#but that's a different enzyme pathway
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i'm medicated now and caffeine still does literally nothing because of my aforementioned-several-times-in-the-notes liver enzyme issue that metabolises it too fast
this is not an adhd post. yes adhd contributed to the lack of mental effect from caffeine and in hindsight it is hysterical nobody noticed i have understimulation syndrome, but that isn't solely - or even mostly - why
caffeine has no physical or mental effect on me, even with massive doses of amphetamine, because it LITERALLY noclips through my liver like a bethesda game. like physically.
a fun and fucked up fact about me is that when i was in sixth form (16-18), approximately 10 years prior to being diagnosed ADHD, i drank SO MUCH store brand energy drink that 2 things happened
1) It became such an obvious and well known Thing about me that my tutors started putting "too much red bull can kill you" news articles on the walls. These were not present in rooms I didn't have classes in. It was not a college-wide initiative. That was for me, specifically. Nobody said it but we all knew.
2) Several friends suggested, in all seriousness, I contact the Guinness Book of Records to set a record for "most caffeine consumed with no physical effect" after I had 3x 1 litre bottles in about an hour and my heart rate was still exactly the same and nothing about my demeanour had changed at all. Meanwhile Ryan had 1 bottle and was physically vibrating. Because he's normal.
(I didn't do it because it would require having a medical professional present the whole time to verify and like absolutely nobody with a medical degree is going to do that in good conscience)
#i ALSO metabolise amphetamine too fast#but that's a different enzyme pathway#that i have to take another drug to slow down a bit#the caffeine one remains unaltered#other people with adhd who have NORMAL livers will still experience physical effects such as: increased heart rate / mild laxative effect#i do not. it is simply never in my system#if i slam back enough of it FAST enough i get the adhd 'now i am eepy' effect#but it's short lived#the volume required and fast turnaround have nothing to do with my adhd and everything to do with my liver being an overachieving asshole
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— Pinnacle [ tsukishima kei university au series ]
— and i don’t know how it gets better than this ; let’s take a look on how a month of a relationship would be like
author’s notes : no mention of (y/n), written in second person pov, semi alternative universe, timeskip!tsukishima, college life, not proofread, english is not my first language
[ masterlist ] | [ ask daleelah go to box box 🐭 ]
Do you want to have lunch in the cafeteria?
As you were packing up your notes and preparing to head back to the dorm after a long day of classes, your phone buzzed softly in your pocket.
The text was from Tsukishima, and your heart did a little flip as you read it. It had only been two minutes since your class ended, and he was already asking to meet up. A small smile tugged at your lips as you began typing back.
My mom just sent me lunch 🥹
Heading to dorm now
you quickly replied, trying hard to suppress the giddiness that threatened to spill over. It had been a month since you started dating, and even though the relationship still felt new and exciting, there was a comforting familiarity in the way Tsukishima showed his affection—always understated, never excessive, but undeniably present.
The phone buzzed again.
Stop walking. I’m behind you.
You froze mid-step, instinctively turning around to see him standing there, his tall frame leaning casually against a nearby lamppost. His expression was as unreadable as always, but the faint smirk on his lips gave him away. Your cheeks warmed with the blush that spread across your face, and your smile bloomed wider.
Tsukishima walked toward you, closing the distance with a calm, measured pace. When he reached you, his hand gently ruffled your hair, tousling it just enough to make it messy. But before you could protest, he smoothed it back down, his fingers moving with surprising gentleness. You felt a warmth bubble up inside you at the small act of care.
Without a word, he took your hand in his, his long fingers intertwining with yours as you both began walking toward your dorm. His grip was firm, steady, and familiar. It was these small gestures that always caught you off guard—how someone as stoic as him could show affection in such quiet, tender ways.
As you walked, he glanced down at you.
“So, how was class?” he asked, his tone casual but interested.
You shrugged lightly, trying to think of something coherent to say despite the fluttering in your chest. “It was okay, I guess. We had a lecture on enzyme kinetics today. It’s... complicated. We’re learning about how different substrates affect reaction rates and how to calculate Vmax and Km using Lineweaver-Burk plots. It’s kinda overwhelming.” You chuckled, trying to play it off, but the truth was, biochemistry wasn’t getting any easier. The second semester was filled with more challenging topics—metabolism, enzyme mechanisms, and signal transduction pathways. Sometimes it felt like your brain was spinning in circles trying to keep up.
Tsukishima’s thumb brushed over the back of your hand in a soothing motion. “Hmm, sounds like you’re managing,” he commented, his voice low and cool, but there was an underlying sense of approval in his words. “Just don’t overthink it.”
You nodded, appreciating his subtle encouragement, even if it was delivered in the most Tsukishima way possible.
When the two of you reached your dorm, you invited him inside. “You can sit down,” you said, motioning to the low table as you slipped off your shoes. “I’ll get us some tea.”
Tsukishima didn’t argue, simply settling himself comfortably at the table. He stretched out his long legs under the table, leaning back with that same calm, collected demeanor. You poured two glasses of iced barley tea, setting them down on the table along with the meal your mom had sent. Two plates of rice, grilled mackerel, miso soup, and some side dishes—enough for the both of you.
“I’m glad you came with me to the dorm,” you said, sitting across from him. “Finally, someone can help me eat all of this food. My mom keeps sending more than I can finish.”
Tsukishima let out a soft sigh, clearly unimpressed by your complaint, but he said nothing. Instead, he picked up his chopsticks and muttered a quiet, “Itadakimasu,” before digging in.
“Itadakimasu,” You started eating as well, savoring the familiar flavors of homemade food. But halfway through, you felt your hair falling into your face, getting in the way as you tried to eat. You pushed it back with your hand, annoyed, but it kept slipping forward again.
Tsukishima’s gaze shifted toward you, and without saying a word, Tsukishima stood up and walked over to your desk. You looked up, confused, but before you could ask what he was doing, he grabbed a hairpin from the top drawer. Moving with quiet precision, he came over and gently swept your hair back, securing it in place with the pin. His fingers brushed against your temple as he worked, and you felt your face heat up, your heart pounding in your chest.
“There,” he said simply, stepping back as if nothing had happened, as if tying your hair was just another mundane task. But the subtle softness in his actions didn’t go unnoticed by you.
You sat there, momentarily stunned by the unexpected act of care. Your face felt like it was on fire, but you managed a small, “Thank you,” before quickly looking down at your food, hoping he wouldn’t notice how flustered you were.
Of course, Tsukishima noticed. He always did. But instead of teasing you about it, he simply returned to his seat and resumed eating, as if tying your hair was no big deal. Still, the softness of the gesture lingered in the air between you, a quiet reminder of the tenderness he hid behind his stoic exterior.
A few moments passed in comfortable silence before Tsukishima spoke again, his tone as cool and casual as ever. “I’m going grocery shopping after this. Want to come?”
You almost choked on your rice at the sudden question, nodding a bit too enthusiastically in response. “Yeah, I’ll come,” you said, trying to sound calm, even though your heart was still fluttering from earlier. You avoided his gaze, focusing on your food instead, hoping he wouldn’t notice how nervous he still made you.
But of course, he noticed. You caught the faintest hint of a smirk on his face before he resumed eating, completely unfazed. And somehow, that only made your heart race even faster.
The clinking of silverware against the plates was the only sound between you and Tsukishima as you both finished dinner. It was a quiet moment, but not awkward—just the kind of comfortable silence that had begun to settle naturally between you two. You were about to gather the dishes when Tsukishima leaned back, glancing at you with a knowing look.
“You can go change. I’ll wash the dishes,” he said, his voice carrying that soft, direct tone that you’d come to recognize as one of his small acts of care.
You blinked, a little surprised, your hand freezing just as you were about to reach for the plates. Did he know that you had planned to rush to the sink—hoping to clean up quickly so you could change and head to the grocery store with him? The realization that he had noticed, or perhaps just anticipated your routine, made your heart warm slightly. But before you could protest or offer to help, Tsukishima stood up, gathering the dirty plates himself, his long fingers deftly handling the stack as he carried them to the sink.
For a moment, you just watched him—admiring the subtle way his back muscles shifted beneath his shirt, his movements smooth and efficient as he began rinsing the dishes. A soft sigh escaped you as you thought about how thoughtful he was. Being romantic and naturally kind were two different things, right? But with Tsukishima, the lines always seemed to blur. Maybe he wasn’t the overly affectionate type, but his quiet actions spoke volumes.
“You’re going to change, or just stand there staring?” His voice pulled you from your thoughts, and your face immediately warmed in embarrassment. Tsukishima wasn’t even looking at you, but he’d sensed it all.
With a quick jump, “I-I’m going!” you grabbed a fresh set of clothes from your drawer and hurried to the bathroom to change. You could hear the faint sound of water running and plates clinking as he washed the dishes, and you couldn’t help but feel a little guilty for letting him do it.
Once you’d collected your clothes, you changed in the bathroom, letting the coolness of your new outfit calm your sudden rush of emotions. The fact that he had noticed such small details about you, that he had even anticipated your next move, made your heart race in a way you weren’t used to.
When you stepped out of the bathroom, feeling refreshed in your clean clothes, Tsukishima was already waiting by the door. His tall figure leaned casually against the doorway, his eyes flicking to you briefly before he reached out his hand. You took it quickly, slipping on your sneakers with your free hand, the warmth of his palm making you feel slightly more at ease.
As you both stepped outside into the early evening air, the streets were quiet, bathed in the soft glow of the setting sun. Tsukishima unlocked his car with a beep, and as he always did, he opened the passenger door for you, gesturing for you to get in first. You couldn’t help but smile as you slid into the seat, appreciating the small gesture.
He walked around to the driver’s side and got in, starting the car with a low rumble. As he pulled out onto the street, the golden sunlight filtering through the trees created an almost dreamlike atmosphere inside the car. You snuck a glance at him—his profile lit by the warm light, the subtle focus in his eyes as he drove, his grip steady on the steering wheel. There was something comforting about being next to him like this, in the quiet space that only the two of you occupied.
“Didn’t think you were the type to leave dirty dishes behind,” he said, a faint smirk tugging at his lips as he looked at you sideways.
You laughed softly, squeezing his hand lightly in return. “I didn’t plan on it! You just swooped in so quickly.”
He hummed in acknowledgment, his eyes focused ahead. “Thought I’d spare you from rushing around.”
You smiled at his words, appreciating how well he knew you. He always seemed to understand the little things you didn’t even realize about yourself.
There was a beat of silence before he spoke again, this time in a quieter tone. “You want to get ice cream after I’m done with groceries?” he asked, glancing at you briefly before parking the car.
The mention of ice cream caught you off guard, and before you could even think about it, your face lit up with a grin. “Yes, please,” you answered eagerly, though you tried to keep your tone polite, not wanting to seem too excited. But Tsukishima noticed anyway, the faintest hint of a smile pulling at the corners of his lips.
“Thought you’d like that,” he muttered, a bit of teasing in his voice as he unbuckled his seatbelt and got out of the car. You couldn’t help but feel a bit giddy as you followed him into the store, his hand slipping into yours once more as if it was second nature.
The cool air of the grocery store greeted you as the automatic doors slid open. Tsukishima walked beside you, casually pushing the cart with one hand, while his other hand remained intertwined with yours. It was a small gesture, but it made your heart flutter. You glanced around the store, noting how brightly lit it was, rows of fresh produce on one side, aisles of packaged goods on the other. The slight hum of people moving about and the soft background music made the atmosphere feel almost peaceful.
Tsukishima paused for a moment, glancing at the list on his phone before steering the cart toward the vegetable section. His brows furrowed slightly in concentration, his long fingers tapping at the screen. You watched him for a moment, admiring how focused he seemed even with something as mundane as grocery shopping. It made you smile—how someone so seemingly distant and cool could still care about the little details.
“What?” Tsukishima asked, catching your gaze.
You quickly looked away, feeling your cheeks heat up. “Nothing, just… you look really serious about those vegetables,” you teased, trying to hide your fluster.
He raised an eyebrow, glancing down at the pile of vegetables in front of him. “Well, we need good ones. I’m not buying anything that’ll go bad in a day,” he replied, his tone neutral, though there was a hint of amusement in his eyes.
When he reached the hygiene aisle, he turned to you unexpectedly, “What hair product do you use?”
You blinked, surprised by the question. “Uh, I just buy whatever shampoo catches my eye each month. But my mom got me this hair mask and said I should use it every week.”
“What hair mask?” he asked, curiosity clear in his tone.
You walked a few steps to the shelf where the product was and pointed to a tub. “This one. It smells like cocoa,” you explained, trying not to sound too self-conscious.
Tsukishima took the container, examining it for a moment. “Why’s it so expensive for a hair product?” he mumbled under his breath. You couldn’t help but laugh softly at his confusion.
Suddenly, he reached out and gently picked up a strand of your hair, bringing it closer to his nose. “I was curious because your hair always smells nice,” he said casually, placing the container back on the shelf and moving to the next item. You stood there momentarily, blushing at the compliment, even though he had said it so nonchalantly.
Trying to hide the warmth creeping up your face, you fell back into step behind him, the interaction replaying in your head. After he finished collecting everything on his list, you both made your way to the cashier. The line moved slowly, but Tsukishima handed you his card before you had a chance to say anything.
“Go ahead and get the ice cream. I’ll meet you there after I pay for this,” he said, nodding toward the ice cream shop across the street.
Your face lit up at the suggestion. “What flavor do you want?” you asked, barely able to contain your excitement.
“Surprise me,” he replied with a small smile, clearly amused by your enthusiasm.
You grinned widely and, holding onto his card, headed toward the ice cream shop, trying to decide on the perfect flavor combination that would do the “surprise” justice. Tsukishima, meanwhile, watched you leave with a soft chuckle, shaking his head at how effortlessly happy you seemed when it came to something as simple as ice cream.
You looked over the options, your eyes drawn to the more unique flavors. “One cup of vanilla yuzu and one cup of blueberry sea salt, please,” you told the employee with a polite smile.
There was something thrilling about trying new flavors—your mom had always been the type to stick to the basics, buying you plain vanilla or chocolate, often with the cautionary “what if you don’t like it and throw it away?” But today, you wanted something different, something adventurous.
As you received the cups, Tsukishima walked into the shop, immediately spotting you. You smiled instinctively when you saw him, feeling a rush of warmth at the sight of him. He pointed toward a small table near the window, a cozy spot bathed in the fading golden light of the evening. You followed him as he pulled out a chair for you to sit first—a small, but appreciated gesture that made your heart skip.
Once you were both settled, Tsukishima glanced at the ice cream cups you placed on the table. His eyes shifted to you with mild curiosity. “What’s this?”
You grinned, practically buzzing with excitement to see how he’d react to the flavors. “Just try it,” you urged him, sliding one of the cups toward him.
He picked up the small plastic spoon and dipped it into the vanilla yuzu first, bringing the bite to his lips. His expression remained neutral, but you noticed the way his eyes softened slightly as he savored the taste, the sweetness of vanilla melding with the citrusy sharpness of yuzu.
“It’s good,” he said simply, placing the spoon down.
Your smile widened. “Yeah? Try this one,” you added, offering him a spoonful of the blueberry sea salt.
As he leaned in and took the spoon from your hand, you suddenly remembered the time he had casually sipped from your cup of hot chocolate before you got in a relationship. The memory made your cheeks flush slightly, and you quickly turned your attention back to your own ice cream, feeling the heat rise to your face.
Tsukishima hummed quietly in approval as he tasted the blueberry, though he didn’t comment further. His calm demeanor never wavered, but you could tell he preferred the first flavor from the subtle way his attention shifted back to the vanilla yuzu cup.
For a while, the two of you ate in comfortable silence, the sounds of the shop around you blending into the background. The occasional clink of spoons against the cups, the soft hum of conversation from other customers—it all felt peaceful, like time had slowed down just for you two.
After a few more bites, Tsukishima broke the silence. “I’m gonna be busy for the next two days,” he said, his tone casual, but his gaze fixed on you. “You okay with that?”
You smiled, shrugging nonchalantly. “Of course. We used to see each other by coincidence, remember? I can manage two days without you,” you replied, your voice light and playful.
Tsukishima’s lips curled slightly in amusement, his eyes glinting with a teasing edge. “Yeah—thought I should give you the experience of missing your boyfriend’s presence now that you have one.”
The teasing tone made your heart skip a beat, and before you knew it, you were playfully nudging his side, laughing at his comment. Tsukishima smirked, though there was a warmth behind it—a quiet understanding that, despite his teasing, you’d miss him more than you were letting on.
sorry i didn’t upload it sooner, and i missed kei’s birthday—bit i promise to post about it tomorrow, so i hope you guys still wait for this story to finish 🥹🥹
it’s been so hectic guys—but i miss writing and see your comments—they always lighten up my mood 🫶🏻✨🤧
tagslist (free to mention) ; @theweirdfloatything @snowthatareblack @ilovemymomscooking @nayiiryun @knightofmidnight @kozumesphone @scxrcherr @thechaosoflonging @monya-febrjack
#daleelah writings 🐭#haikyuu x reader#tsukishima kei x reader#haikyuu x you#kei tsukishima x reader#tsukishima x you#haikyu x reader#jjk x reader#haikyuu au#college au#haikyuu fluff#haikyuu tsukishima#haikyuu fanfiction#haikyuu!!#hq tsukki#hq smau#hq x you#hq x reader#hq fluff#hq fanfic#hq#tsukishima x y/n#tsukishima fluff#tsukishima x reader#tsukishima kei#hq tsukishima
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also preserved at the archive
By: Jessica Wildfire
You don't need me to tell you how bad it's getting.
I'll tell you anyway, though.
As we drown in endless waves of Covid that generate millions of infections and thousands of deaths per week, our leaders have effectively stripped away every tool we have. They prefer a society that sacrifices themselves for short-term economic and political gains and then becomes ripe clientele for the pharmaceutical industry. They collude with the media to push out a daily barrage of misinformation aimed exclusively at ensuring we continue to work, shop, and vacation, because that's what they care about. Meanwhile, they do absolutely nothing about pandemics on the way as dozens of diseases spread out of control, at levels 10 times worse than normal. As the World Health Organization sounds alarms, telling us "we have arrived in the post-antibiotic era," and that we faced a future pandemic up to 20 times worse than Covid, our leaders focus on vibes. That last part should get our attention. Yes, we are here. We have arrived in the time when superbugs aren't responding to antibiotics. If that weren't bad enough, they're preying on our weakened immune systems.
And bird flu has likely gone human to human.
But it's not hopeless.
Four years ago, we looked to plants to protect us from pathogens because vaccines and treatments weren't coming anytime soon. The minute those vaccines and antivirals came out, most people forgot all about plants. They reverted to their old assumptions that plants were for hippies.
Well, here we are again.
Our vaccines and treatments are failing, and when they work they're often in short supply, or we can't even get access to them. Moms and dads are rolling out the NyQuil in little cutesie Facebook posts, along with all the pills that treat the symptoms but leave the disease itself to roam free all over your body.
We can do better.
As we mask while demanding clean air and better medicine, it's time to revisit those plants and see what they can do.
Do they even work?
Yeah, they do.
A 2024 review of studies in Viruses identified 10 different plant compounds with broad antiviral properties and effectiveness specific to Covid (and in many cases several other viruses). As they write, "plat-derived molecules can tackle viruses by acting on different aspects of their infection process" and "inhibit coronavirus/host protein pathways" by blocking them. The authors initially identified 45 different compounds and then narrowed them to the 10 most effective.
Plants work because they contain terpenoids, flavonoids, phenols, and alkaloids that all demonstrate "high anti-viral potential against SARS-CoV-2 particles" as well as other viruses. They do this in a variety of ways that work across variants because they block virus entry while also tamping down replication and essentially "stopping its life cycle."
Sounds good to me...
Let's get into it.
First, ginkgo biloba contains two bioflavonoids called quercetin and rutin that can block Covid's 3CLPro BS PL-pro enzymes, as demonstrated in two different studies that looked at how they bind to parts of the spike protein. According to an article in Nature, 3CLPro plays a central role in virus replication, specifically for Covid. Ginkgo also contains kaempfero that inhibits Covid's envelope protein E, "consequently suppressing virus activity and proliferation." G. Biloba also brings an anti-inflammatory effect that can help with recovery as well.
Second, turmeric and curcumin "can either bind directly to the receptor binding domain of the viral S-proteins or secure ACE2 receptors of the hosted cell." Basically, they stop viral entry into your cells. As the authors write, a curcumin derivative called bi-demethoxycurcumin "displayed the best binding affinity" to spike proteins.
It also works on the original SARS virus.
Third, a common spice called artemesia annua demonstrated antiviral activity in clinical trials. The group who took an artemisia compound called artemisinin-piperaquine "took significantly less time to reach undetectable levels of SARS-CoV-2 than the controls." In fact, artemisinins "are known for their extended-spectrum antiviral activity." An artemisia derivative called artesunate has shown effectiveness against both DNA and RNA viruses including hepatitis and HIV.
Artemesia compounds work similar to ginkgo by latching on to five different parts of the spike protein "which might explain its remarkable binding affinity." In addition to flavonoids like quercetin, researchers have identified di-caffeoylquinic acid as doing a lot of the heavy lifting here. Like curcumin, these flavonoids also bind to ACE2 receptors on your cells and protect them. Medical researchers are working on refining these compounds into artenimol, a single high-potency compound for giving to patients.
Fourth, nigella sativa (black cumin seeds) have shown antiviral activity by disrupting viral RNA transcription. Carvacrol and nigellidine extracted from these seeds "can block ACE2 receptors, thus inhibiting the SARS-CoV-2 entry into the host cells."
Fifth, ginger (6-gingerol, 8-gingerol, 10-gingerol) can inhibit parts of the Covid spike protein. Specifically, it's the bioactive compounds geraniol, shogaol, zingiberene, and zingiberenol that do the blocking.
Sixth, garlic (allium sativum) shows antiviral activity. It contains compounds called allicin, ajoene, and garlicin that work against several viruses in the same ways as the other compounds, by targeting spike proteins, disrupting transcription, and protecting your cells' entry channels.
Next:
Cinnamon at 50 ug/ml operates the same way as the other compounds, by blocking host cell entry and viral replication. Rosemary (rosmarinus officinale) shows effectiveness in blocking viral activity, even in a study that compared it to the antivirals remdesivir and favipiravir.
Want an unusual suspect?
It's dandelion.
Dandelion extract has shown to be "effective against influenza virus infection" and in higher concentrations "showed efficacy against spike proteins... and its different mutants" in human lung and kidney cells, while also helping to prevent the cytokine storm that's often so deadly in the acute stage. Here in particular, studies have shown that dandelion extract works regardless of the variant.
Finally, oregano (origanum vulgare) extract demonstrates antiviral activity against many DNA and RNA viruses, including Covid and HIV. As the authors write, extracts "showed remarkable efficacy against equine influenza virus, canine coronavirus, RS, and H1N1. In fact, it can inhibit up to 74 percent of viral activity at certain sites.
Again, carvacrol does the heavy lifting.
I've looked at other supplements and extracts with antiviral properties. They include grapeseed extract, grapefruit seed extract, olive leaf extract, echinacea, St. John's-Wort, and elderberry.
A 2024 study found that oleuropein, found in olive leaf extract, demonstrates high antibacterial activity at 130 mg/ml and high antifungal activity at 65 mg/ml. Another 2022 study found that oleuropein showed significant effectiveness against Covid in hospitalized patients when they were given 250-500 mg every 12 hours for five days. (No real difference between 250 and 500 mg.) The study also reviews previous research that oleuropein has shown effectiveness against other viruses, including HIV and influenza. It works the same way as other flavonoids, lectins, secoiridoids, and polyphenols, by blocking ACE2 receptors.
A 2022 study reviews available research on elderberry (sambucus nigra), confirming antiviral activity against HIV, flu, and coronaviruses. As the researchers write, adults in clinical trials "showed a significant reduction in symptoms, averaging 50 percent." Elderberry has also shown the ability to stimulate the production of immune cells. A 2019 study confirms that elderberry works against flu via "multiple modes of therapeutic action," including the inhibition of replication and host cell entry. An extensive 2021 study looking at prior research found that high-quality elderberry extracts enriched with anthocyanin work especially well.
A 2022 study in Nature found that a mixture of St. John's Wort (hypericum perforatum) and Echinacea showed significant antiviral activity against Covid. Specifically capsules with .9 mg of St. John's "can significantly reduce SARS-CoV-2 viral load," peaking at 36 hours after the start of treatment.
St. John's Wort works just fine on its own. The authors stress the importance of maintaining its concentration if you add other compounds like echinacea.
That said, a 2022 study in Frontiers in Pharmacology found that echinacea at 4,000 mg for 10 days led to a substantial reduction in viral load and fewer hospitalizations when used to treat Covid patients.
Here's a chart docs.google.com/spreadsheets/d/1cTJ3lXHPUW7AyrZPXQb63IjmhVbahRm_7Y5IMxKcqO8/edit?usp=sharing&ref=okdoomer.io
You can also look up most of these supplements and extracts on Mount Sinai's health library. They'll give you a good breakdown. It's a good idea to talk with a doctor if you're skeptical or not sure about interactions with other drugs, or look at the studies on your own. The studies linked in the sheet provide the most detailed dose information I can find, usually presented in a table. Duration runs around two weeks for an acute illness and 3-4 months for chronic infections like HIV.
Do I think it's sustainable to take high amounts of supplements all year long to ward off all kinds of airborne diseases, for the rest of our lives? Not really. That's why we absolutely need clean indoor air, masks, better vaccines, and better treatments. Until then, at least we have this information.
List of studies raindrop.io/JW_Lists/alternative-treatments-47681852
So there you have it.
If you've been wondering whether this stuff really works, the answer appears to be a loud yes. We need more research on dose amounts, but the studies all point in the direction of taking as much as you can while staying within the safe limits, for the duration of any time you feel at risk of getting sick.
Most of these extracts work against multiple viruses. They also help regulate your immune system and push it toward a less inflammatory response.
That's good to know.
My family has been using some of these supplements for several years, and it might explain why we've managed to steer clear of Long Covid. We still wear N95 masks everywhere. We advocate for clean air and better vaccines, along with better treatments. In the meantime, it looks like we can up our supplement game and that it's actually going to bring some benefit.
This isn't magic.
These plant compounds work the same way as many of the antivirals on the market. Medical researchers have been researching the antiviral properties of plants for decades, and cultures have used them for thousands of years. Given our current outlook, they're worth taking seriously.
Use what you can.
#mask up#covid#pandemic#covid 19#wear a mask#public health#coronavirus#still coviding#sars cov 2#wear a respirator
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Wondering why PCOS is not considered medically to be under the CAH umbrella (since CAH is a group of conditions involving hyperandrogenism), does anyone happen to know the reason?
Is it the vagueness regarding the cause of PCOS, is it the amount of misunderstanding and misinformation surrounding PCOS, is it intersexism and misogyny? Or even a combination of these?
Looking at the literature, PCOS is indistinguishable from CAH without extensive bloodwork, and often CAH is misdiagnosed as PCOS due to less widespread knowledge of not only CAH's existence (despite it being extremely common) but also due to doctors rarely ever testing for anything that is not 21-OHD, if they decide to run tests at all. (Many PCOS patients are diagnosed without any tests or with only an ultrasound to check for ovarian cysts, which is not actually useful as any kind of evidence towards a PCOS diagnosis at all)
In fact, 3bHSD CAH at one point was even considered to be a type of PCOS rather than CAH. If the two are so similar, and CAH is already an umbrella term, why the distinction between PCOS and CAH at all?
If it's due to treatment implications, that doesn't seem to work because treatment implications are different even within different variations within the CAH umbrella and even further within the same CAH variation. My treatment needs and goals are different from someone with another CAH enzyme deficiency, because the location of the deficiency on the steroid pathway changes a lot about what your symptoms are and how to manage it. Someone with 3bHSD CAH may build up pregnenolone, while someone with 21-OHD CAH may build up progesterone, for example, and these can cause very different outcomes for physical health and needs. There's also vastly different implications between classic, non-classic, and salt-wasters.
Us all being lumped under CAH has never stopped us from accessing the different treatment we need for whichever variation we have. Being grouped under an umbrella label does not mean we are all suddenly the exact same and have the same needs. This is true across all umbrella diagnoses and across spectrum disorders, and CAH is not any different.
A person with XY chromosomes and 3bHSD CAH may have ambiguous genitalia while a person with XX chromosomes and 3bHSD CAH may have completely "typical-appearing" or only slightly virilized genitals, some people with CAH may be infertile while others have no issues with fertility, some have ovarian cysts and some do not, some will go through "typical" puberty and others will have ambiguous or "opposite-sex" puberty, so on.
What vast amount of differences are there between PCOS and CAH that are not present between 21-OHD and 3bHSD, 11-beta, and StAR? PCOS and NCAH can even be more alike to each other than CAH variations can be to other CAH variations.
When we have studies which struggle to differentiate PCOS from CAH even on a biochemical level, why are we so confident in saying that PCOS is not yet another CAH presentation, or that it does not belong underneath that umbrella?
TERFs don't touch this post, I don't want to hear your shit today.
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Albinism
Albinism is a disease that causes a defect in the normal synthesis or transport of melanin. There are a couple different types, but the main distinction is the difference between oculocutaneous albinism (OCA) and ocular albinism.
Oculocutaneous Albinism
OCA is caused by an autosomal recessive mutation. There are seven different mutations that can cause albinism, though OCA1 to 4 are the common ones (with OCA2 being the most common). All of these different mutations affect the melanin pathway (the chemical reaction steps to turn phenylalanine into melanin).
OCA1 is caused by a mutation in the tyrosinase gene, which causes a lack of an enzyme in the melanin production pathway. There are actually two types of OCA1, with one having no tyrosinase, and the other having reduced tyrosinase. OCA1 is the most extreme form of albinism, which gives a person very pale skin, white hair, and light eyes.
The OCA2 gene (located on chromosome 15) encodes for the P protein, which is a transporter of a melanin precursor. This gene also has a large role in the color of iris a person will have. Those with OCA2 will have light skin, lighter brown or blond hair, and light colored eyes.
So basically, someone with a defect in either one of the transporters or enzymes of the pathway will not be able to have their melanocytes produce normal melanin. This leads to pale skin, white hair, and light-colored eyes (but it is a spectrum depending on the exact type).
Ocular Albinism
Ocular albinism is an X-linked mutation (a portion of the X chromosome is mutated). This means it affects males more than females. It causes loss of pigmentation in the iris. OA1 is the most common, and is associated with uncontrolled eye movements. OA2 is associated with color and night blindness. There is also a third type that is associated with deafness, but sometimes that also happens with OA1.
A fun fact: there is a type of albinism that only affects non-human animals called leucism. This leads to a partial loss of pigmentation that affects the hair, scales, feathers, and skin of the animal, but not the eyes. You can see this in white lions that have normally-colored eyes and noses.
Albinism and Eyesight
Now onto the role melanin plays in eye function. Albino people have poor eyesight as a result of their melanin deficiencies. But why? We're going to have to go into some eye stuff to answer this question.
So your retina has two parts: temporal and nasal (two halves, one closer to your temple and one closer to your nose). The input from each half is processed with the opposite half from the other eye. I have another post that explains this better. So, the optic nerves meet at the optic chiasm, with some fibers staying on the same side, and other fibers crossing over. Mammals with forward-facing eyes have larger temporal retina than mammals with lateral-facing eyes (like a guinea pig). About half of the optic fibers also remain uncrossed at the chiasm because of this.
Most people with albinism have almost all of their fibers cross at the chiasm, which is essentially a misrouting of very important sensory information. The eye structure is also changed with albinism, as most albino people have poorly formed fovea (the depression in the center of the retina where vision is the sharpest). They also have more blood supply than normal to the foveal area (it is supposed to be avascular). The retinal macula is usually poorly developed and there is a reduction in cone density (what allows you to see color).
Stereovision is also impaired, which is the ability to discern three-dimensional information about objects using the difference between the inputs from each eye. Those with albinism are also more likely to have nystagmus (involuntary eye movement) and strabismus (crossed eyes).
Albinism and Hearing
Now, onto the ear. The eye and ear are very intimately connected. The ear lets the eye know where to look for threats. This means that the visual and auditory spaces within the brain interact. Fun fact: when blind people are asked to localize sounds, the visual cortex is more engaged than the auditory cortex. Albino animals have fewer binaural cells, and more difficulty visually locating the source of sounds. A lot of the stuff related to this goes beyond the scope of what I want to explain here, but just understand that melanin is important for the development of both the auditory and visual systems of the brain.
Albinism and Immune Function
Finally, I want to discuss the immune system. Melanocytes are important cells for immune function, and release a lot of immune-promoting factors. For some reason, a lot of people think of those with albinism as having weak immune systems or being sickly. If you'll notice what I said earlier about the cause of albinism, it is a lack of transporters or enzymes in the melanin pathway. Not the lack of melanocytes. People with albinism still have these cells, it is only their ability to produce melanin that is impaired.
However, there are immune conditions that affect melanocytes, such as Chediak-Higashi syndrome. This is an autosomal recessive disorder that affects lysosomal trafficking proteins, and causes lysosomal function to be impaired. People with this disease will have frequent infections, platelet function impairment, as well as albinism. This means that albinism does not cause immune deficiency, but is a symptom of conditions that also affect the immune system.
#medicine#med student#medical school#med studyblr#med school#character traits#biology#medical writing#albinism#ocular posting#immune system
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What’s the difference between Pfizer/BioNTech, Moderna, and Novavax COVID-19 vaccines?
The Pfizer-BioNTech and Moderna COVID-19 vaccines use mRNA as the active ingredient. The mRNA is converted by our cells into the antigen, in this case, the spike protein of SARS-CoV-2.
The vaccine contains the mRNA, which is synthesized in the lab using a DNA template, the building blocks of RNA, and the enzyme that puts those building blocks together into the right order. mRNA is the molecule template for every protein in every organism. The mRNA sequence is a code for our cells to link amino acids together into functional proteins
mRNA is very fragile, so it is encased in a lipid nanoparticle (LNP) that protects it until it gets into our cells. When the vaccine is administered, the mRNA is released and is used to synthesize the spike protein which is displayed by cells that produced it. That spike protein is recognized by our innate immune cells like dendritic cells and macrophages as well as B cells, which initiates immune response and generation of memory immunity.
In contrast, Novavax is a protein-based vaccine, which contains the prefabricated antigen - the spike protein - instead of the template for it. To make the antigen, we turn cells into protein-producing factories in the lab.
Novavax uses Sf9 cells (moth cells) infected with an insect-specific virus that has been genetically engineered to contain the gene for the spike protein of SARS-CoV-2. These viruses will hijack the cellular machinery of the Sf9 cells to produce lots of spike proteins and baby viruses. Those will continue to reproduce and produce proteins, which will be harvested, purified, and formulated with the other ingredients in the final vaccine.
When the vaccine is injected, the antigen will be recognized by the same innate immune cells listed above, which will trigger the same immune response pathway.
While the vaccines use different technologies, ingredients, and manufacturing processes, the immune responses center around recognition of the spike protein and generating adaptive immune responses targeting that antigen.
#novavax#covid#covid 19#sars cov 2#vaccines#vaccine#vaccination#get vaccinated#long covid#illness#chronic illness#covid vaccine#mrna#jn.1#kp.2#sf9#Novavax vaccine#mrna vaccine#Pfizer-BioNTech#Moderna#moderna vaccine#pfizer vaccine#pfizer
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Mitochondria can come in two different types, according to a surprising new finding. The newly discovered ability of mitochondria to split into two different forms resolves a longstanding mystery of how mitochondria can simultaneously provide cells with energy and essential building blocks, even when resources are limited.
Read the paper: Cellular ATP demand creates metabolically distinct subpopulations of mitochondria
The team behind the work hope that this ability could help explain how some cancers can thrive, even in hostile conditions.
0:00VOICE OVER: Believe it or not, both of these structures are actually mitochondria.0:06CRAIG THOMPSON: We were as surprised as everyone that there would be this mechanism of mitochondria to become specialised subpopulations.0:15VO: It turns out that mitochondria come in two different types, which could help explain how they can produce energy and make important building blocks of cells at the same time, even when resources are limited.0:32CRAIG: And that was impossible to explain. If the standard chemistry works and there are all these enzymes in one compartment that breaks the laws of thermodynamics, it should have compromised the others. So, there has to be some explanation for this.0:50VO: Mitochondria are known as the powerhouse of the cell for good reason.0:56CRAIG: They are responsible for the bulk of our ability to make ATP, the molecule that provides the energy source for all activities that cells do.1:06VO: But it's become clear over the last few years that that's not all they do.1:11CRAIG: Mitochondria are essential for other things in our body, and that is synthetic reactions that build the building blocks of proteins and lipids that allow us to engage in cell division and cell repair.1:24VO: Now, that makes sense when there are plenty of resources around. But when resources are limited, like if a cell is damaged, for instance, that's been hard to explain.1:36CRAIG: Once the mitochondria is limited for the nutrients with which to make ATP or to engage in synthesis of molecules as precursors, it's got to choose whether it burns it to CO2 and water where it can't get them back. That allows you to make ATP or it takes those molecules and use them as building blocks to build things, using the same energy that otherwise would go to ATP production.2:01VO: So to figure out how this is possible, Craig and the team took cells and starved them of resources. When they did so, they found that the mitochondria were separating into two very different subpopulations. One, an expert in making ATP and looks quite familiar to the one you know from school.2:21CRAIG: So the mitochondria that are enriched in ATP synthesis become the perfect mitochondria that you want to put in a textbook to explain how mitochondria are an energy factory. They have highly ordered cristae. They’re really efficient at making the super complexes that allow you to make ATP, and they're the perfect ones to take a picture of. If you were to show the classic mitochondria, we all learned about in school.2:46VO: The other were less textbook ready, but they were experts at making the cell building blocks.2:53CRAIG: The other population actually still has the double membrane of a classic mitochondria, but it's filled with filaments of proteins.3:00VO: These proteins seem to be key, as Craig in the team narrowed down what was allowing this division of labour to one specific protein that is at the center of these filaments.3:12CRAIG: There was one linchpin protein that was necessary to make the judgment between these two pathways. That gene has a terrible name and no one knows really much about. It's called pyrroline-5-carboxylate synthase.3:25VO: And these two types of mitochondria may be key to help researchers understand things like cancer.3:33CRAIG: And what we show in the paper. One of the most severe cancers, as they grow, the tumour cells acquire these segregated mitochondria that allows them to maintain their growth.3:43VO: Linking this strange mitochondrial behaviour and cancer will need more work, which Craig and the team are pursuing. But for now, it's fair to say that these little organelles that we all know from school are a lot more complicated than we thought, and likely have more mysteries to uncover in the future.
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Exploring the Marvels of Biological Macromolecules: The Molecular Machinery of Life (Part 2)
Amino Acids: The Building Blocks
Proteins are composed of amino acids and organic molecules that contain an amino group (-NH2), a carboxyl group (-COOH), a hydrogen atom, and a distinctive side chain (R group). There are 20 different amino acids, each with a unique side chain that confers specific properties to the amino acid.
Primary Structure: Amino Acid Sequence
The primary structure of a protein refers to the linear sequence of amino acids in the polypeptide chain. The genetic information in DNA encodes the precise arrangement of amino acids.
Secondary Structure: Folding Patterns
Proteins don't remain linear; they fold into specific three-dimensional shapes. Secondary structures, such as α-helices and β-sheets, result from hydrogen bonding between nearby amino acids along the polypeptide chain.
Tertiary Structure: Spatial Arrangement
The tertiary structure is the overall three-dimensional shape of a protein, determined by interactions between amino acid side chains. These interactions include hydrogen bonds, disulfide bridges, ionic bonds, and hydrophobic interactions.
Quaternary Structure: Multiple Polypeptide Chains
Some proteins, known as quaternary structures, comprise multiple polypeptide chains. These subunits come together to form a functional protein complex. Hemoglobin, with its four subunits, is an example.
Protein Functions: Diverse and Essential
Proteins are involved in an astounding array of functions:
Enzymes: Proteins catalyze chemical reactions, increasing the speed at which reactions occur.
Structural Proteins: Proteins like collagen provide structural support to tissues and cells.
Transport Proteins: Hemoglobin transports oxygen in red blood cells, and membrane transport proteins move molecules across cell membranes.
Hormones: Hormonal proteins, such as insulin, regulate various physiological processes.
Immune Function: Antibodies are proteins that play a crucial role in the immune system's defense against pathogens.
Signaling: Proteins are critical in cell signaling pathways, transmitting information within cells.
Protein Denaturation and Folding
Proteins are exquisitely sensitive to environmental changes. Factors like pH, temperature, and chemical agents can disrupt protein structure, leading to denaturation. Proteins can sometimes refold into their functional shape if conditions return to normal.
Protein Diversity
The vast diversity of proteins arises from the combinatorial possibilities of amino acid sequences, secondary structure arrangements, and three-dimensional conformations.
Proteins, the versatile and intricate macromolecules, are the workhorses of biological systems. These molecules, comprised of chains of amino acids, are central to nearly every aspect of life, orchestrating various functions, from catalyzing chemical reactions to providing structural support. Let's delve into the remarkable world of proteins.
#science#biology#college#school#education#student#medicine#doctors#health#healthcare#biochemistry#molecular biology#proteins
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Health update
I am feeling much better in general.
I'm in my luteal phase, so I do expect to experience some additional skin inflammation. However my face and neck have remained 100% clear despite this. 4 weeks ago they were inflamed.
So the DIM supplement is really helping me make improvements.
I've read that DIM supplements are safe to take longterm as well as the other nutrients in the supplement I have that support estrogen metabolism and liver detoxification pathways. I do not drink and I don't eat a lot of junk food, but a liver support supplement can be very helpful. DIM removes the harmful estrogens that contribute to estrogen dominance, PCOS, endometriosis, uterine fibroids, breast cancer, ovarian cancer, hormonal cystic acne and skin rashes, and insulin resistance. We are exposed to these harmful estrogens, known as xenoestrogens, on a daily basis. It is found in plastics, receipts, and drinking water. It's been reported to cause early puberty in girls and dumping plastic waste into lakes has been shown to cause hormonal imbalances in frogs such as feminization and infertility. It makes sense because many plastics contain BPA which is an endocrine disruptor.
I am drinking reverse osmosis water and am eating organic foods that are on the dirty dozen list such as strawberries, blueberries, tomatoes, and spinach. I try to use non-irritating skin and hair and teeth and body care products. It's impossible to avoid "toxins" 100% and it's worth being realistic. That's why I want to incorporate liver detoxification support.
The supplement I'm taking is expensive, but it is worth it. I take other supplements too and I can get cheaper yet good quality versions of those. I like my supplement because it contains DIM and other ingredients to support phase 1, 2, and 3 liver detoxification since DIM alone isn't enough.
I'm happy I am healing because I used to deal with severe skin inflammation. My face, neck, and ears are clear. My hands need a bit. But at least they look better than they did 4 weeks ago. I'm going to heal.
While I'm healing I also really want to help my dog heal too. He's a senior dog with colitis and IBS. So we cant to support his gut health with some supplements.
I've been drinking aloe juice as usual. I've been taking digestive enzymes before larger and my first meals each day. I feel they make a huge difference and I don't feel as bloated.
However, enzymes aren't the only thing that play a role in digestion. Stomach acid (HCl) does too. I know it is also helpful. I do not know if I need it though, and whether which one is better. I heard of a baking soda stomach acid test, but idk how I feel about doing that. But I've also heard that if you take betaine HCl and you experience burning, then you don't need it. If you don't experience burning, then you need it.
I can look for a supplement that combines both HCl and enzymes to get the benefits from both. I'll do my research. I know I can benefit from enzymes for sure because they help with fat absorption and I have issues with that. HCl is good for protein breakdown.
I'm getting a new toothpaste that contains nano-hydroxyapatite. I'm looking forward to using it in conjunction to my regular fluoride toothpaste. You can absorb fluoride through your toothpaste without swallowing it by sublingual absorption. I wonder if the same can happen with the minerals in the nano-hydroxyapatite toothpaste. I'll try it out.
Again I'm not sure why I have low phosphorus levels. Phosphorus tends to be rich in foods rich in protein and fats. So again, enzymes can help here and so can HCl potentially.
I'm sure the liver support supplement can help because the liver is also a digestive organ and can help with the digestion process along with enzymes and HCl.
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Targeted Therapy:
Precision or targeted therapies encompass medications engineered to disrupt specific molecules implicated in the progression of cancer. In contrast to conventional chemotherapy's broad impact on fast-dividing cells, precision therapies selectively target cancer cells while preserving healthy tissue integrity. These drugs aim at various molecular pathways involved in cancer development, including signaling cascades, angiogenesis, and DNA repair mechanisms.
An illustrative example of precision therapy is the application of tyrosine kinase inhibitors (TKIs) in treating specific cancer types like non-small cell lung cancer (NSCLC) and chronic myeloid leukemia (CML). TKIs hinder the activity of particular tyrosine kinases, crucial enzymes in cancer-promoting cell signaling pathways. By obstructing these kinases, TKIs effectively inhibit tumor growth and extend patient survival.
Likewise, monoclonal antibodies represent another form of precision therapy, binding to specific proteins on cancer cell surfaces, initiating immune-mediated tumor destruction. These antibodies can also be combined with cytotoxic agents or radioactive isotopes to heighten their anti-cancer properties.
Personalized Chemotherapy:
While precision therapies are central to personalized medicine, tailored chemotherapy remains vital in cancer treatment. Tailored chemotherapy involves customizing traditional cytotoxic drugs to suit the unique characteristics of each patient's tumor. This may involve adjusting drug doses, combining different agents, or selecting chemotherapy regimens based on tumor biology and patient-specific factors.
One approach to tailored chemotherapy utilizes predictive biomarkers to identify patients likely to respond positively to specific chemotherapy drugs. For example, certain mutations in the BRCA genes are associated with increased sensitivity to platinum-based chemotherapy in breast and ovarian cancers. By identifying these biomarkers, oncologists can identify patients who will benefit most from a particular chemotherapy regimen while minimizing potential toxicity for others.
Furthermore, progress in pharmacogenomics, which explores how genetic variations affect drug response, has provided insights into individual differences in drug metabolism and toxicity. By analyzing patients' genetic profiles, oncologists can predict their likelihood of experiencing adverse effects or poor response to chemotherapy drugs, enabling personalized dose adjustments and treatment optimization.
Early cancer detection and management is important for an improved success rate in cancer treatment. You can undergo regular health checkups to get diagnosed for cancer at an early-stage. There are many good hospitals in Mumbai that offer health checkup packages for cancer screening, such as a full body health checkup at Saifee Hospital Mumbai, which is one of the best hospitals in the country.
#chemotherapy#personalized chemotherapy#targeted therapy#full body health checkup#regular health checkups#cancer screening#cancer detection
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Benefits Of Clove Tea: Explore 8 Impressive Benefits
Herbal tea, as known to all, carries great medicinal value. Among the different kinds of herbal teas, clove tea is an important one. Clove Tea carries a strong flavor and a wide range of health benefits. The use of clove has been plentiful throughout history. Clove has a great many medicinal properties. There is no doubt that the use of clove in tea yields the best results. Here we offer you a sneak preview of the benefits Of Clove Tea.
8 Benefits Of Clove Tea
1. Antioxidant Powerhouse
Clove tea enhances antioxidants owing to its antioxidant content. This injection prevents oxidative stress and promotes wellness. Free radical-neutralization clove tea protects cells against aging and chronic illnesses.
Beyond its excellent flavor, clove tea’s antioxidants make it a complete beverage. Cloves’ natural safeguards empower health with every drink. Clove tea is a pleasant approach to increase immunity and health frequently or sometimes.
2. Immune System Support
Vitamin- and mineral-rich clove tea promotes immunity naturally. This vitamin C-rich herbal infusion boosts immunity. Eugenol and bioactive chemicals in cloves enhance immunity.
Vitamin C in clove tea enhances immunity and prevents infections. This herbal tea’s immune-boosting effects are improved by adding it. This infusion works as a natural health aid by strengthening the body against external threats.
Vitamin C and eugenol work together to improve immunity in clove tea. Together, these bioactive chemicals improve immunity and combat infections. Thus, drinking clove tea regularly is a delightful and healthy investment.
Since robust immune systems safeguard health, clove tea is a great daily supplement. Clove tea tastes great and helps people remain healthy.
3. Digestive Aid
Tea with cloves has long been used to calm and aid digestion. Carminative tea helps with bloating and gas. Since it relieves these issues, clove tea is calming after meals.
Clove tea increases digestive enzyme production. Natural digestive stimulant, this infusion promotes food digestion and nutrient absorption. Clove tea aids digestive enzymes.
After bloating and gas, clove tea may relieve nausea and indigestion. Cloves form a warm, aromatic beverage that relieves post-meal aches. Mild and organic clove tea aids digestion without medication.
Clove tea aids digestion after meals. Both for its fragrance and digestive effects, clove tea is tasty. Clove tea’s natural remedies ease post-meal symptoms and support digestion. This is one of the Important Benefits Of Clove Tea.
4. Anti-Inflammatory Properties
Cloves’ anti-inflammatory properties help chronic inflammation. Eugenol, the major ingredient in clove oil, is anti-inflammatory. Cloves may relieve inflammation naturally.
Eugenol, clove oil’s major component, reduces inflammation. The chemical reduces systemic inflammation by altering inflammatory pathways. Many chronic diseases include inflammation, therefore drinking clove tea may help.
Regular clove tea consumption treats arthritis and inflammatory bowel problems. Clove tea’s anti-inflammatory properties treat inflammation naturally. Regularly drinking clove tea may reduce chronic inflammatory pain.
Clove tea adds a rich, aromatic taste to inflammation control. Cloves’ anti-inflammatory properties may make a pleasant drink a complete chronic disease treatment.
5. Dental Health Elixir
Tea made from cloves maintains the dental therapy tradition. Long-standing antibacterial and analgesic properties make cloves strong dental pals. Clove tea promotes comprehensive oral health using cloves’ natural ingredients.
Antibacterial clove tea soothes teeth. It fights oral microorganisms to prevent cavities and gum disease. Clove tea protects teeth and gums naturally and proactively.
Beyond prevention, clove tea improves dental ache. Tea’s analgesic properties soothe toothaches and other oral discomfort naturally. Clove Tea’s oral health strategy covers prevention and comfort.
Clove tea tastes good and is a traditional mouthwash. Old wisdom and modern comfort make clove tea ideal for natural smile care. The tea’s delightful smell promotes a comprehensive and time-tested approach to oral health by highlighting cloves’ ancient advantages.
Aldo Check: How To Use Clove Water For Hair Growth? Benefits & Side Effects
6. Blood Sugar Regulation
Patients at risk of diabetes may benefit from clove tea’s blood sugar-regulating properties. This new study emphasizes cloves’ bioactive components, including eugenol, and their insulin-like effects, suggesting better glycemic control.
Due to its insulin-like effects, clove bioactive components including eugenol are researched. Clove tea may manage glucose levels, according to this research. Eugenol’s effects on insulin pathways add to clove tea’s health benefits as insulin is essential to glucose metabolism.
Clove tea may improve metabolic health, but further research is required. Early study suggests clove tea may improve metabolic health, particularly glucose control. Clove tea may cure diabetes as the study continues.
Studies show that clove tea may impact metabolic health as well as taste. As scientists investigate its intricate mechanisms, clove tea and its bioactive components offer hope for natural blood sugar regulation.
7. Pain Relief And Headache Remedy
Natural painkiller clove tea. Clove tea’s anti-inflammatory and numbing qualities relieve headaches, muscle, and joint pain. This makes it a diversified and comprehensive natural remedy for many diseases.
Clove tea reduces inflammation and discomfort from several conditions. Clove tea relieves stress and inflammation headaches. The tea’s analgesic effects relieve extreme physical exertion, muscle strains, and joint discomfort.
Clove tea’s stress-relieving properties go beyond comfort. The tea soothes stress-prone people naturally. Relaxing clove tea is a terrific self-care addition.
Clove tea for pain enhances overall wellness. Clove tea is pleasant and calming, helping to reduce life’s stresses. Each warm, fragrant sip supports physical and mental well-being.
8. Respiratory Wellness
Clove tea relieves congestion and coughing. Expectorants like cloves clear mucus and alleviate respiratory issues. The tea’s antimicrobial qualities also combat infections, improving lung health overall.
The expectorant qualities of clove tea reduce respiratory congestion. Facilitating mucus evacuation reduces coughing and congestion. In addition to being warm and aromatic, clove tea may help with respiratory difficulties.
The antimicrobial properties of clove tea protect the respiratory system. By battling infections, the tea avoids respiratory issues, particularly in cold weather. Clove tea helps respiratory health, whether for a sore throat or seasonal prevention.
For organic respiratory health, clove tea is a proactive option. Cloves warm and soothe the body and lungs with each sip. Drinking clove tea is a delicious respiratory hygiene routine.
Read More: Is Ginger Tea Good For Constipation? Benefits Of Ginger Tea
Conclusion
The multifaceted benefits of clove tea will, no doubt, attract health-conscious persons. It is the kind of drink that offers a boost to the body and mind. Modern researches confirm the fact that clove tea is a great relief for those suffering from low immunity, bad digestion, inflammation, etc. The therapeutic nature of clove tea offers great relief in every possible matter.
References
Clove Based Herbal Tea: Development, Phytochemical Analysis and Evaluation of Antimicrobial Property https://www.jpsr.pharmainfo.in/Documents/Volumes/vol11issue09/jpsr11091905.pdf
Reichling J (2010) Plant-microbe interactions and secondary metabolites with antibacterial, antifungal and antiviral properties. In: Wink M (ed.) Annual Plant Reviews Volume 39: Functions and Biotechnology of Plant Secondary Metabolites. 2nd edition. Oxford: Wiley-Blackwell, pp. 214–347. https://doi.org/10.1002/9781444318876.ch4
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feeling so awkward i stayed after class because i had to finish something which was due at 12 and this other lecture started and i have one at 12 in a different building and this one finishes at 12:30. and i feel so bad just walking out in the middle. but also they are saying some multi enzyme pathways shit and i don't know anything about this like at all
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How Does Ayahuasca Affect The Brain
Ayahuasca, an ancient medicinal brew used by the indigenous people of the Amazon, has witnessed a surge in popularity in recent years. Its increased use in urban settings, once scarce two decades ago, has prompted extensive research into its components. This has especially intrigued the scientific community, which is exploring its potential therapeutic applications, particularly in the realms of psychiatry and neurology.
Over the last decade, Ayahuasca research has flourished, shedding light on its primary constituents—DMT (Dimethyltryptamine) and the Beta-carbolines (Harmine, Tetrahydroharmine, and Harmaline)—resulting in a deeper understanding of its cerebral mechanisms and effects.
Must Read Blog: What is Ayahuasca
Components of Ayahuasca: Ayahuasca derives its main alkaloid substances from two plants: Banisteriopsis Caapi vine, yielding Beta-carbolines (Harmine, Tetrahydroharmine, Harmaline), and Psychotria viridis leaves, known as chacruna, providing N, N-dimethyltryptamine (DMT). Both components collaborate to induce psychoactive effects that facilitate altered states of consciousness, contributing to mental, emotional, and spiritual healing.
DMT and its Significance: DMT, a crucial component in Ayahuasca, shares a structural resemblance with serotonin (5-HT). Classified as an endogenous trace neurotransmitter, DMT is naturally present in the body, albeit in low quantities. Serotonin, a neurotransmitter, plays a pivotal role in various bodily functions, and comprehending its functions provides insights into Ayahuasca's impact on the brain.
Serotonin and Neural Communication: Serotonin interacts with at least 14 different receptor types in the brain, each with specific functions and signaling pathways. Neurons in the raphe nuclei are the primary sources of 5-HT, with various pathways forming from these neurons. Ayahuasca, containing DMT, acts on brain areas similar to serotonin, affecting neuronal receptors. Beta-carbolines in Ayahuasca also function as neurotransmitters, binding directly to stimulated brain areas or inhibiting serotonin degradation through monoamine oxidase-A (MAO-A) inhibition.
Monoamine Oxidases (MAO) and Ayahuasca: MAOs are enzymes controlling neurotransmitter availability, influencing DMT when orally ingested. Ayahuasca's Beta-carbolines act as MAO inhibitors, temporarily blocking MAO action. This inhibition enables DMT to reach the brain, elevating serotonin, noradrenaline, and dopamine levels.
Effects on the Brain: Ayahuasca's impact on the brain is intricate and varied. The brew takes effect approximately 30 minutes after consumption, inducing a transient introspective state marked by dream-like visions, personal memory recollection, and intense emotions. Research suggests associations between Ayahuasca intake and modulation of neuronal plasticity, influencing the brain's capacity to form new connections.
Substances in Ayahuasca and Their Effects: DMT, harmaline, and tetrahydroharmine exhibit antioxidant effects at the cellular level. Harmine and harmaline increase dopamine concentration, potentially beneficial for Parkinson's disease management. Harmine demonstrates anti-inflammatory effects, while DMT promotes neurogenesis and has protective effects on cells against oxidative agents.
Psychological and Behavioral Effects: Ayahuasca consumption has been linked to increased creativity, ethical lessons, and profound subjective experiences fostering connections with the self and the 'source.' It enhances introspection, reduces stress, improves judgment processing, and induces changes in perception, ultimately aiding in the management of anxiety, depression, and addictions.
The Default Mode Network and Ayahuasca: Ayahuasca's effects extend to the default mode network in the brain, impacting self-recognition, thoughts about others, memories, and emotional processing. Studies indicate significant activation in specific brain regions, alterations in neurophysiology, and increased "decentering" ability post-Ayahuasca consumption.
Conclusion: Research into Ayahuasca's brain mechanisms and neurotransmitter functions underscores its therapeutic potential. Reported benefits include improved mood, cognitive processes, introspection, stress management, impulse control, and creativity. Ayahuasca's effects on neurogenesis, myelination, and antioxidant activity at the neuronal level further emphasize its potential to facilitate emotional processing and enhance psychological well-being.
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Biostimulants: Tailoring Solutions for Crop Performance Enhancement
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HEREDITARY FORM OF EPILEPSY ASSOCIATED WITH PYRIDOXAMINE 5'-PHOSPHATE OXIDASE DEFICIENCY IN A CHILD by Plotnikova I.A in Journal of Clinical Case Reports Medical Images and Health Sciences
SUMMARY
The article presents a clinical case of focal epilepsy with a status course of seizures associated with a genetic mutation in exon 1 of the PNPO gene, which led to pyridoxamine-5'-phosphate oxidase deficiency. The diagnosis was made late due to the misinterpretation of symptoms, which complicated the course of the disease. Despite the fact that the first symptoms in the form of seizures appeared at the age of 1 month, only at the age of 5 the diagnosis was verified by doing targeted DNA sequencing. At the moment, the patient is receiving substitution therapy in the form of pyridoxal phosphate 300 mg/day, which enabled unstable clinical remission. Right now, it is impossible to achieve complete control over the convulsive syndrome without a strict diet: dairy-free, meat-free, egg-free and low-protein fat-free food. Currently, further search for treatment methods continues to improve the patient's quality of life and ensure stable remission. A detailed analysis was given for further genetic verification based on the amino acid profile of the patient, and the rehabilitation potential was determined based on topical neuropsychological diagnostics performed on a non-verbal child.
Key words: focal epilepsy; Pyridoxal 5′-phosphate; vitamin B6; PNPO; vitamin B6-dependent epilepsy, neuropsychological diagnostics.
INTRODUCTION
Vitamin B6-dependent epilepsies are aheterogeneous group of autosomal recessive diseases that are caused by mutations of five different genes involved in vitamin B6 metabolism [1]. Vitamin B6 is present in many forms in the human diet, but only pyridoxal-5 -phosphate (PLP) plays a vital role in the metabolism of a number of neurotransmitters, especially the inhibitory mediator gamma-aminobutyric acid. Code errors leading to a lack of pyridoxal-5'-phosphate manifest as B6-dependent epilepsy, including pyridoxamine-5-phosphate oxidase (PNPO) deficiency, which affects the synthesis and recycling of pyridoxal-5'-phosphate [2,3]. Neonatal manifestation in the form of acute encephalopathy with biphasic epileptic seizures (or status epilepticus) is the main symptom of the disease. The first phase (early attacks) is accompanied by fever and a temporary recovery of consciousness and the development; the second phase is a global cognitive dysfunction (late attacks).
Resistance to traditional antiepileptic therapy requires patient's lifelong treatment by pharmacological doses of vitamin B6 in the form of pyridoxine (PN) or a biologically active form of pyridoxal-5’-phosphate [1,4].
Case reports of PLP deficiency, verified not only clinically, but also by exome sequencing, are quite rare as well as the methods for studying molecular markers of alpha-aminoadipic semialdehyde and pipecolic acid in body fluids [5–7]. The complexity of diagnosis is caused by multiple disorders in newborns, especially in case of a slow and incomplete response to pyridoxine [8].
Recent studies have shown that the main enzyme defect in pyridoxine-dependent epilepsy is caused by alpha-aminoadipic acid semialdehyde dehydrogenase in the pathway of cerebral lysine degradation. The accumulating compound, alpha-aminoadipine semialdehyde (alpha-AASA), is in equilibrium with delta-1-piperidine-6-carboxylate (P6C). P6C inactivates pyridoxal-5’-phosphate, causing severe cerebral insufficiency. Although treatment of pyridoxal 5'-phosphate deficiency can successfully control seizures, most patients develop some degree of disability, regardless of early diagnosis and treatment. Very few patients with normal intelligence have been reported [7].
Objective: to analyze the course of epilepsy with pyridoxamin-5’-phosphate oxidase deficiency in an 8-year-old patient with diagnosis verification by clinical exome sequencing.
MATERIALS AND METHODS OF RESEARCH.
The analysis of primary medical documentation from 2013 to 2021 of a patient born in 2013 was performed. We reviewed the materials on the topic using PubMed search engines for the period 2014-2021, correlation of literature data with a specific clinical case.
RESEARCH RESULTS AND THEIR DISCUSSION.
A clinical case
Girl, 8 years old, was born from IV pregnancy of a woman with a burdened obstetric history. At the age of 1 month, tonic-clonic convulsions were first noted during sleep: gaze adversion to the left, lasting 30 seconds - 1 minute; afterwards there was up to 4 seizures per day, daily. At the age of 1 year, she was hospitalized 4 times on an emergency basis for convulsive seizures. The child was observed by a neurologist-epileptologist with a diagnosis of perinatal damage to the central nervous system, recovery period. Valproic acid was prescribed at a dosage of 50 mg/kg per day, oxcarbazepine 300 mg/day, without an effect of therapy. At the age of 2 years, she was hospitalized three times in the intensive care unit due to the status course of an epileptic seizure with a rise in temperature to febrile numbers. Neurological diagnosis at that time was: symptomatic epilepsy with complex partial seizures, status course of generalized convulsive seizures. On electroencephalography (EEG): moderate diffuse changes in the bioelectric activity (BEA) of the brain in a disorganized type. The patient's condition worsened. At the age of 3 years, she was observed in the State Autonomous Healthcare Institution of the Sverdlovsk Region "Children's City Clinical Hospital No. 9, Yekaterinburg" with the same diagnosis; the dose of oxcarbazepine was increased to 500 mg/day, valproic acid to 300 mg/day with no significant clinical effect. At the age of 4 years, she was hospitalized three times in the intensive care unit about epileptic seizures, without the effect of anticonvulsant therapy. Concomitant diseases at age 4 were: severe osteoporosis of the visible parts of the skeleton; pathological compression fracture of the body Th11; hepatomegaly; moderate expansion of the common hepatic, common bile ducts; enlargement of the gallbladder; a pronounced increase in the size of the kidneys, pancreas; diffuse changes in the parenchyma of the kidneys, a single cyst of the right kidney; unspecified form of caries; chronic gingivitis. Computed tomography of the abdominal aorta and its branches showed no evidence of hepatic artery stenosis. Autonomic dysfunction of the sinus node was noted: sinus arrhythmia with episodes of bradycardia. There were also small anomalies in the development of the heart: a functioning foramen ovale, additional chords of the cavity of the left ventricle.
DNA sequencing was carried out in 2017. Genetic mutations that were identified are described in patients with epilepsy associated with pyridoxamine 5'-phosphate oxidase deficiency and, based on the totality of information, regarded as pathogenic - a mutation in exon 1 of the PNPO gene (chr17: 46019139A> T, rs370243877), leading to amino acid replacement at position 33 of the protein (p.Asp33Val, NM-018129.3, mutation frequency in the ExAC control sample 0.0235%); as probably pathogenic - a previously undescribed heterozygous mutation in intron 3 of the PNPO gene (chr17:46022086G>A, rs766037058), leading to disruption of the splicing site and synthesis of the full-length protein (c.363+5G>A, NM_018129.3, OMIM: 610090, the value of the algorithm for predicting its influence on the function of AdaBoost splicing sites is 1.000).
A heterozygous mutation was also found in exon 4 of the EARS2 gene (chr16:23546678A>T), leading to a premature translation termination site at codon 163 (p.Tyr163Ter, NM_001083614.1). Such mutations have been described in patients with combined oxidative phosphorylation deficiency type 12 (OMIM: 614924). In this case (when no second mutation in the gene is detected), the result is regarded as an option with uncertain clinical significance, however, the mutation may be related to the phenotype. The parents did not undergo a genetic examination.
Prescribed treatment was: pyridoxine hydrochloride intramuscularly, then - pyridoxal phosphate at the rate of 10-50 mg / kg /day. On the 7th day after the start of treatment, the patient's consciousness was assessed as clear, she was able to sit up independently and stand with support. Her seizures stopped, appetite improved, during rehabilitation positive dynamics in neuropsychic development was noted with an expansion of the range of motor activity, the appearance of gaming activity, emotions and attempts to pronounce individual sounds.
At the age of 5 years 1 month there was a new epileptic seizure. The dose of pyridoxal phosphate was increased to 600 mg/day, convulsive attacks stopped. Concomitant diseases at age 5 were perianal dermatitis, vulvitis, continuously recurrent leukocyturia. Subsequent courses of medical rehabilitation was prescribed with positive dynamics.
In 2019, hyperkinesis (blinking), tremor, restlessness reappeared; in the summer were tonic-clonic seizures with vocalization, lasting 15-20 minutes and the status course of an attack, operculations, loss of appetite. By the end of the year, there was constant nausea and a gag reflex at the sight of food, vomiting with yellow mucus and a sour smell once every 5-7 days, accompanied by febrile fever, the smell of "rotten cheese" from the scalp and excrements during attacks. Motor clonic seizures appeared with a frequency of once every 1-2 months, symmetrical chill-like tremor - up to 3-5 times a day. Periodic episodes of psychomotor agitation, stereotyped movements were also noted.
Neurological status. There are bradypsychia, delayed psycho-motor development, coordination disorder. Patient does not pronounce words, speech is active only during the game-vocalisms, self-service skills are not formed. Autism spectrum disorders with general speech underdevelopment of level 1, psychomotor alalia were noted. Cerebral, meningeal symptoms are negative. The gait is uncertain. Cerebellar tests are negative. Cranial nerves: palpebral fissures D=S, pupils D=S, pupil reaction to light: direct D=S, consensual D=S. The volume of movement of the eyeballs is complete D=S, there is no nystagmus. The face is symmetrical D=S. There is no language deviation. Swallowing, phonation are not disturbed. Muscle tone: arms - reduced D=S, legs - normal D=S. Tendon reflexes: from the arms and legs increased D=S. There are no pathological foot signs, pelvic functions are preserved. Patient shows signs of slightly asymmetrical (with an accent on the left) motor awkwardness, reduced nutrition (Body weight 21,5 kg).
Results of instrumental and laboratory studies. The following disorders were detected on the EEG prior to the start of etiological therapy: Epileptiform activity in the form of "peak-wave" complexes in the frontal and central-temporal leads, more on the right; slowing down of activity in the temporal zone.
In the biochemical analysis of blood the level of amino acids (µmol/l) is low: alanine 119.30; glutamic acid 72.00; glycine 86.50; ornithine 22.10; proline 87.00. Activity of alanine aminotransferase is 24.9 U/l (reference values 0-29 U/l), aspartate aminotransferase - 26.4 U/l (reference values 0-48 U/l).
Control visit. After the diagnosis was verified by exome sequencing, the patient was prescribed etiotropic therapy: pyridoxal phosphate 300 mg/day. The pre-elevated (1070 nmol/l) plasma concentration of vitamin B6 (pyridoxal-5-phosphate) normalized. EEG data - video monitoring showed moderately severe violations of BEA of the brain; the main rhythm is formed by age; registered regional slowing of the rhythm in the right central-parietal region. Epileptiform activity, clinical paroxysms, EEG patterns of epileptic seizures were not registered.
Final diagnosis: Genetic focal epilepsy due to a mutation in the PNPO gene (chr17: 46019139A> T, rs370243877). The type of attack is focal with impaired consciousness. PNPO developmental and epileptic encephalopathy. Cognitive impairment. Alalia. Motor awkwardness.
Psychological status. Diagnostics of cognitive activity showed that the girl is accessible to contact; she does not speak and comprehension of the speech is shown only in the form of understanding simple commands and simple instructions for the task. The child's object-sensory activity is carried out 100% through visual perception and shape perception, the perception of size is developed by 50%, spatial perception - 12%, color perception is completely absent. The insufficiency of these afferentations is a consequence of the decrease in the “zone of actual development”, which may be attributed to pedagogical neglect. In the motor sphere, gross motor skills are fully formed, fine motor skills are developed by 54%, objective activity is formed by 9%, taking into account the skills of game and constructive praxis, speech function is developed by 25%, self-service skills - by 60%, socialization – by 40%. Psychological diagnostics of the state of higher mental functions was carried out by depicting the structural and functional features of the brain, as a result of which topical insufficiency of brain areas was revealed. Figure 1 shows the level of formation of brain zones.
Figure 1: The degree of formation of brain departments that implement sensory and motor skills.
Despite the pronounced cognitive deficit in the child, the implementation of the program of psychological rehabilitation may expand the "zone of actual development" in the structure of the sensory, subject and pedagogical profile (since there are preserved components of cognitive activity)
DISCUSSION
Patient’s clinical diagnosis was established only at the age of 5 years, based on clinical manifestations and exome sequencing. The primal reduction of the dose of pyridoxal-5'-phosphate provoked a relapse of status epilepticus and a regression of acquired cognitive skills. A subsequent increase of treatment in combination with dietary therapy provided an unstable clinical remission without further improvement in the patient's condition. Such a response to the therapy has also been demonstrated in other studies [6,7].
Although in patients with a typical course of the disease, there is a several-fold increase in the level of glycine and glutamic acid in the blood plasma [1,5–7,9], in our case there is a decrease in glycine to 86,50 µmol/l (norm: 100-400 µmol /l) and other amino acids. Hypoglycinemia is an extremely rare condition, it occurs only in severe hereditary aminoacidopathy, but in our patient, tandem mass spectrometry was performed twice (including against the background of an attack) in 2016 and did not show any data of hereditary aminoacidopathy, organic aciduria, defects β-oxidation of fatty acids. The girl has a positive reaction to the oral intake of amino acid complexes and glycine separately, therefore, additional genetic analysis can be performed for 3-phosphoglycerate dehydrogenase deficiency, the clinical manifestations of which may be encephalopathy and seizures unresponsive to anticonvulsants [10]. Symptoms of this disease can be stopped by joint intake of serine and glycine so this diet may be developed for our patient. The study of vitamin B6 metabolites in de novo serine biosynthesis by Ramos et al (2017) had one group of rats which received a pyridoxine-deficient diet, while the diet of the control group of rats contained a normal amount of pyridoxine. This study has demonstrated a decrease in serine biosynthesis in Neuro-2a cells in vitamin B6 deficient rats. The pyridoxal-5'-phosphate-dependent enzyme phosphoserine aminotransferase (PSAT, EC 2.6.1.52) cannot function fully in conditions of vitamin B6 deficiency, and likely reduces the synthesis of phosphoserine and serine in animals on a pyridoxine-deficient diet. The production of glycine depends on the availability of serine and on the pyridoxal-5'-phosphate-dependent enzyme SHMT, which catalyzes part of the transformation of glycine, and the simultaneous deficiency of serine and pyridoxal-5'-phosphate can reduce its activity and lead to a decrease in the content of glycine in blood plasma [9].
Some authors reported EEG changes in patients with pyridoxine-dependent epilepsy [11]. In our patient, no clear epileptiform activity was registered either before or after the start of treatment with pyridoxal-5'-phosphate; this variant of EEG was also described by other researchers [5,6]. Changes in the brain during magnetic resonance imaging in patients with pyridoxine-dependent epilepsy may vary from normal to diffuse atrophy of the gray and white matter of the hemispheres [2]; in our case no changes were detected.
According to Plecko B. Et al., with late diagnosis stable remission after the appointment of pyridoxal-5'-phosphate is observed only in a few patients [1]. Early treatment is critical to prevent irreversible damage to the central nervous system and shows positive results [1,5,6]. Patients with pyridoxine-dependent epilepsy require lifelong supplementation with pyridoxal-5'-phosphate. Therapeutic doses of the drug vary from 15 to 30 mg/kg/day [1]. The daily requirement for vitamin B6 in infancy is 0.1–0.3 mg. Pyridoxal-5'-phosphate doses up to 500 mg/day are considered safe in children with classical vitamin B6 deficiency, but higher doses may cause reversible sensory and rare motor neuropathy [1], so total daily doses of pyridoxal-5'-phosphate, should not exceed 200-300 mg. There are no data on the optimal dose of the vitamin for long-term treatment. In experimental animals, doses of pyridoxal 5'-phosphate >50mg/kg/d induce ataxia, peripheral neuropathy, and muscle weakness; histological examination demonstrates neuronal damage with loss of myelin and degeneration of sensory fibers in peripheral nerves, dorsal columns of the spinal cord, and descending tract of the trigeminal nerve. In most cases of peripheral neuropathy, the total dose of pyridoxal 5'-phosphate is >1000 mg/day. Some children who take high concentrations of pyridoxal-5'-phosphate develop a persistent increase in transaminases with progression to cirrhosis and hepatocellular carcinoma [3]. To avoid side effects, a fixed effective dose should be used. However, studies showed that daily doses up to 1100 mg/day and 50 mg/kg/day to achieve a state without epileptic seizures did not cause any side effects when they were divided into 4–5 doses per day [12]. In our case the doses of pyridoxal-5'-phosphate less than 600 mg/day induces epileptic seizures and cognitive disfunction. Some mutations in the genes encoding of pyridoxamine-5-phosphate oxidase may require the combined treatment with pyridoxal-5'-phosphate and pyridoxine [12,13]. It is possible that such treatment will have a positive response in our patient as well.
Another interesting feature of this clinical case is an intolerance of the patient to many products: remission occurs only on a low-protein, low-fat diet with the exclusion of dairy, meat products and eggs. Similar dietary restrictions are observed in ALDH7A1 deficiency (antiquitin deficiency), which often accompanies PNPO gene mutation. In our case ALDH7A1 deficiency was excluded by exome sequencing [13,14]. However, a lysine-restricted diet can also be effective for homozygous mutations in the PNPO gene in some patients [14]. As an example of a diet, the recommendations of Koelker and Ross on glutaric aciduria type I can be used [15].
The patient also has a high content of vitamin B6 in plasma (775.0 nmol/l), which is typical response to an intake of pyridoxal-5'-phosphate (described levels of vitamin B6 in plasma: 400 nmol/l, 1060 nmol /l and 624 nmol/l) [12,18]. It is not known why some patients continue to have seizures even when taking high doses of pyridoxal-5'-phosphate, while others grow almost normally [1,7,19]. The long-term prognosis for this patient remains unclear. For our patient a clarifying genetic study with modification of pharmacological treatment and diet is required, considering that the girl does not tolerate protein hydrolysates and an unstable clinical remission only on a low-protein low-fat diet with the exclusion of dairy, meat products and eggs.
CONCLUSIONS
DNA diagnostics using the method of sequencing of exome regions of the genome is a key method for early verification of the diagnosis of epilepsy in newborns and young children, which in combination with the therapy can improve the prognosis.
The presence of heterozygous mutations in this clinical case suggests other metabolic deficits, which complicates the selection of treatment and requires additional examination of the exome.
To ensure stable remission, nutritional correction is required to compensate for deficient conditions during severe elimination measures, as well as the selection of the minimum sufficient dosage of pyridoxal-5'-phosphate in combination with pyridoxine hydrochloride.
Topical neuropsychological diagnostics and psychological correction based on intact higher mental functions makes the recovery of the patient possible.
Conflict of Interest: The authors of this article have confirmed that there are no conflicts of interest or financial support to report.
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#focal epilepsy#Pyridoxal 5#phosphate#vitamin B6#PNPO#vitamin B6-dependent epilepsy#neuropsychological diagnostics#DNA#aheterogeneous#alpha-aminoadipine#semialdehyde#Plotnikova I.A#jcrmhs
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so i was reading this article in the failing new york times
which for those of you without a free subscription from your college, they talk about GMO trees being planted for carbon capture despite no peer reviewed studies on whether the mutants are even better than wild type. but what particularly interested me is what they did to the poplars: they’re trying to fix RuBisCO.
(for those of you who did not take intro botany, RuBisCo is the enzyme used in photosynthesis to actually stick the carbon dioxide the plant breathes in to molecules in the plant. it’s the reason almost everything on earth is alive but it evolved before there was much oxygen in the atmosphere so it constantly fucks up and adds oxygen instead of CO2, creating toxins that plants waste energy detoxifying. its also slow as fuck but they dont talk about fixing that)
linked was this wild article from 2019, in which three alternate metabolic pathways were added to tobacco to break down the glycolate produced by RuBisCO fucking up. they literally built pathways out of various different enzymes used by different species to try and get glycolate into something useful for the plant. and it worked??? and they grew faster in a field experiment??? absolute sci-fi shit going on here.
that being said the living carbon planting DOES need to have more supervision because planting trees that can 1) grow faster and 2) reproduce asexually in the wild sounds like a monoculture waiting to happen even if theyre not expected to breed, assuming their untested claims are true. potential for huge bottom-up trophic cascades that need to be accepted before rolling this out to more places.
#imo fine plant them on some fucked up land and see what happens. but we are also 3 steps from things that could fuck up the atmosphere and#give us giant bugs again.
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