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Joe Rogans physique, particularly his midsection, garnered widespread attention during his Sober October weigh-in in 2019. Many observers pointed out his protruding midsection and speculated that it could be linked to his daily intake of human growth hormone. Recently, at the UFC 300 event, when Rogan was standing alongside Daniel Cormier, Megan Olivi, and Jon Anik, his posture and his bodys appearance, concerns were raised online again about the possible impact of HGH and TRT on Rogans physique.

Rogan too has been open about his usage of substances he began taking at 39 to aid recovery and maintain his musculature. However, though he has been in great shape for so many years, it could be due to his height being around 5-foot-6 that makes his belly noticeable. Palumboism or the bubble gut has caused eyebrows to be raised at Joe Rogans midsection.

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The term Palumboism describes the condition of a visibly bulging belly associated with HGH use, and was coined in reference to bodybuilder David Palumbo, who first brought the issue to light with his bubble gut. This condition especially occurs in bodybuilders when the muscles on the sides of the abdomen thicken and make it difficult to hold the stomach. According to a few studies, it was reported that this condition could occur because of insulin use, use of HGH, and high calorie/carb diet. Pregnant abs is another term used to describe this condition.

But what exactly are HGH and TRT? Human growth hormone is a small protein that is prepared in the pituitary gland. This hormone influences a persons height and helps build bones and muscles. To enhance their physique, bodybuilders consume this hormone in large doses along with other performance-enhancing drugs (PEDs) such as insulin and anabolic steroids. This causes a rare condition called the HGH gut. And, Testosterone Replacement Therapy, is the method used to treat low testosterone in the body.

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Synthetic forms of HGH have long been abused by athletes for muscle building and injury recovery due to their difficulty in getting detected by drug tests. However, attributing Rogans midsection solely to HGH use may be oversimplifying. Rogans commitment to transparency about his supplement use, along with his stocky physique and training regimen, suggests other factors at play. Without more information, its challenging to attribute his midsection solely to HGH.

In one of the episodes of JRE, in hisconversation with his guest, Andrew Schulz, comedian, Rogan explained that he takes HGH to maintain his vitality, increase muscle mass reduce fat, which was similar to his testosterone replacement therapy. So when HGH is consumed in excess, it could lead to irregular growth of all muscles in the midsection.

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Since the hormone contains high insulin levels, it can result in the storage of visceral fat behind the stomach, causing it to grow outwards. If the bodybuilder follows a high-carb diet, it will further contribute by storing glycogen in the blood and attracting water which will lead to a bloated appearance. This is another reason why bodybuilders with HGH gut cannot suck their gut in and perform stomach vacuums.

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Palumboism can affect both men and women who abuse PEDs. However, it is more common among men who consume higher dosages. Apart from Joe Rogan a few other bodybuilders who also were affected by this condition are, Phil Heath, Big Lenny, Kai Greene, and Ronnie Coleman.

Since this is not an untreatable illness or disease, there are reports that Palumboism can be prevented if the person avoids abuse of PEDs and HGH injections. They should instead focus on eating healthy and training regularly. However, without enough evidence, it is difficult to draw definitive conclusions about the cause of Rogans physique. Nevertheless, his commitment to fitness and martial arts remains unwavering and continues to inspire and captivate audiences worldwide.

Excerpt from:
What Is Wrong With Joe Rogan's Gut? Does UFC Commentator Have Palumboism Because of TRT and HGH? - EssentiallySports

Doha, Qatar: The Emergency Department at Hamad General Hospital has improved the average waiting time for patients to be seen by a doctor, according to a senior official.

Prof. Aftab Mohammad Umar, Chair of Emergency Medicine at Hamad Medical Corporation (HMC) speaking to The Peninsula yesterday, said efforts made to improve the level of care provided to patients at the Emergency Department have contributed to reducing the median waiting time for patients to be seen by a doctor to between 15 to 25 minutes from arrival.

The time is considered very good compared to emergency departments in the region, according to Prof. Aftab.

We have implemented new changes in operations and in the flow of patients, said Prof. Aftab, explaining about the reasons for the improvement in waiting time.

The Emergency Department at Hamad General Hospital treated more than 1,700 cases during the first three days of Eid Al Fitr holidays.

About 50% of the cases were with minor problems and the most common complaints were related to gastrointestinal system.

Prof. Aftab explained that HMC follows the Canadian Triage and Acuity Scale (CTAS) which allows prioritising patients based on their medical condition.

Critical cases receive immediate attention upon arrival at the Emergency Department, they have zero waiting time, he said.

Low priority cases will be seen by a doctor at an average of 15 to 20 minutes, said Prof. Aftab, adding that the waiting time is subject to change depending on the condition and number of patients visiting the Emergency Department at a given time.

According to Prof. Aftab, almost 50% of the cases at the Emergency Department present with conditions which are at low acuity. CTAS is considered the most predominantly accepted method for grouping patients according to the severity of their condition. Patient acuity refers to the severity of an illness or medical condition. It is often used to designate which patients should be seen first. A high-acuity patient is one who is severely ill and should receive care before others.

Prof. Aftab also noted that all emergency departments across HMC operate around the clock, seven days a week, with a medical team consisting of consultant physicians and specialists. They are scheduled according to patient volumes throughout the day.

We have medical teams ready around the clock to handle all cases, he said. The Ambulance Service, trauma and emergency departments across HMC hospitals and paediatric emergency centres provide care to patients with the most critical, life-threatening conditions.

Some 11 Urgent Care Units operated by the Primary Health Care Corporation (PHCC) provide urgent care services to patients with urgent but non-life-threatening conditions. Among the units, five offer services to adults and paediatrics. HMC and PHCC also operate Urgent Consultation Service helplines.

Here is the original post:
Patient waiting time at HGH Emergency Department improves significantly - The Peninsula

An article published recently in the prestigious journal Nature Medicine documents whats believed to be the first evidence that Alzheimers disease can be transmitted from person to person.

The finding arose from long-term follow-up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards including in Australia from the mid-60s.

The practice stopped in 1985 when it was discovered about 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

CJD is caused by prions infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep), and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Read more: People who lived in the UK in the 'mad cow disease' years may now be able to give blood. The risk of vCJD is tiny

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from about16,000 donated glands.

An average course of hGH treatment lasts about four years, so the chances of receiving contaminated material even for a very rare condition such as CJD became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

The Nature Medicine paper provides the first evidence that transmission of Alzheimers disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimers disease.

They considered other explanations for the findings, but concluded donated hGH was the likely cause.

Given Alzheimers disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimers disease.

Alzheimers disease is caused by presence of two abnormally folded proteins,amyloid and tau. Theres increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimers disease develops, theres likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

Read more: Size of brain area linked with cognitive decline even in people with no other warning signs of Alzheimers disease

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimers disease (defined as occurring before the age of 65) is uncommon, accounting for about 5% of all cases. Below the age of 50 its rare and likely to have a genetic contribution.

The Nature Medicine paper identified five cases that were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long incubation period of Alzheimers disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact its first to demonstrate that Alzheimers disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimers cannot be contracted via contact with, or providing care to, people with Alzheimers disease.

Read more: Young-onset Alzheimers can be diagnosed from as early as 30 and the symptoms are often different

This article originally appeared on The Conversation.

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Alzheimer's may have once spread from person to person, but the risk today is low - Monash Lens

Mike Trout is one of the biggest names in the world of MLB. The player has been known for his performance on the pitch and has mesmerized his fans with it. However, at one point, it was speculated that the Angels star was using human growth hormones (HGH).

However, following the fallout from the Houston Astros sign-steal scandal, the MLB commissioners office shot down this speculation about Trout and the players' association. But even though the league flunked off such speculations, some still believed he was guilty of using it. Legendary Yankee Scott Brosius' son, David Brosius, was one of them.

In January 2020, David, via his Instagram post, publicly accused the 11-time All-Star of using his medical condition as a loophole to take HGH. He also speculated that the league knew everything but looked the other way around because Trout was their 'best player.' His post read (via Bleacher Report):

However, this didn't go so well for the Brosius. He faced much backlash and criticism for his wild accusations towards the 9-time Silver Slugger winner. The next day, he deleted the post and apologized for what he said about the player.

Mike Trout has flunked off possibilities of leaving Angles in a trade move. The 32-year-old has been his team's biggest star ever since joining in 2011.

According to reports, Trout dismissed any idea of him leaving the Angels clubhouse soon. He has made it clear that he has no current intentions to make a trade move until the end of his contract. However, he has kept doors open for every option. Talking about his future at the club, the star said:

With the new season starting in a few more days and the Spring Training ongoing, Trout will look forward to starting on a good note and helping his team reach success and win the championship he desperately longs for.

Original post:
Mike Trout takes HGH for a 'thyroid' condition" - When 11x All-Star outfielder was wildly accused by ex-Yankees ... - Sportskeeda

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimers disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Read more: People who lived in the UK in the 'mad cow disease' years may now be able to give blood. The risk of vCJD is tiny

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material even for a very rare condition such as CJD became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

The Nature Medicine paper provides the first evidence that transmission of Alzheimers disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimers disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimers disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimers disease.

Alzheimers disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimers disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

Read more: Size of brain area linked with cognitive decline even in people with no other warning signs of Alzheimers disease

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimers disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 its rare and likely to have a genetic contribution.

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long incubation period of Alzheimers disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact its first to demonstrate that Alzheimers disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimers cannot be contracted via contact with or providing care to people with Alzheimers disease.

Read more: Young-onset Alzheimers can be diagnosed from as early as 30 and the symptoms are often different

See the original post:
Alzheimer's may have once spread from person to person, but the risk of that happening today is incredibly low - The Conversation

Summary: Researchers report a link between Alzheimers disease and a discontinued medical treatment.

In a new study, they found five cases of Alzheimers in individuals treated as children with cadaver-derived human growth hormone (c-hGH), used in the UK from 1959 to 1985. The treatment, later found to be contaminated with amyloid-beta protein, had been linked to Creutzfeldt-Jakob disease (CJD) and was replaced by synthetic hormones.

This discovery suggests a new dimension in understanding Alzheimers, highlighting the potential for disease-related proteins to be transmitted through medical treatments.

Key Facts:

Source: UCL

Five cases of Alzheimers disease are believed to have arisen as a result of medical treatments decades earlier, reports a team of UCL and UCLH researchers.

Alzheimers disease is caused by the amyloid-beta protein, and is usually a sporadic condition of late adult life, or more rarely an inherited condition that occurs due to a faulty gene.

The newNature Medicinepaper provides the first evidence of Alzheimers disease in living people that appears to have been medically acquired and due to transmission of the amyloid-beta protein.

The people described in the paper had all been treated as children with a type of human growth hormone extracted from pituitary glands from deceased individuals (cadaver-derived human growth hormone or c-hGH).

This was used to treat at least 1,848 people in the UK between 1959 and 1985, and used for various causes of short stature. It was withdrawn in 1985 after it was recognised that some c-hGH batches were contaminated with prions (infectious proteins) which had caused Creutzfeldt-Jakob disease (CJD) in some people. c-hGH was then replaced with synthetic growth hormone that did not carry the risk of transmitting CJD.

These researchers previously reported that some patients with CJD due to c-hGH treatment (called iatrogenic CJD) also had prematurely developed deposits of the amyloid-beta protein in their brains.

The scientists went on to show in a 2018 paper that archived samples of c-hGH were contaminated with amyloid-beta protein and, despite having been stored for decades, transmitted amyloid-beta pathology to laboratory mice when it was injected. They suggested that individuals exposed to contaminated c-hGH, who did not succumb to CJD and lived longer, might eventually develop Alzheimers disease.

This latest paper reports on eight people referred to UCLHs National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London, who had all been treated with c-hGH in childhood, often over several years.

Five of these people had symptoms of dementia, and either had already been diagnosed with Alzheimers disease or would otherwise meet the diagnostic criteria for this condition; another person met criteria for mild cognitive impairment.

These people were between 38 and 55 years old when they started having neurological symptoms. Biomarker analyses supported the diagnoses of Alzheimers disease in two patients with the diagnosis, and was suggestive of Alzheimers in one other person; an autopsy analysis showed Alzheimers pathology in another patient.

The unusually young age at which these patients developed symptoms suggests they did not have the usual sporadic Alzheimers which is associated with old age. In the five patients in whom samples were available for genetic testing, the team ruled out inherited Alzheimers disease.

As c-hGH treatment is no longer used, there is no risk of any new transmission via this route. There have been no reported cases of Alzheimers acquired from any other medical or surgical procedures. There is no suggestion that amyloid-beta can be passed on in day-to-day life or during routine medical or social care.

However, the researchers caution that their findings highlight the importance of reviewing measures to ensure there is no risk of accidental transmission of amyloid-beta via other medical or surgical procedures which have been implicated in accidental transmission of CJD.

The lead author of the research, Professor John Collinge, Director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, said: There is no suggestion whatsoever that Alzheimers disease can be transmitted between individuals during activities of daily life or routine medical care.

The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.

However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.

Importantly, our findings also suggest that Alzheimers and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimers disease in the future.

Co-author Professor Jonathan Schott (UCL Queen Square Institute of Neurology, honorary consultant neurologist at UCLH, and Chief Medical Officer at Alzheimers Research UK) said: It is important to stress that the circumstances through which we believe these individuals tragically developed Alzheimers are highly unusual, and to reinforce that there is no risk that the disease can be spread between individuals or in routine medical care.

These findings do, however, provide potentially valuable insights into disease mechanisms, and pave the way for further research which we hope will further our understanding of the causes of more typical, late onset Alzheimers disease.

First author Dr Gargi Banerjee (UCL Institute of Prion Diseases) said: We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimers disease.

This transmission occurred following treatment with a now obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years. There is no indication that Alzheimers disease can be acquired from close contact, or during the provision of routine care.

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR UCLH Biomedical Research Centre, Alzheimers Research UK, and the Stroke Association.

Note:

If you were treated with the growth hormone (c-hGH) in the UK between 1959 and 1985 and would like further information about this research, please contact the National Prion Clinic via email ([emailprotected]) or by telephone (020 7679 5142 or 020 7679 5036).

Author: Chris Lane Source: UCL Contact: Chris Lane UCL Image: The image is credited to Neuroscience News

Original Research: Closed access. Iatrogenic Alzheimers disease in recipients of cadaveric pituitary-derived growth hormone by John Collinge et al. Nature Medicine

Abstract

Iatrogenic Alzheimers disease in recipients of cadaveric pituitary-derived growth hormone

Alzheimers disease (AD) is characterized pathologically by amyloid-beta (A) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau.

Compelling genetic and biomarker evidence supports A as the root cause of AD. We previously reported human transmission of A pathology and CAA in relatively young adults who had died of iatrogenic CreutzfeldtJakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and A seeds. This raised the possibility that c-hGH recipients who did not die from iCJD may eventually develop AD.

Here we describe recipients who developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms.

Although iatrogenic AD may be rare, and there is no suggestion that A can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures.

As propagating A assemblies may exhibit structural diversity akin to conventional prions, it is possible that therapeutic strategies targeting disease-related assemblies may lead to selection of minor components and development of resistance.

Read more:
Discontinued Medical Treatment Linked to Alzheimer's - Neuroscience News

Uncovering the Link Between Alzheimers and Human Growth Hormone Treatments

A ground-breaking study published in Nature Medicine has shed light on a startling revelation Alzheimers disease may be transmissible under very specific circumstances. This inference was drawn from the long-term observation of patients who had received human growth hormone (hGH) from deceased donors, a practice that ceased in 1985. The particularly interesting aspect of this study is the conceivable connection between Alzheimers disease and prion diseases, which are known to be transmissible.

The discontinued medical practice involved extracting growth hormone from the brain tissue of deceased individuals. This hormone was then administered to patients, typically children, who required it. However, after approximately 200 patients developed Creuztfeldt-Jakob disease (CJD) a condition caused by prions the practice was halted.

Prions, proteins that can fold in multiple structurally distinct ways, can trigger the development of a range of fatal neurodegenerative diseases, including CJD. The study identified five patients with early-onset Alzheimers disease who had received the donated hGH, leading the researchers to conclude that the hGH was the likely cause of the disease in these cases.

While Alzheimers disease is commonly understood as a non-contagious condition, this study indicates that it can be transmitted under extremely rare conditions. In the reported cases, the recipients of the tainted hGH injections developed early Alzheimers disease, showing higher than usual levels of the sticky protein A-beta in their brains. This protein is known to accumulate in the brains of individuals with Alzheimers disease.

It is important to note, however, that the absolute risk of transmission remains very low. The transmission of Alzheimers disease cannot occur through person-to-person contact, but the study does raise concerns about potential risks of transmission through certain medical or surgical procedures.

Despite the small sample size and the need for replication and confirmation, this study opens new avenues for understanding the etiology of Alzheimers disease. The findings suggest that amyloid-beta pathologys transmission in these rare situations may have implications for understanding and treating Alzheimers disease.

The research also underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources. It also paves the way for further research, which may enrich our understanding of the causes of more typical, late-onset Alzheimers disease.

While these findings are undoubtedly intriguing, it is essential to emphasize that the circumstances through which these individuals tragically developed Alzheimers are highly unusual. There is no risk that the disease can be spread between individuals or in routine medical care. Experts have stressed that this does not indicate that Alzheimers disease can be passed between people through everyday activities or routine care, and there is no cause for concern for the health of the general population.

Patients now receive synthetic alternatives to hGH, which have been approved for safety. Therefore, there is no need for the general population to reconsider or forego any medical procedures based on these findings. The study provides an interesting perspective on the transmission of Alzheimers disease but should not cause undue alarm.

Continued here:
Link Between Alzheimer's and Human Growth Hormone Treatments Revealed | Nature Medicine Study - Medriva

Image by Getty / Futurism

Researchers say they've documented the first ever cases of Alzheimer's disease being transmitted between humans and though it only took place in extremely rare and unusual circumstances, it could provide valuable clues into the underlying mechanisms of the terrible disease.

Their findings, published as a study in the journal Nature Medicine, detail how eight adult patients, only five of whom are still alive, likely acquired the disease through a banned medical procedure performed on them as children in which they were administered human growth hormone extracted from a cadaver's brain. Decades later, they're now showing early signs of dementia, with the earliest experiencing symptoms as young as 38 years old.

The researchers suggest that the procedure inadvertently transmitted a protein called amyloid beta that's considered to have a central role in the development of Alzheimer's disease.

They stress that this does not mean Alzheimer's is transmissible like a cough or the flu. It was spread "iatrogenically" StatNews notes, or only as the result of a medical practice in this case a very seldom used but tragically misguided one.

"I should emphasize these are very rare occurrences, and the majority of this relates to medical procedures that are no longer used," study senior author John Collinge, the director of the University College London Institute of Prion Diseases, said in a news brief, as quoted by CNN.

The practice of using cadaver growth hormones today they're synthesized was banned in the 1980s because it caused another terrifying brain disorder: Creutzfeldt-Jakob disease (CJD), which is transmitted through "misfolded" proteins called prions.

CJD, like Alzheimer's, causes dementia but is even more severe and always fatal. Since both can stem from the same medical procedure, the researchers say their findings support the idea that the beta-amyloids behind Alzheimer's can be transmitted in similar ways to a prion disease, which have been long known to pass between humans.

"It looks like what's going on in Alzheimer's disease is very similar in many respects to what happens in the human prion diseases like CJD, with the propagation of these abnormal aggregates of misfolded proteins and misshapen proteins," Collinge told Stat News.

A key detail is that none of the patients were shown to have genetic mutations known to cause early-onset dementia, despite all of them experiencing symptoms at a relatively young age and well before the cutoff age of 65.

Only one patient had genetic data known to cause late-onset dementia. In addition, none were found to have elevated levels of a protein called tau, Stat notes, which is associated with cognitive decline. As it stands, the only known common factor between the patients is the HGH procedure they received.

The sheer rarity of the circumstances means that it will be tough to bear out the study's findings. Nonetheless, it's already raised useful questions over the nature of Alzheimer's, the exact cause of which remains elusive.

More on neuroscience: Smoking Cigarettes Does Something Horrifying to Your Brain, Scientists Find

Excerpt from:
Alzheimer's Spread Through Growth Hormones Extracted From Cadavers, Scientists Say - Futurism

Sections of mouse brains from the 2018 study. Top line shows control subjects inoculated with synthetic growth hormone, lower two lines show subjects inoculated with c-hGH. E and h show CAA while f and i show amyloid beta plaque deposition. Credit: Purro et al, 2018/UCL

Five middle-aged people have been diagnosed with Alzheimers disease as a result a now-discontinued medical treatment the patients received in childhood, according to a new study. This is the first evidence of Alzheimers disease in living people that appears to have been medically acquired.

Alzheimers disease is typically caused by a buildup of amyloid-beta protein as an individual ages. However, these patients appear to have acquired the disease in middle age due to transmission of the amyloid-beta protein as part of medical treatment decades prior.

The patients described in the new Nature Medicine paper, now between 38 and 55 years old, had all been treated as children with a type of human growth hormone extracted from pituitary glands from deceased individualsknown as cadaver-derived human growth hormone, or c-hGH.

c-hGH was used to treat at least 1,848 people in the UK between 1959 and 1985 for various causes of short stature. It was withdrawn in 1985 after scientists recognized that some c-hGH batches were contaminated with prions (infectious proteins) after some patients contracted Creutzfeldt-Jakob disease (CJD).

This latest paper focuses on eight people at the National Hospital for Neurology and Neurosurgery in London who had all been treated with c-hGH in childhood, often over several years. Five of them had symptoms of dementia, and either had already been diagnosed with Alzheimers disease or would otherwise meet the diagnostic criteria. A sixth person met the criteria for mild cognitive impairment.

All patients were between 38 and 55 years old when they started displaying neurological symptoms. The unusually young age at which the symptoms developed suggests the patients did not have the typical Alzheimers, which is associated with old age. Additionally, for five patients in which samples were available for genetic testing, researchers were able to rule out inherited Alzheimers disease.

As c-hGH treatment is no longer used, there is no risk of any new transmission via this route. There have been no reported cases of Alzheimers acquired from any other medical or surgical procedures.

There is no suggestion whatsoever that Alzheimers disease can be transmitted between individuals during activities of daily life or routine medical care. The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins, said lead author John Collinge, director of the University College London Institute of Prion Diseases and a consultant neurologist at University College London Hospital.

However, the researchers caution that their findings highlight the importance of reviewing measures to ensure there is no risk of accidental transmission of amyloid-beta via other medical or surgical procedures.

In 2018, the same team of researchers showed that archived samples of c-hGH were contaminated with amyloid-beta protein anddespite having been stored for decadesstill transmitted amyloid-beta pathology to laboratory mice when injected. The scientists proposed then that individuals exposed to contaminated c-hGH who did not succumb to CJD in the immediate aftermath might eventually develop Alzheimers disease.

These newest results suggest the researchers 2018 hypothesis was correct.

Overall, the results could have implications for understanding and treating Alzheimers disease in the future, as well as other neurological conditions share similar disease processes to CJD.

Go here to see the original:
Alzheimer's Linked to Discontinued Medical Treatment in UK - Laboratory Equipment

Some recipients of human growth hormone showed signs of Alzheimers disease on their brain scans

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Five people appear to have developed Alzheimers disease after receiving growth hormones from deceased donors brains as children. Although based on a small group of people, this suggests that the condition could theoretically be transmitted during medical procedures. However, measures are in place to prevent this. One expert has also pointed out that this study doesnt definitively prove that these recipients developed Alzheimers in this way.

From the late 1950s until 1985, children around the world with growth issues received injections of human growth hormone, derived from the pituitary gland in the brains of donor cadavers. In the UK, more than 1800 children received this treatment, while around 7700 children did so in the US.

The approach was banned globally when it came to light that some recipients died from a rare condition called Creutzfeldt-Jakob disease after receiving hormones contaminated with misfolded proteins called prions. These cause progressive and irreparable damage to the brain and nervous system by clumping together and making other proteins misfold.

Now, Gargi Banerjee at University College London and her colleagues have uncovered a handful of other people who may have developed Alzheimers disease from these treatments. Similar to prion-related conditions, a key characteristic of Alzheimers is the abnormal build-up of two misfolded proteins in the brain: amyloid-beta and tau.

As part of the UKs National Prion Monitoring Cohort, the team reviewed eight cases where people received batches of donated human growth hormones as children that were later discovered to contain traces of misfolded amyloid-beta.

Of these eight, seven reported cognitive issues in their 40s and 50s. Three of them were diagnosed with Alzheimers disease, while two met the diagnostic criteria for the condition after reporting symptoms such as memory loss and difficulty concentrating. Another two experienced cognitive impairment, while the eighth person had no symptoms, but showed signs of Alzheimers in brain scans. Of the group, six survive.

All the recipients bar one, who only self-reported having cognitive impairment, had elevated levels of misfolded amyloid-beta and tau in their brains.

In another part of their study, the researchers analysed the DNA of five of the recipients, the only ones with samples available, and found that none had a heightened genetic risk of any neurodegenerative condition, suggesting that their symptoms werent inherited.

Writing in their paper, the researchers say there could be alternative explanations for the findings. For example, two of the individuals had an intellectual disability, which has been linked to a heightened risk of dementia, and the recipients initial growth issues may have led to cognitive impairments. But based on the fact that few people have developed early-onset Alzheimers disease after receiving uncontaminated growth hormones, the team concludes that contaminated injections are the most plausible cause.

Its important to recognise that this very rare, acquired form of Alzheimers disease exists, so that people treated with cadaveric growth hormone can get help and support should they need it, says Banerjee. There is no suggestion that Alzheimers disease can be transmitted between people during close contact, or by caring for people with Alzheimers disease, or via routine medical care.

The researchers write that the results should prompt both further consideration of public health implications and the primary prevention of [transmissible] Alzheimers disease for example, by ensuring effective decontamination of surgical instruments, which is already routinely done.

They are now working with the UK Health Security Agency and the Department of Health and Social Care to determine how many people who received these hormone injections may be at risk.

Lawrence Honig at Columbia University in New York says that the study doesnt prove that Alzheimers was due to these injections. There were apparently about 2000 persons who received these HGH [human growth hormone] preparations in the UK, and Alzheimers disease biomarker and pathological changes in the 50s are not extraordinarily uncommon, so an association, or causative association, from the injections cannot be certain, he says.

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Contaminated hormone injections may have given five people Alzheimer's - New Scientist

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