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How does eating too much fructose cause obesity?

How does eating too much fructose cause obesity?

In the United States, more than 40% of adults are obese, with approximately 10% having extreme obesity.

Obesity increases the chance of developing a variety of ailments, such as type 2 diabetes, heart disease, and several malignancies.

An energy imbalance between calories consumed and calories burned is the primary cause of obesity.

Obesity, however, may result from more than just calorie intake—it may also result from the calories.

According to recent studies, the simple sugar fructose, which is present in many foods, may be the cause of obesity and other related health issues.

Around 13% of persons globally, according to the World Health Organisation (WHO), are obese. Although obesity rates are rising in low-income nations, the majority are in wealthy nations.

According to National Institutes of Health (NIH) data, 42.4% of adults and 19.3% of children and adolescents in the United States were obese in 2017–18. Additionally, these figures are rising.

Obesity raises the risk of a number of illnesses. It is linked to a poor diet and an unbalanced energy intake, but it may also have a genetic component. These are listed by the NIH as follows:

What connection exists between fructose and obesity?

According to recent study, obesity may not just be caused by an energy imbalance; rather, the source of that energy may be what causes the illness.

According to the study, which was published in Philosophical Transactions of the Royal Society B, fructose may be the cause of obesity because of an evolutionary “survival switch” that makes people store energy from fructose rather than utilize it.

The study’s results were discussed by Dr. Eamon Laird, a postdoctoral research fellow at the University of Limerick in Ireland who was not engaged in the study, he observed:

This is a highly intriguing theory, even though it is only a narrative overview and not a systematic meta-analysis of the available data. It is conceivable that our present energy-dense diets have altered an evolutionary pathway that was advantageous millions of years ago.

Fructose converts to energy reserves.

According to the study, metabolic diseases like obesity may have arisen as a result of overstimulation of an evolutionary-based biological reaction called the “survival switch,” which is meant to safeguard animals before a crisis like hibernation.

Contrary to glucose, which is used as immediate fuel, the researchers contend that fructose causes the body to conserve energy.

This is better for an animal going into long-term hibernation than for a person who has constant access to high-sugar diets.

This “survival switch” may be more detrimental than beneficial in areas where people have easy access to food. People develop fat reserves as a result of the constant availability of high-fructose foods, which causes obesity and related health issues.

Metabolic effects of fructose

What causes fructose to make the body store energy rather than use it?

Adenosine triphosphate, or ATP, is often utilised and swiftly replaced from nutritional intake or fat storage. ATP is the chemical that supplies energy to power all cell operations.

Fructose, on the other hand, lowers the amount of ATP present in cells and hinders the production of ATP.

A chain of chemical processes that stop the mitochondria of the cell from making more ATP and put them under oxidative stress are triggered when ATP levels fall low enough.

Fructose consumption increases appetite in addition to lowering ATP levels. Once deposited as fat, these extra calories. The ATP levels eventually rise once more, but the fat reserves are still there.

Repeated exposure to oxidative stress causes mitochondrial dysfunction to become persistent over time. The body of a mammal that is hibernating adjusts to the low ATP levels by lowering the resting metabolic rate.

Without reducing calorie consumption, this lower energy usage leads to weight increase in persons who still have access to plenty of food.

Dr. Laird concurred that this theory could help to explain the rise in obesity.

He said, “I agree it could be one component. But obesity and metabolic syndrome are complex conditions; there is seldom just one contributing cause. Lack of exercise, unhealthy eating habits, vitamin deficiencies, socioeconomic causes, and even risk factors related to one’s race and ethnicity are all significant risk factors.”

Therefore, even if fructose did affect obesity, it would only have a minor impact overall, he continued.

Dietary sources of fructose

Although fruit naturally includes fructose, which gives it its sweetness, a normal Western diet also contains a variety of additional sources of fructose.

The majority comes from table sugar, high fructose corn syrup (HFCS), a sweetener manufactured from cornflour, and sucrose, a molecule composed of glucose and fructose chemically bound together.

Fructose can make up to 55% of HFCS. To transform the glucose in corn syrup into the sweeter-tasting fructose, manufacturers must add enzymes.

Since the fructose in HFCS is present as free molecules, it is absorbed more quickly than it is in table sugar.

HFCS is included in practically all processed foods and many other foods. They consist of:

  • sodas
  • fruit juices with added sugar
  • crackers
  • ready-made meals
  • salad dressings and condiments
  • a few pastries and bread.

According to the scientists, the growth in sugar consumption, particularly that found in processed foods, fructose-sweetened beverages, and carbohydrates with a high glycemic index (GI), is related to the global epidemics of obesity and diabetes.

Must you stay away from foods high in fructose?

Although he was not involved in the study, Dr. Mir Ali, a bariatric surgeon and medical director of the MemorialCare Surgical Weight Loss Centre at Orange Coast Medical Centre in Fountain Valley, California, stated that for people who are overweight or obese, “any source of sugar, including non-processed sugars, such as those found in fruits, can have a similar effect on the body.”

We advise our patients to minimize all sources of sugar, including fruits,” the doctor added.

However, Dr. Laird cautioned that most people should not worry excessively about fruit’s sugar content: Most of us don’t consume enough fruits, despite the fact that doing so would benefit our overall health by providing fibre, vitamins, and minerals. The modest amounts of fruit we do consume would probably not amount to much.

However, he continued, “The main risk probably arises when the fructose is highly concentrated and added to other foods (these foods often contain high fat, high sugar, and low nutrition), which could result in an increased risk of obesity.”

So maybe avoid that processed snack since it’s probably laden with fructose to help lower your risk of becoming obese.


For Type 2 Diabetes medications that have been suggested by doctors worldwide are available here

Time limited eating helps in weight loss & type-2 diabetes.

Time limited eating helps in weight loss & type-2 diabetes.

According to recent studies, type 2 diabetics who practise time-restricted eating may experience weight loss and better blood sugar control.

According to a new randomized controlled research, those who restrict their eating to the eight hours from midday to eight o’clock lose more weight than people who lower their overall calorie intake by calorie counting.

However, experts advise patients to work closely with their doctor because certain medications and dietary needs may affect how beneficial a patient’s diet plan is.

In a recent study, people who restricted their eating to the hours between noon and eight o’clock lost more weight than those who merely cut their caloric intake overall by counting calories.

Despite the growing popularity of time-restricted eating, no studies had previously specifically examined an eight-hour meal window in people with type 2 diabetes.

In the study, 57 people with type 2 diabetes and obesity were divided into three groups: one group adhered to time-restricted eating, another group engaged in calorie restriction, and the third group acted as the control group.

The people in the time-restricted eating group could only eat between midday and 8 p.m., whereas the people in the calorie-restriction group could eat whenever they wanted as long as they kept track of their calories.

While the control group maintained eating normally without any special modifications, their objective was to cut their caloric consumption by 25% of what was needed to maintain their current weight.

Eating within a time limit reduces body weight.

The time-restricted eating diet resulted in a 3.55% weight loss in comparison to the control group during the course of the six-month study, according to the researchers.

To put this into perspective, it would mean that a person who weighs 275 pounds would have lost about 10 pounds.

Contrary to expectations, the calorie-restricted group did not significantly lose weight when compared to the control group.

In comparison to the control group, the time-restricted eating and calorie restriction groups both showed lower blood sugar levels (HbA1C), with decreases of about 0.91% and 0.95%, respectively.

The researchers also looked into whether these dietary approaches may lower blood pressure, lower LDL cholesterol, and lower fasting glucose levels, which are all cardiometabolic risk factors.

The weight loss brought on by time-restricted eating, however, did not reach the 5% mark usually linked with improvements in these parameters.

An interview with experts, Vicky Pavlou, registered dietitian nutritionist, University of Illinois at Chicago doctoral student, and author of the study, said, “We found that eating all calories within an 8-hour window is a good alternative to calorie counting for people with type 2 diabetes who want to lose weight and improve their A1C.”

“In comparison to the calorie counting group, the time-restricted eating (TRE) group dropped 4.28% of their body weight in six months. In both groups, the HbA1C was lowered by 1%, the expert said.

Calorie restriction versus intermittent fasting

Studies have previously examined the effectiveness of various dietary strategies among obese people. The prospective effects of time-restricted eating in individuals with obesity and type 2 diabetes, however, have not been studied.

75 obese persons with type 2 diabetes participated in the new study, which was directed by Vicky Pavlou, a doctorate student at the University of Illinois at Chicago who is also a registered nurse. Three groups of participants, ranging in age from 18 to 80, were created: control, calorie restriction, and time-restricted eating.

The calorie intake needed to maintain a person’s present weight (maintenance calories) was lowered by 25% for those in the calorie restriction group and remained unchanged for those in the control group. At any time of day, they could eat.

The time-restricted eating group, on the other hand, was only permitted to eat between noon and 8 p.m. every day without having a set calorie goal or keeping track of their consumption.

For the first three months of the trial, participants in both groups met with a dietician once per week; for the next three months, they met every other week.

Pavlou stated that the dietician “helped them with any challenges in following the diet and gave general nutrition advice,” emphasizing “the importance of reading labels and understanding calories.”

What kind of diet is best for those who have diabetes?

The researcher who was not engaged in this study, Dr. Seun Sowemimo, a board-certified surgeon at Prime Surgicare in Freehold, New Jersey, stressed that “using a combination of disease management tools is more effective than a single effort.”

Time-restricted eating (intermittent fasting) is a powerful strategy for weight loss and blood sugar control because it allows the body to switch from burning sugar to burning fat, resulting in weight loss,” he claimed.

Additionally, it helps diabetic control and lessens the frequency of blood glucose spikes, which can result in insulin surges.

Consuming whole meals with a high fibre content rather than processed foods with added sugar can also help people with diabetes maintain better blood sugar control. Unlike processed foods with free sugar, which are quickly absorbed and cause increased sugar levels and insulin spikes, natural fibre foods help regulate sugar absorption by allowing for a steady release into the bloodstream. Since the idea that fruit contains a lot of sugar is untrue, I also advise persons with diabetes to eat fresh fruits, stated Dr. Seun Sowemimo

Time-restricted eating “may help improve blood sugar control in individuals with type 2 diabetes,” according to registered dietitian Crystal Scott of Top Nutrition Coaching, who was also not involved in the study.

The insulin response may become more efficient by avoiding constant grazing and giving the body longer periods without food intake,” Scott said. Studies have revealed that time-restricted meals can increase insulin sensitivity, glucose levels, and HbA1c levels, which are indicators of long-term blood sugar control. But it didn’t in this study.

Potential effects on type 2 diabetic patients

Dr. Sowemimo stated that this “study adds another layer of clinical evidence that the timing of food consumption is a major contributing factor to diabetes management, weight loss, and overall well-being.

Patients with diabetes can safely be prescribed time-restricted eating, but they should do so in partnership with their physician,” Dr. Sowemimo stated.

Scott also emphasized the significance of investigating potential confounders, such as participant water intake, activity level, and stress-reduction techniques, as well as their use of diabetes medications.

Many additional factors must be addressed concurrently in order for a study like this one on dietary regimens to be entirely successful, according to Scott.

Scott further emphasized that this study shows there are “easier approaches to weight management that don’t involve tracking every piece of food,” even though people may recognize the necessity to implement time-restriction tactics to observe weight loss.


For Weight loss medications that have been suggested by doctors worldwide are available here

Changes in Cholesterol & triglyceride may affect dementia.

Changes in Cholesterol & triglyceride may affect dementia.

Researchers looked into the impact of varying triglyceride and cholesterol levels on dementia risk.

They discovered that varying amounts of triglycerides and cholesterol raise the incidence of dementia by 19% and 23%, respectively. To comprehend how these results might influence patient treatment, more investigation is required.

Globally, dementia affects around 55 million individuals. This number is anticipated to nearly quadruple to 152 million by 2050 as the world’s population ages.

Strategies for dementia prevention are essential for maintaining health. Finding techniques to mitigate potential risk factors that raise the likelihood of dementia is one way to develop these solutions.

Regular medical care includes tests for triglyceride and cholesterol levels. In order to create hormones and cells, the liver produces a form of fat called cholesterol. A form of fat used for energy is triglycerides.

Clinicians may be able to screen patients for dementia risk and maybe stop or delay the start of the disease by looking at the relationship between blood lipids and dementia risk.

Some evidence suggests a connection between cholesterol fluctuation and dementia. Despite conflicting findings in studies on whether high cholesterol levels increase dementia risk.

Future dementia screening methods and treatments may benefit from a deeper understanding of which lipid components raise dementia risk.

To evaluate whether there is a connection between cholesterol levels and the risk of dementia, researchers recently examined medical records.

“While not necessarily altering practice, this study highlights the need to pay close attention to people with fluctuating cholesterol levels. It will need more research to ascertain if this variance is a real factor in the onset of Alzheimer’s disease or only a side effect of dementia,” said Dr. Dmitriy Nevelev, associate director of cardiology at Staten Island University Hospital and a non-participant in the study.

High risk of dementia associated with fluctuating cholesterol

The average age of the 11, 571 participants the researchers gathered for the study was 71. 54% of the participants were female, and none had ever been diagnosed with Alzheimer’s disease or another type of dementia.

All of the individuals had their blood lipid levels checked for several factors at least three times in the five years before to the study. These comprised:

  • cholesterol overall
  • triglycerides
  • LDL, short for low-density lipoprotein cholesterol
  • HDL stands for high-density lipoprotein cholesterol.

Following the participants lasted an average of 12.9 years. 2,473 people experienced the onset of dementia during this time.

Based on how much the individuals’ blood lipid measurements changed, the researchers divided the people into five groups.

In the end, they discovered that those with total cholesterol variability in the highest 20% band had a 19% increased risk of dementia compared to those in the lowest 20%.

Those with triglycerides in the top 20% of the range had a 23% higher risk of dementia than those in the bottom 20%.

The findings persisted after taking into account potential confounding variables like education, initial cholesterol levels, and adherence to lipid-lowering therapies, according to the researchers. They also discovered that changes in HDL and LDL did not correspond to a higher risk of dementia.

Why are changes in lipid levels important?

We discussed how varying triglyceride and cholesterol levels may raise the risk of dementia with Dr. James Giordano, Pellegrino Centre professor of neurology and biochemistry at Georgetown University Medical Centre who was not involved in the study.

He stated that it is unclear whether or how varying cholesterol levels affect the risk of dementia. Nevertheless, he talked about plausible mechanisms from his own study.

According to Dr. Giordano’s research, “a number of blood-borne factors may cause changes in inflammatory mediators that affect cerebral blood vessels, nerve, and glial cells of the brain cells that remove waste from the brain and deliver nutrients to neurons.”

“This shift to a pro-inflammatory phenotype might interact with existing genetic predispositions in certain individuals. This may increase the risk of several neurodegenerative diseases, including some types of dementia,” he said.

Dr. Nevelev concurred that there is currently no conclusive explanation for why cholesterol fluctuation may raise the risk of dementia.

The functioning of our blood vessel lining is impaired by endothelial dysfunction, which is caused by cholesterol variability. This impairment contributes to irregular blood flow. According to Dr. Nevelev, “Cholesterol variability is also associated with [the] instability of blood vessel plaque, which can likewise obstruct blood flow and harm brain tissue.

He continued, “This study seeks to account for another possibility, which is the effect of sporadic adherence with cholesterol-lowering medicine.

The study did not take into consideration every factor.

We requested an explanation of the study’s main shortcomings from Dr. Howard Pratt, a board-certified psychiatrist and medical director of Community Health of South Florida who was not engaged in the investigation.

“The study’s participants had higher levels of comorbidity than the non-study control group, which did not. Therefore, there can be confounding factors that are harder to identify. Another drawback of the study is that it only included participants from one area, so it’s still not clear whether the conclusions apply to the entire community, the author pointed out.

The apolipoprotein-E (Apo-E) gene, which may have impacted the results of the study, is one genetic risk factor for dementia that was not taken into consideration, according to Dr. Giordano.

Dr. Nevelev was questioned about the study’s constraints as well. He pointed out that it is vital to know whether triglyceride levels were evaluated in samples that were fasting or samples that were not, as triglyceride levels change while a person is fasting.

He continued by saying that variations in body weight are associated with poor health outcomes and that triglyceride and cholesterol levels are related to body weight.

The researcher said, “It is possible that the observation in this study is reversed perhaps those in the early stages of dementia have changes in behaviour or changes in body weight that lead to significant variation in triglyceride levels.”

What effects does this have on preventing dementia?

UTHealth Houston’s McGovern Medical School professor of neurology and director of the Neurocognitive Disorders Centre, Dr. Paul E. Schulz, who was not engaged in the study, said the following to us:

How to apply the findings of this study to the real world is one important question. There are numerous drugs available that lower triglycerides or cholesterol, but I am not aware of any that do the same for fluctuations. Conversely, nutrition has a huge role in managing diabetes. I also wonder if dietary adjustments could also assist lower triglyceride or cholesterol fluctuations, which would lower the risk of dementia.

But given the overwhelming evidence that lower cholesterol is linked to a lower risk of Alzheimer’s disease, he added, “I would still advise people at risk for Alzheimer’s disease to think about taking their statin if their doctor prescribes it to lower their risk for developing Alzheimer’s disease.”


For Cholesterol medications that have been suggested by doctors worldwide are available here

Exercise & weight loss can improve obesity and prediabetes.

Exercise & weight loss can improve obesity and prediabetes.

According to new research, people who are overweight and have prediabetes may benefit significantly from regular exercise when accompanied with weight loss via diet.

The goal of the study was to ascertain whether exercise had benefits in addition to those provided by diet-only weight loss.

The study examined two groups, one of which followed a diet plan plus exercise training and the other of which followed a diet plan alone.

According to the findings, the group that combined diet and exercise improved their insulin sensitivity by twice as much as the diet-only group, which is essential for controlling prediabetes.

Researchers from the Centre for Human Nutrition at Washington University School of Medicine in St. Louis, Missouri, examined the results of regular exercise paired with a nutrition programme for people in a recent study.

The individuals’ bodies’ sensitivity to the hormone insulin, which regulates blood sugar levels, was tested by the researchers.

According to the findings, those who made changes to their eating and exercise routines saw a twofold increase in their insulin sensitivity compared to those who only made dietary changes.

This indicates that their bodies used insulin to regulate blood sugar levels more effectively.

The participants’ muscles were also examined by the researchers, and they discovered that the group that changed their diet and exercise regimens had higher expression (activity) of genes related to the production of new mitochondria, which are cells’ energy factories, energy metabolism, and the development of new blood vessels.

They discovered no discernible differences between the two groups in terms of the amounts of specific amino acids or particular inflammatory blood indicators.

The composition of their gut bacteria also changed similarly in both groups, which can have an impact on general health.

Exercise for managing and treating obesity

We spoke with Dr. Sergio P. Ramoa of Atrius Health, who was not a part of the study, and he stated that “despite the growing focus and treatment of obesity and diabetes, diabetes-related mortality increased in the first 20 years of the 21st century.”

“The approach to treating obesity has altered, with a focus on treating it like a chronic illness like hypertension or asthma. There have been considerable advancements in the treatment of weight reduction and weight maintenance, according to Dr. Sergio P. Ramoa, as a result of changes in social, educational, and therapeutic attitudes.

In his statement, Dr. Romoa said that “This article demonstrates why exercise continues to be a pillar of not only weight management treatment but the overall health of the community.”

“Exercise should always be used in conjunction with pharmaceutical treatment for persistent lifestyle changes,” he advised.

The National Coalition on Healthcare’s (NCHC) Kelsey Costa, a registered dietitian and health research specialist who was not involved in the study, concurred, saying that “the study findings imply that combining exercise training with a calorie-restricted diet can enhance insulin sensitivity and metabolic health beyond the benefits achieved solely through diet-induced weight loss.”

As Costa said, “It is essential to understand how effectively this combination of therapies can improve metabolic health given what we know about the barriers to exercise in people with obesity.”

For managing prediabetes, insulin sensitivity is essential.

Prediabetes is characterized by persistently elevated blood glucose levels that are not yet high enough to progress to type 2 diabetes.

Although it acts as a warning sign for an elevated risk of getting diabetes, it is frequently preventable or deferred with lifestyle adjustments.

Enhancing insulin sensitivity through exercise

According to Dr. Romoa, “GLUT4, the main insulin-driven glucose transporter, exercise improves insulin sensitivity.”

“GLUT4 is present in adipose and muscular tissue. The amount of these transporters varies depending on a person’s diabetes and obesity condition.

While they drop in adipose tissue, they hold steady in muscular tissue. As a result, exercise can keep enhancing glucose regulation. Due to insulin resistance, adipose tissue can no longer adequately regulate blood glucose. Additionally, exercise will increase the body’s GLUT4 levels. Walking can help lower blood sugar levels, according to Dr. Sergio P. Ramoa.

It was said by Costa that this study showed that “exercise enhances insulin-stimulated glucose uptake, likely due to changes in skeletal muscle biology induced by exercise.”

This includes an improvement in mitochondrial content and function as well as an increase of genes related to substrate oxidation and mitochondrial energy metabolism. The diet plus exercise group consequently saw a more significant rise in muscle insulin sensitivity,” Costa said.

Type 2 diabetes treatment through exercise

Exercise is strongly advised as a main treatment for type 2 diabetes, according to prior research.

Combining 150 minutes per week of moderate to strenuous exercise with dietary and behavioural adjustments can stop, delay, or even reverse the condition.

Exercise of all kinds, including resistance and aerobic training, can regulate blood sugar levels. Small bursts of exercise spread out throughout the day and high intensity interval training are both good.

Exercise in the afternoon or right after a meal, for example, may have additional benefits.

Exercise guidelines that are ideal Working with healthcare experts is crucial for personalised diabetes management because individual aspects are continuously being researched.

Costa stressed “the significance of integrating a calorie-restricted diet with exercise training to enhance metabolic health and physical function.”

Exercise caution

Be sure to consult your doctor before beginning a new workout routine. Make sure you drink enough water before, during, and after the activity.

To keep your blood sugar levels within the desired range, be sure to closely monitor them as well.


For Diabetes medications that have been suggested by doctors worldwide are available here

Is high BMI linked with an increased risk of death?

Is high BMI linked with an increased risk of death?

The validity of body mass index (BMI) as the only predictor of all-cause mortality is further questioned by a recent study.

The majority of earlier research, according to the study’s authors, rely on more dated data that isn’t sufficiently diverse, so they’re hoping the current study may remedy that.

A BMI that indicates overweight or obesity can increase the chance of developing several chronic, fatal diseases, but it may not be a reliable predictor of mortality as a whole.

According to a recent study, it is advisable to take into account a person’s body mass index, or BMI, together with other risk variables when forecasting all-cause death. As an independent variable, BMI might not be a reliable predictor of premature death.

There was no variation in the risk of death from all causes among persons in the healthy and overweight BMI categories, from a BMI of 22.5 to 27.4, according to the research.

However, the study found that in persons with a BMI greater than 30, the risk of all-cause death rose by 21% to 108%.

No appreciable increase in mortality was observed in older persons between BMIs of 22.5 to 34.9, the higher range indicating obesity.

Older statistics on BMI and early death are displaced by new data.

Data from the 1970s that concentrated on non-Hispanic white adults formed the basis of the majority of research on BMI and mortality.

The new study examined more recent, comprehensive data while keeping in mind the changes in lifestyles since that time, including the rise in overweight and obesity, and sought a more varied study population sample.

Self-reported BMI data from 554,332 American individuals who took part in the National Health Interview Survey from 1999 to 2018 and data from the 2019 US National Death Index were used in the analysis.

The average age was 46, there were equal numbers of males and women, and 69% of the population identified as non-Hispanic white, while 12% identified as non-Hispanic Black.

Among the individuals, 35 percent had a BMI between 25 and 30, which is normally regarded as overweight, and 27.2 percent had a BMI of 30 or more, which is categorised as obesity.

A total of 75,807 fatalities were reported throughout the average follow-up period of 9 years and the maximum follow-up period of 20 years.

Why BMI is a poor indicator of health?

We spoke with Dr. Pedro J. Caraballo, medical director of the Mayo Clinic Clinical Decision Support Programme, who was not engaged in this investigation.

“It is extremely debatable whether or not BMI alone should be used to define obesity or health. Different types of obesity that may have an impact on health have clearer definitions. BMI may be easily calculated and found in any medical records, though.

A person’s BMI is calculated by dividing their weight in kilogrammes by the square of their height in metres.

However, BMI ignores other aspects of the body, such as the ratio of fat to muscle, how fat is distributed throughout the body, and metabolic health. For instance, having excess fat around the waist raises your risk of getting sick.

“[BMI] does not distinguish between muscle mass and fat mass, and some individuals, like bodybuilders, may have a high BMI because of more muscle mass,” said Dr. Dagfinn Aune, a research associate in the Faculty of Medicine, the School of Public Health at Imperial College London in the United Kingdom, who was not involved in this study.

Despite these drawbacks, according to Dr. Aune, BMI performs a good job of capturing the elevated risk of chronic disease and mortality that is connected to obesity at the population level.

BMI as a measure of obesity is “not a suitable tool”

Dr. Aune provided a lengthy list of chronic diseases linked to an oversized BMI. These included kidney stones, gallstones, diverticular disease, coronary heart disease, stroke, heart failure, sudden cardiac death, atrial fibrillation, hypertension, type 2 diabetes, and a dozen distinct cancers.

Additionally, preeclampsia, gestational diabetes, gestational hypertension, stillbirth, and infant death are just a few of the pregnancy issues that are linked to being overweight or obese while pregnant, according to Dr. Aune.

The results of this study are outdated in Dr. Caraballo’s eyes. He referenced his own research, which “showed that BMI is an independent risk factor only in extreme values, very low (20) or very high (>40), with risk stratification based on comorbidities.”

Multiple studies, according to Dr. Caraballo, have found that mild to moderate obesity “may help survival when considering a specific subpopulation that is under stress.”

He noted various papers on this subject for “heart disease, kidney disease, cancer, stroke, and rheumatoid arthritis, etc.” and concluded that maintaining energy reserves may be beneficial for people.

According to Dr. Visaria, “the United States has undergone a significant transformation since the 20th century in terms of racial/ethnic makeup, age distribution, healthcare access and treatments, and sociocultural behaviours.”

It is crucial to comprehend the relationship in a more modern population since all of these can affect the association between BMI and all-cause mortality, he said.

Dr. Visaria further emphasized the importance of utilizing the most rigorous techniques to eliminate bias and ensure that observational data is as nationally representative as feasible.

Lower risk of older adults having greater BMI

Dr. Visaria proposed theories as to why this would be the case, given that older adults did not exhibit an increased mortality risk up to a BMI of 35.

We believe that the decline in bone mineral density and sarcopenia that occurs as people age have a role in this. Despite having large quantities of fat, losing these two types of weight can cause you to have excessively normal BMIs, he warned us.

Because of their maintained bone and muscle mass, those with higher BMIs may actually be in better health.

What factors predict total mortality more accurately?

According to Dr. Caraballo, the link between fat and mortality is extremely convoluted.

“Obesity by itself, in the range of mild to moderate, may not be an independent risk factor,” he said. “However, obesity is a significant risk factor for the emergence of numerous metabolic disorders that, over time, raise the mortality risk (diabetes, heart disease, etc.). People may also put on weight when they have a chronic illness because they do less exercise and eat poorly.

In his recommendation, Dr. Visaria said that “physicians should consider supplementing BMI with other measures such as waist circumference, waist-to-height ratio, and waist-to-hip ratio.”

According to Dr. Visaria’s study, “We show that waist circumference significantly modifies the association between BMI and all-cause mortality.”

Dr. Visaria stated, “Bioimpedance scales are another alternative to determine total body fat percent, but they still need to be verified and are known to have some mistakes. Additionally, doctors should consider patients’ cardio-metabolic health factors like blood pressure, blood sugar, and cholesterol levels when interpreting adiposity measurements.


For Obesity medications that have been suggested by doctors worldwide are available here

Higher doses of Ozempic improve blood sugar, weight loss?

Higher doses of Ozempic improve blood sugar, weight loss?

According to experts, glucagon-like peptide 1 (GLP-1) medications like Ozempic, often referred to as semaglutide, can aid in weight loss in those who are obese.

For weight loss, Ozempic is not FDA-approved. There is also the brand Wegovy, which is semaglutide.

Wegovy and Ozempic should not be used by persons who are not diabetic or obese for any reason, including to shed minor amounts of weight, according to experts.

In the latter part of 2017, the FDA approved the use of the GLP-1 medication Ozempic in people with type 2 diabetes. But lately, it’s made news for other reasons as well: Benefits of purported weight loss and scarcity.

“People are talking about them because there is a trend where celebrities and influencers are increasingly turning to off-label use of GLP-1 medications like Ozempic for weight loss by people who are not obese or diabetic,” claims Dr. Rekha Kumar, an endocrinologist in New York City and the head of medical affairs at the weight management program Found.

This, according to Kumar, is very troubling.

“The trend of medispas, boutique weight-loss clinics, and illegal telehealth businesses liberally prescribing to people who don’t meet criteria is not only irresponsible prescribing, but it may also prevent the medication from reaching those who need it most,” Kumar claims.

By responding to the following frequently asked questions regarding Ozempic, Kumar and other professionals distinguished fact from fantasy.

What is Ozempic?

Dr. Angela Fitch, FACP, FOMA, president of the Obesity Medicine Association and chief medical officer of knownwell, a weight-inclusive healthcare firm, says that Ozempic is a brand name for the medication recognised as semaglutide.

Ozempic is an injectable medicine for persons with type 2 diabetes, according to Kumar. The FDA first approved it for 0.5 mg or 1 mg dosages. The FDA authorized a higher dose of 2 mg in 2022.

According to Kumar, it helps the pancreas produce insulin, which decreases blood sugar levels.

Adverse effects of semaglutide

All GLP-1 medications, as pharmacological agents, have the potential to have side effects, according to Dr. Jay Shubrook, professor of the Primary Care Department at Touro University in California.

According to Dr. Shubrook, these “are frequently dose-dependent and can be more obvious during dose changes.”

In any case, typical adverse effects of semaglutide “include an excessive loss of appetite, nausea, and less frequently, vomiting or diarrhoea. Most patients only experience temporary adverse effects, he noted.

He pointed out that teaching patients to eat slowly and mindfully, as well as how to control their portions, can lessen the negative effects of semaglutide.

Is Ozempic an FDA-approved weight-loss product?

No. “Ozempic is only approved for diabetes,” claims Dr. Charlie Seltzer, a Philadelphia-based medical professional who is board-certified in both internal medicine and obesity.

But here’s where some of the ambiguity arises. “The active ingredient, semaglutide, is approved for weight loss under the trade name Wegovy,” claims Seltzer.

Elon Musk tweeted about Wegovy’s assistance with his weight loss in October 2022.

Distinction between Wegovy and Olympic

Semaglutide and injectables are both sold under the trade names Ozempic and Wegovy. They aren’t precisely the same, though.

“Wegovy is FDA-approved for the treatment of overweight and obesity,” claims Kumar. “Wegovy was developed specifically for the treatment of overweight and obesity,” according to the manufacturer. “It contains a higher dose of semaglutide, [2.4 mg], than Ozempic.”

Does Ozempic aid in shedding pounds?

Kumar points out that Wegovy’s dosing was employed in the studies on semaglutide and weight loss, including one from 2021 that showed that once-weekly doses of 2.4 mg of semaglutide could lower body weight when paired with dietary and lifestyle modifications.

“[In the] study,] those who took the medication and made lifestyle changes lost almost 15% of their body weight, on average, compared to 3% in the placebo group,” Kumar claims.

So certainly, semaglutide may aid in weight loss, at least at a greater dose of 2.4 mg. Although Seltzer observes that the two medications function similarly, it is uncertain whether the 0.4 mg dosage difference between Ozempic and Wegovy is significant.

As food takes longer to leave the stomach and suppresses hunger, ozempic prolongs satiety, according to Seltzer. “It does nothing magical to the metabolism.”

In addition, Kumar points out that despite what some celebrities and social media influencers may say, these medications are not intended for those who just want to drop a few pounds.

“Normal-weight patients without diabetes might lose weight if they take GLP-1s, but the risks of the medication outweigh the benefit of weight loss just to be thin versus treating a disease,” says Kumar. “GLP-1s have not been studied in this population, and with this type of inappropriate use, we probably will see more side effects.”

Is Ozempic safe?

For adults with type 2 diabetes, ozempic is typically regarded as safe in doses up to 2 mg, however doctors agree that some people shouldn’t take it.

“It should be avoided in many populations, including but not limited to people with a history of pancreatitis, people who have had medullary thyroid cancer, or who are at increased risk for medullary thyroid cancer,” says Seltzer.

If you are a good candidate for Ozempic, your doctor can help you decide. Furthermore, some persons might suffer negative effects. According to Fitch, typical ones include:

  • nausea
  • constipation
  • dizziness
  • reduction in appetite
  • diarrhea

Can you regain weight after using semaglutide?

Patients who quit taking 2.4 mg dosages of semaglutide had gained back two-thirds of the weight they had lost one year after stopping, according to a trial of nearly 2,000 patients published in 2022.

The same problems that got the people into difficulty in the first place will still exist once the drug is stopped or loses its effectiveness, according to Seltzer, and the weight will quickly regain.

Fitch concurs,

Whatever you do personally to aid in weight loss, Fitch advises, “You have to keep doing it, or the weight will come back.” “The human body was created in this manner. It is constructed to safeguard its weight at all costs. Care for the elderly is crucial.

“Since obesity is a chronic disease, you must treat it chronically, ongoingly, and in a coordinated, comprehensive way,” adds Fitch. For a comprehensive approach to metabolic health, weight control, and primary care, patients must collaborate with their doctor.

What other therapies are there for obesity?

First, Fitch emphasises the need of being nonjudgmental and emphasising joint decision-making in all obesity treatments.

According to Fitch, “obesity is a lifelong chronic disease and should be treated in a compassionate and thorough patient-centered way, such as shared decision making around taking medication or having surgery with the risks and benefits in mind.”

Although diet and exercise are frequently suggested as first-line therapy, they are not always effective.

“Obesity is a complex disease with many factors,” explains Fitch. “We add in other treatments to help patients live longer, healthier, better quality lives when lifestyle changes are not enough.”


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Can antibiotics help in reducing endometriosis symptoms?

Can antibiotics help in reducing endometriosis symptoms?

Researchers discovered that compared to less than 10% of individuals without the ailment, approximately two-thirds of patients with endometriosis have higher levels of a particular bacterium around their uterus.

The researchers observed that the levels of the bacteria and the development of endometriosis-related lesions were decreased after administering antibiotics to endometriosis-affected mice.

To determine whether the results apply to people, however, more research is required.

In the disorder known as endometriosis, uterine lining-like cells proliferate outside of the uterus. Along with symptoms like discomfort and nausea, this can result in the production of scar tissue and inflammation in the pelvic area as well as different organs.

In the entire world, endometriosis affects about 10% of people of reproductive age who were born female. There is presently no cure for the illness, though various therapies can assist control it. Additionally, there is no method to avoid the illness.

Millions of people worldwide could have their health and quality of life improved as a result of further endometriosis research.

Recently, scientists discovered that treating mice with a particular bacterium may lessen lesions related to endometriosis. Science Translational Medicine included the findings in one of its issues.

Not a part of the study, Dr. Marc Winter, medical director of Hoag’s minimally invasive surgical gynaecology, told us:

Fusobacterium, a type of bacteria, is implicated in this study from Japan as a potential agent encouraging the development of inflammatory cells that cause inflammation, scar tissue, and pain related to endometriosis. This finding may prompt the addition of particular antibiotics as an essential component of endometriosis therapy.

Fusobacterium in endometriosis

Starting with fibroblasts from four patients with endometriosis and four individuals without, the researchers performed a genomic study. Cells known as fibroblasts help repair wounds and create connective tissues.

They discovered that individuals with endometriosis had much higher levels of the transgelin (TAGLN) gene. It also codes for a protein known as transgelin, which is involved in cell reproduction and is crucial for the growth of the illness.

The expression of TAGLN, which may result from a bacterial infection, can be upregulated by inflammation. According to prior studies, patients with endometriosis have much higher levels of some bacterial genera than healthy people.

The researchers next evaluated the frequency of a bacterium known as Fusobacterium within and outside of the uteruses of 79 people with and 76 people without endometriosis to examine how the presence of these bacteria in the uterine effects endometriosis.

Fusobacterium was found in higher concentrations in the uterine endometrial tissue of 64.3% and the endometrial tissue that had grown outside the uterus of 52.4% of patients with endometriosis. Only 7.1% of those without the disease had higher concentrations of the bacteria in their uteri.

The scientists then looked into whether Fusobacterium encouraged endometriosis in nine mice models of the disease. They discovered that Fusobacterim-exposed animals had higher uterine lesions than control mice.

In contrast, animals without Fusobacterium did not produce as many uterine lesions. This discrepancy persisted even after oestrogen stimulation, which medical professionals believe may induce tissue resembling uterine lining to develop outside of the uterus.

Treatment with antibiotics lessened symptoms

The final goal of the study was to see whether antibiotics could eliminate Fusobacterium in mice and lessen endometriosis symptoms.

To do this, scientists treated endometriosis-affected mice models with metronidazole and chloramphenicol for a total of five days. After a week, they discovered that the mice no longer had Fusobacterium and that transgelin expression had decreased close to the uterus.

They added that animals given antibiotics had less and smaller endometrial lesions than mice not given antibiotics.

According to the researchers’ findings, both antibiotics might be effective in treating endometriosis. However, they pointed out that it is uncertain why Fusobacterium infects some people.

Endometriosis bacteria are unknown.

We discussed the limits of the study with Dr. Karnika Kapoor, a family doctor from Medical Offices of Manhattan who was not engaged in it.

Since mice don’t have a menstrual cycle and don’t naturally develop endometriosis, the mouse model employed in this study has some inherent limitations, according to the researcher.

She said that there is insufficient evidence in the study to support the theory that endometriosis is promoted by Fusobacterium near the uterus after retrograde menstruation, which occurs when the period flows upward via the fallopian tubes and is thought by some researchers to be a possible cause of the disorder.

The authors were careful to make it clear that their analysis could not establish causation, Dr. Stringfellow did observe. This is an important distinction.

“More research is required to prove that Fusobacterium is a causal agent. To ascertain whether other microbial species might have a harmful function, more investigation is also required, he added.

Treatment with antibiotics can slow the spread of endometriosis.

These two studies provide evidence that antibiotic therapy can slow the spread of endometriosis and stop the early development of endometriotic lesions.

The bacterial ecosystem in the mice given antibiotic treatment was also examined by the researchers. Mice with endometriosis who were not given antibiotics had a greater variety of bacteria in their guts.

The mice that received antibiotic treatment had the least bacterial variety.

For endometriosis, metronidazole might be more efficient.

The effectiveness of metronidazole and neomycin as a stand-alone endometriosis treatment was also investigated by the researchers. Lesions on the mice receiving metronidazole were less severe than those on the mice receiving neomycin.

Additionally, the lesions in the mice receiving metronidazole exhibited fewer inflammatory components.

Finally, mice with endometriosis treated with metronidazole were fed endometriotic mouse faeces. Endometriotic lesions developed and resembled those from endometriosis animals given aspartame in their drinking water in terms of mass and volume.

This shows that the bacterial population in the gut can affect how endometriosis develops and spreads.

Future treatments for endometriosis

Dr. Kapoor discussed the limitations of the available endometriosis treatments today.

The current endometriosis treatment options rely on hormone medication, which prevents women from becoming pregnant while receiving care. The removal of endometrial lesions raises concerns since there is a high recurrence rate, which is an option for people with recurring pelvic pain, she said.

“This research appears to point to a possible Fusobacterium-related mechanism of endometriosis, and that antibiotic elimination is a treatment possibility. If antibiotic therapies for endometriosis are found to be beneficial in subsequent research, we could be able to use them in our clinical practise. Karnika Kapoor, M.D.

Dr. Winter concurred that the discoveries might result in fresh therapeutic approaches. “The function of Fusobacterium in promoting endometriosis may result in a completely new strategy for treating it. Further research is required to understand the contribution of Fusobacterium to the development of endometriosis, according to him.

He said, “The use of a widely prescribed antibiotic metronidazole may be a key in improving the efficacy of endometriosis treatment.”

Further research is required.

If similar effects also occur in humans, more research is needed to confirm this. There may be new endometriosis treatments developed if gut bacteria can affect the onset and course of endometriosis in humans.


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Longer naps may increase the risk of obesity & hypertension

Longer naps may increase the risk of obesity & hypertension

According to research, those who nap during the day for longer than 30 minutes appear to be more likely to be obese and have high blood pressure.

They observed that persons with shorter naps are less likely to develop high blood pressure.

Longer naps, according to specialists, may play a role in these illnesses because they can disturb both eating and sleeping patterns at night.

More than 30-minute naps during the midday may raise blood pressure, increase body mass index, and worsen diabetes and heart-related diseases, according to research.

The prevalence of high blood pressure was lower among people who took what are known as “power naps,” which are midday sleep sessions lasting 30 minutes or fewer.

Researchers from Brigham and Women’s Hospital in Boston evaluated more than 3,000 adults from a Mediterranean population—where midday naps, known as “siestas,” are common—for a recent study that was published in the journal Obesity.

The duration of siestas and their association with metabolic syndrome and obesity were investigated by the researchers.

According to studies, those who take siestas of at least 30 minutes are more likely than those who don’t to have higher blood pressure, a higher body mass index, and other diseases linked to diabetes and heart disease.

Additionally, compared to people who did not take a siesta, those who took brief naps were less likely to exhibit elevated systolic blood pressure. “Not all siestas are the same,” said Marta Garaulet, Ph.D., MS, a senior study author and a visiting professor in the Brigham and Women’s Hospital Division of Sleep and Circadian Disorders. “The health effects of a nap can depend on the length of time, position of sleep, and other particular factors.”

Obesity and Naps

According to Garaulet, the group previously conducted research in the UK and discovered that siestas were linked to a higher risk of obesity. The next step was to examine siestas in a nation where afternoon naps were more prevalent in culture.

According to Garaulet, “in this case, Spain, as well as how the duration of siestas is related to metabolic health.” The group notes that there are more than 1 billion obese people in the world, which is a rising health risk.

In the course of metabolic processes, how people digest food has a connection to fat accumulation in the body. Researchers suggested that studying how habits, such as napping, alter certain metabolic pathways, could contribute in the understanding of how habits affect health.

Findings from the napping research

The group looked at information from 3,275 persons in the Murcia region of Spain.

Participants at the University of Murcia had their baseline metabolic parameters assessed, and information about their naps and other lifestyle elements was gathered. No siestas, shorter than 30 minutes, and more than 30 minutes were the categories into which the subjects were split.

In comparison to those who did not take siestas, subjects who took longer naps had higher body mass indices and were more likely to have metabolic syndrome (MetS).

The extended nap group exhibited greater waist circumference, fasting glucose levels, systolic blood pressure (SBP), and diastolic blood pressure values as compared to the no-siesta group. Longer siestas were linked to later nighttime eating and sleeping, more energy consumed during lunch, and smoking.

Sleep and obesity

A lot of study has been done on the relationship between sleep and obesity, according to Becca Krukowski, PhD, a professor at the University of Virginia School of Medicine.

In contrast, Krukowski noted, “This article adds knowledge about sleep and health risks in a cultural context where naps are promoted among healthy people, across the lifespan, while also considering other potentially related factors, such as nap length and eating patterns.”

According to Krukowski, it’s probable that the health issues led to the lengthier sleeps rather than the other way around. The direction of these correlations cannot be determined from this study because it is cross-sectional. It’s likely that obese people sleep less soundly at night and require longer naps as a result.

The study, according to Krukowski, might be a first step towards more illuminating research.

“Previous studies have shown that weight loss interventions improve sleep quality,” said Krukowski. It could be interesting to look at whether weight loss is impacted by sleep therapies, such as controlling nap length and increasing nocturnal sleep.

More study is required on napping

The authors of the study acknowledged that it’s possible that some factors—rather than siestas per se—might be a result of obesity rather than being caused by siestas, as evidenced by a prior investigation of data from the UK Biobank that found a causal link between napping and obesity, particularly abdominal obesity, which they refer to as the most harmful type.

The link between siestas and health indices was found to be mediated by a number of statistically relevant lifestyle factors, according to the authors.

They urge further investigation into whether a little siesta is preferable to a long one, especially for people who smoke, have bad habits like sleeping in late or delaying meals, or who have delayed sleep patterns.

The Brigham’s Division of Sleep and Circadian Disorders’ Frank Scheer, PhD, a senior neuroscientist and professor in the Medical Chronobiology Programme, commented on the study’s findings in a statement. “This study shows the importance of considering siesta length and raises the question of whether short naps may offer unique benefits,” he said. Numerous institutions are starting to recognise the advantages of quick naps, mostly for work productivity but also more and more for overall health.


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Analyze the links between BMI, obesity & cognitive ability.

Analyze the links between BMI, obesity & cognitive ability.

According to the World Health Organisation (WHO), there were more than 650 million obese adults in the world as of 2016. Obesity has been linked in the past to an increased risk of cognitive deterioration.

Evidence from University College London researchers challenges the idea that fat and cognitive capacity are causally related.

Around the world, more than 1.9 billion adults were obese in 2016, with more than 650 million of those adults suffering from obesity, a disease in which a person’s weight is over normal ranges and may lead to various health issues.

According to current estimates, 167 million adults and children will be overweight or obese by 2025. A multitude of disorders, including diabetes, cardiovascular disease, hypertension, osteoporosis, rheumatoid arthritis, and cancer, have been linked to obesity in previous studies, including these.

Furthermore, previous research has connected obesity to a higher risk of cognitive deterioration.

The causal relationship between obesity and cognitive performance has now been called into question by University College London academics. They contend that common family variables have tainted the research linking cognitive aptitude and BMI.


If a person’s present weight is excessive for their height, they are considered obese. The body mass index (BMI) is the most popular metric for determining a person’s level of obesity.

This tool determines if an adult is obese or not based on their height and current weight:

  • BMI less than 18.5 indicates underweight.
  • Suitable BMI range: 18.5-24.9
  • BMI of 25 to 29.9 indicates obesity
  • obesity: a BMI of 30 or above

Children and teenagers need a different BMI calculator, which considers height, age, and gender to evaluate obesity because they are still developing.

The BMI measurement is not without problems, though. It is unable to distinguish between muscle and fat when weighing someone. Additionally, it disregards a person’s race, overall body composition, or bone density.

Cognitive function and obesity

Lead author of this study and senior research fellow at the Centre for Longitudinal Studies at University College London in the U.K., Dr. Liam Wright, Ph.D., states that there are several reasons why the research team decided to investigate the causal relationship between cognitive capacity and obesity:

“Over the past forty years, there has been a significant rise in the prevalence of obesity, but BMI hasn’t increased uniformly throughout the population. Therefore, it is crucial to understand why some people are more predisposed to obesity than others.

Additionally, there is a substantial body of research in the field of cognitive epidemiology that demonstrates a connection between cognitive function and practically every measure of health and health behaviour, including obesity.

Unfortunately, the majority of the cognitive epidemiology literature employs observational research designs that may be biassed and fail to show causal effects, according to Dr. Wright. “There are some compelling theoretical arguments for why cognitive ability might have a causal effect on health, but regrettably, these arguments are based on observational research designs,” she said. Because a sibling design could take into account some of the variables that can skew relationships found in previous research, we felt it was crucial to investigate for a relationship between cognitive capacity and BMI.

Examining siblings to reduce bias

Dr. Wright and his research group evaluated data from four distinct young population cohort studies carried out in the United States that included 12,250 siblings from 5,602 homes. Each participant’s data were tracked from youth to age 62.

The scientists were able to take into consideration unobserved characteristics associated with family background by analysing the relationship between cognitive capacity and BMI among families.

“Sibling designs account for factors that are shared between siblings by design,” Dr. Wright said. They don’t require the measurement of these factors, which is both a benefit and a drawback because it is difficult to determine which common factors actually contribute.

With this qualification, he continued, “There are four main factors that we thought might be significant: genetics (siblings share 50% of DNA), parental socioeconomic class (wealth, location, etc.), parenting styles (particularly regarding dietary choices), and parental cognitive ability (cognitive ability could operate indirectly!). “Once more, we didn’t directly examine these.”

According to Dr. Wright, they predicted that these variables would make general population studies more biassed and lead to weaker relationships than in earlier studies, which is exactly what they found.

However, he cautioned, “remember that sibling designs have their own flaws, including the ability for siblings to influence one another, for example, by modelling one another’s behaviour. This may imply that our findings are also skewed, albeit downwardly and smaller than the actual causal effect.

Association between BMI and cognitive ability

When the researchers evaluated the data from study participants who were not related, they discovered that, after accounting for family socioeconomic status, the change in teenage cognitive capacity from the 25th to the 75th percentile was associated with an estimated 0.61 kg/m drop in BMI.

And when the researchers analyzed the information from siblings, they discovered that the change in BMI from the 25th to the 75th percentile of teenage cognitive ability was only correlated with a 0.06 kg/m drop in cognitive capacity.

The relationship between cognitive capacity and BMI was less pronounced when siblings were compared than when the entire population was, according to Dr. Wright, but he was not surprised by this given the overall characteristics he mentioned.

However, he noted, “I was shocked at how little of an association there was when comparing siblings. As said, there are strong arguments to support the idea that cognitive ability has an impact on health and health-related decision-making“.

“Two possibilities for this small association are that one, our results were biassed towards finding smaller associations (e.g., by siblings influencing each other), and two, reflective decision-making isn’t as important in determining BMI as other factors like satiety, etc.,” Dr. Wright continued. Both of these are hypothetical.

Unproven causality

As a parent and a neurologist, Dr. Segil claimed that he has never observed a connection between obesity or a healthy weight and cognitive aptitude in people.obese

The purpose of this study, according to Dr. Segil, “is to argue that people with higher cognitive abilities, who have a higher socioeconomic position, have made healthier decisions.” Additionally, it’s possible that people’s cognitive function increases as their BMI decreases when they make healthier decisions.

He continued, “I do not believe that there is any evidence linking obesity to cognitive function. And I believe that their research’s use of siblings or other family members who are in a similar social economic situation to real-life situations such as brothers or sisters or siblings is realistic.”

After reading this study, Dr. Segil stated that he would be curious to know whether maternal or paternal obesity had a greater impact on adolescent cognitive development.

As a result of reading this, they claimed that adolescent cognition is linked to a lower adult BMI, he continued. So I’m keen to know if stronger adolescent cognitive abilities are related to the maternal and paternal BMI. Does having a thin or fat parent, using the same dataset, alter their children’s cognitive ability?I was shocked, though, by how little of an association there was when comparing siblings. As mentioned, there are strong arguments to support the idea that cognitive ability has an impact on one’s health and decision-making in relation to their health.


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Can hormones predict the possibility of weight loss?

Can hormones predict the possibility of weight loss?

In addition to being one of the world’s greatest killers, obesity is linked to several medical disorders. The majority of people who do succeed in losing excess weight do so only to gain it back, which frequently frustrates attempts to shed excess weight through lifestyle changes.

Understanding the complicated function that hormones play in this process may aid in the creation of effective long-term treatments for obesity.

Now that higher levels of the hormone neurotensin have been connected to greater weight loss maintenance in obese individuals, this information provides another hint as to how to rebound weight gain might be controlled.

It has long been understood that while many people who struggle with overweight or obese can lose excess weight through lifestyle changes like diet and exercise, it can be difficult for many of them to keep it off.

The World Health Organisation (WHO) views obesity as an epidemic since it causes more than 4 million deaths annually. Many of these fatalities are thought to be preventable with weight loss. For instance, it has been demonstrated that a weight loss of 5–7% can halt or delay the onset of type 2 diabetes.

Sadly, up to 80% of people who lose weight through diet and exercise gain back every bit of the weight they previously did. In the past, this weight increase has been attributed to a lack of self-control or a failure to follow weight maintenance plans.

A higher level of the hormone neurotensin may be associated with a superior capacity to maintain weight loss in obese people who have recently lost weight, according to the most recent research, which gives a fresh explanation.

Do we regain weight after weight loss?

The assumption that the body would return to a predetermined weight despite weight loss or growth has been proposed as one theory to explain why people experience rebound weight gain.

Bariatric surgeon Dr. Mir Ali of Orange Coast Medical Centre in Fountain Valley, California, who also serves as the center’s medical director, explained:

According to the set point theory, there is a weight that your body prefers to maintain at all times (within 5 to 10 pounds). This set point can be influenced by a variety of factors, including age, heredity, sex, health issues, and degree of activity. But it’s unclear what mechanisms might be at work in this observation.

The importance of hormones in hunger regulation has just recently come to light, despite the WHO reporting a rise in the number of persons with obesity starting in the 1970s. Only in 1999 was ghrelin, a hormone that promotes the desire to eat, separated and identified. Its ability to control hunger, fat storage, and energy regulation is now well documented. It also has interactions with other hormones like insulin which are important in regulating energy and storing fat.

Researchers have postulated that the fact that ghrelin levels tend to increase after weight reduction brought on by diet and exercise may be the cause of “rebound weight gain.” Contrarily, after bariatric surgery, which has a lower rate of rebound weight gain than diet and exercise-based therapies, levels of this hormone drop.

Less than 20 years ago, in 2004, researchers found that ghrelin and leptin, a hormone that controls satiety and long-term energy balance, interact. Since then, it has been shown that obese individuals have leptin resistance, which makes them less susceptible to its appetite-suppressing benefits.

looking into the neurotensin hormone

Recently, the focus has shifted to a different hormone termed neurotensin and its potential contribution to weight gain following weight reduction. The brain and intestines both generate this hormone. Previous studies have demonstrated that neurotensin levels rise following bariatric surgery, much like other hormones that control hunger and energy expenditure.

According to Dr. Gina Leinninger, an associate professor of physiology at Michigan State University who studies how the body manages its energy and how it affects obesity in people.

The possibility that neurotensin could modify body weight has drawn increasing attention. We were aware from earlier studies that neurotensin could cause animal models to eat less and move around more, two behaviors that might help them lose weight.

Higher neurotensin levels following meals may be associated with an individual’s likelihood of maintaining weight loss, according to a group of Danish researchers. In mice and obese adults, they also demonstrated a drop in neurotensin levels following weight loss.

Effects of neurotensin on preserving weight loss

8 obese mice were kept on a regular diet as controls, while 9 obese mice were placed on a calorie-restricted diet for 8 days. After the animals were put to sleep, the scientists collected samples from the duodenum, jejunum, ileum, and proximal colon to examine the levels of neurotensin expressed in those regions.

The goal of the calorie-restricted diet for mice was to promote weight loss that was comparable to what was shown in the 8-week human research.

The amounts of neurotensin in the jejunum region of the small intestine were much lower in the mice whose access to food was restricted, the researchers discovered.

The next step was to examine how a group of 42 obese patients responded to an extremely low-calorie diet plan of roughly 800 calories per day for eight weeks. Following this regimen, participants lost 12.3 kg on average. Participants underwent testing to see how their leptin, insulin, ghrelin, and neurotensin levels changed in the three hours following a meal after these 8 weeks.

For a further 52 weeks, researchers gave this group of participants instructions to eat a diet with a calorie restriction (600 fewer calories than their daily requirements).

Researchers examined data for a subcohort of participants from both groups—those who had lost over 3% weight during the maintenance period and those who had gained at least 5% of their initial weight loss—in order to examine the effect of hormones on weight loss maintenance.

After the initial 8-week weight loss phase, they discovered that those who had initially displayed a higher level of neurotensin in the three hours following a meal were more likely to have continued to lose weight during the maintenance phase.

What does this indicate for the management of obesity?

The Metabolism research is the first to link variations in circulating neurotensin to better/more sustained weight loss results in humans, and it suggests that (in the future), manipulating the neurotensin system might be helpful to support and/or optimise weight reduction. Dr. Leinninger acknowledged that there is still much to learn before that objective can be met.

In her own research, Dr. Leinninger examined the areas of the brain that neurotensin affects and if these areas are involved in the management of energy and obesity. That will be the focus of the following research steps.

How neurotensin can regulate weight and, more particularly, where in the body it acts, are the next great unanswered mysteries. We have some promising results in my lab’s investigation into how and where in the brain neurotensin can affect body weight, she said.


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