultz LI. 2014. Semen quality, infertility and mortality in the USA. Hum Reprod 29: 1567-1574.
  3. Eisenberg ML, Li S, Cullen MR, Baker LC. 2016. Increased risk of incident chronic medical conditions in infertile men: analysis of United States claims data. Fertil Steril 105: 629-636.
  4. Latif T, Kold Jensen T, Mehlsen J, Holmboe SA, Brinth L, Pors K, Skouby SO, Jorgensen N, Lindahl-Jacobsen R. Semen quality is a predictor of subsequent morbidity. A Danish cohort study of 4,712 men with long-term follow-up. Am J Epidemiol. Doi: 10.1093/aje/kwx067. (Epub ahead of print]
  5. Levine H, Jorgensen N, Martino-Andrade A, Mendiola J, Weksler-Derri D, Mindlis I, Pinotti R, Swan SH. 2017. Temporal trends in sperm count: a systematic review and meta-regression analysis. Hum Reprod Update pp. 1-14. Doi: 10.1093/humupd/dmx022.

SOURCE

From: Marcus W Feldman <mfeldman@stanford.edu>

Date: Monday, July 31, 2017 at 8:10 PM

To: Aviva Lev-Ari <aviva.lev-ari@comcast.net>

Subject: Fwd: text of sperm count essay

Psycho-Social Effects of Poverty, Unemployment and Epigenetics on Male Well-being, Physiological Conditions as POTENTIAL effects on Sperm Quality and Quantity and Evidence of its effects on Male Longevity

The Voice of Carol GrahamSergio Pinto, and John Juneau II , Monday, July 24, 2017, Report from the Brookings Institute

  1. The IMPACT of Well-being, Stress induced by Worry, Pain, Perception of Hope related to Employment and Lack of employment on deterioration of Physiological Conditions as evidence by Decrease Longevity

  2. Epigenetics and Environmental Factors

The geography of desperation in America

Carol GrahamSergio Pinto, and John Juneau II Monday, July 24, 2017, Report from the Brookings Institute

In recent work based on our well-being metrics in the Gallup polls and on the mortality data from the Centers for Disease Control and Prevention, we find a robust association between lack of hope (and high levels of worry) among poor whites and the premature mortality rates, both at the individual and metropolitan statistical area (MSA) levels. Yet we also find important differences across places. Places come with different economic structures and identities, community traits, physical environments and much more. In the maps below, we provide a visual picture of the differences in in hope for the future, worry, and pain across race-income cohorts across U.S. states. We attempted to isolate the specific role of place, controlling for economic, socio-demographic, and other variables.

One surprise is the low level of optimism and high level of worry in the minority dense and generally “blue” state of California, and high levels of pain and worry in the equally minority dense and “blue” states of New York and Massachusetts. High levels of income inequality in these states may explain these patterns, as may the nature of jobs that poor minorities hold.

We cannot answer many questions at this point. What is it about the state of Washington, for example, that is so bad for minorities across the board? Why is Florida so much better for poor whites than it is for poor minorities? Why is Nevada “good” for poor white optimism but terrible for worry for the same group? One potential issue—which will enter into our future analysis—is racial segregation across places. We hope that the differences that we have found will provoke future exploration. Readers of this piece may have some contributions of their own as they click through the various maps, and we welcome their input. Better understanding the role of place in the “crisis” of despair facing our country is essential to finding viable solutions, as economic explanations, while important, alone are not enough.

https://www.brookings.edu/research/the-geography-of-desperation-in-america/?utm_medium=social&utm_source=facebook&utm_campaign=global

 

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Trends in Sperm Count

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

There has been a genuine decline in semen quality over the past 50 years. There is lot of controversy about this as there are limitations in studies that have attempted to address it. Sperm count is of considerable public health importance for several reasons. First, sperm count is closely linked to male fecundity and is a crucial component of semen analysis, the first step to identify male factor infertility.

Reduced sperm count is associated with cryptorchidism, hypospadias and testicular cancer. It may be associated with multiple environmental influences, including endocrine disrupting chemicals, pesticides, heat and lifestyle factors, including diet, stress, smoking and BMI. Therefore, sperm count may sensitively reflect the impacts of the modern environment on male health throughout the life span.

This study provided a systematic review and meta-regression analysis of recent trends in sperm counts as measured by sperm concentration (SC) and total sperm count (TSC), and their modification by fertility and geographic group. Analyzing trends by birth cohorts instead of year of sample collection may aid in assessing the causes of the decline (prenatal or in adult life) but was not feasible owing to lack of information.

This rigorous and comprehensive analysis found that SC declined 52.4% between 1973 and 2011 among unselected men from western countries, with no evidence of a ‘leveling off’ in recent years. Declining mean SC implies that an increasing proportion of men have sperm counts below any given threshold for sub-fertility or infertility. The high proportion of men from western countries with concentration below 40 million/ml is particularly concerning given the evidence that SC below this threshold is associated with a decreased monthly probability of conception.

Declines in sperm count have implications beyond fertility and reproduction. The decline reported in this study is consistent with reported trends in other male reproductive health indicators, such as testicular germ cell tumors, cryptorchidism, onset of male puberty and total testosterone levels. The public health implications are even wider. Recent studies have shown that poor sperm count is associated with overall morbidity and mortality. While the current study is not designed to provide direct information on the causes of the observed declines, sperm count has been plausibly associated with multiple environmental and lifestyle influences, both prenatally and in adult life. In particular, endocrine disruption from chemical exposures or maternal smoking during critical windows of male reproductive development may play a role in prenatal life, while lifestyle changes and exposure to pesticides may play a role in adult life.

These findings strongly suggest a significant decline in male reproductive health, which has serious implications beyond fertility concerns. Research on causes and implications of this decline is urgently needed.

 

REFERENCES

Temporal trends in sperm count: a systematic review and meta-regression analysis 

Hagai Levine, Niels Jørgensen, Anderson Martino‐Andrade, Jaime Mendiola, Dan Weksler-Derri, Irina Mindlis, Rachel Pinotti, Shanna H Swan. Human Reproduction Update, July 25, 2017, doi:10.1093/humupd/dmx022.

Link: https://academic.oup.com/humupd/article-lookup/doi/10.1093/humupd/dmx022.

Sperm Counts Are Declining Among Western Men – Interview with Dr. Hagai Levine

https://news.afhu.org/news/sperm-counts-are-declining-among-western-men?utm_source=Master+List&utm_campaign=dca529d919-EMAIL_CAMPAIGN_2017_07_27&utm_medium=email&utm_term=0_343e19a421-dca529d919-92801633

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