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Several fruits and berries are considered superfoods for their physical and mental health benefits such as improved heart health, boosted brain function, lowered symptoms of depression and anti-inflammatory impacts.

On average, people who eat more berries seem to live a little bit longer, Eric Rimm, professor of epidemiology and nutrition at Harvard T.H. Chan School of Public Health, told The Washington Post. Rimm suggests incorporating fruits and berries to a healthy diet every day to reap benefits.

Here are five superfood fruits and berries with mental and physical health benefits.

Blueberries boast benefit for both mental and physical health. Research shows eating blueberries can improve brain function, lower symptoms of depression and aid in maintaining a healthy heart.

Much of the power of blueberries lies in their colors. The deep-blue hue comes from anthocyanin, a phytochemical whose abilities may help protect the body from heart disease and Type 2 diabetes, offering cancer-fighting benefits, promote gut health and reduce inflammation, reports the Mayo Clinic.

A one-cup serving of blueberries contains 25% of the recommended daily value for vitamin C and 4 grams of dietary fiber, but only 80 calories.

Adding just a handful of blueberries to your daily diet could improve brain function, found a study from Kings College London. Researchers asked participants to consume wild blueberry powder for a duration of 12 weeks. Individuals who consumed the blueberry powder experienced improved memory and increased accuracy on attention tasks.

Regularly eating blueberries can also help relieve anxiety and ease feelings of depression because they are rich in antioxidants, per WebMD. A study from the British Journal of Nutrition found that adolescents who took daily wild blueberry supplements reported lower symptoms of depression.

Despite common misconceptions, avocados are actually single-seeded berries, per Healthline. They are an excellent source of healthy fat, fiber, potassium, magnesium and vitamins B, C, E and K.

Avocados contain several nutrients including carotenoids, monounsaturated fats, potassium, and fiber that have been associated with a reduced risk of chronic diseases, especially when included as part of a balanced nutritious diet, per Harvard Health.

Frequently eating avocados is heart-healthy, according to a 30-year study published in the Journal of the American Heart Association. Researchers found that those who regularly ate avocados experienced a significantly reduced risk of developing cardiovascular disease compared to individuals who rarely ate avocados.

The study also noted that individuals who ate avocados at least twice per week experienced a 21% lower risk of coronary heart disease, compared to those who rarely or never eat avocados.

Professional athletes report drinking tart cherry juice to aid in reduced inflammation and muscle pain, per The Washington Post. Studies show that tart cherries and tart cherry juice have a similar impact to anti-inflammatory drugs.

The anti-inflammatory and antioxidant properties of cherries work like nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen for reducing or preventing pain, registered dietitian Carly Sedlacek told Cleveland Clinic.

A study from the Journal of the International Society of Sports Nutrition found that runners who consumed cherry juice throughout the week before a race experienced significantly less muscle pain.

Tart and sweet cherries may also improve sleep. A review from the journal Nutrients found that cherries high levels of melatonin, serotonin and tryptophan aided in increasing quality and quantity of sleep.

Acai is a nutrient-dense berry loaded with antioxidants. Research shows these unique berries improve cholesterol, protect cognitive function, reduce cancer risk and support liver health.

Acai berries are one of the richest natural sources of anthocyanins, the antioxidant that give the berries their deep purple color.

Anthocyanins (provide) anti-inflammatory effects in the body, (and) may help reduce the risk of chronic diseases such as heart disease, diabetes, and cancer, registered dietitian Kristen Nicolai told Everyday Health. They also protect against free radical damage known as oxidative stress, which can lead to chronic and acute conditions.

Eating acai berries could protect the brain as it ages. One animal study reported that acai might help improve memory while aging. Another study, published in the journal Molecular Neurobiology, found that acai berries might have an anti-inflammatory, neuroprotective impact on Parkinsons disease. Researchers found that acai supplements were able to mitigate Parkinsons disease through reducing the loss of dopamine.

Oranges, grapefruits, lemons, limes, clementines and pomelos are all citrus fruits. These zesty fruits offer a great source of fiber, may protect against cancer, boost heart health, improve cognitive function in older adults and aid in maintaining a healthy heart.

Citrus fruits are also one of the best dietary sources of vitamin C.

Citrus fruits, including oranges, lemons, limes, grapefruits and clementines, are an excellent source of vitamin C. And vitamin C supports your immune system, which plays a role in maintaining healthy skin, bones and blood vessels, reports the Mayo Clinic. Citrus fruits contain soluble and insoluble fiber, both of which provide great benefits.

A study from the American Journal of Lifestyle Medicine linked the consumption of vitamin C found in citrus fruits with decreased duration and severity of the common cold. Researchers found that those who took vitamin C supplements while suffering from a common cold experienced shortened illness by 8% in adults and 14% in children.

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Superfood fruits and berries with mental and physical health benefits to add to your diet - Deseret News

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Summary: A new pilot study presents a compelling case for the ketogenic diet as a dual-action treatment for individuals with serious mental illnesses like schizophrenia and bipolar disorder, who often suffer metabolic side effects from their medication. The research shows how adopting a ketogenic diet not only mitigates these metabolic issues but also significantly improves psychiatric conditions.

Participants adhering to a high-fat, low-carbohydrate diet experienced weight loss, reversed metabolic syndrome, and saw a 31% improvement in psychiatric assessments. This innovative approach underscores the potential of dietary interventions in enhancing both physical and mental health, offering hope for a more holistic treatment strategy.

Key Facts:

Source: Stanford

For people living with serious mental illness like schizophrenia or bipolar disorder, standard treatment with antipsychotic medications can be a double-edged sword. While these drugs help regulate brain chemistry, they often cause metabolic side effects such as insulin resistance and obesity, which are distressing enough that many patients stop taking the medications.

Now, a pilot study led by Stanford Medicine researchers has found that a ketogenic diet not only restores metabolic health in these patients as they continue their medications, but it further improves their psychiatric conditions.

The results,publishedMarch 27 inPsychiatry Research, suggest that a dietary intervention can be a powerful aid in treating mental illness.

Its very promising and very encouraging that you can take back control of your illness in some way, aside from the usual standard of care, saidShebani Sethi, MD, associate professor of psychiatry and behavioral sciences and the first author of the new paper.

The senior author of the paper is Laura Saslow, PhD, associate professor of health behavior and biological sciences at the University of Michigan.

Making the connection

Sethi, who is board certified in obesity and psychiatry, remembers when she first noticed the connection. As a medical student working in an obesity clinic, she saw a patient with treatment-resistant schizophrenia whose auditory hallucinations quieted on a ketogenic diet.

That prompted her to dig into the medical literature. There were only a few, decades-old case reports on using the ketogenic diet to treat schizophrenia, but there was a long track record of success in using ketogenic diets to treat epileptic seizures.

The ketogenic diet has been proven to be effective for treatment-resistant epileptic seizures by reducing the excitability of neurons in the brain, Sethi said. We thought it would be worth exploring this treatment in psychiatric conditions.

A few years later, Sethi coined the term metabolic psychiatry, a new field that approaches mental health from an energy conversion perspective.

Meat and vegetables

In the four-month pilot trial, Sethis team followed 21 adult participants who were diagnosed with schizophrenia or bipolar disorder, taking antipsychotic medications, and had a metabolic abnormality such as weight gain, insulin resistance, hypertriglyceridemia, dyslipidemia or impaired glucose tolerance.

The participants were instructed to follow a ketogenic diet, with approximately 10% of the calories from carbohydrates, 30% from protein and 60% from fat. They were not told to count calories.

The focus of eating is on whole non-processed foods including protein and non-starchy vegetables, and not restricting fats, said Sethi, who shared keto-friendly meal ideas with the participants. They were also given keto cookbooks and access to a health coach.

The research team tracked how well the participants followed the diet through weekly measures of blood ketone levels. (Ketones are acids produced when the body breaks down fat instead of glucose for energy.)

By the end of the trial, 14 patients had been fully adherent, six were semi-adherent and only one was non-adherent.

Feeling better

The participants underwent a variety of psychiatric and metabolic assessments throughout the trial.

Before the trial, 29% of the participants met the criteria for metabolic syndrome, defined as having at least three of five conditions: abdominal obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure and elevated fasting glucose levels. After four months on a ketogenic diet, none of the participants had metabolic syndrome.

On average, the participants lost 10% of their body weight; reduced their waist circumference by 11% percent; and had lower blood pressure, body mass index, triglycerides, blood sugar levels and insulin resistance.

Were seeing huge changes, Sethi said. Even if youre on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, the insulin resistance. I think thats very encouraging for patients.

The psychiatric benefits were also striking. On average, the participants improved 31% on a psychiatrist rating of mental illness known as the clinical global impressions scale, with three-quarters of the group showing clinically meaningful improvement. Overall, the participants also reported better sleep and greater life satisfaction.

The participants reported improvements in their energy, sleep, mood and quality of life, Sethi said. They feel healthier and more hopeful.

The researchers were impressed that most of the participants stuck with the diet. We saw more benefit with the adherent group compared with the semi-adherent group, indicating a potential dose-response relationship, Sethi said.

Alternative fuel for the brain

There is increasing evidence that psychiatric diseases such as schizophrenia and bipolar disorder stem from metabolic deficits in the brain, which affect the excitability of neurons, Sethi said.

The researchers hypothesize that just as a ketogenic diet improves the rest of the bodys metabolism, it also improves the brains metabolism.

Anything that improves metabolic health in general is probably going to improve brain health anyway, Sethi said. But the ketogenic diet can provide ketones as an alternative fuel to glucose for a brain with energy dysfunction.

Likely there are multiple mechanisms at work, she added, and the main purpose of the small pilot trial is to help researchers detect signals that will guide the design of larger, more robust studies.

As a physician, Sethi cares for many patients with both serious mental illness and obesity or metabolic syndrome, but few studies have focused on this undertreated population.

She is founder and director of themetabolic psychiatry clinicat Stanford Medicine

Many of my patients suffer from both illnesses, so my desire was to see if metabolic interventions could help them, she said. They are seeking more help. They are looking to just feel better.

Researchers from the University of Michigan; the University of California, San Francisco; and Duke University contributed to the study.

Funding: The study was supported by Baszucki Group Research Fund, Keun Lau Fund and the Obesity Treatment Foundation.

Author: Nina Bai Source: Stanford Contact: Nina Bai Stanford Image: The image is credited to Neuroscience News

Original Research: Open access. Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial by Shebani Sethi et al. Psychiatric Research

Abstract

Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial

The ketogenic diet (KD, also known as metabolic therapy) has been successful in the treatment of obesity, type 2 diabetes, and epilepsy. More recently, this treatment has shown promise in the treatment of psychiatric illness.

We conducted a 4month pilot study to investigate the effects of a KD on individuals with schizophrenia or bipolar disorder with existing metabolic abnormalities. Twentythree participants were enrolled in a singlearm trial.

Results showcased improvements in metabolic health, with no participants meeting metabolic syndrome criteria by study conclusion. Adherent individuals experienced significant reduction in weight (12 %), BMI (12 %), waist circumference (13 %), and visceral adipose tissue (36 %).

Observed biomarker enhancements in this population include a 27 % decrease in HOMAIR, and a 25 % drop in triglyceride levels. In psychiatric measurements, participants with schizophrenia showed a 32 % reduction in Brief Psychiatric Rating Scale scores.

Overall Clinical Global Impression (CGI) severity improved by an average of 31 %, and the proportion of participants that started with elevated symptomatology improved at least 1point on CGI (79 %). Psychiatric outcomes across the cohort encompassed increased life satisfaction (17 %) and enhanced sleep quality (19 %).

This pilot trial underscores the potential advantages of adjunctive ketogenic dietary treatment in individuals grappling with serious mental illness.

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Keto Diet May Improve Mental Health Symptoms - Neuroscience News

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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

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Mark C. Markowski, MD, PhD

In this interview, Mark C. Markowski, MD, PhD, discusses bipolar androgen therapy (BAT), including its advantages and disadvantages, trials that have evaluated the treatment, and what some next steps may include. Markowski is an associate professor of oncology at Johns Hopkins University in Baltimore, Maryland.

We've been doing a lot of work at Johns Hopkins using high-dose testosterone therapies to treat patients with metastatic prostate cancer. It's probably been going on for more than a decade, at least with preclinical studies, and eventually moving into clinical trials. When you treat a patient with metastatic prostate cancer, the backbone of therapy is hormone suppression. We're lowering testosterone levels, trying to get them as low as possible, because testosterone fuels the cancer to grow. When we remove it from the equation, PSA levels go down and that tumor starts to shrink. As a result, patients can live a long time and do very well. But there are also can be a lot of toxicities associated with hormone-based therapies, and so trying to develop non-castrating therapies has been a goal of ours. As I said, when we lower testosterone levels in a patient with metastatic prostate cancer, the cancer will initially respond, but inevitably will become resistantthis is called castration resistance. At the end of the day, even during castration resistance, we think the cancer still wants to signal through the androgen receptor; it still wants to use that testosterone receptor to drive its growth. And it will do so in a number of different ways to get around the testosterone suppression. It can mutate the receptor, it can make more of the receptor, it could splice the receptor so that it doesn't even need testosterone to bind to it anymore, and that cancer will grow. What we've discovered is when you use high-dose testosterone therapy, for lack of a better term, there's just too much electricity flowing through that circuit, and we think we're overwhelming the cancer. By signaling through that testosterone pathway again after potentially years of experiencing a low testosterone environment, this will lead to apoptosis, cell death, and tumor regression. And so, we're trying to take advantage of how it becomes resistant to castration and then really whacking that cancer down by giving it high-dose testosterone therapy that is just too much for the cancer to handle.

We've conducted a number of clinical trials over the years. Initially, we did pilot studies, so very small numbers of patients to test for safety. Weve been treating metastatic prostate cancer with testosterone suppression for the past 80 years. So, when you propose using high-dose testosterone therapies, it can be a bit alarming to move it forward in patients. We did an initial study with etoposide and bipolar androgen therapy. In this trial, it looked like the testosterone therapy by itself worked such that chemotherapy was not necessary. We subsequently moved on to doing different groups of patients, such as patients at different stages of their cancer care. By testing bipolar androgen therapy before and after different novel androgen receptor targeting therapies, we have begun to tease out where bipolar androgen therapy may fit in the treatment paradigm for patients with metastatic prostate cancer? Is it after abiraterone [Zytiga]? Is it after enzalutamide [Xtandi]? After chemo? Where should we employ this kind of testosterone therapy? These questions remain unanswered, but we are getting closer. The largest clinical trial to date was the TRANSFORMER study [NCT02286921], which was a randomized phase 3 study for patients with metastatic castration-resistant prostate cancer after having cancer progression on abiraterone. Patients were randomized to the bipolar androgen vs enzalutamide. The primary end point was radiographic progression-free survival. What we learned from that study was that bipolar androgen therapy certainly works on its own. We can induce clinical responses, PSA decreases, and tumor regression. But when you compare them head-to-head, the results look similar with the enzalutamide. Enzalutamide had similar response rates and a similar radiographic progression-free survival compared to bipolar androgen. It was somewhat disappointing that the primary end point was not met, but when we started to look at secondary end points, we began to better understand that bipolar androgen may prime the tumor to respond to the next line androgen receptor inhibitor. It's not only that the bipolar androgen may work on its own. But it's also that the testosterone therapies may sensitize the patients to other novel androgen receptor targeted therapies. I think when we were designing the TRANSFORMER study, we were looking at testosterone by itself vs enzalutamide by itself. But when we looked at the data, those patients that got testosterone then crossed over to enzalutamide did very well. And there was actually an overall survival benefit when we looked at patients receiving bipolar androgen followed by enzalutamide vs those who just received enzalutamide by itself. That was a secondary end point, so it wouldn't change the standard of care, but at least it was cluing us in to the mechanism here, that it may not just be the bipolar androgen therapy that works, even though it does in certain patients; they do very well. But when they have cancer progression on the testosterone, we really can take advantage of that sensitization effect with next line treatment And so, we may want to prime patients between oral AR-targeted therapies with the testosterone therapy, and I think that was the lesson that we learned from TRANSFORMER.

I think we're still working on that and trying to identify where bipolar androgen therapy would be best suited. We've done a number of trials; like I said, the TRANSFORMER study. We also just completed the COMBAT study [NCT03554317], which was a combination of bipolar androgen with the immune checkpoint inhibitor nivolumab [Opdivo]. The eligibility for the COMBAT study was that patients had to have cancer progression on at least 1 AR-targeted therapy, but there was no limit in number of therapies. And so, we actually got a very heterogeneous population of patients in terms of treatment; some were early phase, early in their clinical disease course, and some were heavily pretreated with a number of oral AR-targeted therapies and even chemotherapies. And so, we got to look at some of the response rates to testosterone therapy in a bunch of different clinical states of prostate cancer. There did not appear to be an advantage of treating early vs later; it seemed like if the testosterone was going to work, it was going to work for however long it was going to work for, irrespective of the number of therapies. So, it's not exactly clear where we should implement it. It seems to work reasonably well wherever we choose to use it. But I think, in a little bit more general terms, mixing in the bipolar androgen after an AR-targeted therapy will sensitize patients to that next line of AR-targeted therapy. We've learned over the years that trying to move from an oral AR-targeted therapy like abiraterone straight to enzalutamide is not the best treatment approach. There should be something in the middle there, whether it's chemotherapy or something else. But that may be a spot where testosterone therapies would become useful to see if we can get you to sensitize to that second AR-targeted therapy.

We're trying to understand that. Conventional wisdom would suggest that the harder you've been targeting that AR-targeted pathway, the more likely you may be to benefit from the testosterone. So, the more pressure you put on the androgen receptor over time, perhaps we can take advantage of giving the bipolar androgen therapy, and that's been our hypothesis. We have not found clear, convincing evidence that the line of AR-targeted therapies will either improve or worsen outcomes. We're looking into that. What we're trying to do now is pool all the patients that we've treated over a number of clinical trials and even off clinical trials to answer this question. If we have 500 to 700 patients with various degrees of prior treatment, we may be able to at least retrospectively get a signal to say, which patients responded best to bipolar androgen. We're trying to figure that out. But I think right now, that's unclear, and we don't have that answer.

That's the million-dollar question right now. We're going over the data from the COMBAT study. The best part about that study is that we took serial biopsies from patients, so we have actual tissue that we can study from before testosterone and during testosterone. We have serial blood draws; we have a lot of time points where we're collecting specimens for patients to try to answer that question. Dr. Laura Sena, Dr. David Sanin, and others have begun to analyze some of that data. I think it's no surprise that when we study the androgen receptor and androgen receptor signaling, we're starting to see a pattern of who's going to respond to bipolar androgen. Its not just in patients who have the highest level of androgen receptor -That doesn't appear to be the case. But the data suggest that those patients that have high signaling through the androgen receptor - so if you can give them a score for androgen signaling, those that had the highest androgen receptor scorehad the best response to testosterone. From a practical perspective, that makes sense; those patients who are heavily dependent on the androgen receptor pathway may see the most benefit using a drug that's clearly hitting the androgen receptor pathway. I think that's what we found so farthat high AR signaling will predict response. We're also finding that bipolar androgen therapy can reduce MYC expression. MYC is a common oncogene in many cancers, not just prostate cancer. We found that those patients who respond deeply to bipolar androgen had very significant declines in MYC protein expression. There are still some pieces to put together there. So I think if I'm going to answer this a little bit more succinctly, patients with tumors that had high AR signaling did better on bipolar androgen, and those that we found had the most robust MYC decrease in protein expression also did very well. The relationship between AR and MYC is there, and we're trying to explore that further.

I think it's received attention. I think people are interested in the topic. The beauty of bipolar androgen is that it's relatively cheap. Injections of testosterone are somewhere in the range of $20 to $30 a month. For cancer treatments, that's remarkably inexpensive. I think there's a cost effectiveness to it. I think it's very safe. And then, in terms of the side effects of bipolar androgen, many of the "side effects are actually positive changes. Hot flashes go away, they have more energy, they get more libido, they can have erections, and this is all during the course of received treatment for metastatic prostate cancer. I think people are interested in it based on the quality-of-life perspective, the cost efficiency of it. But I also think providers need to see concrete data showing that bipolar androgen is superior to whatever cancer treatment that we're comparing it to. I think each trial that we do, we're clearly seeing signal and the treatment seems safe. What we're still trying to identify is what's the right sequence so that we can inform treatment. That kind of parlays into ongoing clinical trials with bipolar androgen. And I think the one trial that I will highlight is the STEP-UP trial [NCT04363164]. This trial involvespatients with metastatic castration-resistant prostate cancer who received prior treatment with abiraterone. They get randomized to 1 of 3 groups. They can go into the enzalutamide-only group, so they go straight from abiraterone to enzalutamide. That was 1 of the control groups in the TRANSFORMER study. And then there are 2 experimental arms. In 1 of these arms, patients get bipolar androgen therapy until progression, and then enzalutamide until progression. The third arm is a kind of flip-flop; patients receive bipolar androgen therapy for a period of time, then enzalutamide, then bipolar androgen and back to enzalutamide. The hope here is that this trial is going to be a more definitive study to really show the benefit of bipolar androgen therapy because TRANSFORMER didn't build that second piece, the enzalutamide treatment, into the primary end point. So if STEP-UP is positive and shows a clear difference vs enzalutamide alone, then I think the way patients with metastatic prostate cancer are treated is going to change. Bipolar androgen will get more attention, and more people are going to do it. I think the other part of this conversation is that there is some concern about providers and patients doing testosterone therapy off label and on their own without clear clinical guidance. It's great to get attention for your work, but we're also a bit concern that providers are just going to do it in patients because testosterone is FDA approved affordable. But we worry about safety and monitoring. How do you follow those patients? It can be a little tricky because we're using testosterone. Testosterone can signal through AR, and those cancers can make more PSA. Well, that rise in PSA may not reflect tumor growth, so do you manage that in patients? It becomes a little bit tricky. We've gotten good experience with managing these patients, like I said, over the past 10 years, sowe kind of know what patterns we're looking for. Whereas if you don't have experience, we just worry about safety. It's a double-edged sword. It's nice to get attention; I think it is getting attention. But we also worry about people going out and doing it without the proper guardrails in place.

As we learn more about mechanism, which we're understanding from the COMBAT study, we're trying to find logical partners to put with bipolar androgen therapy. I think there are 2 directions that we're going in. One is bipolar androgen by itself and the sensitization to other AR therapies story, and I think STEP-UP is going to tell that story. And then there's another direction that is somewhat open endedwhat are logical partners to pair with bipolar androgen? How do we make bipolar androgen therapy work better? Can we figure out a way to keep MYC levels down for longer? Can we pair testosterone with some MYC inhibitor or some suppressor of MYC expression to make it work better? It's possible. Are there other logical pairs of treatments that go with bipolar androgen? Yes, absolutely, and we're trying to figure those out as we go. I think it's a 2-pronged approach. One is the conventional approach, which is STEP-UP. And then as we dig through the data from our prior studies to say what makes sense to pair with bipolar androgen? We are working those out right now.

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Bipolar androgen therapy in prostate cancer: Current evidence and next steps - Urology Times

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A recent study published in the journal Psychopharmacology shows that men currently using anabolic-androgenic steroids face challenges in accurately recognizing facial expressions of emotion, especially those of anger and disgust. This effect appears to be more pronounced among individuals with steroid dependence.

Anabolic-androgenic steroids, synthetic variations of the male hormone testosterone, are widely known for their use among athletes and bodybuilders to enhance physical performance and muscle mass. Despite their popularity, anabolic-androgenic steroids come with a host of potential side effects, including significant impacts on mental health and cognitive functions.

Prior studies have associated anabolic-androgenic steroids use with increased aggression, anxiety, depression, and personality disorders. Intriguingly, these behavioral changes may stem from impaired social cognitive functions, such as recognizing and interpreting others emotionsa crucial skill for effective non-verbal communication and empathy.

Motivated by the gap in understanding the specific impact of anabolic-androgenic steroids on emotional recognition, researchers conducted this study to better understand the effects of steroid use and dependence on the ability to recognize facial expressions of emotion accurately. They hypothesized that anabolic-androgenic steroid use would correlate with diminished accuracy in emotional recognition, potentially mediated by altered hormone levels.

Our team has previously investigated the role of anabolic steroids in recognizing emotions from biological movement and theory of mind video tasks, so we were interested in how people who use(d) steroids recognize emotions from facial expressions, said study author Morgan Scarth, a postdoctoral researcher at Oslo University Hospital.

We were also interested if fluctuations in hormone levels could explain any differences in emotional recognition abilities. The ability to recognize and respond to other peoples emotions may have implications for social behaviors.

The study cohort comprised 171 adult men engaged in heavy resistance training, divided into two main groups: those who had used anabolic-androgenic steroids (94 participants) and a control group with no history of steroid use (77 participants). The steroid group was further categorized based on current usage status into those currently using steroids (On) and those who had ceased use (Off).

Participants underwent a comprehensive evaluation including emotional recognition tasks, hormone level measurements, and assessments for anabolic-androgenic steroid dependence. Emotional recognition was tested using a computerized task where participants identified emotions from facial expressions. Hormone levels were analyzed from blood samples, focusing on the serum free testosterone index (FTI) among others.

Men who were currently using steroids demonstrated a significantly lower ability to accurately recognize facial expressions of anger and disgust. This indicates that steroid use may impair individuals capacity to interpret these particular negative emotions, which could have implications for social interactions and communication.

The researchers further identified that individuals with a dependence on steroids showed a worse recognition of fear compared to those without such dependence. This suggests that beyond the general effects of steroid use, developing a dependence on these substances might be associated with additional deficits in social cognition.

The researchers did not find evidence that FTI levels significantly mediated the impact of steroid use on the ability to recognize facial expressions of emotion. This indicates that while testosterone levels are altered by steroid use and correlated with changes in emotion recognition, they do not fully explain the observed deficits in recognizing certain emotions.

Men who are currently using anabolic steroids may have a reduced ability to recognize negative facial emotional expressions, specifically anger and disgust, Scarth told PsyPost. This effect does not seem to be explained by fluctuations in the hormone levels measured in the study. Men who had previously used anabolic steroids but have quit did not seem to have the same deficits, suggesting that this effect may be temporary.

However, the study is not without its limitations. The specificity of the sample all male, heavily involved in resistance training, and primarily Norwegian limits the generalizability of the findings to broader populations, including females and those from other cultural backgrounds. Additionally, the cross-sectional design precludes conclusions about causality, and the presence of unmeasured confounding variables could influence the observed relationships.

The study is cross-sectional, so we cannot make any claims that steroid use causes impaired emotion recognition, Scarth explained. Also, we do not account for the specific types of anabolic steroids used, nor the duration of use or how recently steroids were used prior to completing the emotion recognition task, which may have some impact on social cognitive abilities.

Looking ahead, the research team aims to delve deeper into the neurological impacts of anabolic-androgenic steroids, with a particular focus on how these substances affect brain aging and cognitive functions over time. By unraveling the nuanced ways in which synthetic hormones influence our minds and social lives, this line of inquiry holds the promise of informing more effective interventions for those affected by steroid use and dependence.

The research group is continuing to investigate how anabolic steroids impact the brain and cognition, and is particularly interested in the effects of anabolic steroids on brain aging, Scarth said.

The study, Supraphysiological testosterone levels from anabolic steroid use and reduced sensitivity to negative facial expressions in men, was authored by Morgan Scarth, Lisa Evju Hauger, Per Medbe Thorsby, Siri Leknes, Ingunn R Hullstein, Lars T. Westlye, and Astrid Bjrnebekk.

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Steroid use linked to diminished emotional recognition skills in men - PsyPost

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Published on Mar 30, 2024 06:48 PM IST

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Published on Mar 30, 2024 06:48 PM IST

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Published on Mar 30, 2024 06:48 PM IST

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Published on Mar 30, 2024 06:48 PM IST

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Published on Mar 30, 2024 06:48 PM IST

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Published on Mar 30, 2024 06:48 PM IST

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4 supplements for losing weight with PCOS: Dietitian shares tips - Hindustan Times

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STEPHEN A. SMITH has undergone a dramatic physical transformation over the last year, after a series of health issues prompted him to make some major changes to his lifestyle. In a recent wide-ranging interview with biologist and 10X Health founder Gary Brecka on his

"That was me a year ago, ladies and gentlemen," he said, over an image of himself before he began his weight loss journey. "Yeah, that was your boy Stephen A. I can't even tell you how bad I was. Nearly 30 percent body fat. A cholesterol level over 300. And .1 point away from being a full-blown diabetic. And that was after I had Covid, which damn near killed me."

"This is a year later," he continued, showing off his visibly leaner appearance. "As you can see, times have changed."

While Smith tends to be a very private person outside of his work as a sports anchor, he felt compelled to share his health journey and be transparent, in the hopes that it will encourage others to take proactive action in their own lives.

Smith revealed that a year after beginning the process of changing his diet and increasing his physical activity, he is no longer pre-diabetic, his blood sugar is normal, and he's gained around 6 pounds of lean muscle.

He also addressed the rumors that his recent weight loss has been aided by the controversial diabetes medication Ozempic, which has become popular as a "diet drug" in wealthy circles.

"I've had people come up to me man, you know, that Ozempic must be good," he said. "I'm like, I didn't take that! I'm doing cardio six days a week, weightlifting five days a week, I take my supplements and vitamins, but I'm not doing that."

He added that his mindset with regards to exercise has also changed dramatically, saying: "I went from being conniving and slick and trying to avoid the gym to being pissed off that I missed going to the gym."

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Stephen A. Smith Opens Up About Weight Loss Transformation - Men's Health

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Everybody was happy except my GI tract

Vicki Webb Pouncey, a 58-year-old breast cancer patient from Melbourne, Florida, tried three of the drugs over the last few years, under the supervision of both her nurse practitioner (who discovered Pouncey was insulin resistant) and her oncologist, who worried her extra weight might drive a recurrence.

She first tried the low-dose pill Rybelsis, but after several weeks had zero results. So she tried Wegovy using a discount coupon for a six-month supply.

On the Wegovy, I lost 40 pounds right away and my numbers all started to improve, she said. Cholesterol, blood sugar, insulin resistance that all looked better. But then the coupon ran out and I couldnt get any more so I went back on the Rybelsis.

Again, her weight loss stalled. So her providers suggested she try Ozempic. Immediately, pounds started to come off again.

I lost weight and my labs looked great, she said. Everybody was happy except my GI tract.

The drugs can have considerable side effects. Ozempic lists the most common as nausea, diarrhea, abdominal pain, vomiting and constipation. Zepbound lists the same plusindigestion, injection site reactions, fatigue, allergic reactions, belching, hair loss and heartburn. It also mentions the potential for kidney failure; gallbladder problems; pancreatitis; low blood sugar; changes in vision and depression.

At first, Pouncey only had nausea and diarrhea a few days after her weekly shot; then it started happening more often.

The drug absolutely diminished her food cravings and her sweet tooth, she said, and she felt healthier, at least for a while. But Ozempic may have been too effective.

There were days when I had to make myself eat, she said. At one point, I think I became malnourished because of all the nausea and diarrhea. But my lab numbers were beautiful so I stayed on it.

After several months, though, the GI issues became a daily ordeal and she started to have pain on her right side. Now, there were only good hours, not good days, she said.

She stopped the Ozempic and went to her doctor about the pain. He ordered a CT scan, thinking shed developed pancreatitis, one of the noted side effects. Instead, the CT scan found metastatic breast cancer in her liver, which led to more scans and more tumors.

The scans also detected nodules on her thyroid, which have yet to be biopsied. The metastatic breast cancer treatment is her primary concern, she said.

She absolutely does not attribute her metastatic recurrence to the weight-loss drugs.

I understand the difference between correlation and causation, she said. The thyroid nodules are the only thing I would associate with it. And it lists that in the risk factors on the label.

Even with the all the suffering, Pouncey said the drugs were beneficial. All told, she lost 80 pounds; her cholesterol, insulin resistance and blood sugar improved dramatically and she was even free of the joint pain caused by her anti-hormone drugs.

Once I got rid of processed sugar and carbs, my joint pain almost resolved itself, she said. And losing the weight took the pressure off my knees.

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The new weight-loss drugs and cancer - Fred Hutchinson Cancer Center

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The Gila monster is a poisonous North American lizard that measures around 50 centimetres and sports a distinctive coat of black and orange scales. This lethargic reptile, which mostly dwells underground and eats just three to four times a year, is the unlikely inspiration for one of pharmas biggest blockbusters: a new generation of weight-loss drugs that has patientsand investorsin a frenzy. Originally made for diabetes, evidence is growing that they also have benefits in diseases of the heart, kidney, liver and beyond.

Since the late 1980s scientists believed that a gut hormone called glucagon-like peptide-1 (GLP-1), which is secreted by the intestines after a meal, could help treat diabetes. GLP-1 increases the production of insulin (a hormone that lowers blood-sugar levels) and reduces the production of glucagon (which increases blood-sugar levels). But GLP-1 is broken down by enzymes in the body very quickly, so it sticks around for only a few minutes. If it were to be used as a drug, therefore, patients would have faced the unwelcome prospect of needing GLP-1 injections every hour.

In 1990 John Eng, a researcher at the Veterans Affairs Medical Centre in The Bronx, discovered that exendin-4, a hormone found in the venom of the Gila monster, was similar to human GLP-1. Crucially, the exendin-4 released after one of the monsters rare meals is more resistant to enzymatic breakdown than GLP-1, staying in its body for hours. It took more than a decade before exenatide, a synthetic version of the lizard hormone, created by Eli Lilly, an American pharma giant, and Amylin Pharmaceuticals, a biotech firm, was approved to treat diabetes in America. This breakthrough spurred other firms to develop more effective and longer-lasting GLP-1 medications as a treatment option for diabetes, beyond injections of insulin.

Scientists had also been aware that GLP-1 had another side-effect: it slowed the rate of gastric emptying, which allows food to stay in the stomach for longer and suppresses appetite. But the potential weight-loss benefits were not seriously pursued at first. It was only in 2021 that Novo Nordisk, a Danish firm, showed data from a clinical trial where overweight or obese patients were put on a weekly dose of its GLP-1-based diabetic drug, semaglutide, which was then being marketed under the name Ozempic, for 68 weeks. The results were dramaticparticipants had lost 15% of their body weight, on average.

The medicines that mimic the GLP-1 hormone then became blockbusters. With close to half of the worlds population expected to be obese or overweight by 2030, according to the World Obesity Federation, demand for these drugs is surgingBloomberg, a data provider, estimates that these medications will hit $80bn in yearly sales by then. The market is projected to grow by 26% per year in the next 5 years, compared with16% per year for oncology drugs and 4% per year for immunology medicines, the two other biggest areas.

So far only three GLP-1 drugs have been approved to treat obese or overweight individuals: liraglutide and semaglutide, developed by Novo; and tirzepatide, made by Lilly. But the market has already attracted a wave of competitors (see chart 1). Bloomberg tracks close to 100 wannabe drugs in the development pipeline. Most new therapies hope to outdo semaglutide and tirzepatide by crafting drugs that are easier to take, cause fewer side-effects or deliver more effective weight loss (see chart 2).

Start with convenience. Both semaglutide and tirzepatide are injections that need to be taken weekly. Stop the dose and most of the weight returns within a year. Amgen, a large American biotech firm, is developing an anti-obesity drug that relies on doses once a month, and hopes the weight-loss effects will last even after treatment ends. AMG133 activates receptors for GLP-1 while blocking receptors of glucose-dependent insulinotropic polypeptide (GIP), a hormone secreted in the small intestine in response to food intake that stimulates the production of both insulin and glucagon. The company is now conducting clinical trials to find out if patients can, over time, be gradually weaned towards smaller doses.

Switching from injections to pills would also make the drugs a lot more tolerable for those who dislike needles. Novo is working on an oral version of semaglutide that works just as well as its jabs. But the pill requires 20 times the amount of the active ingredient as the injection, and must be taken daily. With semaglutide in short supply, Novo has had to push back the oral versions launch. Lilly also has a daily pill that targets GLP-1 receptors called orforglipron in late-stage clinical trials.

Another drawback of GLP-1-based medicines is the nausea and vomiting that frequently accompanies their use. Zealand Pharma, a Danish biotech firm, is developing a drug that is based on a different hormone called amylin, produced in the pancreas along with insulin in response to food intake. But unlike GLP-1, which suppresses appetite, amylin induces satiety, or the feeling of fullness after a meal.

Adam Steesburg, boss of Zealand, says that in most people a hormone called leptin is released from fat tissue that signals to the brain that the body is full. Obese individuals are insensitive to that hormone. Clinical studies have shown that analogues of amylin can make people sensitive to leptin again, helping them to stop eating earlier. Feeling full, rather than lowering appetite, may also reduce the feeling of nausea. Mr Steesburg says that results from early-stage trials suggest that its drug could achieve similar weight loss as GLP-1 drugs, but with less nausea and vomiting.

Besides pesky injections and nausea, a bigger concern is that patients on these drugs do not just shed fat, they also lose lean muscle mass. Some patients drop almost 40% of their body weight in lean mass, a serious concern for older patients. To counter this, companies are trying out, alongside GLP-1 drugs, medicines originally designed to treat muscle atrophy.

Regeneron, an American pharma company, is testing drugs that block myostatin and activin, proteins that inhibit muscle growth in the body. Taken with semaglutide, the combination can potentially boost the quality of weight loss by preserving lean muscle. Similarly, BioAge, a California-based biotech, is testing a drug that activates the apelin receptor that can be taken alongside Lillys tirzepatideApelin, a hormone secreted after exercise that acts on skeletal muscle, the heart and the central nervous system to regulate metabolism and promote muscle regeneration. In obese mice, the combination led to greater weight loss compared to tirzepatide alone, while preserving lean body tissue.

The slimming drugs arent just for shedding pounds. Because obesity is linked to over 200 health issues, including strokes, kidney problems and fatty liver, GLP-1 drugs are proving useful for more than just obesity.

A recent clinical trial by Novo that ran for five years and enrolled more than 17,500 participants found that semaglutide cut the risk of serious heart issues like heart attacks, strokes, or death from heart disease by 20%. Novo believes that the heart benefits of the treatment are not due to weight loss alone, because the reduction in the risk of cardiovascular problems occurred early, before patients lost weight. In March semaglutide was approved by the US Food and Drug Administration for reducing the risk of heart disease in obese or overweight people, the first time a weight-loss medication has been approved for this purpose. Results from another clinical trial have shown that semaglutide reduced the risk of kidney-disease-related events by 24% in patients with type-2 diabetes.

Another weight-loss drug, survodutide, being developed by Boehringer Ingelheim, a German drug company, and Zealand, has shown promising results in being able to treat a serious liver condition called metabolic dysfunction-associated steatohepatitis (MASH). This is caused by the build-up of excess fat in the liver and can lead to liver cancer or liver failure. In a recent trial of 295 patients, 83% saw significant improvement in their condition when treated with survodutide, compared with 18% of those on a placebo. Survodutide targets receptors for GLP-1 and glucagon. Waheed Jamal from Boehringer Ingelheim says that there is evidence that glucagon breaks down more fat in the liver compared with GLP-1 and reduces fibrosis (build up of excessive scar tissue in the liver).

While a lot of focus has been on the action of these medicines on improving metabolic health, scientists are now uncovering that these drugs also engage with the brain and immune system, by interacting with GLP-1 receptors in the brain.

Daniel Drucker, a diabetes researcher at Mount Sinai Hospital in Toronto, found that in mice suffering from extensive inflammation throughout the body, GLP-1 drugs reduced the condition, but only when the receptors in the brain werent blocked. When the brain receptors in mice were either blocked or genetically deleted, the anti-inflammatory properties of the drugs were lost. This suggests that the GLP-1 drugs tame inflammation by acting on the brain cells.

For some this suggests that these drugs might be useful for treating brain disorders that are characterised by inflammation, such as Alzheimers disease and Parkinsons disease, both of which are characterised by inflammation in the brain. Since 2021, Novo has been conducting a clinical trial involving more than 1,800 patients to test whether semaglutide helps patients with early stages of Alzheimers. This study is expected to be completed by 2026.

Dr Drucker sees the anti-inflammatory qualities of GLP-1 medications as key to their versatility. He notes that besides Alzheimers and Parkinsons, chronic inflammation is a factor in many complications for people with type-2 diabetes and obesity, and affects organs like the kidneys, heart, blood vessels, and liver. If these drugs eventually help in treating these conditions, Dr Drucker believes that their inflammation-reducing properties could explain part of their success.

The appetite-suppressing effects of these drugs has also raised interest in their ability to curb cravings for other substances. Researchers in Denmark investigated the effect of GLP-1 drugs on people with alcohol-use disorder. In the study of 130 people, they found no difference between patients who used the drugs (alongside therapy) compared with those using a placebo. However there was a reduction in alcohol consumption in obese patients. When the researchers looked at the brain activity of the patients by showing them pictures of alcoholic drinks, for those in the placebo groups the reward centres of their brains lit up. For patients on GLP-1 drugs, the activity of the brain in the areas associated with reward and addiction was attenuated, indicating a direct brain effect. Some researchers are now actively exploring whether the drugs might have an impact on how people use other addictive substances such as tobacco or marijuana.

All of these findings are still early. Developing new drugs is costly and time-consuming. There are steep failure rates. Successes in the lab may not work in people, and results in small groups may not replicate in larger ones. But with the potential to treat dozens of conditions well beyond obesity and diabetes, hope around the new drugs will only grow.

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Could weight-loss drugs eat the world? - The Economist

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Summary

After losing over 400 pounds, 1000-lb Sisters star Tammy Slaton has been experimenting with the boho fashion aesthetic and posting them on social media. When the series premiered in 2020, Tammy weighed 725 pounds at her heaviest, but she has since gone through an extraordinary weight-loss journey. After a health scare that landed her in the hospital and a medically induced coma, Tammy decided she had to change her life. She checked herself into rehab, where, through diet and exercise, she lost enough weight to qualify for bariatric surgery.

After losing 400 pounds, the 1000-lb Sisters season 5 star is living an entirely different life. Before Tammy lost weight, her mobility was limited, and her size made her a prisoner in her own home. Now, she travels with her family, tries new things, and celebrates new milestones at every turn. Tammy has especially enjoyed experimenting with style and fashion since losing weight, trying on clothes and looks that weren't available to her at her previous size.

In January, Tammy posted a TikTok of herself singing a duet with fellow TikTok creator @Crazyjen1998. In the side-by-side split screen, the women are singing along to a remake of Rachel Platten's "Fight Song." The power anthem is the perfect background tune to the last few years of Tammy's life. Despite the triumph of losing weight, Tammy suffered a tragedy during 1000-lb Sisters season 5, when her husband, Caleb Willingham, sadly passed away from complications due to obesity. She had to fight hard to stay on track with her weight-loss despite being devastated by the loss.

" Looking good girl!! Proud of you."

In January, Tammy posted a TikTok clip of herself showing off her outfit of the day. In the clip, she's wearing a wildly colorful tie-dye top that screams flower power. In a nod to another of Tammy's weight-loss milestones, she's also wearing jeans, which would have been impossible before Tammy lost all of the weight. At her former size, she would never have been able to find a pair of denim jeans. In the clip, Tammy lifts her shirt slightly to show off that her jeans have a zipper and front button closure, as opposed to an elastic waistband.

" You are doing great and you look AMAZING!"

Fans of the 1000-lb Sisters star took to the comment section to offer their support to Tammy. "Looking good girl!! Proud of you," wrote one fan, while another reiterated, "you look amazing!! I love that shirt!!" Though the internet isn't known for kindness in the comment section, the Slatons have always had a great relationship with their supportive fan base. Another fan wrote, "You are doing great and you look AMAZING!"

In a TikTok Tammy posted in July 2023, she's wearing fun rope bracelets and is ready for spring in her floral printed top. The 1000-lb Sisters star is also wearing layered boho chic necklaces, including the treble clef necklace she has often been spotted wearing lately. Her full face of skillfully applied makeup shows how much slimmer Tammy's face is than it used to be before she lost over 400 pounds. There are no comments in the comment section because it's locked, but the clip has over 5,000 likes.

Tammy isn't the only Slaton who has gotten in on the weight-loss action since the show premiered. Her sister and fellow 1000-lb Sisters star, Amy Slaton, has lost over a hundred pounds as well. Additionally, Tammy and Amy's step-brother, Chris Combs, has lost over 150 pounds, while their step-sister, Amanda Halterman, has lost over 300 pounds. Though the Slatons have lost over a thousand combined pounds over the years, they are all still planning and working on losing more weight while inspiring others with their incredible journeys.

Tammy Slaton

Lost 400+ pounds

Diet, exercise, weight loss surgery

Amy Slaton

Lost 125+ pounds

Diet, exercise, weight loss surgery

Chris Combs

Lost 150+ pounds

Diet, exercise, weight loss surgery

Amanda Halterman

Lost 300+ pounds

Weight loss surgery

Misty Slaton

Unknown

Wants weight-loss surgery

In August 2023, Tammy posted a video clip of herself to Instagram, and in the clip, Tammy is singing along with Taylor Swift's "Shake It Off." The lyrics "Haters gonna hate, hate, hate, hate, hate, hate" are intended for the haters in the comment section commenting negatively about Tammy's body since losing weight. Many of the criticisms come from people who point out that Tammy has a lot of extra skin since losing weight, while others want Tammy to fix her teeth. Too many people have forgotten that if they can't say anything nice, it's best to say nothing at all.

" she cant win guys. when she was overweight you hated her and then when she loses weight you make fun of the way her body looks. What is she supposed to do?"

Though some people in the comments still had plenty to say about the extra skin Tammy has since she has lost over 400 pounds. The positive comments far outnumber the negative comments. One Instagram user said it best, writing, "she cant win guys. when she was overweight you hated her and then when she loses weight you make fun of the way her body looks. What is she supposed to do?" The 1000-lb Sisters star is shaking off all the criticism with a smile on her face.

1000-lb Sisters seasons 1-5 can be streamed on MAX and Discovery+.

Sources: Tammy Slaton/TikTok, Tammy Slaton/TickTock, Tammy Slaton/TikTok, Tammy Slaton/Instagram

1000-lb Sisters follows sisters Amy Salton-Halterman and Tammy Slaton in their home in Dixon, Kentucky, covering their daily lives, weight loss attempts, and subsequent weight loss surgery. The show covers such moments as attempts to have children, medical visits, and dramatic emergency room visitations. The family wrestles with supporting their daughters and their weight loss efforts while struggling with their own life troubles.

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1000-Lb Sisters: Tammy's Best Hippie Outfits After Extraordinary Weight Loss Milestone (You'll Love Her Boho Clothes) - Screen Rant

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