How brain regulates fat burning

Scientists have discovered a molecular switch in the brain that regulates fat burning and could provide a way to control weight gain following dieting. Monash University researchers have identified a molecular switch in the brain that potentially controls the human body's capacity to store fat, particularly after long periods of "famine" or weight loss-a process that underlies yo-yo dieting, where the body regain the weight lost caused by dieting.

Being able to control this switch may be a therapy for obesity and other metabolic disorders such as Type 2 diabetes. Associate Professor Zane Andrews and his colleagues at the Monash Biomedicine Discovery Institute have identified a protein in mice, called carnitine acetyltransferase (Crat), in hunger-processing brain cells that regulate fat storage after dieting.

During dieting, the body burn more fat to provide enough energy. But at the same time the brains fight to conserve energy and, as soon as food becomes available, the body switches from burning to storing fat and instead uses ingested calories from food.

The international research team discovered the Crat protein and developed a mouse that had this protein genetically switched off. These mice, when fasted or fed after a fast, consume their fat reserves at a greater than normal rate.

Repeated dieting, or yo-yo dieting, may lead to weight gain because the brain interprets these diets as short famines and urges the person to store more fat for future shortages. For the first time the Crat protein in hunger-processing brain cells has been identified as the switch that instructs the body to replace the lost weight through increased fat storage.

Manipulating this protein offers the opportunity to trick the brain and not replace the lost weight through increased appetite and storage of fat, regulating this protein can ensure that diet-induced weight loss stays off rather than sneaking back.
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Links between gut bacteria and obesity

A new Johns Hopkins study of mice with the rodent equivalent of metabolic syndrome has added to evidence that the intestinal microbiome-a "garden" of bacterial, viral and fungal genes plays a substantial role in the development of obesity and insulin resistance in mammals, including humans.

Highlighting the potential to prevent obesity and diabetes by manipulating levels and ratios of gut bacteria, and modifying the chemical and biological pathways for metabolism-activating genes.

Metabolic syndrome, a cluster of conditions including obesity around the waist, high blood sugar and increased blood pressure, is a risk factor for heart disease, stroke and diabetes. While no precise cause for metabolic syndrome is known, previous studies of Toll-like receptor 4 (TLR4), a protein that receives chemical signals to activate inflammation, have suggested that TLR4 may be responsible in part for its development.

TLR4 signaling in different cells and their association with the bacterial environment could result in different effects on the development of metabolic syndrome. To determine whether TLR4 specifically in the intestinal epithelium (layer of cells that line the small and large intestines) would cause the development of metabolic syndrome, the research team ran a series of experiments on normal mice and mice genetically modified to lack TLR4 in their intestinal epithelium.

The researchers fed both groups of mice "standard chow," with 22 percent fat calories, for 21 weeks. Compared to normal mice, those lacking TLR4 showed a series of symptoms consistent with metabolic syndrome, such as significant weight gain, increased body and liver fat, and insulin resistance. The researchers then fed both groups of mice a high-fat diet comprised of 60 percent fat calories for 21 weeks to find out whether diet would affect the development of metabolic syndrome.

The genetically modified mice gained significantly more in weight and had greater body and liver fat than the normal mice. To confirm the role of TLR4 expression in the intestinal epithelium, the researchers genetically modified three more groups of mice: one group expressed TLR4 only in the intestinal epithelium, another group lacked TLR4 in all body cells and the third group lacked TLR4 only in white blood cells.

All groups ate standard chow, and all groups had similar body weight, body and liver fat, and glucose tolerance compared to normal mice. Compared with normal mice, belly and small intestine fat was higher in mice lacking TLR4 only in the intestinal epithelium. This, the researchers say, provides further evidence that deleting TLR4 specifically from the intestinal epithelium is required for developing metabolic syndrome.

To investigate the role the bacterial makeup of the gut had on the mice, they administered antibiotics to the normal and TLR4 intestinal epithelium-deficient mice. Antibiotics significantly reduced the amount of bacteria in the intestinal tract and prevented all symptoms of metabolic syndrome in the mice that lacked TLR4 in their intestinal epitheliums.

This shows that bacterial levels can be manipulated to prevent the development of metabolic syndrome. To further explore the role of intestinal epithelial TLR4 on the development of metabolic syndrome, the research team analyzed fecal samples from the TLR4 intestinal epithelium-deficient and normal mice.

The team found that specific clusters of bacteria that contribute to the development of metabolic syndrome were expressed differently in the deficient mice than in normal mice. They also determined that the bacteria expressed genes that made them "less hungry" and thus less able to digest the nutrients present in the mouse chow. This resulted in a greater abundance of food for the mouse to absorb, which contributed to obesity.

The researchers then analyzed the genes expressed in the lining of the intestinal mucosa-the site at which food absorption occurs in normal and TLR4 intestinal epithelium -deficient mice. Of note, the team determined that important genes in the perixisome proliferator-activated receptor (PPAR) metabolic pathway were significantly suppressed in the deficient mice.

Administering antibiotics prevented the differences in gene regulation between the two groups of mice, as did administering drugs to activate the PPAR signaling pathway. The bacterial sensor TLR4 regulates both host and bacterial genes that play unrecognized roles in energy metabolism leading to the development of metabolic syndrome in
mice.
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Breast cancer therapies linked to heart failure

According to American Heart Association, women should consider the risks and benefits of any therapies that may hurt hearts during breast cancer treatment, patients should have a conversation with their doctor about the side effects of the treatment. Some treatments for different types of cancer may pose heart risks, but they are growing more common for breast cancer patients.

Side effects can include abnormal rhythms, valve problems or heart failure, where the heart slowly weakens and can't pump effectively. Symptoms may not appear until long after treatment ends.
Herceptin and similar drugs for a specific type of breast cancer can cause heart failure. Sometimes it's temporary and goes away if treatment is stopped, but it can be permanent.

Radiation can affect arteries and spur narrowing or blockages. Other drugs can lead to abnormal heart rhythms or artery spasms, which can cause chest pain and possibly lead to a heart attack. Some research suggests that powerful new drugs that harness the immune system to fight cancer may in rare cases cause heart damage, especially when used together.

Certain chemotherapies such as doxorubicin, sold as Adriamycin and in generic form, might be less risky if given more slowly, rather than all at once. Some research suggests that a drug called dexrazoxane may minimize damage if given to women with advanced breast cancer who are getting high doses of doxorubicin.

Cancer patients should make sure doctors are monitoring their heart before, during and after breast cancer treatment. Common risk factors of breast cancer are: obesity, smoking, sedentary lifestyle and eating of junk food.
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Sound sleep leads to healthy weight

Sleep can foster healthier eating habits, sleeplessness is one of the lifestyle factors that can contribute to obesity. For the study, researchers led by Wendy Hall, from the department of nutritional sciences at King's College, recruited 42 people who habitually got less than seven hours of sleep a night.
Half of the people received a 45-minute personalized sleep consultation, which provided them with tips to improve their sleep. The goal was to extend their sleep by as much as an hour and a half each night. The other half received no advice and served as the control group.

All participants were equipped with a wrist-worn motion sensor that kept track of how much they slept each night, as well as the amount of time they spent in bed before falling asleep. They also kept food diaries to track what they ate. Sleep and diet were monitored for a week. Nearly 9 in 10 of the people who received advice increased their sleep time during the week. No significant changes in sleep patterns occurred among those in the control group.

Those who got more sleep wound up with a 10-gram reduction in their daily intake of added sugars, the researchers found. But over time those added sugars can add up, especially if sleeplessness also keeps a person from being more active in their daily life. Sleeplessness could influence a person's food choices-hunger-dampening hormone called leptin which is secreted when people enter the deeper stages of sleep, lack of sleep could mean that people's appetites are instead being driven by ghrelin, which is known as the "hunger hormone.''

People with insomnia tend to develop a lack of inhibition due to their sleeplessness, it becomes harder to resist certain foods and other things. For sound sleep, avoid caffeine and alcohol about four to six hours before bedtime, eat a moderate amount in the evening, so you don't go to bed too full or too hungry.
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Severe obesity linked to gene mutations

Researchers have discovered mutations in a gene related to obesity, offering new treatment possibilities in the fight against the global epidemic. The new study, led by Imperial College London  focused on children suffering from obesity in Pakistan, where genetic links to obesity had been previously identified by the team in about 30% of cases.

This link of genes to obesity is due to recessive mutations that are more likely to be inherited and passed on to children in a region like Pakistan because of the high level of consanguinity (inter-family relationships) in its population. This is because parents who are closely related are more likely to be carrying the same mutation, so a child may inherit from both sides, causing the mutation to take effect.

This new study used genome sequencing and found mutations in one specific gene related to obesity: adenylate cyclase 3 (ADCY3). When mutations occur in ADCY3, the protein it codes for forms abnormally and doesn't function properly. This leads to abnormalities relating to appetite control, diabetes, and even sense of smell.

Early studies into ADCY3 tested mice that were bred to lack that gene, found that these animals were obese and also lacked the ability to smell, known as anosmia. When we tested our patients, we found that they also had anosmia, again showing a link to mutations in ADCY3.

ADCY3 is thought to impact a system that links the hypothalamus to the production of hormones that regulate a wide variety of biological functions, including appetite. This research also found a link between ADCY3 mutations and obesity, a
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Excess fat upsets heart cells

A University of Iowa study has identified how excess fat in the heart, a common feature in diabetes and obesity, can harm the cells' essential ability to produce energy. Researchers believe the mechanism may contribute to the two- to five-fold increased risk of heart failure in people with diabetes. The heart is the most energy-hungry organ in the body. Just like a combustion engine burning fuel to power the pistons, healthy heart cells consume fuel molecules to create the necessary energy to keep the heart pumping.

This essential energy production takes place inside mitochondria, the self-contained "powerplant" organelles inside cells. Although mitochondria in a healthy heart primarily use fatty acids as fuel, they can easily adapt to use other fuel molecules as needed, including glucose, lactate, and ketone bodies. Diabetes, however, reduces the heart muscle's metabolic adaptability and causes heart cells to overuse fat as a metabolic fuel.

 Cardiac lipid overload leads to numerous small, misshapen mitochondria that don't produce energy as efficiently as normal mitochondria. Previous research from the UI team has suggested that problems with mitochondrial energy production may play a role in heart failure associated with diabetes. Diabetes increases the risk of heart failure and one of the cardinal manifestations of the hearts of people with diabetes is the tendency to overuse fat as a metabolic fuel, which ultimately leads to mitochondrial and cardiac damage.

 Increasing the amount of fat (lipid) that the heart consumes leads to dramatic changes in the structure and function of the mitochondria in the heart. These studies provide a new window into how these changes to mitochondria could occur in the lipid-overloaded heart. The UI team used genetically modified mice that mimic the increased fatty acid uptake (lipid overload) that characterizes diabetes to investigate the consequences of cardiac lipid overload on mitochondria. A novel 3-D electron microscopic cellular imaging technique developed by colleagues in Germany allowed the researchers to directly observe the structural changes to the mitochondria - rather like putting on a virtual reality headset inside the cardiac muscle cell.

 In the mouse model, lipid uptake to heart is doubled. This modest increase resulted in mitochondria that became thinner and more twisted than mitochondria in healthy heart cells. These structural changes (almost like a noodle snaking through the heart) lead to an appearance of mitochondrial fragmentation when imaged by conventional electron microscopy. The study also revealed the molecular cause of the change in mitochondrial structure. Prolonged lipid overload leads to increased levels of damaging substances called reactive oxygen species (ROS). The excess ROS disrupts the mitochondrial network by altering the activity of several important proteins that help control the size and shape of mitochondria.

Removing the excess ROS by overexpressing a molecule that helps "mop up" ROS molecules restored normal-looking mitochondria, which worked properly, despite the lipid overload. Using the same approach to remove ROS in normal heart cells led to mitochondria that were four times as large as normal, suggesting that ROS levels are inversely proportional to mitochondria size. The findings suggest that cardiac lipid overload disrupts normal mitochondrial structure, which may impair energy production and compromise heart function.
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Effects of obesity on bone marrow cells

According to new research, obesity causes durable and harmful changes to the hematopoietic stem cell compartment-the blood-making factory in human body. Blood stem cell compartment is made up of numerous cell subsets, age and environmental stresses can lessen the healthy diversity of cells in human blood-making machinery. This can include skewing blood cell formation toward myeloid cells and possibly promoting pre-leukemic fates.

Obesity related stresses alter the cellular architecture of the hematopoietic stem cell compartment and reduce its long-term functional fitness. Tests in obese mice show these effects are progressive and that some of the harmful manifestations persist even after researchers normalize the animals' weight through dietary controls. Alterations of the body's blood-making system appear to be linked to over- expression of a transcription factor called Gfi1- a regulatory gene that controls other genes. The researchers show that oxidative stresses in the body caused by obesity drive overexpression of Gfi1.

 This produces a lasting alteration of hematopoietic stem cell compartment and molecular mayhem. The study also provides groundwork to investigate how lifestyle choices, such as diet, can durably impact blood formation and may contribute to the development of blood cancer. Hematopoietic stem cells are an important tool for treating leukemia and other blood diseases.
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Habits that increase the risk of cancer

Forty per cent of cancer deaths could be prevented with simple lifestyle changes. Quitting smoking, eating healthier and boozing less would stop the disease. Scientists suggest habits responsible for cancer with tobacco proving the biggest burden. Other habits, includes excessive UV radiation, obesity and not exercising enough can be blamed.

Researchers at the QIMR Berghofer Medical Research Institute, Brisbane, said the total amount is greater than 38 per cent because many deaths involved two factors. Even 'small improvements' would reduce the risk of dying prematurely from cancer, the Australian researchers claimed. Their findings, which also highlighted irresponsible sun tanning as a cause, were derived from an analysis of cancer deaths.

Obesity and infections were responsible for five per cent of the deaths while not exercising enough was blamed for 0.8 per cent.Dr David Whiteman, lead researcher of the study published in the International Journal of Cancer, found that the bad habits fueled 41 per cent of cancer deaths in men and 34 per cent in women because men smoke and drink more, spend more time in the sun and don't eat healthy foods.

The researchers concluded that the following eight habits are responsible for 38 per cent of cancer deaths. Researchers at the QIMR Berghofer Medical Research Institute, Brisbane, said the total amount is greater than 38 per cent because many deaths involved two factors. The habits are-Smoking, Poor diet, Boozing, UV radiation, Obesity, Infections, Inactivity and Hormones.
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Anti-stress compound reduces obesity and diabetes

Stress protein found in muscle has a diabetes promoting effect. For some time, researchers have known that the protein FKBP51 is associated with depression and anxiety disorders. It is involved in the regulation of the stress system – when the system does not function properly; mental disorders may develop. Now, researchers have discovered a new, surprising role for this protein: It acts as a molecular link between the stress regulatory system and metabolic processes in the body.

FKBP51 influences a signaling cascade in muscle tissue, which with excessive calorie intake leads to the development of glucose intolerance- the key indicator of diabetes type 2. An unhealthy diet, rich in fat means stress for the body. If FKBP51 is increasingly produced in the muscle it leads to reduced absorption of glucose – as a result, diabetes and obesity may develop.

If FKBP51 is blocked, diabetes will not develop, even if too many calories are consumed or the body is still stressed. Less FKBP51 in the muscle tissue means reduced glucose intolerance and thus maintenance of normal metabolism. The protein FKBP51 can be pharmacologically blocked by antagonist compounds
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Dangers of painkiller drugs

Commonly prescribed painkillers need to be given for shorter periods of time to reduce the risk of obesity and sleep deprivation. Findings show that medications commonly used to treat pain, like gabapentinoids such as gabapentin, pregabilin and opiates, increased the risk of obesity and were associated with poor sleep.

Scientists assessed the cardio-metabolic health - the inter-relationship between metabolic and cardiovascular disease in many participants. Body Mass Index, waist circumference and blood pressure were compared between those taking painkillers for chronic, non-cancer pain and cardio-metabolic drugs, compared to those prescribed cardio-metabolic treatment only. Conditions that can require the use of this treatment include migraine, diabetic neuropathy and chronic lower back pain.

Findings of the new study show people on opiates and cardio-metabolic drugs reported 95% rates of obesity, 82% 'very high' waist circumference and 63% hypertension, as opposed to those on cardio-metabolic drugs only. Results suggest that chronic pain medications should be prescribed for shorter periods of time to limit serious health complications. Opioids are recognised as being among the most dangerous prescription painkillers because they are addictive which can lead to them being abused.

Patients can require continuous use of the drugs to feel normal and avoid symptoms of withdrawal.
In the last decade, the number prescribed has doubled and long-term use has become increasingly controversial as the medication causes sleep disorders, daytime sedation and accidental overdose.

There are a number of possible reasons why opioids can be associated with significant weight gain and obesity. For example, they can act as a sedative which makes patients less active and they have been shown to alter taste perception with a craving for sugar and sweet foods. Opioids are also known to worsen snoring and untreated sleep apnea, as well as causing problems with nocturnal hypertension.
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Link between obesity and diabetes

Researchers have identified a major mechanism by which obesity causes type 2 diabetes, which is a common complication of being overweight. In obesity, insulin released into the blood by the pancreas is unable to pass through the cells that form the inner lining of blood vessels.

As a result, insulin is not delivered to the muscles, where it usually stimulates most of the body's glucose to be metabolized. Blood glucose levels rise, leading to diabetes and its related cardiovascular, kidney and vision problems.

 A major problem in obesity is the delivery of circulating insulin to the muscle, this problem involves immunoglobulins, which are the proteins that make up circulating antibodies. The researchers found that obese mice have an unexpected chemical change in their immunoglobulins.

The abnormal immunoglobulins then act on cells lining blood vessels to inhibit an enzyme needed to transfer insulin from the bloodstream into the muscle. Type 2 diabetes patients have the same chemical change, and if immunoglobulins from a type 2 diabetic individual is given to a mouse, the mouse will becomes diabetic.
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Using mouthwash increases the risk of obesity and diabetes

Using mouthwash twice a day significantly raises the risk of obesity and developing type 2 diabetes, according to a new study. Swilling with the anti-bacterial fluid could be killing beneficial microbes which live in the mouth and protect against the conditions. People who used the product twice a day were around 55 percent more likely to develop diabetes or dangerous blood sugar spikes.

Popular mouthwash solutions include ingredients that kill good and bad bacterial. Most of these antibacterial ingredients in mouthwash are not selective- they do not target specific oral bacteria-instead, these ingredients can act on a broad range of bacteria.
Researchers looked at overweight people who were at risk of developing diabetes. Over the study period, around 17 per cent developed diabetes or pre-diabetes, but that rose to 20 per cent for those using mouthwash once a day, and 30 per cent for those using it in the morning and evening.

Helpful bacteria in the mouth can protect against obesity and diabetes, as it helps the body produce nitric oxide. This important molecule helps trillions of our cells to communicate with each other by transmitting signals throughout the entire body and regulates insulin levels and our metabolism. Commonly-used mouthwashes typically contain powerful bacteria-killing formulas including cetylpyridinium chloride, chlorhexidine, triclosan, alcohol, fluoride, peroxide and essential oils. However, the researchers warn killing off good helpful bacteria also makes room for harmful bacteria to thrive.
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Drinking of alcohol and metabolic factors increase the risk of liver disease

There is an increasing burden of liver disease and liver cancer. The metabolic syndrome and heavy alcohol consumption are associated with increased risks of liver disease, although only a minority of patients with early-stage liver disease (e.g. fatty liver) develop liver failure or liver cancer. Few general population studies have analyzed metabolic predictors of such severe liver complications.

Researchers studied which metabolic factors best predict severe liver complications. Their analysis included people without liver disease who participated in the Finnish population-based Health 2000 Study (2000-2001). The researchers analyzed follow-up data on liver-related hospital admissions, mortality, and liver cancer from national registers.

Some of the participants experienced a severe liver event during follow-up. Factors predictive of liver events were older age, female gender, alcohol use, diabetes, LDL cholesterol, and insulin resistance. Among individuals who consumed higher amounts of alcohol (average alcohol use ?210 g/week for men, ?140 g/week for women), diabetes was the only significant predictor.

Among those who consumed less or no alcohol, older age, alcohol use, smoking, abdominal obesity, LDL cholesterol, and insulin resistance were significant predictors. Alcoholic liver disease ALD and non-alcoholic liver disease NAFLD are considered separate entities, distinguished from each other by an arbitrary threshold of average alcohol intake.

This diagnostic approach assumes that alcohol intake does not affect the course of NAFLD and that the metabolic syndrome is the hallmark of NAFLD is not a factor in ALD. This study reveals that alcohol is a relevant risk factor even when alcohol consumption is within the limits currently used to separate NAFLD from ALD.

Liver disease should perhaps not be considered in terms of mutually exclusive entities of ALD and NAFLD, because in a large number of patients with liver disease, the effect of alcohol is difficult, and sometimes impossible, to separate from the effect of metabolic factors.

 Alcohol use and metabolic factors are taken into account at the same time in order to identify individuals with a high risk for severe liver complications. For a comprehensive liver-risk assessment, lipid abnormalities, abdominal obesity, insulin resistance, diabetes, and alcohol use should all be considered at the same time.
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Effects of parents' lifestyle on their children

The importance of parents' characteristics for their children's health is explained by poor living conditions in childhood lead to poverty in adulthood-which affects health and
the transmission of sound or ill health to children. Beyond the obvious common genetic inheritance across generations, parents' health also has an impact on their children's health by imparting habits and lifestyles.

Our research found that if a parent smoked when their child was young, the child was much more likely to smoke as an adult. A person's obesity in later life was more frequent when their parents were smokers and had a problem with alcohol. Obesity was one not only associated with parents having a problem with alcohol it was also associated with parent being smoker. If a person's father smoked when they were 12, they were almost twice as likely to smoke than people whose father did not smoke at all.

If mothers smoked, it increased the risk of their daughters smoking – but not their sons. The risk that a person would smoke was also higher among those whose father was a manual worker, and who had experienced periods of poverty during their childhood. Our findings should give pause for thought to those who devised the new NHS plans to stop smokers or obese patients from having surgery unless they quit smoking or lose weight.

The decision assumes that these patients' poor health is self induced, so they are made to choose between facing the consequences of their lifestyle or demonstrating a commitment to change. These sorts of public health policies don't take into account that lifestyle is strongly associated with circumstances beyond a person's control, especially their childhood circumstances and their parents' health and lifestyles.

Restricting their access to treatment appears especially unfair when people do not have equal opportunities to be in good health and to adopt healthy lifestyles. People would only be responsible for the share that isn't linked to their childhood conditions or their parents' choices. The study shows that, even without making this distinction between responsibility and true responsibility, the control of people on their health choices and their health status is limited.
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Dangers of taking energy drink

Short-term benefits of energy drink can be outweighed by serious health risks which include risk-seeking behavior, mental health problems, increased blood pressure, obesity and kidney damage. The health risks suggests they are harmful to health and should be limited through more stringent regulation by restricting their sales to children and adolescents.

Most energy drinks consist of similar ingredients-water, sugar, caffeine, certain vitamins, minerals and non-nutritive stimulants such as guarana, taurine and ginseng. Some can contain up to 100 mg caffeine per fluid ounce, eight times more than a regular coffee at 12 mg. A moderate daily caffeine intake of up to 400 mg is recommended for adults, but little research exists on tolerable levels for adolescents and children. Energy drinks are often marketed as a healthy beverage that people can adopt to improve their energy, stamina, athletic performance and concentration, but researchers discovered that they have  health consequences.

 The health risks associated with energy drinks are mostly attributed to their high sugar and caffeine levels. They range from risk-seeking behavior, such as substance misuse and aggression, mental health problems in the form of anxiety and stress, to increased blood pressure, obesity, kidney damage, fatigue, stomachaches and irritation.
Mixing energy drinks with alcohol leads to consumption of more alcohol than drinking alcohol alone, leading to dehydration and alcohol poisoning.
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Traumatic event increase a woman's risk of obesity

According to a new study, women who have experienced traumatic events are more likely to become obese. Researchers discovered that the more traumatic events women reported experiencing in the last five years, the more likely they were to become obese. Obesity can leads to elevated risk for cardiovascular disease, diabetes, stroke, and other serious health problems.

As much as 20 percent of people who experience trauma develop post traumatic stress disorder PTSD, but women are twice likely to suffer from the disorder as are their male counter parts. Stress from sources like bullying and economic strain has well-documented links to eating disorders, including over-eating and obesity. Since women are more prone to both extreme stress or PTSD and obesity, the study authors suggest that more attention needs to be paid to these relationships.

The researchers analysed data on both the women’s body mass indexes BMI and self-reported stress. The divided stressors into two categories: Significant traumatic events like physical violence or the death of a child that could have occurred any time in their lives and still be affecting them, and ‘negative life events’ that had occurred in the last five years.

Living through just one traumatic life event increased the risk of obesity by 11 percent, over that of women who reported no traumatic events. Those that had experienced four or more ‘negative life events’ were at a 36 percent greater risk of obesity.Women are living longer and are more at risk for chronic illnesses, such as cardiovascular disease, obesity is related to increased risks of heart attack, stroke, diabetes and cancer, and contributes to spiraling healthcare costs.
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Low testosterone levels reduces the risk of prostate cancer

Men with low testosterone may not develop prostate cancer. Reducing testosterone hormone could reduce the risk of the cancer. Scientists who examined different men discovered that those with the lowest testosterone levels were 20 per cent less likely to get the cancer.

One in eight men will develop prostate cancer, with approximately 46,700 cases a year. But little is known about what causes the disease, unlike most cancers, it does not seem to be linked to obesity, exercise, smoking or alcohol.

Prostate cancer tumours need testosterone to grow, men with lower levels are less likely to get the illness. Reducing the levels of testosterone could unravel ways to diagnose and treat fatal prostate cancers before they can do any harm.
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Obesity increases the risk of knee dislocation

Knee dislocations occur when the knee is disrupted because of multiple torn ligaments in the joint. Typically, this happens in vehicle crashes or contact sports like football. There is an increase in knee dislocations among obese patients with an increased risk of vascular injury to the main artery that runs down the leg behind the knee.

The symptoms of a kneecap dislocation will vary based upon how the injury occurred as well as the severity of the damage to the knee joint. Common symptoms are : immobility, bruising repositioning of the patella, pain when standing and swelling.

Vascular injury is a severe complication because if undiscovered and untreated, it can lead to amputation of the leg. The odds of vascular injury during a knee dislocation were twice as high among obese or morbidly obese people than for normal-weight people.

Orthopaedic and emergency medicine clinicians should have a heightened awareness for the potential of a knee dislocation in the obese patient following a low-energy fall. If you have torn ligaments with dislocation call your doctor immediately, do not attempt to reset your knee. You may need to have surgery depending on the severity of the tear.
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How bones affect appetite and metabolism

Human skeleton is more than the structure supporting the muscles and other tissues, it produces osteocalcin hormone. The hormone affects how we metabolize sugar and fat. It increases insulin production which reduces blood glucose levels, it can also protects us from obesity by increasing the use of energy.

Changes in blood concentrations of osteocalcin may stave off the development of diabetes. Osteocalcin is produced by osteoblasts, the cells responsible for making human bones. The hormone builds up in bone, and then, through a series of chemical reactions, is released into the blood.

Inactive osteocalcin has one more piece than active osteocalcin. The researchers examined in mice the different enzymes present in cells where osteocalcin was produced. Furin causes osteocalcin to become active and the hormone is then released into the blood.

When there was no furin in bone cells, inactive osteocalcin built up and was still released, but this led to an increase in blood glucose levels and a reduction in energy expenditure and insulin production. The absence of furin reduced the mice's appetite, osteocalcin has no effect on appetite, the existence of a new bone hormone that controls food intake.
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How obesity causes breast cancer

Obesity leads to the release of cytokines into the bloodstream which impact the metabolism of breast cancer cells, making them aggressive to treatment.
Severe overweight can lead to various health impairments. Besides inducing cardiovascular diseases, obesity for example also promotes the development of cancer and metastases.

ACC1 acetyl-CoA-carboxylase 1, a central component of fatty acid synthesis. ACC1 mediates the chemical addition of carbon dioxide to acetyl-CoA, which results in malonyl-CoA. This reaction is the first and speed determining step in the fatty acid synthesis of all living organisms.

ACC1 enzymes is a key component of fatty acid synthesis, its function is impaired by the cytokines leptin and TGF-β. The levels of these cytokines are increased particularly in the blood of severely overweight people.

Fatty acid precursors promote metastasis. The inhibition of ACC1 leads to the accumulation of the fatty acid precursor acetyl-CoA. This precursor is transferred to certain gene switches that in turn increase the metastatic capacity of cancer cells by activating a specific gene program.

Scientists used human tissue from breast cancer metastases to show that ACC1 was less active. When the scientists blocked the unknown signaling pathway with an antibody directed against the leptin receptor, this led to a significantly reduced metastatic spread of breast cancer tumors in an experimental model.
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