Category: Health

Sept. 20, 2022 – On Monday nights, while millions of viewers are marveling at the whirlwind romance of “Bachelor” couples and their extravagant dates, glamorous dresses, and fitted suits, one mental health expert will beking notes on the relationship behavior the contestants .

Diane Strachowski, EdD, a licensed cognitive behavioral psychologist and couples therapist, uses media psychology to share dating and relationship takeaways from “Bachelor” episodes via her Instagram platform.

Fans of the franchise — also known as “Bachelor Nation” — become invested in the relationship journeys of “Bachelor” couples, which can present valuable opportunities for self-reflection, according to Strachowski.

“I’m using the show as a catalyst to start conversations about ‘What is good coupling? What is a good relationship? What are good determinations on what makes for a viable relationship?’” says Strachowski, who has dubbed herself the “Bachelor psychologist.”

Even after two decades, the “Bachelor” franchise garners a minimum of 3 million viewers on any given episode. This summer, fans are reacting to two bachelorettes — Gabby Windey and Rachel Recchia — in one season for the first time ever.

The success rate of couples from the franchise is about 30% — out of the 75 “Bachelor” couples, 24 are still together. The emotional and physiological implications of the competition component of the show can play a major role in successful, and unsuccessful, matchmaking.

“It’s cortisol and endorphins and dopamine and serotonin. It’s all those neurotransmitters, chemicals that we see in all relationships when falling in love,” says Strachowski, who lives in Menlo Park, CA, in the Bay Area. The show, however, amplifies these effects vs. “real-life,” where couples often move at a slower pace.

“The dates themselves are filled with adrenaline: bungee jumping, helicopter rides. All of these experiences bond couples together because your heart is racing and because that feels like excitement, that feels like love.”

“Bachelor” stars often pledge to “follow their heart” in their decision-making. But, it’s much more complex than that, says Strachowski.

“’It’s got to be a head, heart, gut decision, not just to who you’re attracted to,’” Strachowski says. “That’s why we see some of these couples breaking up. They haven’t had enough time to really go through a profound decision-making process.”

Boosting “Bachelor” Couples Success Rate

It’s critical that “Bachelor” leads and contestants understand the difference between chemistry and compatibility, says Kelle Carver, a marriage and family therapist and owner of The Honored Place Therapy in Kansas.

“They feel similar when you’re in the beginning stages. Chemistry feels like this person meets every one of my needs and that they’re perfect for me. Chemistry can also be when you get out of that honeymoon phase, mystery, right? The dynamics that you came from and your family system or from generations past,” says Carver.

Compatibility is something much deeper, says Noreen Dupriest, owner of Simply Be Marriage and Family Psychotherapy, also in Kansas. True compatibility allows each partner to be secure in who they are, so fixating on similarities can also be a dating pitfall.

Sometimes, differences can actually work in a couple’s favor. The therapists give the example of attachment styles, or how someone makes emotional bonds with others. While there are four styles, they highlight anxious vs. avoidant attachment.

Avoidant attachment: Person appears confident, yet they struggle to display or accept emotional

Anxious attachment: Person is more emotionally needy, fears that others don’t want to be with them.

“Anxious attachment is, ‘I’m not enough or will they see me?’ They typically look for, and are very compatible with, a person with avoidant attachment. That avoidant attachment fears abandonment so much that they can rescue that anxious attachment,” says Dupriest.

Bachelor Stars Reflect on True Love Post-Show

“Bachelor” franchise stars also shared their experiences in exclusive interviews with WebMD. Season 20 Bachelor Ben Higgins says compatibility questions came to a head post-show, and he soon realized what he truly needed in a partner.

“It changed for me where I wanted somebody who had a heart for people, was genuine, was caring. Someone who would stand beside the people who feel like the least of these, no matter what. I knew if they felt that way towards other people, they would feel that way towards me,” he says.

Ashley Iaconetti-Haibon, who hosts the “Almost Famous Podcast” alongside Higgins, says romantic sparks in her relationship with fellow “Bachelor in Paradise” cast member-turned-husband Jared Haibon came to a head after the two had gotten to know each other a little better.

“I think a lot of people think that chemistry is something that you feel right off the bat. In my relationship with my husband in “Bachelor in Paradise,” it was interesting because I knew there was compatibility. But my nerves got in the way of chemistry,” says Iaconetti-Haibon, who also owns Audrey’s Coffee House and Lounge in Rhode Island.

Life post-show can become challenging, and couples often need more time before saying “I do,” Higgins says.

“I think it’s [the show] a great way to meet somebody who can potentially become your lifelong partner. I don’t know anybody that’s gotten right off the show — even if they’re so confident in that moment that this is the person for them — and says ‘Hey, let’s get married next week,’” says Higgins, author of Alone in Plain Sight: Searching for Connection When You’re Seen but Not Known.

Things have changed greatly since the franchise began and “Bachelor” stars often gain a social media following from the show. While this can raise eyebrows about a person’s motives for applying, season six Bachelorette Ali Fedotowsky-Manno says the answer isn’t black and white – nor does it have to be.

“At the end of the day, if someone’s on the show and they’re not really into you, you’re going to be able to sniff that out. If somebody’s on the show for fame and they actually fall in love with you, you’ll feel that too,” she says.

The fact that there have been a number of successful “Bachelor” franchise couples is notable within itself, according to Fedotowsky-Manno, who is also co-owner of 1to3 Life Hydration Accelerator, a low-calorie electrolyte drink mix.

“If you look at the statistic a little bit differently and think about, out of all the men you’ve met in your life, that you randomly met at a bar, how many did you end up dating and how many did you end up engaged to?” she says.

Higgins says that although his “Bachelor” journey didn’t end in true love, his experience ultimately led him to his wife, Jessica.

“How I found my wife was, post-show, looking at, OK, this is what I thought during the show when I had 30 people to get to know and work alongside to see if we could work. This is what I looked for then. That didn’t work for me. What can I look for now? And I found it.”

Be Unapologetically Yourself

Being authentic and presenting the truest version of yourself can save “Bachelor” relationships, and “real-life” couples, from turmoil down the line, says Strachowski.

“If I pretend that I’m the cool chick that doesn’t need anything, eventually I will blindside my partner. I can only sustain that ‘pretend me’ for so long. Ask for what you want and need. No apologies.”

Decentralized clinical trial company Curebase is partnering with Meru Health on a three-year clinical trial to study the effectiveness of Meru’s 12-week treatment program aimed at reducing depression among primary care patients. 

Meru Health’s smartphone-based, therapist-guided treatment program targets depression, burnout and anxiety, while Curebase provides a decentralized clinical trial platform connecting researchers with trial participants, streamlining the paperwork and allowing for remote study management. 

The two-phase trial will begin with a proof-of-concept phase, where 15 patients will use Meru Health’s treatment program. Another 15 will undergo traditional treatment methods, such as face-to-face therapy, antidepressants or combination therapy, under the supervision of their primary care physician.

Once the proof-of-concept phase concludes, the two companies will collaborate for a randomized controlled trial (RCT), which will include 300 participants and eight primary care clinics within the U.S.  

During the RCT, Curebase and Meru Health will collect electronic patient-reported outcomes for analysis. After participants complete the treatment program, researchers will monitor their progress for up to a year to evaluate the sustained effects of the Meru’s treatment program compared to standard treatment methods. 

The trial was funded by the National Institutes of Health’s Small Business Innovation Research program and is slated to begin recruitment in autumn 2022. It’s expected to conclude by spring 2023. 

“Too many people who are struggling with mental health issues also struggle with gaining access to effective treatment and our solution was created to help these people,” Kristian Ranta, founder and CEO of Meru Health, said in a statement. “Curebase is an ideal partner for us because the company’s DCT platform and support services allow us to focus on the clinical aspects of these trials, while treating participating patients at a variety of locations.”

THE LARGER TREND

A number of digital health companies offer technology for conducting decentralized clinical trials, including Medable, Reify Health and THREAD. Curebase recently closed a $40 million Series B funding round, bringing its total raise to $59 million.

Digital mental health continues to be a popular clinical area for investment, even as overall digital health funding has declined so far in 2022. Meru raised $38 million in Series B equity and debt funding last year, following an $8.1 million Series A in 2020. 

“Meru Health’s smartphone-based mental health program shows tremendous potential for bringing effective and accessible treatment to the growing population of depression and anxiety patients,” Curebase CEO and founder Tom Lemberg said in a statement. “We’re excited to be working with Meru Health on clinical research that has the potential to benefit millions of Americans.”

By Cara Murez HealthDay Reporter


HealthDay Reporter

WEDNESDAY, Sept. 21, 2022 (HealthDay News) – In a report issued Tuesday, the U.S. Food and Drug Administration acknowledged numerous shortcomings in its response to the infant formula shortage earlier this year.

“For things that are critical to the public health, if you don’t have some understanding of how all the pieces fit together, then when you get into a crisis or a shortage you have a real problem,” FDA Commissioner Robert Califf told the Associated Press. “To a large extent, that’s what happened here.”

Among the problems highlighted in the report were outdated data-sharing systems, while staffing and training for food inspectors was below normal. The agency also had poor insight into the supply chains and manufacturing procedures for infant formula.

The 10-page report comes eight months after the agency closed Abbott’s infant formula plant in Michigan amid safety concerns and reports of illness in infants. The review was led by a senior official who interviewed roughly 60 agency employees.

Although a whistleblower had tried to warn the FDA about problems in September 2021, the agency didn’t investigate until the following February.

By then, four infants were ill and two had died. The FDA is still investigating whether there is a connection between those infants and the formula, the AP reported.

“Whistleblower complaints come into the agency in many different ways, from many different sources,” Dr. Steven Solomon, director of the Center for Veterinary Medicine and the person who oversaw the review, told the AP. “One of the actions we’ve already taken is to make sure that however they come into the agency, they get triaged and escalated to the right leadership levels.”

Mail delays were one of the reasons the FDA didn’t learn about the complaint earlier, according to information the agency gave Congress. Another was a failure to escalate the whistleblower allegations.

The FDA’s “inadequate processes and lack of clarity related to whistleblower complaint” likely contributed to delays, according to the report.

Shipping issues experienced by “third party delivery companies” further caused delays in testing bacterial samples and the agency struggled with its testing capacity for the rare but potentially deadly cronobacter bacteria that was linked to the infant formula outbreak.

Continued

Still more issues were caused by the pandemic, both when the agency missed inspections after removing inspectors from the field and also because of COVID cases among agency staff, the report said.

The FDA plans to seek new authority that would require companies to provide samples and records on manufacturing supply chains, quality and safety.

The report also asked for funding from Congress to improve infant formula inspections and standards. This would increase funding and hiring authority for new experts in the FDA’s food division, as well as improve technology to share data on FDA inspections, consumer complaints and testing results.

Still, the report doesn’t go far enough, Scott Faber, of the Environmental Working Group, said in a statement.

“This internal evaluation treats the symptoms of the disease rather than offering a cure,” Faber said. “Nothing in this evaluation addresses the fragmented leadership structure that led to critical communication failures.”

The problems at the Abbott plant in February triggered significant formula shortages and resulted in the United States airlifting about 80 million bottles of formula from other countries.

More information

The U.S. Centers for Disease Control and Prevention has more on cronobacter .

Many, many millions of years ago, an HIV-like virus wriggled its way into the genome of a floofy, bulgy-eyed lemur, and got permanently stuck.

Trapped in a cage of primate DNA, the virus could no longer properly copy itself or cause life-threatening disease. It became a tame captive, passed down by the lemur to its offspring, and by them down to theirs. Today, the benign remains of that microbe are still wedged among a fleet of lemur genes—all that is left of a virus that may have once been as deadly as HIV is today.

Lentiviruses, the viral group that includes HIV, are an undeniable scourge. The viruses set up chronic, slow-brewing infections in mammals, typically crippling a subset of immune cells essential to keeping dangerous pathogens at bay. And as far as scientists know, these viruses are pretty uniformly devastating to their hosts—or at least, that’s true of “all the lentiviruses that we know of,” says Aris Katzourakis, an evolutionary virologist at the University of Oxford. Which means, a long time ago, that lemur lentivirus was likely devastating too. But somewhere along the way, the strife between lemur and lentivirus dissipated enough that their genomes were able to mix. It’s proof, says Andrea Kirmaier, an evolutionary virologist at Boston College, that lentivirus and host “can coexist, that peace can be made.”

Détentes such as these have been a fixture of mammals’ genomic history for countless millennia. Scientists have stumbled across lentiviruses embedded in the DNA of not just lemurs, but rabbits, ferrets, gliding mammals called colugos, and most recently, rodents—all of them ancient, all of them quiescent, all of them seemingly stripped of their most onerous traits. The infectious versions of those viruses are now extinct. But the fact that they posed an infectious threat in the past can inform the strategies we take against wild lentiviruses now. Finding these defunct lentiviruses tells us which animals once harbored, or might still harbor, active ones and could potentially pass them to us. Their existence also suggests that, in the tussle between lentivirus and host, the mammal can gain the upper hand. Lemurs, rabbits, ferrets, colugos, and rodents, after all, are still here; the ancient lentiviruses are not. Perhaps humans could leverage these strange genetic alliances to negotiate similar terms with HIV—or even extinguish the modern virus for good.

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When viruses assimilate themselves into animal genomes in a heritable way, a process called endogenization, scientists generally see it as “kind of a mistake,” says Daniel Blanco-Melo, a virologist at the Fred Hutchinson Cancer Center. Once cemented into one host, the virus can no longer infect others; much of its genome may even end up degrading over time, which is “certainly not what it evolved to do.” The blunders usually happen with retroviruses, which have RNA-based genomes that they convert into DNA once they enter cells. The flip allows the viruses to plug their genetic material into that of their host, which is then forced to manufacture its pathogen’s proteins alongside its own. Sometimes, a retrovirus will inadvertently stitch itself into the genome of a sperm or an egg, and its blueprints end up passed to its host’s progeny. If the melding doesn’t kill the animal, the once-pathogen can become a permanent fixture of the creature’s DNA.

Over time, the human genome has amassed a horde of these viral hitchhikers. Our DNA is so riddled with endogenous retroviruses, ERVs for short, that they technically occupy more space in our genomes than bona fide, protein-manufacturing genes do. But on the long list of ERVs that have breached our borders, lentiviruses are conspicuously absent, in both our genomes and those of other animals; up until the mid-aughts, some scientists thought lentiviruses might not endogenize at all. It wasn’t a totally wonky idea: Lentiviruses have complex genomes, and are extremely picky about the tissues they invade; they’re also quite dangerous, not exactly the kind of tenant that most creatures want occupying their cellular real estate. Or perhaps, some researchers posited, lentiviruses were endogi-capable, but simply too young. If they had only begun infecting mammals within the past few hundreds of thousands of years, there might not have been time for such accidents to occur.

Then, some 15 years ago, a team led by Katzourakis and Rob Gifford, an evolutionary virologist at the University of Glasgow, discovered an endogenous lentivirus called RELIK in the genomes of rabbits and then in hares, a hint that it had lodged itself in the animals’ mutual ancestor at least 12 million years before. In an instant, the lentivirus timeline stretched, and in the years since has kept growing. Scientists have now identified endogenous lentiviruses in a wide enough array of mammals, Gifford told me, to suspect that lentiviruses may have been a part of our history for at least 100 million years—entering our very distant ancestors’ genomes before the demise of the dinosaurs, before the rise of primates, before the land masses of North and South America kissed. “That tells us just how long virus and host have been connected,” Katzourakis told me. Through those eons, lentiviruses and the mammals they afflict have been evolving in concert—the pathogen always trying to infect better, the animal always trying to more efficiently head its enemy off.

Knowing that lentiviruses are so deeply laced into our past can help us understand how other mammals are faring against the ones that are still around today. Two species of monkeys, sooty mangabeys and African green monkeys, have spent so much evolutionary time with a lentivirus called SIV—the simian version of HIV—that they’ve grown tolerant of it. Even when chock-full of virus, the monkeys don’t seem to suffer the severe, immunocompromising disease that the pathogen induces in other primates, says Nikki Klatt, a microbiologist and an immunologist at the University of Minnesota. The key seems to be in the monkeys’ ultra-resilient, fast-healing guts, as well as their immune systems, which launch more muted attacks on SIV, keeping the body from destroying itself as it fights. Such immunological shrugs could enable certain retroviruses to eventually endogenize, says Lucie Etienne, an evolutionary virologist at the International Center for Infectiology Research, in Lyon, France.

Many mammals have also developed powerful tools to prevent lentiviruses from reproducing in their bodies in the first place—proteins that can, for instance, mess with viral entry or replication, or prevent new viral particles from busting out of already infected cells. Viruses, too, can mutate and evolve, far faster than animals can. That’s given the pathogens plenty of chances to counteract these defenses; HIV, for instance, has no trouble sidestepping or punching through many of the shields that human cells raise against it.

Read: Could genetics be the key to never getting the coronavirus?

But take the equivalent immune-defense protein from a monkey, and HIV “cannot degrade that,” says Michael Emerman, a virologist at the Fred Hutchinson Cancer Center. Other primates have had different infectious histories from ours, which have shaped their immune evolution in distinct ways. Studying those primates’ genomes—or maybe even the genomes of mammals that are carrying lentiviruses as neutered genetic cargo—might eventually inspire therapies that “augment our immunity,” Emerman told me. At the very least, such experiments could point scientists to lentiviruses’ common weak spots: the parts of the virus that ancient immune systems once targeted successfully enough that their hosts survived to tell the tale. “Evolution has already taught us the best places to target retroviruses,” says Maria Tokuyama, a virologist at the University of British Columbia. “Why not push for the types of interactions that we already know have worked?”

Another, perhaps more radical idea might yet give way to an HIV cure: speeding the path toward endogenization—allowing lentiviruses to tangle themselves into our genomes, in the hopes that they’ll stay permanently, benignly put. “We could figure out a way to silence the virus, such that it’s there but we don’t care about it,” says Oliver Fregoso, a virologist at UCLA. One of the holy grails of HIV research has always been cooking up a vaccine that could prevent infection—an extraordinarily difficult thing to do. But if some sort of gentle armistice can be reached, Boston College’s Kirmaier told me, “maybe we don’t need to go that far.”

Cedric Feschotte and Sabrina Leddy, virologists at Cornell, are among those pushing for such an intervention. They’re capitalizing on HIV’s tendency to go dormant inside cells, where it can hide from some of our most powerful antiretroviral drugs. The virus essentially “plays dead,” Leddy told me, then reawakens when the coast is clear. But if HIV could be silenced stably, its rampage would end when it jammed itself into the genome. “We’re hoping to emulate this natural path that ERVs have taken,” where they’re effectively locked in place, Leddy said. The imprisoned viruses could then be excised from cells with gene editing.

The idea’s ambitious and still a way off from yielding usable treatments. But if it works, it could produce an additional perk. After setting up shop inside us, our viral tenants can start to offer their landlord benefits—such as fighting off their own active kin. In recent years, researchers have found that some animals, including cats, chickens, mice, primates, sheep, and even humans, have been able to co-opt proteins from certain endogenous retroviruses to create blockades against incoming viruses of similar ilk. Blanco-Melo and Gifford were part of a team that made one such discovery in 2017, describing an ERV that ancient monkeys and apes might have used to strip viral entryways off the surfaces of their cells. When encountering an ERV-ed-up host, the infectious, still-pathogenic version of that ERV would no longer have been able to get in.

Eventually, the active retrovirus “just went extinct,” Blanco-Melo told me—an outcome that he thinks could be attributable to the antics of its endogenous counterpart. It’s a devious move, essentially a way to “turn the virus against itself,” Kirmaier said. This sort of friendly-fire tactic may already be at work among lentiviruses, duking it out inside and outside host genomes: Species with endogenous lentiviruses usually aren’t bedeviled by active lentiviruses, at least none that has been identified yet, Fregoso told me. With any luck, the same could someday be true for HIV, the virus little more than a memory—or an idle fragment in our cells.

Our skin performs many roles. It helps manage body temperature, keeps out bacteria and other bugs, and is key to our sense of touch.

Skin unites us all in these common functions, but our skin also varies in ways that show up cosmetically.

Your skin tone can affect how soon you’ll develop wrinkles and sunspots. It can also influence whether you’re more prone to hyperpigmentation, darkened areas on your skin.

Skin tone isn’t simply a matter of race, since people from the same background can have widely varying skin color. Race and ethnicity usually aren’t an accurate reflection of skin tone, says Anna Chien, MD, an associate professor of dermatology at the Johns Hopkins University School of Medicine.

Doctors refer to “skin types” ranging from 1 to 6. Skin type 1 is the palest, which always burns and never tans. Mid-tones, such as type 4, are light brown, tan easily, and rarely burn. The darkest, Skin type 6, is deeply pigmented and never burns. This range of skin types is also called “Fitzpatrick skin typing,” named for the doctor who developed it. It’s based on how much pigment is in someone’s skin and how their skin reacts to sun exposure.

Learn from three dermatologists how skin tone can affect our skin care routines.

Sun Damage

Doctors call sun damage “photoaging,” which includes the wrinkles and sunspots that can come with sun exposure.

This tends to happen “a little more quickly” in people who have lighter skin types, Chien says. “And they are more prone to skin cancers.”

In contrast, people with darker skin tones “often do have delay in the signs of photoaging. And they also have a lower risk of skin cancer,” says Julia Mhlaba, MD, an assistant professor of dermatology at Northwestern University Feinberg School of Medicine. “That pigment actually provides sun protection.”

But it’s important to keep in mind that a lower risk of skin cancer doesn’t mean zero risk. “All skin can get skin cancer,” says Shani Francis, MD, a dermatologist in the Los Angeles area.

Misconceptions that people with darker skin don’t get skin cancer are dangerous because that can lead to a delayed diagnosis or misdiagnosis. “We definitely can see skin cancer in darker-skinned individuals,” Chien says. “And unfortunately, because this isn’t often talked about … the skin cancer may be found later when it’s much more progressed.”

In people with darker skin, cancers can also occur in places “where patients typically don’t get exposed to sun, like the bottoms of the hands and the feet,” Mhlaba says.

Universal Need: Sunscreen

All skin tones require sunscreen with an SPF of at least 30 – every day, rain or shine – to help prevent skin cancer and slow photoaging.

“We always recommend sun protection because even in darker-skinned individuals [and in] folks who say, ‘I never burn; I always tan,’ they’re still getting the damage in the skin,” Chien says.

If you’re outdoors for long periods, use at least an SPF of 60, Chien says. Reapply often, especially if you’re active, sweating, swimming, or getting wet.

Physical blocker sunscreens with zinc oxide or titanium dioxide offer the best protection, according to the experts. But on darker skin, these products aren’t always cosmetically elegant.

“It can cause white film on the skin, which is challenging for individuals with darker skin tone,” Chien says. She recommends tinted sunscreens that might better match their skin tone.

Tinted sunscreen may offer further benefits. In darker-skinned people, longer wavelengths beyond UV rays can be more damaging than in people with lighter complexions, Chien says. “The tint can actually protect against a little bit of the longer wavelength that their skin could be more sensitive to,” she explains.

Beyond Sunscreen

Don’t rely on sunscreen alone. “I always tell my patients sunscreens aren’t perfect,” Chien says. “We need to reapply and combine [it] with other measures.”

That includes wearing sunglasses and long-sleeved shirts, avoiding peak sun, looking for shade, and wearing wide-brimmed hats. She calls it a “multi-modal approach to sun protection.”

And don’t count on SPF in makeup alone to give you enough protection, Chien says. “The SPF they achieve in a lab setting – usually they’re applying a fairly thick amount of that makeup, so it doesn’t really mimic day-to-day use.”

What to Know About Retinol and Retinoids

Regular use of sunscreen and moisturizer can help slow signs of aging. And so can using a retinoid or retinol on your skin.

“These are vitamin A derivatives that can either be purchased in over-the- counter versions or they can be prescribed by a dermatologist at higher strengths,” Mhlaba says. “They do a lot of things: They’re used to treat acne. They can help with pigmentation. But they can also help in terms of smoothing out fine lines and preventing wrinkle formation.”

People with darker skin tones can use higher-strength retinoids but must start slowly to avoid irritating their skin, Mhlaba says. “If they do develop irritation, it can cause hyperpigmentation more easily than in patients with lighter skin types,” she explains.

Her advice: When you start using a retinol or retinoid, apply only a small amount to your face, and do that every few days at first. Follow up with a moisturizer to help curb any skin irritation.

Hyperpigmentation

Wearing sunscreen on the face not only slows photoaging, Mhlaba says, but can also help stop hyperpigmentation from getting worse.

Hyperpigmentation can happen in all skin types, but it’s more common in people of color, Mhlaba says.

“It can occur from acne scars or eczema or at sites of trauma, and then there are other conditions that lead to hyperpigmentation, like melasma,” she says. Melasma appears as darker patches of pigmentation, especially on the face.

Sun exposure can worsen hyperpigmentation – another reason why sunscreen is key. Products that can treat hyperpigmentation include vitamin C serum or vitamin C-containing products, glycolic acid, azelaic acid, and niacinamide, Mhlaba notes.

For melasma, dermatologists can also prescribe hydroquinone-based compounds or oral medications.

Dryness

Dry skin can affect all skin tones. “But if your skin is darker, dry skin is light white, and so there’s more contrast. It’s much more noticeable,” Francis says. That dry appearance comes from the scales of shedding skin.

Darker skin that becomes dry could benefit from “a really good, thick moisturizer, something that could help to rebuild the [skin] barrier,” Chien says.

Don’t judge a product by how thick it looks in the container. What matters more is how thick it is on your skin, Francis says. She suggests looking for ingredients such as ceramides, glycerin, castor oil, petroleum jelly, and hempseed oil.

Smooth moisturizer over damp skin after showering or bathing. “It will keep the water in the skin,” she says.

Sensitivity

People of all skin tones can have problems with sensitivity. “Stick with really bland products,” Chien says. Choose unscented products, and stay away from those labeled antibacterial.

“Keep the skin care regimen pretty simple: just a gentle face wash, a bland moisturizer, something with an SPF built in for the daytime, and just a plain moisturizer in the evening,” she says.

People with sensitive skin can spot-test a product behind their ear or upper inner arm to make sure they don’t react to the product, Chien says.

She recommends “not adding in a lot of serums or anti-aging products. A lot of those can be irritants.”

If people with sensitive skin want to exfoliate, “It’s a little more patient-specific in terms of what their skin will tolerate,” Mhlaba says. Physical exfoliators can be too harsh. But “if you’re talking about a chemical exfoliator, I would definitely recommend starting slowly and working up to using it daily, if needed. Sometimes, even just … once a week, depending on the product, could be enough.”

“Look for things with salicylic acid, glycolic acid,” she says. “A lot of topical creams will have that. That is a good way to exfoliate.”

Contributed by: Anjali Dharra

Introduction

Did you know today we have completed 35 years of ozone layer protection? You must be surprised and thinking about whether it’s been that long since we protected our ozone layer; a molecule (strong antioxidant) that proves to be a safeguard for life on the planet.

September 16 is commemorated as ‘World Ozone Day’ every year to spread awareness among current and future generations for protecting the lower region of the earth’s atmosphere.

The theme for World Ozone Day 2022:

September 16 is marked to observe the completion of 35 years of the Montreal Protocol. ‘Montreal Protocol@35: global cooperation protecting life on earth‘ is the theme for the year 2022. It is the day that tells people why it is important to save the ozone layer, as it protects mankind from harmful radiation emitted by the sun.

World Ozone Day history

The Montreal Protocol Corporation was developed in 1987 to reduce the concentration of ozone-depleting compounds in the atmosphere and to halt their use, manufacturing, and import in order to safeguard the earth’s ozone layer. Then, in 1994, the UN General Assembly adopted September 16 to be observed as World Ozone Day.

You must have heard that the ozone layer is depleting day by day. There are so many reasons behind the ozone layer depletion and the ozone hole, including:

• Chlorofluorocarbons or CFCs 
• Natural gases
• Nitrogenous compounds
• Unregulated launch of Rockets

Let’s take a pledge on ‘World Ozone Day‘  to make as many possible attempts to preserve the ozone layer for ourselves and our future generations.

When was World Ozone Day first celebrated?

World Ozone Day was first celebrated on September 16, 1994, when the UN General Assembly declared it an important worldwide event. This is also the day when the Montreal Protocol Corporation was launched in 1987.

Did you know how World Ozone Day is celebrated? People all over the world hold talks and seminars to spread awareness about the ozone layer so that people can get as much information about the present situation as possible and start taking necessary steps.

What is the ozone layer?

The ozone layer is the lowest portion of the earth’s stratosphere that contains a large proportion of ozone.  Ozone is a strong antioxidant that is made of three molecules of oxygen and is often referenced as O3 (far more so than oxygen).

Did you know the ozone layer has the potential to imbibe 97-99% of the harmful ultraviolet rays emitted by the sun that can affect the life of humankind on earth?  Because of this fact, the ozone layer protects the earth from harmful ultraviolet rays.

If the ozone layer is depleted, the human population would develop a number of skin diseases as well as have a weakened immune system to fight against infections.

One must know how the ozone is formed. Heat and sunlight cause chemical reactions between hydrocarbons such as nitrogen oxides and volatile organic substances resulting in the formation of the ozone layer. These reactions can develop near the surface or high in the atmosphere.

What is ozone layer depletion?

Ozone layer depletion is the thinning of the ozone layer in the earth’s upper atmosphere. This mainly happens when chlorine and bromine in the atmosphere come into contact with ozone and destroy this strong antioxidant (ozone molecules).

Did you know one chlorine atom can destroy 100,000 ozone molecules? Yes, it happens, and they destroy more easily and quickly than they create.

What are the major concerns about ozone layer depletion?

Scientists have identified a hole in the ozone layer over Antarctica. This has drawn their attention to numerous environmental problems and solutions as a result. Chlorofluorocarbons, carbon tetrachloride, methyl bromide, and hydrochlorofluorocarbons are the primary causes of the ozone hole.

A few of the well-known ozone-depleting substances and the sources from which they are released are:

Chlorofluorocarbons or CFCs

Chlorofluorocarbons, or CFCs, are the main concern for ozone layer depletion and the ozone hole. Chlorofluorocarbons are manufactured chemicals released by solvents, air conditioners, spray aerosols, dry cleaning agents, and refrigerators, to name a few.

All these chemicals release chlorine atoms and destroy ozone molecules. 

Nitrogenous substances

The nitrogenous compounds NO2, NO, and N2O are largely to blame for the ozone layer’s thinning.

Unregulated rocket launches

According to studies, the ozone layer is destroyed considerably more quickly by uncontrolled rocket launches than it is by CFCs. By 2050, the ozone layer might have lost a significant amount of its thickness if this is not regulated.

Natural factors

It has been discovered that some natural processes, such as solar flares and stratospheric winds, degrade the ozone layer. However, it only contributes to 1 to 2% of the ozone layer loss.

The ozone layer is being destroyed due to volcanic eruptions as well.

What if there is no ozone layer?

The depletion of the ozone layer has ample adverse effects on the environment as well as human beings.

Impacts on human health

As the ozone layer thins, people will be directly exposed to the sun’s dangerous UV radiation. Humans may have severe health problems as a result, including skin conditions, cancer, sunburns, cataracts, rapid ageing, and weakened immune systems.

Impacts on animals

Animals that are directly exposed to UV light develop skin and eye cancer.

Impacts on the environment

Strong UV radiation may prevent plants from growing, blooming, or performing photosynthesis. The detrimental effects of UV light must also be endured by the woodlands.

Impacts on marine life

The impact of damaging UV light exposure on plankton is significant. Higher in the aquatic food chain are these. The species that are part of the food chain are also impacted by the destruction of plankton.

Possible solutions to ozone layer depletion

There are many programmes in place by the governments of many nations to stop the destruction of the ozone layer, which is a severe concern. To stop the ozone layer from being destroyed, however, action must also be taken on a personal level.

The following are some ideas that could aid in stopping this issue on a worldwide scale:

Don’t use ozone-depleting substances (ODSs)

The use of ozone-depleting chemicals should be decreased. For instance, replace halon-based fire extinguishers with alternatives, avoid using CFCs in refrigerators and air conditioners, etc.

Reduce the use of vehicles

Cars produce a lot of greenhouse gases, which contribute to ozone depletion and global warming. Therefore, it is best to limit the usage of automobiles as much as possible.

Utilize green cleaning supplies

The majority of cleaning solutions contain chemicals that release chlorine and bromine into the air and have an impact on the ozone layer. To conserve the environment, natural alternatives should be used in their place.

Nitrous oxide use ought to be prohibited

The usage of dangerous nitrous oxide, which is harming the ozone layer, should be outlawed by the government. To reduce its use, nitrous oxide’s negative consequences and the goods that emit the gas should be made known to the public.

Final thoughts

We have one earth and one ozone. We should “Act as a Whole to Protect the Hole”. The fear of its continuous depletion has propelled mankind to advance attempts to preserve our atmosphere and shield ourselves from the sun’s rays.

As it is said by Saint Rampal Ji – “The world looks at the scientists. Why not pray to the supreme God who made science”?

We should understand this and take as many possible steps in order to preserve the natural beauty: OZONE; a molecule that saves us from so many health and environmental consequences.

As the depletion of the ozone has been happening for a long time it can cause major health and skin setbacks, therefore it is advisable to go for genetic testing to know about any predispositions or you can go for a full body health checkup to keep track of your health and body vitals.

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Contributed by: Rachna Arya

Carbohydrates have developed a negative reputation through time. Some trendy diets would have you believe that they are linked to type 2 diabetes, weight gain, and a number of other health issues.

It is true that refined grains and processed diets high in sugar frequently lack the necessary vitamins and minerals. Numerous nutrient-dense, fibre-rich meals, however, might really be highly beneficial for your health.

Although some people may benefit from low-carb diets, there is no need to completely exclude high-carb items.

What are high-carb foods?

Quinoa

Quinoa is often regarded as a superfood or a super grain or healthy carbs. It is a very healthy edible seed that has higher levels of numerous minerals and plant components than many cereals. Although cooked quinoa is a high-carb food containing 70% carbohydrates, it is also a fantastic source of important nutrients, including fibre, manganese, protein, folate, magnesium, fibre and protein.

Quinoa has been associated with a number of health advantages, including improved blood sugar management and heart health. It also doesn’t contain any gluten, making it a well-liked wheat substitute for individuals following a gluten-free diet. Due to its relatively high protein and fibre content, quinoa is also highly satisfying. It may therefore support good weight management and intestinal health.

Oats

Oats have been recognised as an extremely healthful and nutritious cereal. They are a terrific source of many beneficial nutrients, and they contain a high concentration of soluble fibre and dense nutrients. Raw oats contain 70% carbs. Oats are also a relatively good source of protein and the content of protein is much higher than most grains. Research also suggests that eating oats may have potential health benefits ranging from improved immune health to reduced risk of obesity, heart disease and cholesterol levels. Eating oats may also lower blood sugar levels and support healthy weight management. 

Bananas

Bananas are a popular fruit that has astonishing health benefits. One large banana provides roughly 31 grammes of carbohydrates, either in the form of starches or sugars. Additionally rich in vitamins B6 and C, bananas also contain a number of advantageous plant components. Bananas may assist to control blood pressure and enhance heart health due to their high potassium content.

Resistant starch and pectin, which promote digestive health and feed the good bacteria in your gut, are also present in reasonable proportions in unripe and less-ripe bananas.

Sweet potatoes

Sweet potatoes are a delicious, nutritious vegetable. One-half cup of mashed, cooked sweet potatoes with their skin on contains about 20.7 grams of carbs, which consists of starch, sugar, and fibre. Sweet potatoes are loaded with vitamin A, vitamin C, and potassium. What’s more, they’re also packed with powerful antioxidants 9 like beta carotene and other important phytonutrients.

Blueberries

Blueberries are frequently regarded as a superfood due to their rich content of antioxidants. There are many science-backed benefits of blueberries, consisting of high amounts of many vitamins and minerals, including vitamin C, vitamin K, and manganese.  

According to numerous studies, blueberries are a good source of antioxidant substances that can help shield your body from harmful free radicals. 

Apples

Apples are renowned for their incredible health benefits. They are a wonderful source of fibre, antioxidants, and vitamin C. The phytochemicals and fibre in apples have antioxidant effects that help heart health and blood sugar control, among other health advantages. 

Apples are a very significant source of antioxidants, plant components, vitamin C and several other nutrients. Eating apples may help you control your blood sugar, as well as lower your risk of heart disease. According to preliminary studies, apple consumption has also been found to lower your risk of developing some cancers.

Final thoughts

The notion that all carbohydrates are bad is untrue.  However, not all carbohydrates are good for you either. A balanced diet should contain both simple and complex carbohydrates. 

Just choose your carbohydrates wisely. Avoid low-nutrient desserts, think about the amounts of sugar and fibre, and concentrate on whole grains, fruits, and vegetables that are healthful. When you go shopping, try to look for the foods mentioned above as these are examples of healthy complex carbs. And one thing you should always be mindful of is to get your full body health checkup done regularly. There are a host of packages available here that you can choose to keep track of your health and be a step ahead of diseases.

Also,  it is advised to have frequent preventive health check-ups to keep an eye on overall health, especially your cholesterol levels.

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Contributed by: Anjali Sharma

Understanding Alzheimer’s

Alzheimer’s disease is the most common and progressive type of dementia. Dementia is a condition that negatively affects memory, thinking capacity, and the ability to communicate effectively. People suffering from Alzheimer’s may also experience language problems and impulsive or unpredictable behaviour.

According to a study conducted by the Alzheimer’s & Related Disorders Society of India (ARDSI), India had around 3.7 million cases of Alzheimer’s disease in 2010 and the number is expected to rise to 7.6 million by 2030. At present, approximately 5.3 million Indians live with dementia, and the most common cause is Alzheimer’s disease. 

The condition usually affects people aged 65 years or above, but it can also impact the brain health of people in their 30s or 40s. When any person below the age of 65 years is affected by Alzheimer’s, the condition is termed early-onset (or younger-onset) Alzheimer’s disease. 

The disease got its name from Dr. Alios Alzheimer who identified this condition in 1906. World Alzheimer’s Day is observed on 21st September every year, and the theme for 2021 is ‘Know Dementia, Know Alzheimer’s’.

In this article, we will reflect on the causes and symptoms of Alzheimer’s disease and the measures you can take to manage the condition, once diagnosed.

Causes & risk factors of Alzheimer’s disease 

Although the exact cause of Alzheimer’s disease is still unknown, experts have identified several risk factors which include:

People aged 65 years or above are more prone to get affected by Alzheimer’s disease.

There is a slightly higher risk of getting affected by Alzheimer’s disease if your parents or siblings are suffering from this condition.

Having one or both of these risk factors does not necessitate that you can get affected by the disease, but it increases the risk levels of being afflicted by Alzheimer’s 

Symptoms of Alzheimer’s

Being a progressive condition, Alzheimer’s symptoms worsen over time. The symptoms do not occur at once and appear gradually over months or years. If the symptoms develop in hours or days, immediate medical attention is required as it can be a sign of stroke. These symptoms include:

• Repeating questions or conversations
• Losing track of everyday objects
• Inability to remember appointments or events
• Wandering or getting lost
• Lessened understanding of safety and risks
• Difficulty in making decisions
• Difficulty in completing stage-based tasks, such as getting dressed
• Problem with recognition
• Problem with speaking, reading, or writing
• Personality and behaviour, such as being compulsive, angry, upset, or loss of interest in activities

Stages of Alzheimer’s disease

Alzheimer’s disease is a progressive condition that includes three stages:

In this stage, Alzheimer-affected people develop memory problems and cognitive difficulties.

In this stage, the part of the brain responsible for language, senses, reasoning, and consciousness is damaged in affected people.

This last stage of Alzheimer’s is a condition in which plaques and tangles are present in the brain of affected people, causing the brain tissue to deteriorate. Plaques are clumps of a protein (beta-amyloid) found in the brain which disrupts the communication between nerve cells. Tangles are abnormal accumulations of a protein (tau) inside the neurons.

How best to manage Alzheimer’s

Alzheimer’s disease is a progressive ailment and unfortunately, it does not have any cure so far. Though, there are medicines available that can help delay the aggravation of dementia symptoms and manage behavioural issues. However, certain management techniques can also be practised to help manage the impact of Alzheimer’s 

Here are some tips for caregivers/relatives of Alzheimer’s patients:

• Keep things simple and ask or say one thing at a time
• Maintain a daily routine to help the patient understand where certain things happen
• Gain the trust of the patient that he/she is safe with you
• Learn from their expressions about their feelings. For example- say, “you seem worried!” and wait for the answer
• Don’t argue or try to reason with the patient
• Don’t show frustration or anger towards the patient 
• Make the patient laugh whenever possible
• If the patient has a habit to walk, take him/her to a safe place to walk
• Give the patient some light snacks to eat while walking. This will help prevent weight loss
• Try to distract or keep the patient occupied with light music, singing, dancing, or any other activity that makes him/her happy
• Ask for the patient’s help in easy domestic works like folding clothes or setting table for a meal to keep their motor skills active

Diagnosis of Alzheimer’s disease

If a person has Alzheimer’s, he/she may experience personality and behavior changes that are primarily noticed by friends or family members. If the symptoms are similar to those mentioned above, the doctor may carry out the following diagnoses. 

• Cognitive and memory tests: This will help in understanding the patient’s ability to think and remember.
• Neurological function test: To test the balance, senses, and reflexes of the patient
• Blood and urine tests
• A brain CT scan or MRI scan

Final thoughts

Alzheimer’s disease is a progressive condition that has no cure yet, and it can affect anyone aged 65 or above. If a person manifests the above-mentioned symptoms, it is recommended to seek immediate medical attention and initiate Alzheimer’s management to slow the worsening of the disease.

The aforesaid tips can also help in managing the condition effectively at home. To manage Alzheimer’s effectively, you need to keep a check on the patient’s overall health by opting for regular overall health screening. 

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The Food and Drug Administration is likely to approve a controversial new drug for ALS by the end of the month.

But it’s still not clear whether the drug, called AMX0035, truly helps people with ALS, a rare and fatal neurological disorder that eventually leaves a person unable to walk, talk, swallow and breathe.

In March, the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee concluded that a study of 137 ALS patients did not provide “substantial evidence” that AMX0035 was effective.

Then in September, after prodding from FDA officials and an email campaign by patients and their families, the same committee reconvened, and this time recommended approving the drug.

The FDA, which usually follows advisory committee recommendations, has indicated it will make a decision by Sept. 29.

An approval is more likely now that it would have been decades ago, says Holly Fernandez Lynch, an assistant professor of medical ethics and health policy at the University of Pennsylvania.

“The trajectory at FDA has been increased willingness to accept weaker evidence,” she says.

Two old products, one new drug

AMX0035 is a combination of two existing products. One is a dietary supplement called taurursodiol, which can be purchased online.The other is a prescription drug called sodium phenylbutyrate, which is used to treat a rare type of metabolic disorder.

The combination is meant to slow down ALS, which gradually destroys cells in the brain and spinal cord that control voluntary muscle movement.

AMX0035 was developed by Amylix— a company based in Cambridge, Mass. that was founded in 2013 by two graduates of Brown University.

Amylix sought FDA approval of its drug based on a single study of 137 patients with ALS. The results suggested that AMX0035 could extend patients’ lives by several months.

But at a public meeting in March, most experts on the FDA’s advisory committee said they were unconvinced by the study, called Centaur.

“There are many features of Centaur that limit its persuasiveness,” said Dr. G. Caleb Alexander, an epidemiologist at Johns Hopkins University.

“The applicant hasn’t provided robust evidence,” said Dr. Bryan Traynor, a neurologist at the National Institute on Aging.

“The data isn’t as strong as we would hope,” said Dr. Liana Apostolova, an Alzheimer’s expert at Indiana University.

The study was “problematic,” said Dr. Kenneth H. Fischbeck, a neurogenetics researcher at the National Institutes of Health.

It “did not meet the threshold,” said Dr. Thomas J. Montine, a pathologist at Stanford University.

“This study, on its own, doesn’t establish that this drug is effective in the treatment of ALS,” said Dr. Robert C. Alexander, chief scientific officer at the Banner Alzheimer’s Institute.

All six of those committee members voted no, when asked whether the evidence showed the drug was effective. Four other committee members voted yes.

Advice to the advisors

Typically, that kind of response would have been the end of it, at least until Amylix was ready to present data from a much larger study, which is already underway.

But after the March meeting, ALS patients and family members took to the Internet.

“There were thousands of emails that went to the [FDA] commissioner’s office,” says Neil Thakur, chief mission officer at the ALS Association, which helped fund the Amylix study. “There were over 1,100 comments that went to the advisory committee themselves, and also there was a sustained effort from ALS clinical scientific leaders.”

The small clinical trial does have flaws, Thakur said, but the advisory committee should have been willing to overlook those when it first reviewed the evidence in the spring.

“They were asking to hold that drug to the same standard they would hold any drug for any disease that wasn’t fatal and had lots of effective treatments,” he says.

Right now, ALS patients are offered variants of just two drugs: edaravone and riluzole. And even with these drug treatments, they typically die within two to five years after a diagnosis.

From no to yes

The email campaign by ALS patients seemed to have an effect on some FDA officials.

Early this month, the agency took the unusual step of reconvening its advisory committee to reconsider the Amylix drug. And this time, the FDA encouraged committee members to take a different perspective, Thakur says.

“This committee, it was clear that they were being asked to make a decision taking into account the available treatments and the needs of the ALS community,” he says.

The committee also received some additional data on patients in the Amylix study, and data from a study of Alzheimer’s patients who took AMX0035.

When the committee held its second public meeting on the drug, they were offered guidance from Dr. Billy Dunn, who directs the FDA’s Office of Neuroscience. He urged them to consider the plight of patients with ALS, and suggested his agency was open to approving the drug.

“For these serious diseases, like ALS and so many other neurological diseases, the maximum degree of regulatory flexibility is operational,” he said.

The FDA even revised its question to the committee. Instead of asking whether the drug was effective, they asked simply whether it should be approved.

After listening — instead of six no votes, seven of nine committee members decided to vote yes.

Echos of Aduhelm?

The process leading to the yes vote was “fishy,” says Fernandez Lynch, the bioethicist at UPenn.

“The very cynical version of this is that there was some kind of goal of manipulating the advisory committee to vote in a different way,” she says.

“They were swayed by this concern that they might be making the wrong judgment if they recommended FDA not to approve this product,” she says. “But nobody, as far as I heard, said this drug meets the substantial evidence standard.”

The substantial evidence standard was also in question when the FDA was considering the controversial Alzheimer’s drug Aduhelm. The FDA approved that drug last year despite an overwhelming vote from the advisory committee that the standard had not been met.

If AMX0035 is approved, that could send troubling message to pharmaceutical companies, Lynch says.

“The message to companies is that you don’t have to show that your drug works,” she says. “You have to do the bare minimum to show that it might work.”

Analysis by Dr. Joseph Mercola
Fact Checked

• September 21, 2022Download PDF

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