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tteessiiee · 2 months ago

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Health impacts of obesity, death feedee edition

TW: this is dark and very real, do not read if you are not ready to understand the consequences of feedism. And I really mean it. It may be f* scary.

You know I study physiotherapy at med school. And Im also a feedee, feeder, FA... Which means that mine internships in hospitals are pretty heavy and hard for me. I see all the impacts of obesity, or even morbid obesity on people and their health. On their life.

We are all talking about heart-attacks. Sure, your arteries getting clugged, atherosclerosis growing in your body and getting you closer to an early grave. But atherosclerosis does not cause only heart-attacks. It would be nice, wouldn’t it? Feeling your heart struggling, pain in your chest (which you deserve for being the pig you were), and pretty soon there is the end. Death.

But atherosclerosis can also cause strokes. And I don’t think you want that. Part of your brain gonna die, part gonna live. It can affect your motor functions, your ability to feel by touch, your ability to know where and how placed your limbs are, your speech, of course your ability to think. You may die, sure. Or you gonna survive and live way way worse life fully dependant on people around you… Did you know that?

You also might ruin your pancreas. Im sure that many of you already have insulin tolerance way higher than you should. Well diabetes mellitus is incoming if you will not change your lifestyle. It does not only mean that you will need to take insulin! It will also damage your nerves. Neuropathies are very common. DM can lead even to amputations of legs. And also an impact on eyes is very well known, you can become blind. Over all diabetes is a metabolic disease and it has huge impact on your whole body – nerves, organs, veins, everything.

Another effect of our feedee diet - your liver become fattier making it work less. And liver are very important organ! Liver steatosis can become cirrhosis, the organ will be very damaged. Btw it also gonna increase your blood pressure which has significant impact on probability of heart-attacks and strokes. Another thing – there can appear stones in your gallbladder. That is mainly caused by eating too greasy and fatty food. And this also can be very painful situation needing a surgery.

It is proved that obesity increases the risk of cancer, especially cancer in gastro-intestinal tract and urogenitals. One more thing that people do not want.

Not to mention your musculo-sceletal system. Arthrosis in joints (another painful thing restricting your daily life), unfit and stiff muscles, bones easier to break by your weight if you fall… And it will not hurt only when you move. But also when you lie in your bed getting stuffed to the brim once again. Who of you have never ever had back pain, mainly lower-back pain? It is not comfortable, is it? And it only gonna get worse if you don’t exercise.

There are also impacts on your skin but i'm not good in this field so can't say much about it.

I know it is a lot of fun to be a feedee. To gain, get fatter, heavier, softer. Getting out of breath easily? Oh f* yes please, it makes you so horny. But there is a huge impact on your health. Im sure you know it. But maybe you don’t know all the specific things that may happen. This is just a brief list of health complications that obesity brings. So if you are a death feedee, go on! Eat yourself to these diseases if that’s what you want. But be aware that your life probably will not end by a sudden quick heart attack. You will suffer many months and years due to many comorbidities till your body will give up on you. Are you ready for that long pain?

Wanted to let you know so that I can feel better when I actually encourage you to gain. You know, consent means that you agree while being aware of the consequences. If you want me to help you get morbidly obese I wanna be sure I warned you. And maybe (hopefully) this gonna help someone to stop gaining so much if they find out that they would not be happy. Because babes – I don’t want you fat in the first place. I want you happy.

That’s the reason why im drinking 700 kcal hot chocolate made of heavy cream while writing this article. It makes me happy to gain. It makes me happy being fat even though I know all of these things. And it also scares the s*it out of me. I fear it so much. I want it so much. Im not a death feedee in real life, will not let the kink kill me (I hope). But I definitely am a death feedee in fantasies, deep inside and sometimes it is really hard to find the difference between having fun and ruining your body.

••••••••••••••••••••••••••••••••••••

I warned you it gonna be dark and real 🖤

Enjoy your life as you wish 💕 Give fully into hedonism or enjoy the parts of feedism that don't kill you - that is your choice. Your body. Your life. Your death.

~ Tessie

#dark feedism #dark feederism #death feedism.#death feedee #feedism health #health consequences #health concerns #feedee.#feeder.#feederism.#feedism.#feedee girl #gaining #fatter #getting fat #gaining weight on purpose #feederism health #feedism consequences

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mistydeyes · 2 years ago

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141 and what their patient file looks like

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summary: This is what I imagine everyone's favorite pharmacist as well as medics see when they look at 141's medical file.

Based on this pharmacist and 141 interactions

pairing: Task Force 141 x pharmacist!Reader

warnings: medical/pharmacy terminology, medical inaccuracies, swearing, depiction of wounds, mention of substance use disorder and abuse

Terms

PMH - Past medical history - the total sum of a patient's health status prior to the presenting problem

FH - Family history - contributing family history, generally parents and siblings

SH - Social history - contributing social behavior and routine

a/n: not canon at all! this is just a reference for me

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Price

PMH

Height: 1.88 m (6' 2'')

Weight: 93 kg (205 lbs)

Blood type: O+

Extensive physical injuries

21+ stab wounds - 2 required antibiotics for recurrent infection

9x bullet wound - 5x in the extremities, 4x in the chest (no perforation of vital organs), healed without complication

5x abrasion collar - 1 near right eyebrow became infected following medical eval and stitches

3x diagnosed concussion

Aspirin-sensitivity

Previously evaluated for tinnitus and hearing loss

Father - deceased at 76 from liver disease - 50 pack years, mycardial infarction (x2)

Mother - deceased at 84 due to chronic heart failure (CHF) -Glaucoma, asthma, CHF

Sister - Sports induced asthma, hypothyroidism

Negative family history of diabetes, hypertension, and cancer

Smokes - 30 pack years

Drinks regularly - 4-5 hard liquor each weekend; 1 glass of whiskey occasionally

Physically active - Enjoys recreational activities such as hiking, swimming, and biking

Has 1 dog, currently under the care of pt's younger sister

History of monogynous long term relationships, currently single

Medication list + indications

Amoxicillin/Clavulanic acid 625mg - Infection

Morphine 15mg + Ketamine 3mg - IV - Pain

Paracetamol 750mg - Pain

Buproprion SR 150mg - Smoking cessation - not-taking est 2004

Allergies

Aspirin allergy - Reaction: hives and asthma - ONLY PRESCRIBE PARACETAMOL

No environmental, food, or animal allergies

Notes

Patient has denied smoking cessation options

Soap

PMH

Height: 1.88 m (6' 2'')

Weight: 91 kg (200 lbs)

Blood type: O+

7x stab wound - 6 required antibiotics for recurrent infection, 2 MRSA resistant

2x bullet wound - 2x in lower extremities, healed with no complication

6x abrasion collar

2x broken collar bone - healed, with no complication

Lactose sensitivity - Recurrent IBS if ingested

Chipped first left molar following opening a beer with teeth

Father deceased at 68 due to heart failure - Type 2 Diabetes Mellitus, high cholesterol

Mother - Stage I HTN (hypertension)

Sister #1 - Postpartum depression, generalized anxiety disorder

Sister #2 - Elevated cholesterol/triglycerides

Brother - No known chronic health issues

Positive family history of diabetes and hypertension, but no cancer

Drinks regularly and heavily - 8-12 beers and 2-3 glasses of hard liquor each weekend; 1 glass of scotch occasionally

Smokes socially - 5 pack years

Physically active

Close relationship with family, has 4 dogs at home under the care of pt's mothers

Avid fan of The Glasgow Football Club

Medication list + indications

Clindamycin 300mg with ciprofloxacin 400mg - Infection

Amoxicillin/Clauvanic acid 625mg - Infection

Vancomycin 18mg/kg - MRSA resistant infection

Paracetamol 500mg - Pain

Morphine 15mg IV - Pain

Doxycycline 100mg - Acne discontinued in 2004

Allergies

Insect stings - Observed anaphylaxis to childhood bee sting

Notes

Patient demonstrates medication non-adherence, counsel ESPECIALLY with antibiotics

Scored 6 on Alcohol use disorders identification test for consumption (AUDIT C)

Gaz

PMH

Height: 1.86 m (6' 1'')

Weight: 93 kg (205 lbs)

Blood type: B-

3x stab wound - healed, no complications

1x broken collar bone

2x broken femur

Diagnosed concussion - evaluated in Oct. '19

Father - Type 1 Diabetes, high cholesterol

Mother - Vitiligo, Stage 3 breast cancer

Positive family history of maternal cancer and diabetes, but no hypertension

Social drinker - 3-4 beers each weekend

Does not smoke

Physically active - Enjoys morning and evening runs

Enjoys spicy food and tries to introduce into diet

When on leave, enjoys attending concerts and music festivals

Medication list + indications

Piriteze 10mg - Allergic rhinitis

Fluticasone Propionate - 93 mcg/actuation - Allergic rhinitis

Paracetamol 500mg - Pain

Allergies

Seasonal - Pollen and pet dander

β-Lactam allergy - Reaction: anaphylaxis evaluated in '19

Notes

Organ donor

Ghost

PMH

Height: Weight: 1.93 m (6' 4'')

WeighT: 100 kg (220 lbs)

Blood type: AB-

Extensive cuts and scarring to entire body

4+ stab wounds - healed, no complications

Gun shot to lower abdomen - healed, no complications, evaluated in Nov. '22

13+ collar abrasion

2x broken nose

Childhood injury of broken tibia and large toe

Psych eval - History of depression and post traumatic stress disorder, childhood history indicates emotional and physical abuse

Father - status unknown Diagnosed alcohol use disorder

Brother - deceased, cause of death non-contributory - Substance use disorder

Mother - deceased, cause of death non-contributory - Hypertension, thrombophilia (blood clotting disorder)

Positive family history of hypertension, but no diabetes or cancer

Social drinker - 3-4 glasses of hard liquor each weekend

Smokes socially - 10 pack years

Physically active - Enjoys nightly walks

Psych eval - Other squad members act as his emotional support

Expressed interest in cats and tattoo art (FLAGGED: Further input and comments from other medical professionals would be appreciated)

Medication list + indications

Paracetamol 1000mg - Pain

Amoxicillin/Clavulanic acid 625mg - Infection

Morphine 20mg + Ketamine 4.5mg IV - Pain

Mafenide acetate 5% topical - Antimicrobial, burn wounds

Fluoxetine 20mg twice daily - Depression - not taking est 2001

Allergies

NKDA - No known drug allergies

No environmental, food, or animal allergies

Psych recommends evaluation of a pet, such as cat, for pt while on leave

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covid-safer-hotties · 3 months ago

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The Long-term Complications of Covid-19 Infection - Published Sept 13, 2024

Context.— As the Covid-19 pandemic continues into its 4th year, reports of long-term morbidity and mortality are now attracting attention. Recent studies suggest that Covid-19 survivors are at increased risk of common illnesses, such as myocardial infarction, diabetes mellitus and autoimmune disorders. Mortality may also be increased. This article will review the evidence that supports some of these observations and provide an opinion about their validity and their relevance to insured cohorts.

Background Many Covid-19 survivors report protracted symptoms, sometimes lasting 3 years or more. These are collectively called post-acute sequelae of SARS-CoV-2 infection (PASC) or long Covid. They have been frequently described.1–4 In the past year, reports of long-term complications such as atrial fibrillation, heart failure, stroke and pulmonary embolism have emerged. In some reports these established disease entities are erroneously described as long Covid, generating confusion. The distinction is important: illness reported in Covid survivors are not restricted to the long Covid cohort. Thus, they are relevant to the majority of the North American population who have been infected by SARS-CoV-2, and not just the estimated 5-10% of individuals who belong to the long Covid cohort. This paper will examine the reports of increased incidence of cardiovascular diseases in both and will examine the reported long-term increase in mortality.

Cardiovascular disease after 1 and 2 years Multiple studies have reported an increased risk of cardiovascular events at 1 year. A February 2022 analysis of 153,760 US veterans, followed for 1 year after Covid-19 infection, reported an increased risk of cerebrovascular disease (HR 1.53), ischemic heart disease (HR 1.66), thromboembolic disease (HR 2.39) and atrial fibrillation (HR 1.71).5 Risk was greatest in those hospitalized and those with pre-morbid illnesses. However, risk was also elevated in outpatients, who constituted the vast majority of the cohort. These findings have been corroborated in 2 further studies. In a 2023 analysis of 690,000 Covid-19 survivors, drawn from the TriNetX database–self-described as the world’s largest global Covid-19 dataset–there was an increased risk of cerebrovascular disease (HR 1.6), ischemic heart disease (HR 2.8), thromboembolic disease (HR 2.6) and atrial fibrillation (HR 2.4) at 1 year.6 In contrast to the VA study which examined a predominantly older male population, the subjects in this study were younger, with mean age 44, and 57% were female. Risk was higher in the >65 age group and was not limited to inpatients. In a May 2023 Lancet retrospective analysis of 535,000 Hong Kong (HK) and 16,000 UK Covid 19 survivors, similar hazard ratios were recorded for stroke (HR 1.2), ischemic heart disease (HR 1.32), atrial fibrillation (HR 1.31) and deep venous thrombosis (HR 1.74).7 However, it is worth noting that while follow-up was described as 28 months for the HK cohort and 17 months for the UK cohort, the median follow-up for the HK group was 146 days and was 243 days for the UK cohort, somewhat limiting the conclusions of true impact at 1 year. Contradicting these studies, a prospective analysis of 17,000 Covid-19 survivors in the UK Biobank, did not document an increased risk of cardiovascular outcomes amongst outpatients, with the exception of thromboembolic disease (HR 2.7).8 An August 2023 analysis of 138,000 VA Covid-19 survivors followed for 2 years– the longest follow-up period to date– reported that the risk of complications in outpatients had returned to baseline at 6 months.9 In contrast, the risk for multiple cardiovascular and thromboembolic complications in the hospitalized cohort remained elevated at 2 years. None of these 5 studies was limited to individuals with long Covid, but similar findings have been reported in this group: a recent analysis of 13,435 individuals who had been diagnosed with long Covid, based on a typical array of symptoms, reported increased risks at 1 year for ischemic heart disease (HR 1.7), ischemic stroke (HR 2.1) and pulmonary embolism (HR 3.6).10

These studies document a fairly consistent, increased risk of cardiovascular complications among Covid-19 survivors. However, important questions remain. Amongst these: does increasing population immunity and vaccination change the risk? Is the magnitude of risk similar for all SARS CoV-2 variants? Does reinfection increase the risk? Answers to some are available. Vaccination appears to attenuate the risk: a Korean study of 592,000 individuals post-Covid-19 infection, showed that vaccination decreased the risk of heart attack and stroke by approximately 50%.11 This finding was replicated in a large US cohort where major adverse cardiovascular events were reduced by a similar amount for full vaccination, and by 25% for partial vaccination.12 Thus, while vaccination does not eliminate long-term complications, it appears to provide a substantial protective effect.

Reinfection may increase the risk of sequelae. In a large US VA cohort of 440,000 Covid survivors, of whom 40,000 had one or more SARS-CoV-2 reinfections, the risk of cardiovascular disorders was increased (HR 3.02), when compared to a single infection.13 Moreover, this risk was not modified by vaccination.

The impact of different variants is less clear. Most of the described studies were conducted in 2020-2021 when delta and pre-delta variants predominated. It is unclear whether similar outcomes would characterize infection with Omicron variants, which remain dominant in most countries since November 2021. Interestingly, the risk of cardiovascular complications in the cohort of Hong Kong survivors described above, where the Omicron was the prevalent strain, was no different than among the comparator UK Biobank cohort, where pre-Omicron strains were prevalent.7

Is there extra long-term mortality after Covid-19 infection? Extra mortality has been reported by several studies.6,8,14–18 A 2021 US analysis of 400 Covid-19 survivors, documented increased mortality (HR 2.5) at 1 year.14 The additional risk was confined to individuals who had been hospitalized. In 2022, 3 studies reported excess mortality in 3 different countries. The first, an Estonian whole-population study of 66,000 Covid-19 survivors, of whom 8% were hospitalized, reported a 3-fold increase in mortality at 12 months.15 Mortality was particularly elevated in the first 5 weeks following infection. For those over age 60, increased mortality persisted until 12 months (HR 2.8). However, for those less than age 60, mortality was not increased after 35 days. The second, an analysis of 690,000 Covid-19 survivors from the TriNetX database also reported increased 1-year mortality risk (HR 1.6).6 This was largely explained by excess deaths in individuals over age 65; below age 45 risk was not increased. For the outpatient cohort the risk of mortality was lower than that of the comparison group (HR 0.46). The third, a study of 25,000 Covid-19 survivors drawn from the UK Biobank, reported increased mortality risk at 20 months, for those with severe Covid infection (HR 14.7), but also an increased risk for those with mild disease (HR 1.23).16 Stratification by age was not provided.

In 2023 4 further studies reported similar, but at times quantitatively different results. Two analyses drew on the UK Biobank cohort. In the first, a prospective evaluation of 7,800 SARS-CoV-2 PCR positive individuals, increased mortality was reported for the study group at 18 months (HR 5.0), when compared to both a contemporary and an historical cohort.17 For the non-severe cases the mortality risk remained elevated (HR 4.8). The second study, already described above– a comparative analysis of 7600 Covid survivors from the UK Biobank and 530,000 Covid survivors in Hong Kong–reported increased mortality (HR 4.16) after 17 months for the former and 28 months for the latter.7 The risk of mortality was higher in the UK than the HK cohort, a difference the authors posited was due to Omicron being the dominant variant in HK during the study period. The risk remained elevated, but less so, for younger cohorts and for mild Covid-19 infections.

Finally, 2 large US studies recently reported mortality at 2 years. In the first, an analysis of 138,000 US veteran Covid-19 survivors with 5.9 million controls, the risk of death for the hospitalized cohort remained elevated at 2 years (HR 1.29).8 In contrast, the risk of death for the outpatient cohort returned to baseline at 6 months. Breakdown of risk by age-group was not provided. The second study, also of US veterans, reported similar findings. In a cohort of 280,000 Covid-19 survivors the risk of death remained elevated at 2 years (HR 2.0).18 The risk was highest in the first 90 days (HR 6.3) and decreased at 6 months (HR 1.18). Thereafter, the risk in Covid-19 survivors was slightly less than the control group (HR 0.89). A post-hoc subgroup analysis examined and refuted the possibility that accelerated mortality in the control group could have explained the lower mortality in Covid-19 survivors. The risk of death in hospitalized individuals remained elevated at 2 years (HR 1.22).

How Plausible is this Information? The studies described above command attention by virtue of their size and the consistency of their findings in different populations, and in different countries. They are also supported by the observations of long-term pathophysiologic abnormalities following SARS-CoV-2 infection, such as ongoing inflammation, persistence of virus, and immune system dysfunction. However, the negative ledger is also substantial. Observational studies such as these, no matter how well-designed, remain open to many types of bias. Reliance on diagnostic codes, prescription records, laboratory results and tallies of clinical visits, to establish disease incidence, is intrinsically error-prone and makes cross-study comparisons difficult. Perhaps more importantly, the cohorts described above were different in many respects, varying from the older, male-predominant cohort of the US VA system to the younger healthier cohort of the UK Biobank. Further, cohorts were constituted during the first year of the pandemic, at a time when healthcare delivery was disrupted, lockdowns were in effect, vaccination and antivirals were largely unavailable, and population immunity levels were low. Thus, it could be argued that the observed outcomes are better explained by an evolving pandemic, rather than solely SARS-CoV-2 infection. This could also explain the most recent reports that after 2 years of follow-up, the risk of both Covid-19 complications and mortality, in most of those infected (i.e., the non-hospitalized), is no longer elevated. It also evident that most of the reported extra mortality is occurring in the early months following infection, where survival curves separate rapidly.6,10,15,18

Are these findings relevant to an insured population? ‘Partially’ is probably the best answer. The most important observation is that hospitalization, and in-particular an intensive care unit admission, is the dominant risk factor for both morbidity and mortality. This risk appears to persist up to 2 years. The second important risk element is the presence of comorbid conditions. This observation raises the interesting question of what exactly causes the extra mortality. Is it due to ‘protracted’ SARS-Co-V-2 infection or is it caused by a recognized complication of Covid-19, such as pulmonary fibrosis or acute kidney injury? Or is it explained by an aggravation of a comorbid illness? Or is it a complication of long Covid? There is a likelihood that all these mechanisms were at play in the cohorts under study.

For non-hospitalized individuals, and those that are healthy, the evidence for extra morbidity and mortality after the first 3-6 months is far from conclusive. For the long Covid cohort, the evidence for additional mortality requires further supporting evidence. As the prevalence of co-morbid conditions is lower in insured populations, one might reasonably expect, based on current evidence, that longer-term morbidity and mortality due to Covid-19 infection will be minimally affected.

References 1.Davis H, McCorkell L, Vogel, J. et al Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol 21, 133–146 (2023). doi.org/10.1038/s41579-022-00846-2

2.Meagher T. Long COVID - An Early Perspective. J Insur Med. 2021 Jan 1;49(1):19–23. doi: 10.17849/insm-49-1-1-5.1. PMID: 33784738.

3.Meagher T. Long COVID – One year On. J Insur Med. 2022 Jan 1;49:1–6. doi: 10.17849/insm-49-3-1-6.1. PMID: 33561352.

4.Meagher T. Long Covid - Into the Third Year. J Insur Med 2023;50(1):54–58. doi.org/10.17849/insm-50-1-54-58.1

5.Xie Y, Xu E, Bowe B et al Long-term cardiovascular outcomes of COVID-19. Nat Med 28, 583–590 (2022). doi.org/10.1038/s41591-022-01689-3

6.Wang W, Wang CY, Wang SI et al Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks. eClinicalMedicine. 2022 Nov;53:101619. doi: 10.1016/j.eclinm.2022.101619

7.Lam I, Wong C, Zhang, R et al Long-term post-acute sequelae of COVID-19 infection: a retrospective, multi-database cohort study in Hong Kong and the UK. eClinicalMedicine Vol. 60 Published: May 11, 2023. doi: doi.org/10.1016/j.eclinm.2023.102000

8.Raisi-Estabragh Z, Cooper J, Salih A, et al Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank Heart 2023;109:119–126.

9.Bowe, B., Xie, Y. & Al-Aly, Z. Postacute sequelae of COVID-19 at 2 years. Nat Med 29, 2347–2357 (2023). doi.org/10.1038/s41591-023-02521-2

10.DeVries A, Shambhu S, Sloop S et al One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database. JAMA Health Forum. 2023;4(3):e230010. doi:10.1001/jamahealthforum.2023.0010

11.Kim Y, Huh K, Park Y et al Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection. JAMA. 2022;328(9):887–889. doi:10.1001/jama.2022.12992

12.Jiang J, Chan L, Kauffman J, et al Impact of Vaccination on Major Adverse Cardiovascular Events in Patients With COVID-19 Infection. J Am Coll Cardiol. 2023 Mar, 81(9):928–930. doi.org/10.1016/j.jacc.2022.12.006

13.Bowe B, Xie, Y, Al-Aly Z. Acute and postacute sequelae associated with SARS-CoV-2 reinfection. Nat Med 28, 2398–2405 (2022). doi.org/10.1038/s41591-022-02051-3

14.Mainous AG, Rooks BJ, Wu, et al COVID-19 post-acute sequelae among adults: 12 month mortality risk. Front Med (Lausanne). 2021;8:778434. doi:10.3389/fmed.2021.778434

15.Uuskula A, Jurgenson T, Pisarev H et al Long-term mortality following SARS-CoV-2 infection: A national cohort study from Estonia. The Lancet Regional Health - Europe 2022;18:100394 Published online 29 April 2022. doi.org/10.1016/j.lanepe.2022.100394

16.Xiang Y, Zhang R, Qiu G. et al Association of Covid-19 with risks of hospitalization and mortality from other disorders post-infection: A study of the UK Biobank. medRxiv doi: doi.org/10.1101/2022.03.23.22272811

17.Wan E, Mathur S, Zhang R et al Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank, Cardiovascular Research, Volume 119, Issue 8, June 2023, 1718–1727. doi.org/10.1093/cvr/cvac195

18.Iwashyna TJ, Seelye S, Berkowitz TS, et al Late Mortality After COVID-19 Infection Among US Veterans vs Risk-Matched Comparators: A 2-Year Cohort Analysis. JAMA Intern Med. Published online August 21, 2023. doi:10.1001/jamainternmed.2023.3587

#mask up #covid #pandemic #covid 19 #wear a mask #public health #coronavirus #sars cov 2 #still coviding #wear a respirator

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mcatmemoranda · 29 days ago

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CDC recommends everyone ages 75 and older get an RSV vaccine.

CDC recommends adults ages 60–74 who are at increased risk of severe RSV disease get an RSV vaccine.

The RSV vaccine is not currently an annual vaccine. If you have received an RSV vaccine already (including last year), you should not get another RSV vaccine at this time.

You can get one at any time, but the best time to get vaccinated is in late summer and early fall.

Conditions that increase your risk for severe illness include:

Chronic heart or lung disease

Weakened immune system

Certain other medical conditions

Living in a nursing home

To protect infants and some young children, CDC recommends the maternal vaccine (Pfizer’s Abrysvo) for pregnant people during weeks 32–36 of pregnancy, or an RSV monoclonal antibody (nirsevimab) for babies given after birth and for some young children ages 8–19 months.

Adults who get RSV usually have mild or no symptoms. Symptoms are usually consistent with an upper respiratory tract infection, which can include rhinorrhea, pharyngitis, cough, headache, fatigue, and fever. Milder illness in adults typically resolves in 1–2 weeks. However, RSV can also cause severe disease and hospitalization in adults.

RSV can sometimes also lead to exacerbation of serious conditions such as:

Asthma

Chronic obstructive pulmonary disease (COPD)

Heart failure

Epidemiologic evidence indicates that all adults ages 75 or older and adults ages 60–74 with certain risk factors are at increased risk of severe RSV.

Conditions that increase the risk for severe RSV

The following conditions increase the risk of severe RSV:* 

Chronic cardiovascular disease (e.g., heart failure, coronary artery disease, or congenital heart disease [excluding isolated hypertension])

Chronic lung or respiratory disease (e.g., chronic obstructive pulmonary disease, emphysema, asthma, interstitial lung disease, or cystic fibrosis)

End-stage renal disease or dependence on hemodialysis or other renal replacement therapy

Diabetes mellitus complicated by chronic kidney disease, neuropathy, retinopathy, or other end-organ damage, or requiring treatment with insulin or sodium-glucose cotransporter-2 (SGLT2) inhibitor

Neurologic or neuromuscular conditions causing impaired airway clearance or respiratory muscle weakness (e.g., poststroke dysphagia, amyotrophic lateral sclerosis, or muscular dystrophy [excluding history of stroke without impaired airway clearance])

Chronic liver disease (e.g., cirrhosis)

Chronic hematologic conditions (e.g., sickle cell disease or thalassemia)

Severe obesity (body mass index ≥40 kg/m2)

Moderate or severe immune compromise��

Residence in a nursing home

Other chronic medical conditions or risk factors that a health care provider determines would increase the risk for severe disease due to viral respiratory infection (e.g., frailty,§ situations in which health care providers have concern for presence of undiagnosed chronic medical conditions, or residence in a remote or rural community where transportation of patients with severe RSV disease for escalation of medical care is challenging¶)

Source

#RSV

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diabetes-health-corner · 6 months ago

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Long term Complications of Diabetes Mellitus

Failure to control blood sugar will damage the body’s blood vessels, and this damage leads to complications of diabetes. These problems do not happen overnight, but their very insidious nature makes them all the more dangerous.

Read the full blog: https://www.freedomfromdiabetes.org/blog/post/long-term-complications-of-diabetes-mellitus/394

#Complications of Diabetes Mellitus #complications of diabetes #complications of diabetes mellitus #type2 diabetes complications #long term complications of diabetes #microvascular complication of diabetes #number one complication of diabetes #chronic complication of diabetes mellitus #what is complication of diabetes #short term complication of diabetes #most common complication of diabetes #the most complication of diabetes

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viasox · 8 months ago

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#carbohydrates #diabetic friendly #diabetes mellitus #health #diabetic neuropathy #diabetes complications #healthy diet #sugarcontrol #type 2 diabetes

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jcsmicasereports · 1 month ago

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Decreased erythrocyte glyoxalase 1 (GLO1) activity in patients with diabetes with reduced estimated glomerular filtration rate by Dr. Mohsen Kerkeni in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: The glyoxalase enzymes are located in the cytosol of all cells, including erythrocytes, and prevent advanced glycation end products (AGEs) production through the detoxification of the methylglyoxal (MGO). The present study was made to evaluate the GLO1 activity in diabetic patients and it relationship with estimated glomerular filtration rate (eGFR).

Patients and methods: GLO1 activity was measured spectrophotometrically in erythrocytes of 123 participants: 35 healthy subjects and 88 patients with diabetes. Biochemical parameters were measured and eGFR was calculated using the MDRD (Modification of Diet in Renal Disease) formula.

Results: We found no difference in GLO1 activity in patients with diabetes compared to healthy subjects. However GLO1 activity tended to be reduced in diabetic patients with loss renal function. A significant decrease was shown in patients with moderate to severe loss renal function. GLO1 activity was correlated with eGFR, creatinine and urea. Multivariate analysis showed that GLO1 activity was independently associated with eGFR.

Conclusion: GLO1 activity was related with loss renal function in patients with diabetes according glomerular filtration rate.

Keywords: glyoxalase 1, diabetes mellitus, glomerular filtration rate

Introduction

Diabetes is the most important disease in the wild words including type 1 diabetes, type 2 diabetes as known as diabetes mellitus (DM), and gestational diabetes [1-3]. DM is defined by chronic hyperglycemia and affected sugars metabolism caused by impaired insulin secretion [4]. Overweight and obesity are two risk factors or metabolic syndrome for developing DM. Indeed, obesity is characterized by excess body fat which is harmful to health, thus generating significant oxidative stress than chronic inflammation [5]. DM, as chronic hyperglycemia, promotes protein glycation and leads to the formation of advanced glycation end products (AGEs).

AGEs are formed by prolonged duration of hyperglycemia in diabetics and they have long-term toxicity in the body. Indeed, AGEs come from the attachment of sugar to a protein, an amino acid, or a lipid. These toxic products accumulate in all the organs leading to the activation of its RAGE receptors. A high number of publications have reported the AGEs involvement in the development of diabetes complications such as nephropathy, retinopathy, and atherosclerosis [6-8]. These products are not only present, but they also contribute to the severity of the pathology [9, 10]. The pathophysiological mechanisms of the increase in these products are still unidentified, but the formation of these products is done through the precursors of AGEs, also known as highly reactive dicarbonyl stress, the α-oxoaldehydes, such as the methylglyoxal (MGO) has a key role in detrimental effects on cellular function and has a key factor in vascular complications leading to oxidative stress. MGO is metabolized to lactate or acetol [11]. The MGO was detoxified by the glyoxalase system [12]. The glyoxalase system has two enzymes, glyoxalase 1 (EC 4.4.1.5, S-D-lactoylglutathione lyase; GLO1) and glyoxalase 2 (EC 3.1.2.6, D-hydroxyacylglutathione hydrolase; GLO2) [12]. Reduced glutathione is an essential cofactor. GLO1 catalyzes the conversion of the hemithioacetal to the thioester S-D-lactoylglutathione. The GLO2 enzyme catalyzes the hydrolysis of S-D-lactoylglutathione to form the lactate. Reduced glutathione is important for the detoxification of reactive dicarbonyls, especially methylglyoxal [13]. Therefore, we aimed to go deeper in the relation between renal function impairment and the MGO system in patients with type 2 diabetes. So, we measured the enzyme activity of glyoxalase 1 in patients with diabetes according their renal function using estimated glomerular filtration rate.

Materials and Methods

Study population

In a cross-sectional study, we recruited 123 participants (88 with type 2 diabetes) between 2019 and 2021 from CHU Taher Sfar in Mahdia-Tunisia. Data included age, weight, and height, history of diseases, smoking, and alcohol consumption. Patients were asked if they used any medication, and blood was taken. Plasma and erythrocytes cells were stored at -80°C. This study was approved by the ethics committee.

Assessments of biochemical parameters

All the analyzes of the biochemical parameters were carried out in the biochemistry department of the CHU Taher Sfar of Mahdia, These parameters were measured directly after collecting blood samples using enzymatic kits. Estimated glomerular filtration rate (eGFR) was calculated by the MDRD (Modification of Diet in Renal Disease) formula.

Measurement of GLO1 activity

GLO1 activity was measured according to Thornalley et al. [14]. Briefly, hemithioacetal was produced by incubation of MG (20mM) and GSH (20mM) for 30 minutes in an appropriate volume of sodium phosphate buffer (100mM, pH 6.6) at 37°C. The GLO1 activity was calculated and was expressed in Units/mL. One unit was defined as the amount of enzyme that catalyzes the formation of 1 µmol of S-D lactoylglutathione/min under the mentioned assay conditions.

Statistical analysis

Statistical analyzes are carried out by SPSS analysis software. Data were given as mean or median in the case of non-normally distributed data. Group comparisons were performed using the Student’s t-test or Mann-Whitney test, and the correlation coefficient was estimated using the Pearson or Spearman rank-order correlation analysis. Multivariate analysis was performed, and subgroups comparisons were performed by ANOVA test. A P-value < 0.05 was used.

Results

Clinical parameters and GLO1 activity between healthy and diabetic subjects

Clinical parameters and GLO1 activity are shown in Table 1. Patients with diabetes had duration of diabetes between 5 and 17 years and had a high body mass index (BMI) which indicates moderate obesity in most patients. Patients with diabetes showed 48% of hypertension, and 31% of hyperlipidemia. In addition, a significant decrease of renal function, including serum creatinine and eGFR, was shown in patients with diabetes. However, GLO1 activity did not differ between the healthy subjects and patients with diabetes.

Biochemical parameters and GLO1 activity according the loss of renal function

Clinical parameters and GLO1 activity in patients subgroups according eGFR were shown in Table 2 and Figure 1. Patients with diabetes were classified in four subgroup as normal, mild, mild to moderate, and, moderate to severe according eGFR. Duration of diabetes, glucose, and HbA1c did not differ between subgroups. As expected, eGFR was deceased from normal to severe subgroups (P < 0.001). For the GLO1 activity there was no difference between normal and mild group, however, a significant decrease was observed between mild to severe subgroups (P < 0.001).

Data are shown as the mean (SD) or median (range), or number (percentage). **Significantly decreased between each group; P < 0.001 * Significantly decreased between Mild to severe group; P < 0.001

Correlation of GLO1 activity with eGFR and other variables

The GLO1 activity was correlated to eGFR (r = 0.257; P = 0.015) as shown in Figure 2. GLO1 activity was also correlated with serum creatinine (r= -0.328, p=0.002) and urea (r = - 0.300, P = 0.020,). Multivariate analysis showed that GLO1 activity was independently associated with eGFR (b = 0.129, P = 0.038). However, GLO1 activity did not shown any correlation with glucose, HbA1c, cholesterol, and triglyceride.

Discussion

In this study, we examined the activity of GLO1 in patients with diabetes having normal to severe loss of renal function. According to our results, the GLO1 activity profile did not show a significant difference in healthy and patients. The GLO1 activity tended to be decreased with loss of renal function. We found a reduction of GLO1 activity in mild to severe loss of renal function, and was independently correlated to eGFR.

Most studies showed the role of AGEs and their interaction with their receptors, but there are a few studies about the relationships between glyoxalase system, as a antiglycation, and the loss of renal function. The first old study was done by Thornally et al. showed no significant difference in the glyoxalase enzymes between patients with dibetes and controls. However, Thornally et al. showed an increase of methylglyoxal and S-D-lactolglutathione in diabetic patients vs. controls [14]. Data concerning erythrocytes GLO1 activity in diabetes and diabetes complications are relatively scarce, and the results are controversial. Hamoudane et al. showed significantly lower GLO1 activity and glutathione levels in diabetic patients compared to controls. The levels of GLO1 activity were markedly lower in patients with diabetic complications, especially in diabetic patients with nephropathy [15]. In a study by Pacal et al. GLO1 activity was significantly increased in diabetic patients compared to controls, and was higher in nephropathy patients in stages 1-2, and remained decreased in nephropathy patients in stages 3-4 [16]. Our present study confirms the findings of Thornally et al. [14], Pacal et al. [16], Sakhi et al. [17], and Peters et al. [18]. Furthermore, Peters et al. found that GLO1 activity was lower in atherosclerotic carotid artery lesions, and the effects observed are related to the microenvironment of the damaged tissue [18]. We hypothesize that GLO1 activity may affects also the microenvironment location in glomerular and its vascular tissues under chronic hyperglycemia that induce much production of AGEs precursors such as MGO and may inhibits GLO1 enzyme activity. This AGE accumulation has been closely associated with kidney diseases, and aging. Accumulating evidence demonstrates that the progression of renal tubular damage and tubular aging are often correlated with activation of the receptor for the AGE (RAGE)-AGE pathway or decreased activity of glyoxalase 1 [19].

To our knowledge, this is the first study showing the relationships between erythrocytes GLO1 activity and the estimated glomerular filtration rate in patients with diabetes with normal, mild, moderate and severe loss of renal function. The GLO1 activity decreased markedly with patients when they have moderate to severe loss of renal function. The direct pathogenic role of MGO/glyoxalase system in the development of diabetic nephropathy is strongly supported by animal experiments. Overexpression of GLO1 in diabetic rats reduced the production of AGEs, endothelial dysfunction, and also expression of early markers of kidney damage [20]. Interestingly, knockdown of GLO1 in nondiabetic mice induces kidney pathology very similar to diabetic nephropathy [21]. The reduced levels in GLO1 activity may result also from the deceased of glutathione levels but the most biomarker that affects GLO1 activity was the tissues accumulation of α-oxoaldehydes, especially MGO that are formed during cellular metabolic reactions [14]. Recently, it was well described in a review by Schalkwijk and Stehouwer the involvement of the MGO in many diseases [22]. Lowering the MGO levels can provide new therapeutic to reduce AGEs precursors and their accumulation [23-26]. Recent interesting studies are focused on GLO1 inducers as a new therapy [27-29].

Our study has obvious limitations. We have not measured MGO or MGO-derived AGEs due to the lack of technologies in our laboratory. Furthermore, healthy subjects and patients with moderate to severe loss of renal function subgroup showed small size samples.

In conclusion, GLO1 activity in erythrocytes was independently correlated in patients with diabetes having a decreased estimated glomerular filtration rate.

Abbreviations

AGEs: Advanced glycation end products; BMI: Body mass index; DM: Diabetes Mellitus; GLO1: glyoxalase enzyme; HTA: Hypertension; MGO: methylglyoxal

Authors’ contributions

RS, HH, and AM: determined the GLO1 activity measurement, Clinical data, and wrote the manuscript. MK, SA, and AL contributed to the design and the concept of the study. HB measured the biochemical parameters. HZ: provided blood sampling. All authors read and approved the final manuscript.

Declarations

The protocol has been approved by the ethics committees at the CHU Hospital Tahar Sfar Mahdia. All participants signed the informed consent in writing before inclusion in the study.

Competing interests

The authors declare no conflict of interest.

#glyoxalase 1 #diabetes mellitus #glomerular filtration rate #JCRMHS #Clinical Images journal #Journal of Clinical Case Reports Medical Images and Health Sciences (JCRMHS)| ISSN: 2832-1286

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beyondthebloodsugar · 2 months ago

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Diabetes Insipidus and Your Hormones: What's the Connection?

Diabetes Insipidus (DI) might sound complex, but it’s all about how your body manages water. Did you know that hormones play a big role in this process? Let’s break it down.

What is Diabetes Insipidus?

Diabetes Insipidus is a condition that causes frequent urination and extreme thirst. It's not the same as diabetes mellitus, which affects blood sugar levels. With DI, the body can't properly balance fluids, often because of problems with a hormone called vasopressin.

The Role of Vasopressin

Vasopressin, also known as antidiuretic hormone (ADH), is produced in the brain. It signals the kidneys to retain water. If your body doesn’t produce enough of this hormone, you end up losing too much water through urine. Think of vasopressin as a water-saving superhero. Without it, your body feels like a leaky faucet.

Types of Diabetes Insipidus

There are two main types of Diabetes Insipidus:

Central Diabetes Insipidus: This happens when the brain doesn’t make enough vasopressin. It could be due to injury, surgery, or even a tumor.

Nephrogenic Diabetes Insipidus: In this case, the kidneys can’t respond to vasopressin, even if the brain produces it. This can be due to genetic factors or certain medications.

Both types lead to the same result: too much water loss and constant thirst.

Hormonal Connections: More Than Just Vasopressin

While vasopressin is a key player, other hormones also join the party. For example, the body’s balance of sodium and potassium can affect fluid retention and urination. An imbalance in these electrolytes can make symptoms worse.

Another hormone to consider is aldosterone. It helps regulate sodium and water retention in the body. If its levels are off, it can complicate the water balance, making DI harder to manage. These hormones work together in a well-choreographed dance, and if one is out of sync, your body feels it.

Symptoms and Impact on Life

So, how do you know if you have Diabetes Insipidus? Common symptoms include:

Frequent urination

Extreme thirst

Nocturia (waking up at night to urinate)

Dry skin

Living with DI can be challenging. Constantly needing to drink water or rushing to the bathroom can disrupt daily activities. It’s essential to understand these symptoms and their links to hormones to manage the condition better.

Diagnosis and Treatment

Getting diagnosed with DI involves a series of tests. Doctors often check hormone levels and may conduct a water deprivation test, which assesses your body’s ability to concentrate urine. Once diagnosed, treatment focuses on managing symptoms, often with medications that mimic vasopressin.

Conclusion: The Hormonal Balance

Diabetes Insipidus is more than just a thirst issue. It's about understanding the connection between your hormones and fluid balance. By grasping how vasopressin and other hormones work together, you can navigate the challenges that come with DI. Awareness of this connection can lead to better management and a more comfortable life. So, stay informed and empower yourself on this journey!

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