The IRS Wants to Know About Your Cryptocurrency Transactions – Interesting Engineering

Cryptocurrencies, such as Bitcoin, Litecoin, Ethereum, and Ripple, make the U.S. Internal Revenue Service (IRS) nervous. They want to know what you're up to so that they can tax it, and due to COVID-19, you must file your 2019 income tax by July 15, 2020.

On their new Schedule 1 form, the IRS has thrown in a new question: "At any time during 2019, did you receive, sell, send, exchange, or otherwise acquire any financial interest in any virtual currency?"

RELATED: IS NASA DEVELOPING ITS OWN CRYPTOCURRENCY?

Unless you have a death wish, or don't mind doing hard time, you've got to include your cryptocurrency dealings on your income tax filing. We're going to tell you how to do it, but first, a disclaimer.

We're not tax professionals, so take the facts provided below as informational only. Also, those living in countries other than the U.S. may have very different income reporting obligations.

The IRS identifies cryptocurrencies as property, just like collectible coins, valuable paintings, vintage cars, or stocks. Property can appreciate or depreciate in value.

You must report all cryptocurrency transactions and all cryptocurrency, or digital currency income even if you didn't receive a tax form from a cryptocurrency exchange.

While some exchanges, such as the popular site Coinbase, provide a transaction history to every customer, they only provide an IRS Form 1099-K to those customers whose transactions meet a certain dollar amount.

According to the IRS website, "A Form 1099-K includes the gross amount of all reportable payment transactions, and you will receive a Form 1099-K from each payment settlement entity from which you received payments in settlement of reportable payment transactions."

The IRS requires you to report your gains and losses on each of your cryptocurrency transactions. You report cryptocurrency transactions at their fair market value in U.S. dollars.

To calculate your gains and losses, you'll need the cost basis of each transaction, that is, the amount you spent in dollars to buy the cryptocurrency and the amount in dollars that it was worth when you sold it. You can use losses to offset capital gains, thus making losses deductible.

You must pay taxes on cryptocurrency if you:

You don't have to pay taxes on cryptocurrency if you:

Section 501(c)(3) is the portion of the U.S. Internal Revenue Code that allows for federal tax exemption of nonprofit organizations, specifically those that are considered public charities, private foundations or private operating foundations.

On its website, the IRS states that "Only individuals are required to file gift tax returns. If a trust, estate, partnership, or corporation makes a gift, the individual beneficiaries, partners, or stockholders are considered donors and may be liable for the gift and GST taxes."

An airdrop is a usually free distribution of a cryptocurrency token or coin to numerous wallet addresses. Airdrops are done to help newer cryptocurrencies gain attention and new followers.

Recipients are either selected randomly or the airdrop is publicized on bulletin boards or in newsletters. Some airdrops require joining a group, retweeting a tweet, or inviting new users.

Airdropped cryptocurrency should generally be taxable as ordinary income, and valued at its fair market value on the date of receipt. If your exchange doesn't yet support the new coin, meaning it can't be sold, then it isn't taxable.

A fork is an upgrade to a blockchain network. Permanent forks are used to add new features to a blockchain, to reverse the effect of hacking, or to fix bugs, as was the case with the Bitcoin fork that occurred on August 6, 2010, or the fork that separated Ethereum and Ethereum Classic.

Crypto that is received in a fork becomes taxable when it can be transferred, sold, or exchanged. The IRS discusses forks on its Frequently Asked Questions on Virtual Currency Transactions webpage.

Things get even more complicated if you bought cryptocurrency at different times, then sold only a portion of it. You need to choose the cost based on FIFO (First-in-First Out), LIFO (Last-in-Last Out), or the Specific Identification method, which identifies exactly which coins were sold. This IRS page provides information on this choice.

If there is one thing the IRS has a lot of, it's forms. Some of those you may need to use to report cryptocurrency on your income tax include:

If you followed the last link provided, you land on an IRS page with the word "Attention" in red, which is never a good sign. It's followed by several paragraphs, the first of which states: "Copy A of this form is provided for informational purposes only. Copy A appears in red, similar to the official IRS form. The official printed version of Copy A of this IRS form is scannable, but the online version of it, printed from this website, is not. Do not print and file copy A downloaded from this website; a penalty may be imposed for filing with the IRS information return forms that cant be scanned. See part O in the current General Instructions for Certain Information Returns, available at http://www.irs.gov/form1099, for more information about penalties."

If you understood this last paragraph, please let me know so I can put you up for a MacArthur Genius Grant. In the meantime, in July 2019, the IRS sent out over 10,000 letters telling recipients that they owed back taxes, interest, and penalties on their cryptocurrency transactions and that they needed to file amended returns. The IRS also lets recipients of the letters know that they could possibly face criminal prosecution and fines of up to $250,000.

In case you think dabbling in cryptocurrency sounds too complicated, consider this: on March 20, 2020, the value of Bitcoin rose 23% in just 24 hours, reaching $6,172.61.

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The IRS Wants to Know About Your Cryptocurrency Transactions - Interesting Engineering

Can heightened cryptocurrency regulations be a major threat to smaller exchanges? – AMBCrypto English

The announcement of FATFs travel Rule in 2019 came as shocking news to the entire crypto community. As crypto-exchanges were required to submit the originator name, account number, physical address, national identity number of the user, unique identity number, and even the date and place of birth, many of them closed operations, refusing to give away the users information.

Moreover, it was made mandatory that all countries abide by this rule; countries that deny would make it to the blacklist. We are a month away from the FATFs review, while many Asian countries like Singapore, South Korea, and Japan have passed the regulations, others are contemplating the implications.

Canada also recently updated the AML rules, and accordingly, crypto firms in the country are expected to report the transactions above 10,000 CAD to Financial Transactions and Reports Analysis Centre of Canada[FINTRAC]. The question here is How prepared are these crypto firms to comply with these rules?.

In a recent interview with AMBCrypto, Elsa Madrolle, General Manager International at CoolBitX, a blockchain security company commented on the regulations and the plight of the crypto exchanges in Canada. Madrolle stated,

The updated Canadian regulations will be enacted in June 2020 is the first step, and it is largely expected that FINTRAC will announce further regulatory developments down the road, and the crypto industry can expect to receive more clarity and definition on how to operate in the future.

She further shared her thoughts on tightened regulations in Canada and noted that it might result in smaller Canadian exchanges dropping out or be bought out by other leading exchanges which are registered as money services business[MSBs]. But it does give the FINTRACcomplete oversight over all remaining crypto firms, she noted.

While financial authorities will be able to detect and prevent money laundering activities and other criminal activities involving cryptocurrency using the FATFs travel rule, the main concern is still not being addressed. The genuine challenge on the table is Cryptocurrency transactions promise greater levels of privacy, and this is at times the sole reason why many are attracted to the space; they dont want governments to invade their financial privacy.

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Can heightened cryptocurrency regulations be a major threat to smaller exchanges? - AMBCrypto English

CRYPTOCURRENCY MARKET TRENDS ANALYSIS, TOP MANUFACTURERS, SHARES, GROWTH OPPORTUNITIES AND FORECAST TO 2027 3w Market News Reports – 3rd Watch News

The Global Cryptocurrency Market report draws precise insights by examining the latest and prospective industry trends and helping readers recognize the products and services that are boosting revenue growth and profitability. The study performs a detailed analysis of all the significant factors, including drivers, constraints, threats, challenges, prospects, and industry-specific trends, impacting the market on a global and regional scale. Additionally, the report cites worldwide market scenario along with competitive landscape of leading participants.

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Leading Players in the Cryptocurrency Market: Bitfinex, BitFury Group, Bitstamp, Coinbase, Coinsecure, Litecoin, OKEX Fintech Company, Poloniex, Ripple, Unocoin Technologies Private, ZEB IT Service

The Cryptocurrency market analysis is intended to provide all participants and vendors with pertinent specifics about growth aspects, roadblocks, threats, and lucrative business opportunities that the market is anticipated to reveal in the coming years. This intelligence study also encompasses the revenue share, market size, market potential, and rate of consumption to draw insights pertaining to the rivalry to gain control of a large portion of the market share.

Competitive landscape:

The Cryptocurrency Industry is extremely competitive and consolidated because of the existence of several established companies that are adopting different marketing strategies to increase their market share. The vendors engaged in the sector are outlined based on their geographic reach, financial performance, strategic moves, and product portfolio. The vendors are gradually widening their strategic moves, along with customer interaction.

Cryptocurrency Market Segmented by Region/Country: US, Europe, China, Japan, Middle East & Africa, India, Central & South America

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Cryptocurrency Market Update: Bitcoin, Ethereum and Ripple have a bullish start to Saturday, following Fridays drop – FXStreet

The price of BTC/USD has gone up from$9,806.63 to $9,848.50. There is a dip in the RSI, but it is still trending within the overbought zone at 79.63. While this ideally means an upcoming short term bearish correction, we believe that the bulls will continue to consolidate till Tuesdays halving.

The MACD indicates increasing bullish momentum. Ideally, the bulls will want to conquer resistance levels at 10,036 and $10,359.55. On the downside, healthy support lies at $9,500 and $8,780, which must be defended on the face of a sudden bearish onslaught.

ETH/USD is consolidating below the $218 resistance level as it went up from $211.50 to $213.20 in the early hours of Saturday. The price is hovering below the red Ichimoku cloud. The bulls gain enough firepower to enter the cloud by conquering the $227.40 resistance level. On the downside, there are healthy support levels at $207.25 and $198.

The SMA 50 is looking to crossover the SMA 200 to potentially chart the highly bullish golden cross pattern. The MACD shows slightly bearish market momentum.

XRP/USD bulls remained in control for the third straight day as the price went up a bit from $0.2187 to $0.219, trending above the triangle formation in the process. The bulls must garner enough momentum to beat resistance at SMA 200, $0.2284 and $0.2362. The last resistance level will bring the price above the 20-day Bollinger Band.

On the downside, the buyers must make sure that support at $0.2113 and $0.1962 remain strong. The Elliott Oscillator has fallen from 0.026 to0.0163 over the last seven days.

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Cryptocurrency Market Update: Bitcoin, Ethereum and Ripple have a bullish start to Saturday, following Fridays drop - FXStreet

From Competition To Sharing: How Her Childrens Rare Disease Led Sharon Terry To Revolutionize Medical Research – Forbes

Sharon Terry, President and CEO of Genetic Alliance.

Ashoka Fellow Sharon Terry looks back at 25 years of impact that led her from being a homeschooling mom to a genetic researcher and global health leader.

Sharon, in 1994 your two children were diagnosed with a rare genetic disease. That propelled you from a homeschooling mom with a degree in theology to a self-taught genetic researcher with now multiple scientific discoveries. It sounds like a naive question but: How did you do this?

Well, when my kids were diagnosed with this rare disease, I quickly learned that no one knew anything about it. The research available wasnt good, no doctor could really help us. The fear that something was going to happen to my children drove me and trying to keep ahead of the disease.My husband and I realized we would have to start to do research on the disease ourselves and figure out a way forward. We had to turn to ourselves for help, there was no other way.

Where did you get the confidence to do this?

Good question. I didnt really piece the dots together until much later, but I think one thing that ironically helped me was that I had had a very abusive childhood. I had to learn how to survive early. And from that terrible situation grew a confidence. I somehow knew, having survived my childhood years, I could overcome anything else.

You boldly asked Harvard to lend you bench space in their laboratories at night.

Yes. It worked!

And you identified a major problem in scientific research the lack of sharing.

Yes. I quickly learned that one of the biggest impediments was that scientists don't share, they don't collaborate, competition is their driving force. I saw all these researchers that had collected data, but they would hoard it, and not let another researcher see it. So I had to think of ways to break through that system and build a new model one that would encourage accelerated academic collaboration.

How did you do that?

I tracked down individuals suffering from the same condition around the world, and invited them to donate tissue, blood, health records, descriptions of their experience, to set up a database that would invite scientists to collaboratively pursue research on the disease. I knew if I could make a central repository of blood and tissue and DNA, then I could set the rules of the game to be different from what scientists were used to. And I decided my rules were going to be: If you come to my well, you will have to share with the community and with everybody else who takes anything out of the well."

And do you think it was key that you outcompeted them from the get-go with a central repository that was bigger than what they had?

Yes, that is certainly one way to look at it. If, for example, I had only come up with 100 data sets and they had 100, then they would have said, "Eh, well, I don't want to play by your rules." But they knew that we were going to be bigger than them. Because we were open, we were people-centered, and they were regional and closed. I think also people trusted us faster. I was a mom with two kids who had this disease, and was in the same boat they were in.

And your goal was not to outcompete other scientists, but to serve people with diseases.

Right. They knew that we would be in the game longer. A lot of scientists do two, three years of research on one condition, and then they go on to the next disease. In contrast, people knew I would probably work on this condition for the rest of my life.

And they were right. Though in addition, you also included many other genetic diseases into your work.

Correct, when I joined Genetic Alliance in 1996, my goal was to replicate my work and use theblueprint I had created for all sorts of other diseases. Which we did. Today, after almost 25 years, we have over 10,000 organizations that interact with us, and dozens of disease groups that are very, very active, working side by side with us, partnering on research.

A key part of your initial success was to patent the gene you discovered that caused your childrens disease, paradoxically to preserve its open accessibility.

Yes. I was concerned that others might patent the gene and restrict access. I had seen a lot on the way: researchers trying to steal my data, to thaw my samples so theyd be useless to me. When we were succeeding in sequencing the gene, I knew I had to go first. I got the patent and then I turned the patent over to the foundation I had set up. And the foundation licensed it to researchers for a dollar back in the days when we had to license it. Now its free and open, so that doesnt matter anymore.

How do you ensure privacy, and that the benefits of the research get distributed back to the community that contributed the data and samples in the first place?

Any data or samples you share your experience of living with your disease, your electronic health record, and your genomic information is encrypted, stored on the platform and never leaves the system. In lay terms, you keep a string on your data. You always know where it is, you know who's looking at it. Researchers cannot export your data. Neither can they access just your data, they only get access to a big pool of aggregate data. And the fee they pay, based on their size and capacity, and anything they find out based on the research they do, gets passed back and redistributed to the pool in terms of shares in this public benefit corporation established by LunaDNA. Those who contribute data are the shareholders in the B-corp. They receive dividends based on their shares. And, this model cannot be changed without going back the Securities and Exchange Commission with a new plan and then reconsenting everyone.

So patients and nonprofits get remunerated for gains that researchers make based on the data they contributed.

Yes, that happens, and I am very delighted.

What is different for parents or for families with genetic diseases nowadays compared towhen you started?

Today, we have created an infrastructure you can plug into. We created a directory calledDisease InfoSearch, which allows anyone to look up a disease as soon as they're diagnosed, so they get all the support information, all the research information in one place. Furthermore, its easier to take action even when you start from a green field. Lets say you're a mom and a dad, your kid gets diagnosed with a genetic disease, perhaps no one else has done research on it. What we will help you with is to set up a biobank, set up a registry, set up a research consortium, and we help you decide where you want to go, how you're going to get researchers interested.

How have you responded to COVID-19?

We set up aCOVID-19 registry, built on our platform. Any organization gets a branded entry point, and the underlying backend is our registry. But your data is yours. It will not be shared unless you say it can be, and then it will not be ever shared individually, so no one will know your name, your age, etc, and it will never be exported.The communities that are building portals on the platform have a lot of questions. If I have a genetic disease that has lung implications, am I at higher risk of COVID-19? How many of my people have had COVID-19? What kind of services should a non-profit be thinking of giving?We don't have results yet because it's only been up a few weeks, but well have some insights soon.

What is the big opportunity in the field of medical research?

I dearly hope it's going to be that we people take control of what's going to happen with our data and our health. My dream is an encompassing registry, a repository of everyones health information and genotype, where everyone has a string on their data, but it is all available for research. That we overcome the silos that keep us from sharing, and build a common infrastructure for the common good. You can see the complications of the current system in the slow COVID-19response: As much as everyone wants to share, there's no way to share, because the various silos have all kept their data separate from one another, and the federal government doesn't want to go against free enterprise. And my hope is that in 10 years, this will have changed.

I like to say that in another 10 years, smart girl scouts will find the solutions to diseases. We won't be spending one billion dollars with a 95% failure rate, fueled by the goals of big pharmaceuticals. Instead, we'll be just having really smart people play with data and come up with solutions, because information will be freely available, it will be in abundance like air, and we will all win.

___

Sharon F. Terry is President and CEO of Genetic Alliance, an enterprise engaging individuals, families and communities to transform health.Genetic Alliance works to provide programs, products and tools for advocacy organizations and ordinary people to take charge of their health and to further biomedical research. As just a Mom with a masters degree in Theology, she cofounded PXE International, a research advocacy organization for the genetic condition pseudoxanthoma elasticum (PXE), in response to the diagnosis of PXE in her two children in 1994.She is a co-discoverer of the ABCC6 gene, and conducts clinical trials.She is the author of 150 peer-reviewed papers, of which 30 are clinical PXE studies. Her story is the topic of herTED TalkandTED Radio Hour. She is co-inventor of the Program for Engaging Everyone Responsibly (PEER), a cross condition people-centered registry system. She was named one of FDAs 30 Heroes for the Thirtieth Anniversary of the Orphan Drug Act in 2013.In 2019, she won the Luminary Award from the Precision Medicine World Conference.Terry is an Ashoka Fellow since 2009.She is an avid student and facilitator ofGestalt Awareness Practice, offering workshops and individual facilitation. Her daughter and son are why she started down this path. They, their wives, and her granddaughter ground and enliven her.

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From Competition To Sharing: How Her Childrens Rare Disease Led Sharon Terry To Revolutionize Medical Research - Forbes

Infection rates may have links to cancer – Medical News Today

New research suggests the prevalence of infection has links to the development of some types of cancer.

A new study has suggested that before developing some forms of cancer, people experienced increased rates of infectious diseases, such as influenza and pneumonia.

The study, published in the journal Cancer Immunology Research, might help develop diagnostic methods for detecting cancers.

Previous research has indicated that there is a link between immunity, inflammation, and cancer.

Inflammation can promote the development of cancers. This can compromise a persons immune system, which can, in turn, increase inflammation.

Dr. Shinako Inaida, a visiting researcher at the Graduate School of Medicine at Kyoto University in Japan and the corresponding author of the study, explains. Cancer can develop in an inflammatory environment caused by infections, immunity disruption, exposure to chemical carcinogens, or chronic or genetic conditions.

An individuals immunity is thought to be a factor in the development of cancer, but additional research is needed to understand the relationship [between] precancerous immunity, infections, and cancer development. This information may contribute to efforts to prevent or detect cancer.

Consequently, it may be valuable to investigate the relationship between immunity, inflammation, and cancers.

The researchers wanted to understand the relationship between the prevalence of specific infectious diseases that could cause inflammation and cancer development.

To investigate, the authors took their information from a 7-year Japanese social health insurance system database.

The researchers looked at data from 50,749 participants. All the participants were over the age of 30 and did not have any detected immunodeficiency.

The case group comprised 2,354 participants who had developed a form of cancer in the 7th year of the study. The control group consisted of 48,395 people who had no cancer diagnosis during the 7 years of the study, plus an additional final year.

The authors then calculated the prevalence of influenza, gastroenteritis, hepatitis, and pneumonia infections for the two groups.

The authors found a clear link between the prevalence of the four illnesses and the later development of cancer.

The case group experienced significantly higher infection rates than the control group in the 6 years before cancer diagnosis.

Members of the case group experienced higher rates of infection in the year before their cancer diagnosis than those in the control group. During this year, the case group experienced an 18% greater infection of influenza, 46.1% of gastroenteritis, 232.1% of hepatitis, and 135.9% for pneumonia than the control group.

The authors also noted that there was a relationship between different infections and different cancers.

For example, people who developed male germ cell cancers were more likely to have experienced influenza. People who developed stomach cancer were more likely to have had pneumonia, and people who developed blood or bone cancers were more likely to have had hepatitis.

However, as Dr. Inaida points out, [i]nterestingly, we found that infection afflicting a specific organ did not necessarily correlate with increased risk of cancer in the same organ.

The authors point out that the study had some limitations. For example, the data provided limited information on underlying genetic and medical conditions, as well as environmental exposures and different lifestyles. These may have affected the chances of infection and developing cancer.

Nonetheless, by making clear an association between infections, inflammation, immunity, and the development of cancers, future research can look in more detail at the precise mechanisms that govern these relationships.

This may then open the door to better diagnostic methods.

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Infection rates may have links to cancer - Medical News Today

Management of Fertility and Hormonal Health in Women at Risk for Hereditary Gynecologic Cancers – Endocrinology Advisor

Hereditary cancer syndromes account for approximately 5% to 10% of all cancers, including those of the female reproductive organs.1 It is important to identify patients at risk for inherited cancer syndromes to manage and prevent various syndrome-associated malignancies.

The management of women at increased risk for hereditary gynecologic cancer specifically has to take into consideration unique concerns regarding fertility and hormonal health, with the use of appropriate fertility preservation strategies and hormone therapy, according to an evidence-based review by the Society of Gynecologic Oncology and American Society for Reproductive Medicine published jointly in Gynecologic Oncology and Fertility & Sterility.2

The most common conditions associated with gynecologic cancers include hereditary breast and ovarian cancer and hereditary nonpolyposis colorectal cancer, also known as Lynch syndrome.2 Other genetic cancer syndromes that have been linked to increased risk for gynecologic malignancy include Peutz-Jeghers syndrome and Cowden syndrome.1

Hereditary breast and ovarian cancer accounts for approximately 5% of breast cancers and 10% to 25% of ovarian cancers.2 Mutations of the genes breast cancer 1 (BRCA1) and 2 (BRCA2) account for the majority of hereditary ovarian, tubal, and peritoneal cancers.3

Several other pathogenic variants are associated with an increased risk for ovarian cancer but not breast cancer, including variants in BRIP1, RAD51C, and RAD51D. Other pathogenic variants that are associated with an increased risk for breast cancer without a significantly increased risk for ovarian cancer include variants in TP53, CDH1, CHEK2, and ATM.2

Lynch syndrome is associated with increased risk for various solid malignancies other than gynecologic cancers, especially colorectal cancer, with Lynch genes varying in penetrance.2

The International Federation of Gynecology and Obstetrics (FIGO) guidelines detail criteria for genetic risk assessment in hereditary breast and ovarian cancer, based on personal or family history of ovarian and breast cancer, age at diagnosis of the breast or ovarian cancer, or having a close relative with a known mutation or a family history indicative of Lynch syndrome.4

Once a mutation is identified, the patient should be counseled regarding risk-reducing surgery, other risk-reduction strategies, and altered screening.

Screening: Although early detection of malignancies may improve prognosis, there are no effective screening tests for ovarian cancer, even in those at high risk for the malignancy. Transvaginal ultrasound and the cancer antigen 125 (CA 125) test may have a role in these cases.2

Chemoprevention: Several classes of drugs have been investigated for chemoprevention of ovarian cancer, but only oral contraceptives were found to potentially reduce risk for the malignancy. However, several studies have reported a possible increased risk for breast cancer with oral contraceptive in the general population and in women with BRCA1 or BRCA2 mutations.2

Risk-reducing surgery: Women with BRCA1 or BRCA2 mutations should be offered risk-reducing salpingo-oophorectomy by age 35 years or when childbearing is complete, but some countries recommend surgery at age 40 years or at an age that is 5 years younger than the youngest affected family member.4 Women with Lynch syndrome should be offered prophylactic total hysterectomy and bilateral salpingo-oophorectomy after the completion of childbearing, especially after age 40 years, as these measures have been shown to decrease the risk for endometrial and ovarian cancer in this patient population.2

There are multiple fertility-preservation and family-building strategies that can be used to help women achieve their goals, including oocyte and/or embryo cryopreservation; use of donor oocytes, donor embryos, and/or gestational carriers; and adoption.2

Women with BRCA1 or BRCA2 pathogenic variants should be referred early to reproductive endocrinologists, as discussions with physicians and ovarian reserve testing may help inform patients decisions on if and when to pursue fertility preservation.2

Patients have the option to cryopreserve and store oocytes and/or embryos using assisted reproductive technology. Although embryo cryopreservation is an effective strategy for fertility preservation, the success rate is dependent on multiple factors. The use of fertility drugs is not associated with a greater risk for invasive breast, ovarian, or uterine cancer in the general population. There is also no known increased risk for breast cancer with fertility medications in BRCA mutation carriers, but there are limited data on the risk for ovarian cancer in these patients.2

Additional options for parenthood include hormonally priming the uterus for embryo transfer after risk-reducing salpingo-oophorectomy. Even women who have undergone hysterectomy but who have retained ovaries can have children using their own gametes through in vitro fertilization with a gestational carrier. Uterine transplantation is still a novel procedure and its role in fertility preservation has not yet been determined.2

Embryo biopsies for preimplantation genetic testing (PGT) should be offered to carriers of known pathogenic gene variants. Analysis for monogenic/single gene defects (PGT-M) can aid in selecting embryos for intrauterine transfer and serve as an alternative to prenatal testing. However, one study found that only approximately one-third of high-risk women would theoretically use PGT-M themselves.2

Chorionic villus sampling and amniocentesis may be used to assess fetal karyotype and certain chromosomal abnormalities, but as of 2018, it is still considered a screening test primarily for aneuploidy that should not be used for prenatal diagnosis of a cancer risk gene.5

Surgical intervention can result in menopausal symptoms at a young age, including vasomotor symptoms, cognitive changes, increased risk for cardiovascular disease, and osteoporosis. Hormonal therapy may alleviate some of these symptoms, but its use in patients at greater risk for gynecologic and breast cancers is controversial and limited data are available on the safety of hormonal therapy for women with BRCA1 or BRCA2 mutations or those with Lynch syndrome. As the benefits of hormone therapy may outweigh the risks secondary to premature estrogen loss, this option should be considered for women without a personal history of breast cancer.2

Nonhormonal options to reduce vasomotor symptoms include selective serotonin reuptake inhibitors, alpha-2 adrenergic agonists, dietary and lifestyle changes, and alternative medicine approaches.2

Providers who care for women at risk for hereditary gynecologic cancers must consider the impact of these conditions on reproductive and hormonal health, stated the authors of the Society of Gynecologic Oncology and American Society for Reproductive Medicine review. These considerations include discussions about options for cancer prevention, fertility preservation and family planning, and management of early surgical menopause in these patients.

References

1. Ballinger LL. Hereditary gynecologic cancers: risk assessment, counseling, testing and management. Obs Gynecol Clin N Am. 2012;39(2):165-181.

2. Chen L-M, Blank SV, Burton E, Glass K, Penick E, Woodard T. Reproductive and hormonal considerations in women at increased risk for hereditary gynecologic cancers: Society of Gynecologic Oncology and American Society for Reproductive Medicine evidence-based review. Fertil Steril. 2019;112(6):1034-1042.

3. Shaw PA, Clarke BA. Prophylactic gynecologic specimens from hereditary cancer carriers. Surg Pathol. 2016;9(2):307-328.

4. Mutch D, Denny L, Quinn M; for the FIGO Committee on Gynecologic Oncology. Hereditary gynecologic cancers. Int J Gynecol Obstet. 2014;124(3):189-192.

5. American College of Obstetricians and Gynecologists Committee on Practice Bulletins. Practice bulletin No. 163 summary: screening for fetal aneuploidy. Obs Gynecol. 2016;127(5):979-981.

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Management of Fertility and Hormonal Health in Women at Risk for Hereditary Gynecologic Cancers - Endocrinology Advisor

Twin peeks: Stanford inherits twin registry, expanding research options – Stanford Medical Center Report

fTwin studies compare similarities and differences between identical twins with those between fraternal twins. Stronger similarities between identical twins than between fraternal twins are assumed to be rooted in their genes. Significant differences between twin siblings, whether identical or fraternal, point to environmental influences.

Understanding the environmental versus the genetic contribution is a leg up in a long climb. If you find genetic influences dominate, you can drop your search for environmental causes and go after the genes responsible. If theres only a weak genetic basis, you can skip the gene hunt and start tracking down suspected environmental causes. Either way, you save time and money.

It was that economy that spurred the creation of the SRI Twin Registry 25 years ago.

In 1995, SRI researcher Gary Swan, PhD, initiated the registry to further his nicotine metabolism, addiction and cessation research.

Finding more effective ways to help smokers quit has been a major theme of my career, said Swan, who for many years directed SRIs Center for Health Science. Relapse rates following smoking cessation can be as high as 70% among smokers who want to quit.

Now an adjunct lecturer affiliated with the Stanford Prevention Research Center, Swan has authored or co-authored hundreds of papers tied at least in part to the study of twins. These studies allowed him to show, among other things, that about 50% of addiction is genetic, suggesting that treatments to aid smoking cessation can be tailored to individuals rates of nicotine metabolism.

Several Stanford scientists have used the SRI Twin Registry. About a decade ago, Martin Angst, MD, professor of anesthesiology, perioperative and pain medicine, wanted to know whether patients responsiveness to the analgesic effects of opioids varied because of genetic influences. Angst recruited participants from the registry to find out. In a couple of papers published in 2012, he concluded that of five distinct dimensions of opioids action analgesia, euphoria, nausea, respiratory depression and addiction only one of them, nausea, varied in degree largely due to genetic influences.

Meanwhile, Angst told Davis about the SRI Twin Registry. Davis was contemplating a study on the relative contributions of the environment and genes to immune responsiveness.

The twins in the registry ranged from infancy to 90 years old. This allowed Davis to see whether similarities the researchers observed in the immune responses of young twins were stronger than those found in older twins, which would indicate that twins diverging environments, as they moved away from home and from each other, affected their immune response to influenza vaccination.

In 2015, Davis reported inCellthat the environmental contribution in many ways dwarfed genetic factors.

While there are larger twin registries in the United States and one in China with half a million registrants its the only twin registry in Northern California.

But with Swans retirement in 2014, SRI gradually deprioritized the twin registry. In January 2019, with Swans blessing, Lisa Jack, a senior project manager at SRI, asked Davis if he could take over the registry. He responded enthusiastically.

By November, the transfer was a done deal, and the ITI Institute was actively recruiting twin pairs. In late October, the institute sent emails to most of the intact twin pairs from the SRI registry, offering them a mug emblazoned with a colorful logo: Stanford Twins Registry.

But only if they sign up, Davis said.

So far,600 individuals from the SRI registry and about 500 brand-new recruits have climbed aboard.

Davis wants to get the word out to other Stanford researchers, too. In mid-2019, Philip Grant, MD, assistant professor of infectious diseases and the Stanford Twin Registrys newly appointed director, sent out an anticipatory notice alerting the institutes faculty of the registrys impending transfer.

That was a trial run, Davis said. We want to reach the whole community.

Having the registry reside on campus should mean reduced overhead and less paperwork, making it easier for Stanford scientists of all stripes to explore genetic versus environmental influences on all sorts of human traits and outcomes.

Theres a lot of value in having it here, said Michael Snyder, PhD, professor and chair of genetics and the Stanford W. Ascherman, MD, FACS, Professor in Genetics. Having the registry at Stanford will put it right in front of our researchers faces.

You never know all the possibilities until people show up and start doing things, Davis said. People will find all kinds of ways to study twins thattheyhavent thought of yet.

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Twin peeks: Stanford inherits twin registry, expanding research options - Stanford Medical Center Report

Individualized mosaics of microbial strains transfer from the maternal to the infant gut – Newswise

Newswise BIRMINGHAM, Ala. Microbial communities in the intestine also known as the gut microbiome are vital for human digestion, metabolism and resistance to colonization by pathogens. The gut microbiome composition in infants and toddlers changes extensively in the first three years of life. But where do those microbes come from in the first place?

Scientists have long been able to analyze the gut microbiome at the level of the 500 to 1,000 different bacterial species that mainly have a beneficial influence; only more recently have they been able to identify individual strains within a single species using powerful genomic tools and supercomputers that analyze massive amounts of genetic data.

Researchers at the University of Alabama at Birmingham now have used their microbiome fingerprint method to report that an individualized mosaic of microbial strains is transmitted to the infant gut microbiome from a mother giving birth through vaginal delivery. They detailed this transmission by analyzing existing metagenomic databases of fecal samples from mother-infant pairs, as well as analyzing mouse dam and pup transmission in a germ-free, or gnotobiotic, mouse model at UAB, where the dams were inoculated with human fecal microbes.

The results of our analysis demonstrate that multiple strains of maternal microbes some that are not abundant in the maternal fecal community can be transmitted during birth to establish a diverse infant gut microbial community, said Casey Morrow, Ph.D., professor emeritus in UABs Department of Cell, Developmental and Integrative Biology. Our analysis provides new insights into the origin of microbial strains in the complex infant microbial community.

The study used a strain-tracking bioinformatics tool previously developed at UAB, called Window-based Single-nucleotide-variant Similarity, or WSS. Hyunmin Koo, Ph.D., UAB Department of Genetics and Genomics Core, led the informatics analysis. The gnotobiotic mouse model studies were led by Braden McFarland, Ph.D., assistant professor in the UAB Department of Cell, Developmental and Integrative Biology.

Morrow and colleagues have used this microbe fingerprint tool in several previous strain-tracking studies. In 2017, they found that fecal donor microbes used to treat patients with recurrent Clostridium difficile infections remained in recipients for months or years after fecal transplants. In 2018, they showed that changes in the upper gastrointestinal tract through obesity surgery led to the emergence of new strains of microbes. In 2019, they analyzed the stability of new strains in individuals after antibiotic treatments, and earlier this year, they found that adult twins, ages 36 to 80 years old, shared a certain strain or strains between each pair for periods of years, and even decades, after they began living apart from each other.

In the current study, several individual-specific patterns of microbial strain-sharing were found between mothers and infants. Three mother-infant pairs showed only related strains, while a dozen other infants of mother-infant pairs contained a mosaic of maternal-related and unrelated microbes. It could be that the unrelated strains came from the mother, but they had not been the dominant strain of that species in the mother, and so had not been detected.

Indeed, in a second study using a dataset from nine women taken at different times in their pregnancies showed that strain variations in individual species occurred in seven of the women.

To further define the source of the unrelated strains, a mouse model was used to look at transmission from dam to pup in the absence of environmental microbes. Five different females were given transplants of different human fecal matter to create five unique humanized-microbiome mice, which were bred with gnotobiotic males. The researchers then analyzed the strains found in the human donors, the mouse dams and their mouse pups. They found four different patterns: 1) The pups strain of a particular species was related to the dams strain; 2) The pups strain was related to both the dams strain and the human donors strain; 3) The pups strain was related to the human donors strain, but not to the dams strain; and, importantly, 4) No related strains for a particular species were found between the pup, the dam and the human donor. Since these animals were bred and raised in germ-free conditions, the unrelated strains in the pups came from minor, undetected strains in the dams.

The results of our studies support a reconsideration of the contribution of different maternal microbes to the infant enteric microbial community, Morrow said. The constellation of microbial strains that we detected in the infants inherited from the mother was different in each mother-infant pair. Given the recognized role of the microbiome in metabolic diseases such as obesity and type 2 diabetes, the results of our study could help to further explain the susceptibility of the infant to metabolic disease found in the mother. Co-authors with Koo, McFarland and Morrow in the study, An individualized mosaic of maternal microbial strains is transmitted to the infant gut microbial community, published in Royal Society Open Science, are Joseph A. Hakim, UAB School of Medicine; David K. Crossman and Michael R. Crowley, UAB Department of Genetics; J. Martin Rodriguez, UAB Department of Medicine, Division of Infectious Diseases; and Etty N. Benveniste, UAB Department of Cell, Developmental and Integrative Biology.

Support came from the University of Alabama School of Medicine, National Institutes of Health grants CA194414 and NS116559, a UAB Neuro-Oncology Support Fund award, and an American Cancer Society Institutional Research Grant through the ONeal Comprehensive Cancer Center at UAB.

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Individualized mosaics of microbial strains transfer from the maternal to the infant gut - Newswise

The Falsehoods of the ‘Plandemic’ Video – FactCheck.org

The first installment of a documentary called Plandemic stormed through social media this week, promising viewers on its website that the film will expose the scientific and political elite who run the scam that is our global health system. The video appeared across platforms, with individual uploads each garnering hundreds of thousands of views.

But the viral video, running nearly 26 minutes, weaves a grand conspiracy theory by using a host of false and misleading claims about the novel coronavirus pandemic andits origins, vaccines, treatments for COVID-19, and more.

The video is largely an interview with Judy Mikovits, a former chronic fatigue researcher who has lobbed a number of accusations against National Institute of Allergy and Infectious Diseases Director Dr. Anthony Fauci. Mikovits was an author on a controversial 2009 study linking a retrovirus to chronic fatigue syndrome that was published in the journal Science, and then retracted in late 2011 after labs were unable to replicate the results and other issues were brought to light.

That same year, in September 2011, Mikovits was fired from her position as research director at the Whittemore Peterson Institute in Nevada and arrested two months later after the institute alleged she stole a laptop, flash drives and other property with institute information. While Mikovits claims in the documentary that she was held in jail despite being charged with nothing, a criminal complaint from November 2011 shows she was charged with two felonies related to the stolen property. The charges were later dropped.

What followed was a years-long legal battle in which Whittemore won a civil judgment against Mikovits; Mikovits filed for bankruptcy; and Mikovits alleged that Whittemore defrauded the government by misusing federally funded research materials. The latter case was dismissed this year.

Mikovits recently co-authored a book with self-described anti-vaxxerKent Heckenlively, with a forward by vaccine skeptic Robert Kennedy Jr., and has spoken at events aimed at discrediting vaccines.

In the video, she claims, And they will kill millions as they already have with their vaccines. Its unclear what vaccines shes referring to, but vaccines have been credited with saving millions of lives. For instance, according to one estimate by researchers with the Centers for Disease Control and Prevention and the World Health Organization, the measles vaccine has saved more than 20 million lives across the globe from 2000 to 2016 alone.

In the sections below, we break down eight of the false, misleading and unfounded claims aired in Plandemic.

The first part of the video focuses largely on two sweeping, but unrelated, accusations against Fauci, who also has been a fixture at the White House briefings on COVID-19.

Without offering any evidence, the video claims that Fauci was part of a cover-up and that he worked with other doctors to take credit and make money on the AIDS epidemic.

Filmmaker Mikki Willis sets the tone for this section of the video, saying to Mikovits, So Anthony Fauci, the man who is heading the pandemic task force, was involved in a cover-up. Willis, a former model, has a large following on YouTube, where he has previously claimed the novel coronavirus was intentionally released.

He directed the cover-up, Mikovits says. And, in fact, everybody else was paid off, and paid off big time.

But at no point in the video does anyone explain what Fauci supposedly covered up.

We asked Mikovits in a phone interview to explain. She said it was a reference to her 2009research paperthat was laterretracted. Mikovits holds Fauci responsible and claims it was part of a cover-up on the part of the medical establishment to keep hidden her research linking a mouse retrovirus to chronic fatigue syndrome. In the years since the research was first published, Mikovits has expanded its reach, suggesting that it could apply also to prostate cancer, lymphoma, and autism.

The NIAID funded Mikovits initial research related to chronic fatigue syndrome, and, after she was fired, another researcher at Whittemore was awarded the remaining grant money. But there is no evidence that Fauci, personally, had anything to do with it. And the journal that published the paper made no mention of Fauci in its retraction. Rather, it explained it was fully retracting the paper because the results couldnt be replicated, even in the same lab, and there is evidence of poor quality control in a number of specific experiments in the Report.

As for the claim about the AIDS epidemic,that goes back much further. In the early 1980s, Mikovits was working as a technician at the National Cancer Institute. She claimsthat the lab she was in had identified the HIV virus from blood and saliva samples and prepared a paper detailing those findings that was slated for publication.

But, she says in the video, referencing one of the pioneers of AIDS research, Dr. Robert Gallo,Fauci holds up the paper for several months, while Robert Gallo writes his own paper and takes all the credit.

Mikovits could not provide the name of her labs paper or the journal that was going to publish it when we spoke to her, so we couldnt check on that. But heres what we do know about the timeline for AIDS research in the early 1980s:

1981 The Centers for Disease Control and Prevention published an article in its Morbidity and Mortality Weekly Report describing a rare lung infection in five young gay men in Los Angeles. Fauci would later recall seeing that article, saying in a 2011 interview, I remember putting the issue to the side of my desk, thinking, Wow, what a bizarre curiosity. One month later, in July, a second MMWR report came to my desk, and this time, an additional 26 men had it, again all gay, all seemingly healthy, and not only in LA, but now also in San Francisco and New York City. I remember reading it very clearly. It was the first time in my medical career I actually got goose pimples. I knew something was very wrong. It changed the direction of my career.

1982 The CDC used the term AIDS, Acquired Immune Deficiency Syndrome, for the first time.

1983 A group of French researchers identified the virus now known as HIV. Twenty-five years later, Franoise Barr-Sinoussi and Luc Montagnier were awarded the Nobel Prize for that discovery.

1984 A team led by Gallo at the National Cancer Institute published research showing that HIV causes AIDS.

Beyond the unsupported claim that Fauci who didnt become the director of NIAID until 1984 stymied early AIDS research at the National Cancer Institute, Mikovits also claims that he has profited from the epidemic.

Referring vaguely to patents, Mikovits says in the video that Fauci was working with other researchers to take credit and make money on the AIDS epidemic. Its true that Faucis name appears on at least six patents related to AIDS research. But its less clear how much he has profited from them. In 2005, the Health and Human Services Department was criticized for not disclosing how much government scientists were collecting from patent royalties. At the time, Fauci expressed concern over the potential for the appearance of a conflict of interest and said that he donated all of his royalty money to charity.

Mikovits makes a claim that numerous scientists have refuted: that the novel coronavirus was manipulated in a laboratory and is not naturally occurring.

So its very clear this virus was manipulated, these, this family of viruses was manipulated and studied in a laboratory where the animals were taken into the laboratory, she says in the video. And this is what was released, whether deliberate or not, that cannot be naturally occurring. Somebody didnt go to a market, get a bat. The virus didnt jump directly to humans. Thats not how it works. Thats accelerated viral evolution. If it was a natural occurrence, it would take it up to 800 years to occur. This occurred from SARS-1 within a decade. That is not naturally occurring.

The exact origin of the coronavirus is not known, but scientists have said the genetic features of SARS-CoV-2 indicate it was neither created in a lab nor manipulated.

Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus, said an article published in Nature Medicine in March. Instead, the authors said its plausible that the coronavirus originated in one of two ways: natural selection in an animal host before zoonotic transfer, which refers to the spread of disease from animals to humans, or natural selection in humans following zoonotic transfer.

The authors said the possibility of an inadvertent laboratory release of SARS-CoV-2 cannot be ruled out, but they do not believe that any type of laboratory-based scenario is plausible because they had observed all notable SARS-CoV-2 features in related coronaviruses in nature.

In a statement in April, University of Sydney professor Edward Holmes, who was involved in mapping the genome of the coronavirus that causes COVID-19, likewise said: Coronaviruses like SARS-CoV-2 are commonly found in wildlife species and frequently jump to new hosts. This is also the most likely explanation for the origin of SARS-CoV-2.

Holmes said there is unfounded speculation that a bat coronavirus named RaTG13, which was being kept at the Wuhan Institute of Virology, was the origin of the new coronavirus. But, he explained, that is not the case, for several reasons.

In summary, the abundance, diversity and evolution of coronaviruses in wildlife strongly suggests that this virus is of natural origin, Holmes said. He added that more sampling of other animals is needed to resolve the exact origins of SARS-CoV-2.

Mikovits also may give viewers a false impression when she says the novel coronavirus occurred from SARS-1, which is a different coronavirus that caused a global outbreak in 2003.

SARS-CoV, or severe acute respiratory syndrome, is similar but distinct from SARS-CoV-2. The viruses share about 79% of the same genetic make-up, but SARS-CoV-2 is even more closely related (96%) to the bat coronavirus from which Holmes has said SARS-CoV-2 wasnt derived.

Weve already written about a bogus analysis that suggested the new coronavirus could have leaked from a Chinese lab because a portion of its genome is similar to part of a viral vector that was used in previous research on SARS.

Kristian Andersen, the director of infectious disease genomics at the Scripps Research Translational Institute, told us in an email that analysis was completely wrong.

Also on the issue of the Wuhan lab, the video shows a clip claiming that $3.7 million flowed from the National Institutes of Health here in the U.S. to the Wuhan lab in China and that NIAID had already been conducting experiments with the Wuhan lab in the past in regard to coronavirus.

Thats misleading.

The project referenced, as other fact-checkers have previously reported, is actually funding from NIAID to EcoHealth Alliance, a U.S.-based nonprofit that researches emerging infectious diseases. The project was done to examine the risk of future coronavirus (CoV) emergence from wildlife using in-depth field investigations across the human-wildlife interface in China, in particular the risk posed by bats, according to a 2014 description.

NIH records show the project was awarded nearly $3.4 million altogether. Most of the funding was through a five-year grant awarded in 2014, Robert Kessler, an EcoHealth spokesman, said in an email to us. The group was renewed for a second five-year grant in 2019 and received $292,161 but NIH recently terminated the grant.

Of that money, only $600,000 (from the first grant) was given to the Wuhan Institute of Virology, Kessler said. The Wuhan lab was a collaborator that was pre-approved by NIH and the State Department, he added, and one that researchers used to conduct genetic analyses of the viruses.

In each of nearly 30 countries around the world where we work, we collaborate with local institutions, all of which are pre-approved by our federal funders, EcoHealth said in an April 28 statement about the terminated funding. Its been EcoHealth Alliances position for the past 15 years that coronaviruses present a clear and immediate threat to our safety. That seems clearer now than ever before.

The group said its research aimed to analyze the risk of coronavirus emergence and help in designing vaccines and drugs to protect us from COVID-19 and other coronavirus threats. In fact, genetic sequences of two bat coronaviruses that we discovered with this grant have been used as lab tools to test the breakthrough antiviral drug Remdesivir.

So its incorrect, and also lacks context, to claim NIAID gave $3.7 million to the Wuhan lab.

Mikovits falsely claims that if youve ever had a flu vaccine, you were injected with coronaviruses.

Shes wrong, Dr. Paul A. Offit, director of the Vaccine Education Center at Childrens Hospital of Philadelphia, told us in a phone interview. Thats not true.

This person doesnt know what she is talking about, Dr. Lee Riley, professor and chair of the Division of Infectious Disease and Vaccinology at the University of California, Berkeley School of Public Health, told us in an email, adding, I think this person is just seeking publicity.

In an interview, we asked Mikovits what support she had for the claim, and she didnt provide any. She only said that flu vaccines are cultured in chicken eggs and dog kidney cells, and those animals have coronaviruses. Its an extreme leap to then claim animal strains of coronaviruses end up in vaccines tested and approved for people. Mikovits further said she attributes the spread of the novel coronavirus worldwide at least in part to the use of the flu vaccine.

As weve explained before, coronaviruses are a diverse family of viruses, and some, such as canine coronavirus, infect animals. Those arent the same as SARS-CoV-2, the coronavirus that causes COVID-19.

As for influenza vaccines, most are made using hens eggs, Offit explained, and about 10% of vaccines in the U.S. are cell-culture vaccines, which use mammalian cells instead of eggs. Specifically, the process uses Madin-Darby Canine Kidney, or MDCK, cells.

These lines have been around for a long time, Offit said. This is a well-tested cell line that does not contain coronavirus and would never be allowed to.

On its website, the Centers for Disease Control and Prevention has more information on how egg-based and cell-based influenza vaccines are manufactured. A cell-based method that also used eggs at the beginning of the process received Food and Drug Administration approval in 2012, and a fully cell-based process got FDA approval in 2016.

The CDC notes that once vaccines are manufactured, FDA tests and approves the vaccines prior to release and shipment.

This cell-based technology has been used in other U.S. vaccines, including vaccines for rotavirus, polio, smallpox, hepatitis, rubella and chickenpox, the CDC says.

Mikovits also repeats the unsubstantiated claim that the flu vaccines increase the odds by 36% of getting COVID-19, which weve previously covered.

Experts say that there has been no study linking the flu shot to elevated risk for the novel coronavirus. The military study cited by Mikovits involved four types of seasonal coronaviruses thatcausecommon colds, not SARS-CoV-2.

More than that, the results in the study that indicate a flu-vaccinated person had an increased likelihood of testing positive for a seasonal coronavirus do not appear to be adjusted for age groups or seasons. Those factors could affect someones chances of getting a specific virus, regardless of whether or not theyve been vaccinated for the flu.

Multiple scientists have pointed out the same issue in other fact-checks, too, and have debunked the erroneous suggestion that the study looked at SARS-CoV-2.

The Military Health System told us in a statement that the study does not show or suggest that influenza vaccination predisposes in any way, the potential for infection with the more severe forms of coronavirus, such as COVID-19. MHS further said it remains essential for people to obtain the seasonal flu shot each year as it becomes available.

The video makes the unsubstantiated claim that the antimalarial drug hydroxychloroquine is the most effective medication to treat COVID-19, citing a survey of doctors.

Shortly after that, Mikovits says hydroxychloroquine is effective against these families of viruses, referring to the family of coronaviruses, such as COVID-19, but they keep it from the people.

We have covered this ground before when President Donald Trump encouraged the off-label use of chloroquineand its derivativehydroxychloroquine for treatment of COVID-19 patients. Both drugs are used to treat malaria, lupus and rheumatoid arthritis.

But there is only limited evidence that hydroxychloroquine is effective for COVID-19, and it carries potential health risks.

The National Institutes of Health says there is insufficient clinical data to recommend either for or against using chloroquine or hydroxychloroquine for the treatment of COVID-19.

Despite insufficient clinical data, the Food and Drug Administration issued an emergency use authorization, or EUA, order on March 28 that allowed for the drugs to be used as a treatment for some hospitalized COVID-19 patients.

A little less than a month later, the FDA issueda warning against using hydroxychloroquine or chloroquine for COVID-19 outside of the hospital setting or a clinical trial due to risk of heart rhythm problems. The warning came a few days after astudyfoundthat patients at Veterans Health Administration medical centers treated with hydroxychloroquine had an increased mortality risk compared with those that were not treated with the drug.

In the video, Mikovits says, The AMA was saying doctors will lose their license if they use hydroxychloroquine, the anti-malarial drug thats been on the list of essential medicine worldwide for 70 years. Dr. Fauci calls that anecdotal. Its not storytelling if we have thousands of pages of data saying its effective against these families of viruses. This is essential medicine and they keep it from the people.

Its not true that the American Medical Association told doctors they will lose their license if they use hydroxychloroquine for COVID-19. The AMA issued a statement saying it opposed purchasing excessive amounts of chloroquine or hydroxychloroquine for possible COVID-19 treatment. But it also said, Novel off-label use of FDA-approved medications is a matter for the physicians or other prescribers professional judgment.

As for hydroxychloroquines effectiveness against coronaviruses, we have written that at least two studies show that it has antiviral activity against the novel coronavirus in cells grown in the lab. But there is only anecdotal evidence that the drug works in people.

Trump cited in a tweet the results of a small clinical trial in France, but the International Society of Antimicrobial Chemotherapy, which publishes the journal in which the study appeared, later issued a statement that said the article does not meet the Societys expected standard, especially relating to the lack of better explanations of the inclusion criteria and the triage of patients to ensure patient safety.

We cover this more extensively in our story Trump Hypes Potential COVID-19 Drugs, But Evidence So Far Is Slim.

In attacking public health measures taken to address the pandemic in the U.S., Mikovits wrongly suggests that using masks could lead to people infecting themselves with their own breath. Wearing the mask literally activates your own virus, Mikovits said. Youre getting sick from your own reactivated coronavirus expressions and if it happens to be SARS-CoV-2, then youve got a big problem.

Experts were perplexed by what she meant and said the implication that simply breathing through a mask could lead to self-infection doesnt square with science.

Linsey Marr, a professor of civil and environmental engineering at Virginia Tech who studies airborne disease transmission, told us: If youre shedding (breathing out) virus, then youre already infected. Even without a mask, infected people who are shedding virus probably rebreathe some of their own viruses, but there are already billions times more viruses in your body. Hopefully, the mask is protecting other people from your exhalations.

And Lisa Brosseau, an expert on respiratory protection and infectious diseases and a certified industrial hygienist, said in an email that viruses are not activated by anything, as Mikovits suggests.

Viruses instead require living cells in order to replicate, but their viability or ability to replicate isnt affected whether someone is wearing a mask or not, said Brosseau, a former professor at the University of Illinois at Chicago. If anything, viruses in the environment can be rendered non-viable by exposure to certain temperature and relative humidity conditions.

There is nothing magical about our breath that activates or reactivates a virus, Brosseau said.

As weve previously written, while there is little research on cloth masks, the hope is that they can help prevent individuals, even those who do not feel sick, from unknowingly spreading COVID-19 to others. Brosseau said people should frequently wash cloth masks, though, and stressed that masks are not a substitute for social distancing. The CDC notesthe same.

Mikovits says in the video: In 1999, I was working in Fort Detrick and my job was to teach Ebola how to infect human cells without killing them. Ebola couldnt infect human cells until we took it in the laboratories and taught them.

Its not clear what she meant by that, and she didnt explain when we asked about her claim.

But the suggestion that Ebola, which includes six species of ebolaviruses, didnt infect people until 1999, or later, is false.

The first two species, Zaire ebolavirus and Sudan ebolavirus, were discovered after outbreaks in 1976 in Central Africa. Combined, those two viruses, which scientists believe may have come from bats or nonhuman primates (such as chimpanzees, apes, monkeys, etc.), killed about 430 people that year, according to the CDC.

Zaire ebolavirus which is also linked to the largest Ebola outbreak which began in West Africa in 2014 is said to have initially spread in 1976 through the use of contaminated needles and syringes at a hospital in the village where the first infected person was treated. And the Sudan ebolavirus is believed to have started with workers in a cotton factory.

In fact, the CDC says four of the six species of ebolavirus Zaire ebolavirus, Sudan ebolavirus, Ta Forest ebolavirus (formerly Cte dIvoire ebolavirus) and Bundibugyo ebolavirus are known to cause disease in people. And three of the four species were discovered prior to 1999.

A fifth species, Reston ebolavirus, was first discovered in 1989 in research monkeys imported into the U.S. from the Philippines. That species is known to cause disease in nonhuman primates and pigs, but not in people, the CDC says. There have been cases in which individuals developed Reston ebolavirus antibodies, but did not experience symptoms.

The sixth species, Bombali ebolavirus, was discovered in 2018 in a bat in Sierra Leone. It also is not known to infect humans.

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The Falsehoods of the 'Plandemic' Video - FactCheck.org

Its in your genes Whether Covid lands you in hospital or not depends on your body – ThePrint

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When some people become infected with the coronavirus, they only develop mild or undetectable cases of COVID-19. Others suffer severe symptoms, fighting to breathe on a ventilator for weeks, if they survive at all.

Despite a concerted global scientific effort, doctors still lack a clear picture of why this is.

Could genetic differences explain the differences we see in symptoms and severity of COVID-19?

To test this, we used computer models to analyze known genetic variation within the human immune system. The results of our modeling suggest that there are in fact differences in peoples DNA that could influence their ability to respond to a SARS-CoV-2 infection.

When a virus infects human cells, the body reacts by turning on what are essentially anti-virus alarm systems. These alarms identify viral invaders and tell the immune system to send cytotoxic T cells a type of white blood cell to destroy the infected cells and hopefully slow the infection.

But not all alarm systems are created equal. People have different versions of the same genes called alleles and some of these alleles are more sensitive to certain viruses or pathogens than others.

To test whether different alleles of this alarm system could explain some of the range in immune responses to SARS-CoV-2, we first retrieved a list of all the proteins that make up the coronavirus from an online database.

We then took that list and used existing computer algorithms to predict how well different versions of the anti-viral alarm system detected these coronavirus proteins.

Also read: Worlds most accurate antibody test has arrived. Or has it?

The part of the alarm system that we tested is called the human leukocyte antigen system, or HLA. Each person has multiple alleles of the genes that make up their HLA type. Each allele codes for a different HLA protein. These proteins are the sensors of the alarm system and find intruders by binding to various peptides chains of amino acids that make up parts of the coronavirus that are foreign to the body.

Once an HLA protein binds to a virus or piece of a virus, it transports the intruder to the cell surface. This marks the cell as infected and from there the immune system will kill the cell.

In general, the more peptides of a virus that a persons HLAs can detect, the stronger the immune response. Think of it like a more sensitive sensor of the alarm system.

The results of our modeling predict that some HLA types bind to a large number of the SARS-CoV-2 peptides while others bind to very few. That is to say, some sensors may be better tailored to SARS-CoV-2 than others. If true, the specific HLA alleles a person has would likely be a factor in how effective their immune response is to COVID-19.

Because our study only used a computer model to make these predictions, we decided to test the results using clinical information from the 2002-2004 SARS outbreak.

Whats next?

We found similarities in how effective alleles were at identifying SARS and SARS-CoV-2. If an HLA allele appeared to be bad at recognizing SARS-CoV-2, it was also bad at recognizing SARS. Our analysis predicted that one allele, called B46:01, is particularly bad with regards to both SARS-CoV-2 and SARS-CoV. Sure enough, previous studies showed that people with this allele tended to have more severe SARS infections and higher viral loads than people with other versions of the HLA gene.

Based on our study, we think variation in HLA genes is part of the explanation for the huge differences in infection severity in many COVID-19 patients. These differences in the HLA genes are probably not the only genetic factor that affects severity of COVID-19, but they may be a significant piece of the puzzle. It is important to further study how HLA types can clinically affect COVID-19 severity and to test these predictions using real cases. Understanding how variation in HLA types may affect the clinical course of COVID-19 could help identify individuals at higher risk from the disease.

To the best of our knowledge, this is the first study to evaluate the relationship between viral proteins across a wide range of HLA alleles. Currently, we know very little about the relationship between many other viruses and HLA type. In theory, we could repeat this analysis to better understand the genetic risks of many viruses that currently or could potentially infect humans.

Austin Nguyen, PhD Candidate in Computational Biology and Biomedical Engineering, Oregon Health & Science University; Abhinav Nellore, Assistant Professor of Biomedical Engineering & Surgery, Oregon Health & Science University, and Reid Thompson, Assistant Professor of Radiation Medicine, Oregon Health & Science University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Also read: After HCQ, its time for azithromycin and pneumonia drug combo to go under clinical trial

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Its in your genes Whether Covid lands you in hospital or not depends on your body - ThePrint

FDA approves Tabrecta, first targeted therapy to treat metastatic NSCLC – The Cancer Letter

publication date: May. 8, 2020

FDA has granted accelerated approval to Tabrecta (capmatinib) for adult patients with metastatic non-small cell lung cancer whose tumors have a mutation that leads to mesenchymal-epithelial transition exon 14 skipping as detected by an FDA-approved test.

Tabrecta is the first FDA-approved therapy to treat NSCLC with specific mutations (those that lead to mesenchymal-epithelial transition or MET exon 14 skipping).

Tabrecta is sponsored by Novartis.

FDA also approved the FoundationOne CDx assay (Foundation Medicine, Inc.) as a companion diagnostic for Tabrecta. Most patients had tumor samples that were tested for mutations that lead to MET exon 14 skipping using local tests and confirmed with the F1CDx, which is a next-generation sequencing based in vitro diagnostic device capable of detecting several mutations, including mutations that lead to MET exon 14 skipping.

Lung cancer is increasingly being divided into multiple subsets of molecularly defined populations with drugs being developed to target these specific groups, Richard Pazdur, director of the FDA Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the FDAs Center for Drug Evaluation and Research, said in a statement. Tabrecta is the first approval specifically for the treatment of patients with non-small cell lung cancer whose tumors have mutations that lead to MET exon 14 skipping. This patient population now has an option for a targeted therapy, which they didnt have prior to today.

Efficacy was demonstrated in the GEOMETRY mono-1 trial (NCT02414139), a multicenter, non-randomized, open-label, multicohort study enrolling 97 patients with metastatic NSCLC with confirmed MET exon 14 skipping. Patients received Tabrecta 400 mg orally twice daily until disease progression or unacceptable toxicity.

The main efficacy outcome measures were overall response rate (ORR) determined by a blinded independent review committee using RECIST 1.1 and response duration. Among the 28 treatment-nave patients, the ORR was 68% (95% CI: 48, 84) with a response duration of 12.6 months (95% CI: 5.5, 25.3). Among the 69 previously treated patients, the ORR was 41% (95% CI: 29, 53) with a response duration of 9.7 months (95% CI: 5.5, 13.0).

FDA approves daratumumab and hyaluronidase-fihj for multiple myeloma

FDA has approved daratumumab and hyaluronidase-fihj (Darzalex Faspro) for adult patients with newly diagnosed or relapsed/refractory multiple myeloma. This new product allows for subcutaneous dosing of daratumumab.

Darzalex Faspro is sponsored by Janssen Biotech Inc.

Daratumumab and hyaluronidase-fihj is approved for the following indications that intravenous daratumumab had previously received:

in combination with bortezomib, melphalan and prednisone in newly diagnosed patients who are ineligible for autologous stem cell transplant,

in combination with lenalidomide and dexamethasone in newly diagnosed patients who are ineligible for autologous stem cell transplant and in patients with relapsed or refractory multiple myeloma who have received at least one prior therapy,

in combination with bortezomib and dexamethasone in patients who have received at least one prior therapy,

as monotherapy, in patients who have received at least three prior lines of therapy including a proteasome inhibitor and an immunomodulatory agent or who are double-refractory to a PI and an immunomodulatory agent.

Efficacy of daratumumab and hyaluronidase-fihji (monotherapy) was evaluated in COLUMBA (NCT03277105), an open-label non-inferiority trial randomizing 263 patients to daratumumab and hyaluronidase-fihj and 259 to intravenous daratumumab (daratumumab IV). The trials co-primary endpoints were overall response rate and pharmacokinetic endpoint of the maximum Ctrough on cycle 3, day 1 pre-dose. Daratumumab and hyaluronidase-fihj was non-inferior to daratumumab IV in evaluating these two endpoints.

The ORR was 41.1% for daratumumab and hyaluronidase-fihj and 37.1% for daratumumab IV with a risk ratio of 1.11 (95% CI: 0.89, 1.37). The geometric mean ratio comparing daratumumab and hyaluronidase-fihj to daratumumab IV for maximum Ctrough was 108% (90% CI: 96,122).

Efficacy of daratumumab and hyaluronidase-fihj in combination with VMP (D-VMP) was evaluated in a single-arm cohort of PLEIADES (NCT03412565), a multi-cohort, openlabel trial. Eligible patients were required to have newly diagnosed multiple myeloma and were ineligible for transplant. The major efficacy outcome measure, ORR, was 88.1% (95% CI: 77.8, 94.7).

Efficacy of daratumumab and hyaluronidase-fihj in combination with Rd (D-Rd) was evaluated in a single-arm cohort of this trial. Eligible patients had received at least one prior line of therapy. ORR was 90.8% (95% CI: 81.0, 96.5).

FDA accepts NDA for CC-486 in AML indication

FDA has accepted a New Drug Application for CC-486, an investigational oral hypomethylating agent, for the maintenance treatment of adult patients with acute myeloid leukemia who achieved complete remission, or CR with incomplete blood count recovery, following induction therapy with or without consolidation treatment, and who are not candidates for, or who choose not to proceed to, hematopoietic stem cell transplantation.

CC-486 is sponsored by Bristol Myers Squibb. FDA granted the application Priority Review and set a Prescription Drug User Fee Act goal date of Sept. 3, 2020.

The NDA submission was based on the efficacy and safety results of the phase III QUAZAR AML-001 study, which met the primary endpoint of improved overall survival for patients receiving AML maintenance treatment with CC-486 versus placebo.

Often, newly diagnosed adult patients with AML achieve a complete response with induction therapy, however many patients will relapse and experience a poor outcome. Patients in remission are seeking treatment options that decrease the likelihood of relapse and extend overall survival, Noah Berkowitz, senior vice president of Global Clinical Development, Hematology, at Bristol Myers Squibb, said in a statement.

CC-486 is an investigational therapy that is not approved for any use in any country.

Caris Life Sciences submits two PMA applications to FDA for whole exome and whole transcriptome sequencing

Caris Life Sciences has submitted two Pre-Market Approval applications for MI Exome CDx and MI Transcriptome CDx to FDA.

MI Exome CDx, whole exome sequencing (DNA), and MI Transcriptome CDx, whole transcriptome sequencing (RNA), are precision medicine assays that include key companion diagnostic biomarkers with therapy claims, and detect all classes of alterations including genomic signatures for microsatellite instability, tumor mutation burden, and loss of heterozygosity.

MI Exome CDx is a next-generation sequencing-based test utilizing DNA isolated from formalin-fixed paraffin embedded tumor tissue specimens for the qualitative detection of genomic alterations. MI Exome CDx can identify genetic variants (single nucleotide variants, insertions and deletions), copy number alterations, MSI, TMB and LOH.

MI Transcriptome CDx is a next-generation sequencing-based test that utilizes RNA isolated from formalin-fixed paraffin embedded tumor tissue specimens for the qualitative detection of genomic and transcriptomic alterations. MI Transcriptome CDx is a broad, multi-gene panel utilized to identify gene fusions, transcript variants, genetic variants (single nucleotide variants, insertions and deletions), and gene expression changes. FDA granted MI Transcriptome CDx received Breakthrough Device designation in 2019.

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FDA approves Tabrecta, first targeted therapy to treat metastatic NSCLC - The Cancer Letter

Research into the health of unborn babies receives government funding – UNSW Newsroom

A research project that will examine the feasibility of genomic testing has received funding from the Australian Government Medical Research Futures Fund (MRFF).

The two-year project, PreGen, will be led by Associate Professor Tony Roscioli from UNSW Medicine, who is an expert in genomics at Neuroscience Research Australia (NeuRA) and New South Wales Health Pathology.

The funding received will allow PreGen to perform genomic tests in families seen at ten of Australias largest maternity centres. This will assess the benefits made available from antenatal genomic testing.

We do not currently have easily accessible accredited antenatal genomic testing in Australia. Pregnancy abnormalities identified on ultrasound are therefore not usually investigated further with genomic testing to try to find the cause, A/Prof. Roscioli said.

The grant will help to improve knowledge about the conditions causing malformations, improve available testing and promote international collaborations to understand the genetic conditions that may occur in babies.

Prenatal genomic testing allows the cause of some abnormalities to be identified. This information helps families consider available options and could allow clinicians to better manage a babys health after the birth.

There is huge demand for this technology from families and doctors, A/Prof. Roscioli said.

The project will also create training positions to build the workforce required to perform and analyse the results quickly. Further, PreGen will evaluate the psychological support families may require when undergoing genomic testing.

The priorities will be to set up antenatal genomic testing safely around Australia and to expand knowledge about genetic conditions in babies. We will evaluate the counselling that is required to support families appropriately, he said.

UNSW Deputy Vice-Chancellor (Research) Professor Nicholas Fisk, in noting that this grant represented a quantum leap for prenatal genetics, said that rolling out exome and genome sequencing was exactly the sort of translation the MRFF was designed for.

Prof. Fisk,a former President of the International Fetal Medicine Society, said: Fetal abnormalities occur in up to one in 20 pregnancies - this exemplary hi-tech model of care will help parents and their clinicians understand whether imaging findings are just isolated or part of more complex disorders.

PreGen will compliment a related multicentre MRFF grant, Mackenzies Mission, also run out of the Randwick Health Precinct, attesting to UNSWs national leadership in this area.

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Research into the health of unborn babies receives government funding - UNSW Newsroom

New medical foundation invests in COVID-19 research funding – News – The University of Sydney

Snow Medical founder Terry Snow said: COVID-19 has had a devastating effect on Australia and the world this is the biggest thing to hit the globe since 1945 and it will have a lasting impact for years to come. Government has stepped up and now is the time for the community to play a role. All these measures are aimed at getting Australians back to work, making treatment more effective and efficient and getting our economy working again.

Snow Medical chair, Tom Snow, added: We want to help Australias best and brightest to focus their efforts on this huge national and global challenge.

This consortium is particularly notable because of its national reach and collaborative networks it draws on research expertise from over 15 universities and medical research institutes, their affiliated public hospitals, state health departments, public health authorities, pathology services and the Australian Red Cross Blood Service to provide a truly national picture and coordinated approach to beating COVID-19.

Professor Tania Sorrell who is director of the University of Sydneys Marie Bashir Institute for Infectious Diseases and Biosecurity, Infectious Diseases Group head in The Westmead Institute of Medical Research and the lead investigator in CREID said: This very generous donation will help Australia lead in the fight to contain the spread of COVID-19 in the community, better protect health care workers, and offer the best care to individual patients.

Critically, the vision of Snow Medical has enabled CREID and APPRISE to leverage the joint power of their national research networks in the fight against COVID-19.

Professor Sharon Lewin, director of the Peter Doherty Institute for Infection and Immunity (Doherty Institute), a joint venture of the University of Melbourne and The Royal Melbourne Hospital, and chief investigator for APPRISE said: The large injection of funds supports the development of critical national platforms for the current pandemic while building capacity for future pandemics."

Infectious diseases physician and trials expert at the University of Sydneys Faculty of Medicine and Health, Professor Tom Snelling, who will be leading the data science project, said: Australias brisk and effective response to COVID-19 is the envy of many countries but we cant afford to become complacent. This donation will give researchers a critical boost in their race to find and implement science-driven solutions for the pandemic.

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New medical foundation invests in COVID-19 research funding - News - The University of Sydney

Genetics and Weight: Is There an Obesity Gene? – LIVESTRONG.COM

There are many factors at play when it comes to your weight, and genetics is certainly one of them. Every person's body responds differently to food and exercise, and there's some truth to the notion that obesity can run in families.

Genetics and weight are definitely linked, but you're not doomed by your DNA.

Image Credit: Rostislav_Sedlacek/iStock/GettyImages

But what runs in your family may not necessarily be your fate. How your genetics affect your weight is only one piece of the puzzle.

If it seems like some people can eat pizza for breakfast while others gain weight just from looking at sugar, that's because, well, everyone is different thanks in part to genes.

"We inherit all kinds of traits, such as hair and eye color, height and also body type," Keith-Thomas Ayoob, EdD, RD, clinical professor at Albert Einstein College of Medicine, tells LIVESTRONG.com. "If two people both have what might be called a "stocky frame," their kids are probably not going to have frames that are long and lanky."

Like other traits, there's no singular gene connected to weight or obesity. In fact, according to Harvard Health Publishing, more than 400 genes are involved in contributing to obesity.

And while we're not sure exactly how they work, there's definitely a connection between genes and weight. Indeed, a November 2017 study in the International Journal of Obesity found that people with a higher genetic risk of obesity tended to gain more weight from age 20 on than those without this risk.

What we do know: Our genes form the basis for our body's signal and response system, which guides food intake, according to the Centers for Disease Control and Prevention (CDC). One hypothesis is that our bodies are primed to protect us against weight loss because energy, stored in fat, is crucial to survival. So the same genes that helped our ancestors survive food scarcity are still working to protect us, even though most of us have all the food we need and then some.

While most research has focused on how genetic risk affects obesity, more recent research has taken an in-depth look at the links between genetics, obesity and body mass index (BMI) over time.

In one study published January 2020 in JAMA Cardiology, researchers assessed the data on more than 2,500 adults from 1985 to 2010. Using a score based on each participant's DNA, they calculated the genetic risk of obesity for each person and compared it to measurements taken over the course of the 25-year study period. They also monitored each person's BMI over time.

"You may need to adjust your goals to take into account what your body can do [but] lifestyle and your eating style are major players in the obesity war perhaps the main players because they're the only ones over which you can have some control."

Their analysis showed that BMI in young adulthood explained about 52 percent of a person's BMI 25 years later, while genetics explained only about 14 percent. In the end, they concluded that fitness and BMI over time were better indicators of obesity risk than genetics.

Ayoob agrees that having a family history of obesity does not mean you have no control over your BMI.

"It means you may need to adjust your goals to take into account what your body can do and what you should expect," he says. "Lifestyle and your eating style are major players in the obesity war perhaps the main players because they're the only ones over which you can have some control."

Aim for at least 150 minutes of physical activity each week, and remember: Walking counts!

Image Credit: Igor Alecsander/E+/GettyImages

The bottom line? Genes play a role, yes, but lifestyle aka the diet and activity choices you make every day is the best determining factor when it comes to the number on the scale, your BMI and your overall health.

And if your lifestyle isn't the healthiest, it's worth it to make some improvements: The excess fat associated with obesity puts people at risk for other serious conditions, such as cardiovascular disease and stroke.

Here are some suggestions from the experts to get started:

1. Add Weight Lifting to Your Routine

People with a genetic propensity toward obesity can lower their percentage of body fat by raising their metabolism, Robert Herbst, a personal trainer specializing in weight loss, tells LIVESTRONG.com.

To do this effectively, he highly recommends regular weight lifting.

"You should perform compound movements such as squats, lunges, bench press and deadlifts. These cause your metabolism to be elevated for 48 to 72 hours afterward as your body repairs muscle fibers that were broken down during the exercise and builds additional muscle in anticipation of greater loads in the future," he says.

Since muscle is more metabolically active than fat, building more of it helps your body burn more calories, even at rest.

Obesity is diagnosed when your body fat levels are much higher than the healthy range. At the very basic level, too much body fat occurs when more calories come in than go out. So it makes perfect sense to take stock of how and what you eat when confronting obesity.

"Genetics aside, look at the eating habits you grew up with. Are they compatible with having a healthy weight?" Ayoob asks.

A healthy, balanced diet where no food group is restricted is the best approach, he says.

Herbst recommends focusing on whole foods (think: fruits, vegetables and whole grains) and limiting empty-calorie junk foods like soda, chips and sweets.

As part of a healthy eating plan, the National Heart, Lung, and Blood Institute emphasizes staying within your daily calorie goal for weight loss and controlling portion sizes.

Wondering how to calculate your calories for weight loss? Download the MyPlate app to do the job and help you track your intake, so you can stay focused and achieve your goals!

An important part of the equation when making healthy lifestyle changes is making sure those changes are maintainable. Ayoob recommends setting realistic goals and starting off slow.

"Weight loss that is slow and steady, not fast and furious, will win this race," he says. "Give yourself a year. The year will pass anyway, so it's a matter of it passing with progress or just keeping the status quo," he said.

In that time, aim to be purposefully active most days, even if that means just brisk walking, for at least 30 minutes.

He advises his own patients to engage in 30 to 60 minutes of physical activity five or more days a week, with walking being the most common activity.

This is in line with the U.S. Department of Health & Human Services' Physical Activity Guidelines for Americans, which recommend adults do at least 150 minutes of moderate-intensity aerobic physical activity each week along with muscle-strengthening activities at least two days.

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Genetics and Weight: Is There an Obesity Gene? - LIVESTRONG.COM

Michael Jordan’s kids share what it was like to be raised by the NBA legend – CBS Sports

Michael Jordan is an NBA legend, a Hall of Famer, 6-time champion and sneaker king, but to his kids he is first, and most importantly just "dad." Jordan has three children with his first wife Juanita Vanoy, Jeffrey (31), Marcus (29), Jasmine (27). He also has 6-year-old twins Ysabel and Victoria with his wife Yvette Prieto.

"The Last Dance" documentary has given everyone, including his children, a closer look at who MJ was off the court.

The fascination over the unique access to the GOAT's life has a lot to do with how he lived, as well as how private he has previously been. Jordan carefully selected the events he would appear at, rarely shoving himself in the spotlight.

Jasmine told InStyle magazineher dad is "very much a homebody and has always been a private person."

She continued saying, "He just so happened to have chosen a profession that was made for the public eye, and honestly I think if he could've had his same career without the fame, he'd probably still do it. You won't catch him in New York City or L.A. unless it's for business."

His low profile also meant his kids didn't realize just how famous he was.

"I definitely didn't realize growing up who he was. He was "Dad," and that was it." Jasmine said, sharing in her pre-teens she finally searched him online "to see why everyone was so obsessed"

"It didn't hit me that he was the phenomenon that he is," she said. "I would ask him questions all the time like, "Why do you think you're the greatest?" and he would just laugh."

The kids did see the NBA side of Jordan when they were playing pickup games. "He would treat us exactly the same as any other basketball player he was playing," Marcus toldToday, explaining that he would sometimes call his mom to tell her MJ was picking on them.

Sometimes this competitiveness ended in injury. "Jeff was going for a touchdown and, I'll never forget it, my dad tackled Jeff into a glass table and Jeff hit his head," Marcus shared in an interview with The Breakfast Club, adding, "That's the competitiveness. Obviously, it was an accident."

"One of the biggest misconceptions was that he couldn't turn that [competitiveness] off," Jeffrey said. "He definitely could turn it off and be a dad ... But when it was on, it was on."

The kids welcomed the heightened competition. "I wouldn't want him to hold back anything, because that wouldn't make any of us better," Jeffrey said in an interview with Today.

Despite his competitive nature, MJ never pressured his kids to play basketball. Both boys played, but Jordan said he just wanted his kids to be happy. Jasmine tried her hand at basketball, but said her and her dad agreed, the sport wasn't for her.

As far as their personal lives went, Jasmine said they didn't introduce too many people to their dad. When she introduced him to her fiance Rakeem Christmas, she said it was "hysterical" as they were both nervous and unsure what to say.

While all of his kids were encouraged to find their own path to happiness, they each are still in the world of sports, and sneakers.

Jeffrey leads brand digital innovation for the Jordan Brand and Marcus opened the shoe store "Trophy Room." Jasmine works in sports management with Nike and Jordan Brand and previously worked with the Charlotte Hornets.

All three will be featured in episode 10 of the documentary.

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Michael Jordan's kids share what it was like to be raised by the NBA legend - CBS Sports

Jordan hooked up young White Sox teammates with Nike gear – NBCSports.com

Theres a scene in the first 10 minutes of "Space Jam" that shows the opposing catcher tipping pitches to Michael Jordan as the basketball star struggles to hit for the minor league Birmingham Barons. The catcher tells Jordan what pitches are coming and thanks him for signing a basketball for his kid.

Im a hero now, the catcher said.

The movie, of course, is fictional and co-stars cartoon characters like Bugs Bunny, so youd hope the tipping of pitches didnt really happen. But the constant autograph requests certainly did.

I don't know how he didn't get tired of it, but he really didn't, longtimeWhite Sox head trainer Herm Schneider said. He was very generous and kind to everybody.

Schneider, who now holds the title of head athletic trainer emeritus for the White Sox,was charged with getting Jordan ready for his baseball endeavor in 1994, working with him seven days a week during the winter before spring training. And once they all arrived in Sarasota, Floridain the spring of 94, Schneider had a front row seat for a bizarre team dynamic that featured one of the richest, most famous humans on the planet interacting with next-to-broke minor league baseball players.

He blended in very nicely with everybody and tried not to be Michael Jordan the basketball player, Schneider said. He just tried to be Michael the baseball player, and he worked hard at that. He did. He really did.

RELATED:Inside MJ's secret baseball training sessions with Beltin' Bill

It helped that Jordan took care of the younger players and used his deep Nike connections to help them out.

He would see these young guys that had kind of crummy equipment and crummy shoes, and he would tell them, Go tell Herm your shoe size and what size shirt you wear, etc., whatever you need and then Herm will take care of the rest, Schneider recalled.

Suddenly, the head trainer of the White Sox was putting in daily requests to Howard White, who is now the senior vice president of the Jordan Brand.

I would call him with a list that was extremely long and, by golly, the next morning, that stuff was sitting at my desk to distribute to everybody. It was incredible, Schneider said. And this went on daily. I mean, he would pick four or five guys and he would say, Go tell Herm what you need, and I'd call Nike and tell them what Michael wanted them to have. There was never a question asked of like, 'Why so much?' Nothing like that. It was like, OK, it will be there tomorrow.

And then there were the endless autograph requests.

The players, they had shoes, and basketballs, and pictures and everything else. He never really said no to any one of them at all, Schneider said. He just said, Go put it in Herm's office,and after the workout today, I'll go sign them, and then tomorrow morning you can go pick them up in his office.

According to Schneider, the requests never really stopped, and neither did Jordan's generosity.

I'm not embellishing this at all. This is the truth, the trainer said. What I saw was absolutely incredible of how much he signed and how many people were asking.

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Jordan hooked up young White Sox teammates with Nike gear - NBCSports.com

The iconic sneakers that defined Michael Jordan’s title runs – ESPN

May 3, 2020

Nick DePaulaESPN

"It's gotta be the shoes."

For many basketball fans in the 1990s, that wasn't just a line said by Spike Lee's Mars Blackmon character in a commercial -- it was a way of life. Michael Jordan helped turn basketball sneakers into a multibillion-dollar industry.

Episode 5 of "The Last Dance" (9 p.m. ET, Sunday on ESPN and the ESPN App) delves into the global phenomenon that was the Air Jordan sneaker franchise and the off-court business surrounding the Chicago Bulls.

In advance of that episode, longtime designer Tinker Hatfield and Jordan VP of Footwear Gentry Humphrey spoke with ESPN about the iconic Air Jordan line and the sneakers that were on Jordan's feet when he won each of his six championships.

Air Jordan 6

Jordan established himself atop the NBA hierarchy, knocking off Converse icon Magic Johnson and the Los Angeles Lakers in his first NBA Finals. Jordan ushered in a new era in the NBA in an amplified shade of Bulls red -- dubbed "infrared" -- with a molded heel tab inspired by the rear spoiler on his Porsche.

1 Related

"Michael actually started influencing more design power over the process, and I was cool with that," Hatfield said. "He started feeling like his signature look shouldn't have a [toe] tip. He was wearing dress shoes at the time that had a cleaner toe and a molded toe."

Gone was the extra toe panel that defined each of his models to that point, while the heel tab was complemented by a taller, rubberized tongue that allowed for easier entry.

"We always say that if some things are similar from one year to the next, there should always be something that's radically different," Hatfield said.

Air Jordan 7

The VII marked a new chapter for the Air Jordan series, dropping the "Nike Air" branding and iconic swoosh logo entirely.

"I recognized early on that MJ, especially with his Jumpman, I felt could survive and even flourish without a Swoosh," Hatfield said. "It was part of the strategy of mine to sort of create a Brand Jordan before there ever was one."

Hatfield never looked back, sticking with just the Jumpman branding going forward. With angular lines and accent colors inspired by Afropop art and music of the early 1990s, the outsole was highlighted by a dotted halftone traction pattern. While Jordan wore the shoe in black, purple and red during the '92 Finals, it was the Barcelona Olympics edition with gold accents that would define the model.

Air Jordan 8

The reductionist approach of the VI and VII was thrown out the window for the Air Jordan VIII, for which Hatfield used a "baroque design philosophy."

"[It was] adorned, complex and with lots of detail," he said. "It's what was happening in his life at the time, as well. The Bulls were about to win their third straight championship, and everything was getting bigger for Michael, on and off the court."

The only Air Jordan worn by Michael to feature a strap -- two overlapping ones, at that -- the sneaker also featured a cubic dipped graphic heel and a new textured tongue logo.

"It ended up looking like a chenille patch on a letterman's jacket, and by combining that with a sort of a Mercedes Benz-esque Jumpman logo, I think made for an interesting look," Hatfield said. "People probably either loved it or hated it, but at least people had some sort of response."

Air Jordan XI

The Jordan XI is instantly recognizable because of its patent leather accent, a design feature that Jordan himself had pushed for years earlier.

"Michael actually wanted to put patent leather on the IX. We weren't ready for that. When you talk about being comfortable with being uncomfortable -- we were hella uncomfortable," Humphrey said with a laugh.

The patent leather served a performance benefit, providing strategic support in a lightweight solution. The shoe also featured a full translucent bottom, showcasing the carbon-fiber plate that ran from heel to toe.

SneakerCenter explores sneaker culture across sports and entertainment, as told by the athletes, artists, enthusiasts and brands who power the movement. Watch on ESPN+

"The XI became the foundation of what performance greatness was going to be in a truly high-performing basketball product," Humphrey said.

The first time Jordan saw the final sample, the unmistakable look prompted him to predict it would be worn for basketball, sure, but also with tuxedos and suits. Amazingly, the shoe almost never came to be. Hatfield began designing it in 1994, after Jordan had stepped away from basketball. Many at Nike thought the Air Jordan line should stop, but Hatfield and longtime Jordan VP Howard White felt it should continue.

"I've never seen [the Jordan brand] as [only] basketball," White said. "Hope is something that the world needs every day, and they need it in large supplies. And I think Michael Jordan represented that to a lot of people."

Air Jordan 12

The expected move would've been to simply repeat the use of patent leather, the unique shimmery material that made the beloved Air Jordan XI an instant classic. But as Hatfield and Humphrey both often joke about competition and expectations, the brand would rather "zig when they zag."

The Jordan XII was defined by its luxury, with thick, full-grain leathers used throughout, along with contrasting lizard-textured panels and metallic eyelets. Jordan specifically added the "TWO 3" lettering down the tongue. The brand then added its own daringly confident badging along the heel strip, which read, "Quality inspired by the greatest player ever."

The Jordan XII has become forever associated with "The Flu Game." Wearing the red-and-black XII, Jordan poured in 38 points while ill to lead the Bulls to a win over the Jazz in Game 5 of the Finals. The iconic image of an exhausted Jordan leaning on Pippen has since become a hallmark of that Bulls title run.

"No matter how great you are, you always have to be humble enough to accept someone else's hand," White said. "For me, that moment signified the achievement that this brand was built on. It may have been forged in the likeness of an individual, but it took many individuals to bring it into greatness and the light."

Air Jordan 13

When the 13th annual Air Jordan was unveiled at a New York media conference just weeks before the start of the 1997-98 season, launching yet another new sneaker wasn't the main purpose of the day. Jordan was joined onstage by the first five roster members of Team Jordan as the group announced the launch of Brand Jordan. That laid the foundation for what has become a $3 billion brand nearly 23 years later. "CEO Jordan" commercials soon followed.

"People needed to believe that," White said. "They needed to believe, 'Michael Jordan, CEO. Wow, he's the CEO of his brand. Oh my goodness, you can be anything in life.' And those are the building blocks that started it."

The 10-part Michael Jordan documentary "The Last Dance" is here.

Latest updates, full schedule Lowe: How Kukoc remembers the Bulls MacMullan: The Michael Jordan I knew Big moments from episodes 5 and 6

The shoe's design was inspired by a nickname for Jordan that few people outside the NBA used.

"By the guys in the league, he was called the 'Black Cat,'" Humphrey said. "If you think about how he moved on the court, he was pretty relentless. Very smooth, stealthlike, but could strike at any time. It was a pretty good analogy for a player that moved like that."

The sneaker took on a paw-like shape featuring articulated pods. The midsole was wrapped in suede, a first for a basketball sneaker. The green hologram Jordan logo along the heel channeled a panther's peering eyes. The project pulling from MJ's behind-the-scenes persona was fit for Jordan's final season in Chicago, though he had one more surprise in store before leaving the Bulls for good.

Air Jordan 14

When the Bulls returned to Chicago for Game 3 of the Finals, Jordan took to the floor in a never-before-seen model. Long before early online leaks made sneaker surprises a rarity, the curiosity among collectors was rampant.

"We had an opportunity to showcase him in something different," Humphrey said. "Also, knowing that literally, this could be the last dance."

Shifting gears once again, the design inspiration for Hatfield and crew drew from Jordan's new Ferrari 550 Maranello.

The high-gloss midsole and shape mimicked the car's silhouette and body, and the stitched leather panels pulled from the interior's seat construction. An air duct vent could be found along the arch, with molded accents throughout adding to the detailing. The Jumpman was also housed inside of a yellow shield, no small coincidence.

"Tinker did a masterful job of bringing in details that drafted off of the car," Humphrey said.

Jordan went on to wear the sneakers in Games 3, 4 and 6, closing out the Jazz with an iconic Finals-clinching shot to win his sixth championship. With the black colorway not slated to release until March 1999, some nine months later, Jordan's "Last Shot" ramped up anticipation for the sneaker.

"You can't write a better ending," Humphrey said. "It just doesn't get any better than that. Everybody likes to be associated with a winner, and the success that comes with that. It just allowed the brand to evolve to the next level."

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The iconic sneakers that defined Michael Jordan's title runs - ESPN

How Kobe Bryant forged such a strong relationship with Michael Jordan, according to their shared trainer – CBS Sports

Michael Jordan didn't get close to too many players. One of the few he famously did build a relationship with was Kobe Bryant. Kobe spent most of his career drawing comparisons to Jordan, and while he ultimately fell short of Jordan's six championships and general historical standing, he was far and away the closest thing the NBA has ever seen to His Airness since the original's retirement in 2003. That was due in large part to Jordan's willingness to mentor Bryant, as they both discussed in episode 5 of "The Last Dance."

Among the many things the two had in common was trainer Tim Grover. Both were renowned for their work ethic and dedication to the game, and as Grover revealed in an interview on The Jim Rome Show (video at the top), that is what allowed the two of them to become so close.

"The reason Kobe was different in MJ's eyes is because Kobe looked at Michael as a reference book, encyclopedia, whatever you want to call it. He didn't look at him as a fan. He wasn't interested in, 'Mike can I have your shoes after the game? Can I get the signed jersey? Can you do this?' He wanted to absorb the knowledge that MJ had, and MJ would test individuals. He would give them a little, and then he would see if they actually applied it, and if they actually learned it, and if they actually learned to use it.

Then if he did that, and you came back and asked for more, he would give you more, but most people never got past that first stage because they were more enamored by the MJ aura than about the actual learning process of becoming the best basketball player. This was his test to see how dedicated these individuals were for the game. You know Michael, the one big thing he's always big about, 'I don't like individuals, I don't like players, I don't like players, I don't like anybody that disrespects the game.'"

Bryant died in a helicopter crash in January, and Jordan gave an emotional speech at his public memorial. Even if their relationship started with basketball, it grew into something far greater. The two respected one another on the court, and that allowed them to develop a deep friendship off of it.

Continued here:

How Kobe Bryant forged such a strong relationship with Michael Jordan, according to their shared trainer - CBS Sports

Aggregated Oral History of MJ, Isiah feud ruling sports media in 2020 – NBCSports.com

What if Michael Jordan had played in the age of social media?

Its a question as intriguing as it is unanswerable. But with the airing of The Last Dance during a global pandemic that has effectively paused the world as we know it, weve gotten a taste of how the biggest storylines from the NBA of yesteryear would play out in the theater of sports talk/debate television, podcasts, Twitter and the blogosphere.

Chief among those storylines is the public beef between Michael Jordan and Isiah Thomas, which centers around a handful of flashpoint moments throughout each of their careers: The 1985 All-Star freezeout (not depicted or referenced in The Last Dance), the Pistons walk-off without shaking hands after being swept by the Bulls in the 1991 Eastern Conference finals and Isiah Thomas exclusion from the Dream Team of the 1992 Barcelona Olympics a decision that its long been speculated Jordan played a part in.

The latter two points of contention have been blown out across the sports media universe since Episodes 3 and 4 of The Last Dance debuted, with Episode 4 chronicling the Bulls rivalry with the Bad Boy Pistons and the walk-off, and Episode 5 detailing Thomas being left off the Dream Team.

Its been quite a sight to behold. Decades-old controversy, debated with the same fervor as as a present-day free agent signing or public feud.

I hope the full content of what I was trying to express in the admiration we all had for him as a player is shown from my comments, Thomas told The Detroit News on April 14.

Heres an (aggregated) account of how its all gone down since then:

***

The Walk-Off

After falling to the Pistons in the postseason two years in a row, the Bulls finally dethroned their most heated rivals with a sweep in the 1991 Eastern Conference finals. But the real trouble began when, with just under ten seconds left in the decisive Game 4, most of the Pistons players (led by Bill Laimbeer and including Isiah Thomas) walked off their home floor without shaking the Bulls hands. Accounts differ on the exact reasoning behind the move.

John Salley (Pistons center 1986-1992) to Scott Van Pelt on SportsCenter: Bill Laimbeer said, 'Lets hand them the torch the same way the Celtics handed it to us.

Isiah Thomas (Pistons guard 1981-1993) in 2013 on NBATVs Open Court: We had dethroned the Celtics, we had dethroned the Lakers, and we thought that we deserved a little bit of respect as a champion. Everyone and every team could play and act like the Pistons, and adopt our philosophy, except the Pistons.

They (the Bulls) went on a day, day-and-a-half tirade about how we were bad for the game, how we were bad people, how Laimbeer was a thug, and all the time, they were getting ready to win, they were up 3-0. And then they had this press conference just totally disrespecting us as champions.

Thomas in Episode 4 of The Last Dance: Knowing what we know now and the aftermath of what took place, I think all of us would have stopped and said, Hey, congratulations like they do now. I mean, we wouldve done it, of course we would have done it. But during that period of time, thats just now how it was passed. When you lost, you left the floor. That was it.

Michael Jordan (Bulls guard 1984-1993; 1994-1998) in Episode 4: Well, I know its all bulls**t. Whatever he (Thomas) says now, you know it wasnt his true actions then. Hes had time enough to think about it, or the reactions of the public has kind of changed his perspective of it. You can show me whatever you want. Theres no way you can convince he wasnt an a**hole.

Horace Grant (Bulls forward 1987-1994) in Episode 4: Straight up b**ches. Thats what they walked off like.

Thomas to Bill Reiter of CBS Sports: "I was definitely surprised (to hear Jordan call him an a**hole). Because we've been in each other's presence before, and I've never gotten that type of reaction from him. We were even at dinner a couple times and he was always pleasant. Always good to my kids. Always good to my son. He even gave my son a pair of gym shoes.

"The competition that we all had on the floor, I truly just thought it was on the floor."

Chris Broussard (FOX Sports Analyst) on The Association: He (Thomas) was stunned to see Jordan talk about him, use the expletive about him Isiah didnt know that that was coming, and thought that his interactions with Jordan had been cordial over the years.

Shannon Sharpe (FOX Sports Co-Host) on Undisputed: "Listen to Michael talk, listen to his body language and his demeanor. He aint forgot that. Hell never forgive Isiah.

The Shade

Jordan and Thomas public airing of grievances over the walk-off inspired a week of think-pieces, public interviews by Thomas and other members of the Pistons and Bulls, and countless televised Zoom debates. That discourse seemed to reveal deeper fissures in the Thomas-Jordan relationship.

Thomas, to Bill Reiter of CBS Sports: "When you put Jordan and his basketball team in the '80s, they weren't a very successful team. They just weren't. When you talk about Jordan and his team dominating, they dominated the '90s. But when you put him with those Lakers teams and those Pistons teams and those Celtics teams, they all beat him. They just did.

"What separated Jordan from all of us was he was the first one to three-peat. But he didn't three-peat against Magic, Larry and Dr. J."

Thomas is asked by Reiterto give his list of the top five players he played against. This is what he said:

Skip Bayless (FOX Sports Co-Host) on Undisputed: "This is nothing but bitter, bad blood from Isiah Thomas. He still mistakenly holds it against Michael Jordan for keeping him off a Dream Team that he didn't make on sheer ability."

Jordan in Episode 5:I respect Isiah Thomas talent. To me, the best point guard of all time is Magic Johnson and right behind him is Isiah Thomas. No matter how much I hate him, I respect his game.

Bill Laimbeer (Pistons center 1982-1994) on ESPNs The Jump!: They whined and cried for a year and a half about how bad we were for the game. But more importantly, (they said) were bad people. We werent bad people. We were just basketball players winning. And that really stuck with me because they didnt know who we were or what we were about as individuals in our family life."

Will Perdue (Bulls center 1988-1995) on the Bulls Talk Podcast: At the time, I kind of thought it was classless as far as, at least recognize the team that beat you. But later on, as I reflect on that, I thought about, I kinda understand where they were coming from because they just got their ass handed to them, and I can imagine that they were probably in denial.

Isaiah Thomas (NBA player 2011-2020) on Twitter: Yall be tweeting me mad at me like I was tryna hurt Jordan lol

Isiah Thomas repeatedly expressed regret for the incident, saying he paid a heavy price for it, that he would do it differently if given the chance, and even apologizing to the city of Detroit. Had he known the scope of the ramifications of his actions, he said he would have done things differently.

Isiah Thomas on ESPNs Get Up: Being left off the Dream Team, that personally hurt me. In 1980, I was on the Olympic team. As a matter of fact, I was voted the male athlete of the year in 1980 for the USA Olympic team. And the only thing thats missing from my resume is not being on the Dream Team.

If I'm not a part of the Dream Team because of a lapse in emotion in terms of not shaking someone's hand, if that's the reason why I didn't make the Dream Team, then I am more disappointed today than I was back then when I wasn't selected."

The Snub

And then theres the Dream Team controversy. In the 1991-92 season, Thomas age 30 campaign, he made his 11th consecutive All-Star appearance and played 78 games, averaging 18.5 points, 7.2 assists and 1.5 steals per game. To that point in his career, he was a one-time NCAA champion, two-time NBA champion, a Finals MVP and had earned five All-NBA selections. Yet, on the greatest basketball team ever assembled, he was excluded. Conspiracies swirl as to why, with many speculating it was his dispute with Jordan that led to him not being selected.

Isiah Thomas in Episode 5: I dont know what went into that process. I met the criteria to be selected. But I wasnt.

Magic Johnson (Lakers guard 1979-1991; 1995-1996 and Dream Team member): "I know hes hurt During that time, he was one of those top ten players for sure.

Charles Barkley (NBA player 1984-2000, Dream Team member) on ESPNs Waddle & Silvy: I have zero knowledge of why Isiah was left off the team. Obviously, I heard the rumors. I was never asked about Isiah. Michael had never mentioned to me anything about Isiah ever Isiah probably should have been on the team.

Michael Wilbon (ESPN NBA Analyst) on ESPNs The Jump!: My best guess would be, having covered the team and having been there, Im gonna say nine of those guys were just not in favor of hanging out with Isiah Thomas at the time. And thats what that summer was, Rachel (Nichols), it was a big hang out They knew who they wanted to spend the summer with and they knew who they didnt want to spend the summer with. And hanging that on Michael Jordan (alone) is just inaccurate.

Wilbon has since amended this statement, saying on Twitter that he was dead wrong and that nowhere near nine players objected to Thomas inclusion on the team. Thomas responded.

Rod Thorn (chair of the USA Basketball Men's National Team Selection Committee in 1992) on ESPNs Golic & Wingo: When I called Jordan, his first inclination was he didnt know if he wanted to play or not because, as he said, I played on an Olympic team before (in 1988)... 'Its for the younger guys as far as Im concerned.'

So we continued the conversation, and at the end of the conversation, he said, You know something, Ill do it. There was never anything in my conversation with him that had to do with Isiah Thomas. Period.

Jason Hehir (The Last Dance director) on the "Jalen & Jacoby Aftershow":More than one person told me that Joe Dumars is the guard that would have been chosen for the Dream Team because he was a defensive stopper in the backcourt and they had Magic Johnson in the backcourt.

"But I also agree that a lot of guys on that team at that time had beef with Isiah.

Jordan in Episode 5: It was insinuated that I was asking about him, but I never threw his name in there Based on the environment and camaraderie that happened on that team, it was the best harmony. Would Isiah have made a different feeling on that team? Yes.

You want to attribute it to me? Go ahead, be my guest. But it wasnt me.

***

So, yeah, quite the whirlwind. And quite frankly, this merely scratches the surface.

But with the Bulls first three-peat and Jordans meteoric rise (and gambling-related PR foibles) in the rearview after Episode 6, theres a solid chance this news cycle is behind us.

When we tell our grandchildren tales of American sports in the time of coronavirus, this storys break neck, twisting nature will be an essential inclusion. What would it have been like to consume the NBA of the early 1980s and 1990s in the era of social media? We just got something of a taste.

Daniel Santaromita contributed to this aggregation.

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Aggregated Oral History of MJ, Isiah feud ruling sports media in 2020 - NBCSports.com