Body Fat

How come higher blood caffeine is linked to lower body fat and type 2 diabetes risk?

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  • Researchers investigated the effects of a genetic predisposition to high caffeine levels on measures of body fat, type 2 diabetes risk, and cardiovascular risk.
  • They found that a higher genetic predisposition to higher caffeine levels is linked to reduced body fat and type 2 diabetes risk.
  • Further studies are needed to confirm the results.

Caffeine is the most consumedTrusted Source psychoactive substance in the world. The main sources of caffeine consumption include coffee, tea, and soft drinks.

Some studiesTrusted Source show that caffeine intake is linked to weight loss and reduced body mass index (BMI) and fat mass. Caffeine intake may thus lower the risk of conditions linked to overweight or obesity, such as type 2 diabetes or cardiovascular disease.

How much these benefits come from caffeine, however, is unknown. One studyTrusted Source found that the risk for type 2 diabetes decreased by 7% for each additional cup of caffeinated coffee consumed per day, and 6% per cup of decaffeinated coffee.

Understanding more about how caffeine intake influences the development of cardiometabolic conditions could aid the development of dietary strategies to reduce their risk.

Recently, researchers investigated the effect of genetic predisposition to higher caffeine levels in the blood.

They found that a genetic predisposition to higher caffeine levels in the blood is linked to a lower risk for type 2 diabetes.

The study was published in BMJ Medicine.

Slower caffeine metabolism

For the study, the researchers examined data that came from a genome-wide association meta-analysis of 9,876 individuals of mostly European ancestry.

They used the data to examine two common genetic variants — CYP1A2 and AHR genes — in their analysis. These genes slow down caffeine metabolism, meaning that for those carrying the variants, less coffee needs to be drunk in order to have elevated levels of caffeine in their blood, compared to those who metabolize it quickly.

Researchers also collected data on body fat, type 2 diabetes risk, and risk for cardiovascular conditions.

In the end, the researchers found that genetically predicted higher blood levels of caffeine were linked to lower BMI, whole body fat mass, and type 2 diabetes risk.

Through further analysis, they found that 43% of the protective effect of blood levels of caffeine on type 2 diabetes came from weight loss.

They found no strong link between genetically predicted caffeine levels and cardiovascular conditions, including ischemic heart disease, heart failure, and stroke.

Caffeine and weight loss 

When asked how higher caffeine intake may increase weight loss, Dr. Dana Ellis Hunnes, assistant professor at UCLA Fielding School of Public Health, who was not involved in the study, noted that higher caffeine intake increases thermogenesis, or heat production, in the body.

She explained for Medical News Today that “[h]eat production increases calorie burn, and when we burn more calories than we take in, we are more readily able to lose weight and fat.”

Dr. Rohini Manaktala, a cardiologist at Memorial Hermann in Houston, TX, not involved in the study, also told MNT that caffeine causes weight loss by speeding up metabolism.

“This is a dose-dependent process, meaning [that] increasing [the] intake of caffeine […] leads to more fat and calorie burning, which is reflected in weight reduction,” she explained. “Caffeine also inhibits overindulgence in eating by suppressing an individual’s appetite resulting in calorie deficiency which helps in preventing weight gain.”

MNT also spoke with Dr. Mark Guido, an endocrinologist with Novant Health Forsyth Endocrine Consultants in Winston Salem, NC, not involved in the study, to understand how, besides weight loss, caffeine may reduce type 2 diabetes risk.

He said that the science is “mixed” on the topic, but that caffeine may reduce type 2 diabetes risk by altering how the body uses glucose and insulin.

The researchers concluded that higher blood levels of caffeine might lead to weight loss and reduce type 2 diabetes risk.

Limitations 

Dr. Guido noted that the study has significant limitations. He said: “It looked at naturally elevated caffeine levels in people with a certain genetic predisposition, and it does not appear to look at elevated caffeine levels from food or drink. There is a question if these findings would be relevant to increased caffeine levels from food or drink.”

He added that the study only looked at reducing the risk of developing type 2 diabetes as opposed to how caffeine affects those already with the condition.

Dr. Hunnes noted that the results are “not really causal in nature,” as unlike a randomized controlled clinical that studies the “whole person,” it merely studied the effects of genomes.

“It’s sort of like looking at in vitro — in [a] test tube — issues and making assumptions about how it will react in a person,” she noted.

Dr. Manaktala added: “A more robust randomized control study would be beneficial in studying the true clinical and health effects of caffeine. Moreover, the study participants were of European descent. This makes it challenging to extrapolate study findings to the general population in the U.S.”

Implications

Dr. Manaktala called the findings “exciting,” and noted that they mean a “healthy dose” of caffeine may help prevent obesity, a major risk factor for cardiovascular conditions. However, she noted:

“[W]e need to exercise caution before completely accepting the study’s findings and adopting new dietary habits. Most importantly, what we need to remember is that caffeine cannot be a substitute for leading a healthy lifestyle which includes, eating plenty of fruits, vegetables, lean meats, and a moderate intake of carbohydrates/ fats along with daily moderate-intensity physical exercise and careful management of chronic conditions that are risk factors for heart disease.”

Dr. Guido noted that he would not make any different recommendations to his patients based on the study findings.

“I think it is interesting and further studies likely need to be done, but at this time, I don’t think it changes anything regarding recommendations for the prevention of type 2 diabetes,” he said.

“I would not alter caffeine intake based on this study,” he repeated. “It only looked at people with naturally high caffeine, not how much they get from food or drink.”

“We also know that too much caffeine can also have significant harmful effects on health with regard to elevated blood pressure and poor sleep, and in patients who already have type 2 diabetes, caffeine can make their sugars worse,” cautioned Dr. Guido.

Excess Body Fat Can Age Your Brain Faster Than Muscle

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Research shows that maintaining healthy levels of muscle mass has a beneficial effect on your brain and may slow your rate of cognitive aging. Here’s the strategy you should strive for.

STORY AT-A-GLANCE

  • Increasing research shows that maintaining healthy levels of body fat and greater muscle mass has an effect on your brain health and may slow your rate of cognitive aging
  • People with higher amounts of abdominal fat had worse fluid intelligence with age, while those with greater muscle mass were more protected against such declines
  • Women who had greater muscle mass tended to have better scores in fluid intelligence during the study period
  • Past research has linked midlife obesity with an increased risk of mild cognitive impairment, changes in short-term memory and executive functioning and dementia

Staying fit as you age is about far more than aesthetics. Increasing research shows that maintaining healthy levels of body fat and greater muscle mass has an effect on your brain health and even your rate of cognitive aging. It’s known, for instance, that being obese in midlife and early late-life is associated with worse cognitive aging.[1]

What’s more, the amount of muscle and fat you have may be a more important factor in how your level of fluid intelligence decreases over time than your chronological age. Your chronological age, i.e., your age in years, is just a numerical measurement, but your real age is your biological age as dictated by your choices and habits, as well as your modifiable risk factors like levels of muscle and fat.

While many people tend to gain fat and lose muscle mass as they age, this can be largely combated by staying active and eating right — lifestyle choices that will influence your cognitive function significantly.

More Muscle, Less Fat Protects Your Brain

In a study by Iowa State researchers, data from 4,431 adults were examined to compare levels of lean muscle mass, abdominal fat and subcutaneous fat with changes in fluid intelligence — the ability to solve problems in new situations — over a six-year period.[2][3]

Those with higher amounts of abdominal fat had worse fluid intelligence with age, while those with greater muscle mass were more protected against such declines. In fact, women who had greater muscle mass tended to have better scores in fluid intelligence during the study period.

Study co-author Auriel Willette, assistant professor of food science and human nutrition at Iowa State University, said in a news release, “Chronological age doesn’t seem to be a factor in fluid intelligence decreasing over time. It appears to be biological age, which here is the amount of fat and muscle.”[4]

What’s more, the study revealed a link between the immune system and how changes in fat levels affect cognition. Previous research suggests a higher body mass index (BMI) leads to greater immune system activity in the blood, which in turn activates the immune system in the brain, with a negative outcome on cognitive function.[5]

The featured study also found that changes in white blood cells called lymphocytes and eosinophils explained the link between abdominal fat and worsening fluid intelligence in women. In men, basophils, another type of white blood cell, were linked to about half of the link between fat levels and fluid intelligence, the study found.[6]

“Lymphocytes, eosinophils, and basophils may link adiposity to cognitive outcomes,” the researchers explained.[7] Similar research has revealed that overweight and obese individual have greater brain atrophy in middle-age, corresponding with an increase in brain age of 10 years.[8]

How Obesity Affects Your Brain

Obesity has multiple effects on the brain, including anatomically speaking. Obese individuals may have reduced gray matter in brain regions such as the hippocampus, prefrontal cortex and other subcortical regions. Atrophy in the hippocampus, in turn, has been linked to Alzheimer’s disease.[9]

Gray matter is the outer layer of the brain associated with high-level brain functions such as problem-solving, language, memory, personality, planning and judgment. Even in elderly people who are otherwise cognitively normal, obesity is associated with measureable deficits in brain volume in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared to individuals with a normal weight.[10]

Further research published in Radiology found that obesity may lead to alterations in brain structure, shrinking certain regions.[11] Among men, higher total body fat percentage was linked to lower brain gray matter volume. Specifically, 5.5% greater total body fat percentage was associated with 3,162 mm3 lower gray matter volume.

Among men, 5.5% greater total body fat was also associated with 27 mm3 smaller globus pallidus volume, an association also seen in women. In women, 6.6% greater total body fat percentage was associated with 11.2 mm3 smaller globus pallidus volume.

The globus pallidus is a brain region that plays a role in supporting a range of functions, including motivation, cognition and action.[12] Obesity was also associated with changes in white matter microstructure, which may be related to cognitive function.[13]

Cognitively speaking, there’s also a strong link between obesity and deterioration in cognitive function, as well as to other brain disorders such as dementia, anxiety and depression. Further, past research has linked midlife obesity with an increased risk of mild cognitive impairment, changes in short-term memory and executive functioning and dementia.[14]

Obesity-Associated Health Problems Also Harm Your Brain

Obesity’s effects on brain health are also due to its associated health problems, including heart disease, diabetes and atherosclerosis, each of which can have its own deleterious effects on your brain. For instance, as noted in Frontiers in Neuroscience:[15]

“Obesity-derived vascular problems, such as atherosclerosis and arteriosclerosis, which are systemic diseases, are known to affect the steady blood flow of vessels that feed the brain, thus contributing to cognitive impairment or even stroke, where large areas of the brain die due to the stop in the blood flow of a major brain artery caused by a blood clot.”

In terms of diabetes, of which obesity is a key risk factor, having this condition in midlife is associated with a 19% greater cognitive decline over 20 years compared with not having the condition.[16] Even those with prediabetes had significantly greater cognitive decline than those without.

Indeed, “Epidemiological studies have linked type-2 diabetes mellitus with cognitive impairment and dementia, with insulin resistance and hyperglycemia as the probable mechanistic links,” researchers noted.[17]

Coming full circle, eating a highly processed, junk food diet not only increases obesity risk but also can lead to normal but elevated blood sugar levels that, in turn, can lead to impaired glucose metabolism and Type 2 diabetes. Both diabetes and higher fasting glucose levels are linked with lower total brain volume.[18]

Impaired glucose metabolism is then associated with neurodegeneration that impairs cognitive function. This connection begins not in old age but much earlier, such that following a healthy lifestyle in young adulthood may be protective against cognitive decline later.[19]

The Inflammation Connection

Obesity can trigger chronic inflammation in your body, and chronic inflammation in your brain (neuroinflammation) is known to impair neurogenesis, your brain’s ability to adapt and grow new brain cells. It’s also linked to neurodegenerative disorders such as Alzheimer’s disease (AD), and it’s been suggested that “Obesity may serve as an amplifier or initiator of the chronic inflammation observed in AD patients.”[20]

Further, higher levels of inflammatory markers have also been associated with lower brain volume, including “greater atrophy than expected for age.”[21] Excess body fat, particularly visceral fat, is also related to the release of proteins and hormones that can cause inflammation, which in turn can damage arteries and enter your liver, affecting how your body breaks down sugars and fats.

According to a study in the Annals of Neurology, “[A]dipose-tissue derived hormones, such as adiponectin, leptin, resistin or ghrelin, could also play a role in the relation between adipose tissue and brain atrophy.”[22] Further, obesity may also be associated with lower volume in brain regions that regulate food-reward circuitry,[23] possibly influencing overeating.

Strength Training Is Good for Your Brain

While obesity takes a toll on your brain, increased muscle mass protects it, which is likely one reason why strength training has been found to be beneficial for your brain. In other words, your body’s physical strength may serve as a marker of your brain power.

In fact, strength training is known to trigger beneficial neurobiological processes,[24] leading to positive functional brain changes, including in the frontal lobe, with corresponding improvements in executive functions. One systematic review even found that strength training led to less white matter atrophy in the brain, with researchers noting:[25]

“Taken together, during aging processes, a substantial decline in muscular strength, especially in lower limb muscles, occurs, and accumulating evidence suggests that lower muscular strengths are linked to poorer cognitive performance.

Hence, resistance (strength) exercises (a single bout of resistance exercise, also referred to as acute exercise) and resistance (strength) training (more than one resistance exercise session, also referred to as chronic exercise … ) seem to be promising activities to ensure the preservation of physical functioning and cognitive functions with aging.”

Regular strength training, in addition to other forms of exercise and daily activity, is an important strategy for keeping your brain sharp and may help to offset some of the cognitive decline that occurs with age.

5 Fitness tips to lose upper body fat

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Whether you are exercising to lose weight or just to stay fit, the ultimate motive is to burn tons of calories. Burning calories helps you create a calorie deficit and help you drop some kilos. Many pick up an intense workout routine with a motive to come to shape faster. When it comes to exercising for weight loss, it is better to start slow, especially if are new to exercise, says Mandy Narula, a certified sports nutritionist. Which area the body fat will drop is especially dependent upon individual genetics.

Some people will lose fat first from the face some lose it from arms or stomach but in the end if you will remain in calorie deficit and keep doing exercise you will lose weight and reach your desired goals. Here are some fitness tips to lose your upper body fat.

  1. Have an exercise partner- with an exercise partner you will always think twice before skipping your workout session as you given commitment to your better half or friend that we will be going for exercise it is very easy to say no to yourself but to say no to other it is much more difficult.
  2. Schedule your workouts. Keep a calendar that lists specific times for your workouts. Make an appointment with exercise ahead of time, and you won’t have the excuse of running out of time.
  3. Don’t do too much, too fast. Don’t get over-motivated. Lifting weights that are too heavy or starting out with six days a week of aerobic exercise is a mistake. “People end up hurting themselves in the first week and then they give up. It is better to start slow and gradually increase the volume of the workout.
  4. Log your Steps. Logging the time that you work out will help you achieve your weekly goal, even if you get off track one day. It will also inspire you at the end of the week, when you can look back and see what you’ve accomplished.
  5. Cook more often. Portions, and calories, are out of control when you eat out. You’ll almost always consume fewer calories in a meal cooked and eaten at home. Save restaurants for special occasions, and get together with friends for a walk or coffee /Tea instead of a meal.

Your diet and nutrition should be the focus of your weight loss program in the early stages, but exercise matters more for long-term weight maintenance. By committing to an exercise program that you can gradually build on, you can slowly increase your exercise minutes each week to meet your goals and surely you will lose upper body fat.

More body fat linked to lower bone density, especially in men

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High levels of body fat are associated with a lower bone mineral density, with the association more pronounced in men compared with women, according to study data published in The Journal of Clinical Endocrinology & Metabolism.

“While higher BMI is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine, told Healio. “Patients with obesity should still undergo recommended bone density screening, especially if they have other risk factors, such as older age, previous fracture, family history or steroid use.”

Rajesh K. Jain, MD
Jain is an assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine

Jain and colleagues analyzed data from 10,814 adults aged 20 to 59 years who participated in the National Health and Nutrition Examination Survey from 2011 to 2018 and underwent a total body DXA scan. T-scores were calculated to determine total body BMD. Lean mass index and fat mass index were calculated to assess the effects of body composition on BMD.

After adjusting for age, sex, race and ethnicity, height, smoking status, lean mass index and fat mass index, every 1 kg/m2 of lean mass index was associated with a 0.19 higher total body BMD T-score (P < .001). Conversely, each 1 kg/m2 increase in fat mass index was associated with a 0.1 decrease in BMD T-score (P < .001).

The association between fat mass index and BMD T-score differed for men and women. Women had a BMD T-score decrease of 0.08 points for every 1 kg/m2 increase in fat mass index, whereas men had a 0.13 lower BMD T-score with every 1 kg/m2 increase in fat mass index (P for interaction < .001). The association between fat mass index and BMD T-score did not differ by age group. For lean mass index, Mexican American adults had a lower BMD T-score increase of 0.16 for each 1 kg/m2 increase compared with a 0.21 BMD T-score increase for each 1 kg/m2 for white adults (P for interaction = .004). There were no other differences observed between race and ethnicity groups.

“Unfortunately, body composition is not a routine clinical measurement, so we rarely know what a patient’s body fat or body lean mass is,” Jain said. “Factors that correlate with high body fat and low lean mass are often associated with osteoporosis or fractures, and their presence should prompt clinicians to consider osteoporosis screening. This includes, for example, the presence of diabetes or poor performance on physical activity measures, such as grip strength.”

Jain said future research should examine the effects that weight loss may have on BMD.

“In general, weight loss has been associated with bone loss and fractures, but this study suggests the type of weight loss — lean vs. fat mass — may be important in determining if or how much bone loss occurs,” Jain said.

For more information:

Rajesh K. Jain, MD, can be reached at rjain2@medicine.bsd.uchicago.edu.

PERSPECTIVE

Mone Zaidi, MD, PhD, MBA, MACP, FRCP)

Mone Zaidi, MD, PhD, MBA, MACP, FRCP

Over the past two decades, we have worked on the idea that pituitary hormones have diverse functions beyond the unitary actions that appear traditionally in endocrine textbooks. We found, for the first time, that thyroid-stimulating hormone and follicle-stimulating hormone have direct actions on bone. The implication of these studies was that low TSH and high follicle-stimulating hormone levels in hyperthyroidism and after menopause likely contribute to the bone loss hitherto attributed solely to high thyroid hormone and low estrogen levels, respectively (Abe E, et al. Cell. 2003;doi:10.1016/s0092-8674(03)00771-2). 

Correlative studies in cohorts across the globe have shown strong associations between serum TSH or follicle-stimulating hormone, markers of bone remodeling, bone mineral density and fracture risk, independently of thyroxine or estrogen. Focusing on the effects of follicle-stimulating hormone, we developed a targeted follicle-stimulating hormone blocking antibody that prevented bone loss in mouse models (Zhu LL, et al. Proc Natl Acad Sci U S A. 2012;doi:10.1073/pnas.1212806109). Intriguingly, the follicle-stimulating hormone blocking antibody also reduced body fat and converted white adipose tissue to thermogenic beige adipose tissue (Liu X, et al, Nature. 2017;doi:10.1038/nmeth.4436) and, in a separate study, prevented cognitive decline and Alzheimer-like neuropathology in mouse models (Xiong, et al, Nature, 2022; in press).

Our humanized monoclonal follicle-stimulating hormone blocking antibody replicates these actions and has shown promise in preclinical studies toward first-in-human clinical trials in the very near future. Our admittedly ambitious premise is to treat osteoporosis, obesity and neurodegeneration with a single drug.

Mone Zaidi, MD, PhD, MBA, MACP, FRCP

Professor of Medicine and Pharmacological Sciences

Director, Center for Translational Medicine and Pharmacology

Director, Mount Sinai Bone Program

Icahn Sinai School of Medicine at Mount Sinai

Research Reveals How Greater Body Fat is a Risk Factor For Reduced Thinking Memory Ability

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According to recent study, greater body fat is a risk factor for reduced cognitive function for instance how adults process. For the research, they took cardiovascular risk factors like diabetes or high blood pressure, or vascular brain injury into account. The link between body fat and lower cognitive scores remained. This suggested other not yet confirmed pathways that linked excess body fat to reduced cognitive function. The study was published in the journal, ‘JAMA Network open’.Research Reveals How Greater Body Fat is a Risk Factor For Reduced Thinking Memory Ability. Picture Credits: Unsplash

In the study, 9,166 participants were measured by bioelectrical impedance analysis to assess their total body fat.

As well, 6,733 of the participants underwent magnetic resonance imaging (MRI) to measure abdominal fat packed around the organs known as visceral fat, and the MRI also assessed vascular brain injury — areas in the brain affected by reduced blood flow to the brain.

“Our results suggest that strategies to prevent or reduce having too much body fat may preserve cognitive function,” said lead author Sonia Anand, a professor of medicine of McMaster University’s Michael G. DeGroote School of Medicine and a vascular medicine specialist at Hamilton Health Sciences (HHS). She is also a senior scientist of the Population Health Research Institute of McMaster and HHS.

She added that “the effect of increased body fat persisted even after adjusting for its effect on increasing cardiovascular risk factors like diabetes and high blood pressure, as well as vascular brain injury, which should prompt researchers to investigate which other pathways may link excess fat to reduced cognitive function.”

Co-author Eric Smith, a neurologist, scientist, and associate professor of clinical neurosciences at the University of Calgary said that “preserving cognitive function is one of the best ways to prevent dementia in old age. This study suggests that one of the ways that good nutrition and physical activity prevent dementia maybe by maintaining healthy weight and body fat percentage.”

Smith is head of the brain core lab for the two population cohorts used for this new analysis- the Canadian Alliance for Healthy Hearts and Minds (CAHHM) and PURE Mind- a sub-study of the large, international Prospective Urban Rural Epidemiological (PURE) study.

The participants were in the age range of 30 to 75 with an average age of about 58. Just over 56 per cent were women; they all lived in either Canada or Poland. The majority were White European origin, with about 16 per cent other ethnic backgrounds. Individuals with known cardiovascular disease were excluded.

More body fat linked to lower bone density, especially in men

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High levels of body fat are associated with a lower bone mineral density, with the association more pronounced in men compared with women, according to study data published in The Journal of Clinical Endocrinology & Metabolism.

“While higher BMI is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine, told Healio. “Patients with obesity should still undergo recommended bone density screening, especially if they have other risk factors, such as older age, previous fracture, family history or steroid use.”

Rajesh K. Jain, MD
Jain is an assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine

Jain and colleagues analyzed data from 10,814 adults aged 20 to 59 years who participated in the National Health and Nutrition Examination Survey from 2011 to 2018 and underwent a total body DXA scan. T-scores were calculated to determine total body BMD. Lean mass index and fat mass index were calculated to assess the effects of body composition on BMD.

After adjusting for age, sex, race and ethnicity, height, smoking status, lean mass index and fat mass index, every 1 kg/m2 of lean mass index was associated with a 0.19 higher total body BMD T-score (P < .001). Conversely, each 1 kg/m2 increase in fat mass index was associated with a 0.1 decrease in BMD T-score (P < .001).

The association between fat mass index and BMD T-score differed for men and women. Women had a BMD T-score decrease of 0.08 points for every 1 kg/m2 increase in fat mass index, whereas men had a 0.13 lower BMD T-score with every 1 kg/m2 increase in fat mass index (P for interaction < .001). The association between fat mass index and BMD T-score did not differ by age group. For lean mass index, Mexican American adults had a lower BMD T-score increase of 0.16 for each 1 kg/m2 increase compared with a 0.21 BMD T-score increase for each 1 kg/m2 for white adults (P for interaction = .004). There were no other differences observed between race and ethnicity groups.

“Unfortunately, body composition is not a routine clinical measurement, so we rarely know what a patient’s body fat or body lean mass is,” Jain said. “Factors that correlate with high body fat and low lean mass are often associated with osteoporosis or fractures, and their presence should prompt clinicians to consider osteoporosis screening. This includes, for example, the presence of diabetes or poor performance on physical activity measures, such as grip strength.”

Jain said future research should examine the effects that weight loss may have on BMD.

“In general, weight loss has been associated with bone loss and fractures, but this study suggests the type of weight loss — lean vs. fat mass — may be important in determining if or how much bone loss occurs,” Jain said.

For more information:

Rajesh K. Jain, MD, can be reached at rjain2@medicine.bsd.uchicago.edu.

PERSPECTIVE

BACK TO TOP Mone Zaidi, MD, PhD, MBA, MACP, FRCP)

Mone Zaidi, MD, PhD, MBA, MACP, FRCP

Over the past two decades, we have worked on the idea that pituitary hormones have diverse functions beyond the unitary actions that appear traditionally in endocrine textbooks. We found, for the first time, that thyroid-stimulating hormone and follicle-stimulating hormone have direct actions on bone. The implication of these studies was that low TSH and high follicle-stimulating hormone levels in hyperthyroidism and after menopause likely contribute to the bone loss hitherto attributed solely to high thyroid hormone and low estrogen levels, respectively (Abe E, et al. Cell. 2003;doi:10.1016/s0092-8674(03)00771-2). 

Correlative studies in cohorts across the globe have shown strong associations between serum TSH or follicle-stimulating hormone, markers of bone remodeling, bone mineral density and fracture risk, independently of thyroxine or estrogen. Focusing on the effects of follicle-stimulating hormone, we developed a targeted follicle-stimulating hormone blocking antibody that prevented bone loss in mouse models (Zhu LL, et al. Proc Natl Acad Sci U S A. 2012;doi:10.1073/pnas.1212806109). Intriguingly, the follicle-stimulating hormone blocking antibody also reduced body fat and converted white adipose tissue to thermogenic beige adipose tissue (Liu X, et al, Nature. 2017;doi:10.1038/nmeth.4436) and, in a separate study, prevented cognitive decline and Alzheimer-like neuropathology in mouse models (Xiong, et al, Nature, 2022; in press).

Our humanized monoclonal follicle-stimulating hormone blocking antibody replicates these actions and has shown promise in preclinical studies toward first-in-human clinical trials in the very near future. Our admittedly ambitious premise is to treat osteoporosis, obesity and neurodegeneration with a single drug.

Mone Zaidi, MD, PhD, MBA, MACP, FRCP

Professor of Medicine and Pharmacological Sciences

Director, Center for Translational Medicine and Pharmacology

Director, Mount Sinai Bone Program

Icahn Sinai School of Medicine at Mount Sinai

More body fat linked to lower bone density, especially in men

Posted by

0


High levels of body fat are associated with a lower bone mineral density, with the association more pronounced in men compared with women, according to study data published in The Journal of Clinical Endocrinology & Metabolism.

“While higher BMI is generally associated with higher bone density, our study demonstrates that lean and fat mass affect bone density differently and that obesity is not a guarantee against osteoporosis,” Rajesh K. Jain, MD, assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine, told Healio. “Patients with obesity should still undergo recommended bone density screening, especially if they have other risk factors, such as older age, previous fracture, family history or steroid use.”

Rajesh K. Jain, MD
Jain is an assistant professor in the section of endocrinology, diabetes and metabolism and director of the endocrinology fellowship program at the University of Chicago Medicine

Jain and colleagues analyzed data from 10,814 adults aged 20 to 59 years who participated in the National Health and Nutrition Examination Survey from 2011 to 2018 and underwent a total body DXA scan. T-scores were calculated to determine total body BMD. Lean mass index and fat mass index were calculated to assess the effects of body composition on BMD.

After adjusting for age, sex, race and ethnicity, height, smoking status, lean mass index and fat mass index, every 1 kg/m2 of lean mass index was associated with a 0.19 higher total body BMD T-score (P < .001). Conversely, each 1 kg/m2 increase in fat mass index was associated with a 0.1 decrease in BMD T-score (P < .001).

The association between fat mass index and BMD T-score differed for men and women. Women had a BMD T-score decrease of 0.08 points for every 1 kg/m2 increase in fat mass index, whereas men had a 0.13 lower BMD T-score with every 1 kg/m2 increase in fat mass index (P for interaction < .001). The association between fat mass index and BMD T-score did not differ by age group. For lean mass index, Mexican American adults had a lower BMD T-score increase of 0.16 for each 1 kg/m2 increase compared with a 0.21 BMD T-score increase for each 1 kg/m2 for white adults (P for interaction = .004). There were no other differences observed between race and ethnicity groups.

“Unfortunately, body composition is not a routine clinical measurement, so we rarely know what a patient’s body fat or body lean mass is,” Jain said. “Factors that correlate with high body fat and low lean mass are often associated with osteoporosis or fractures, and their presence should prompt clinicians to consider osteoporosis screening. This includes, for example, the presence of diabetes or poor performance on physical activity measures, such as grip strength.”

Jain said future research should examine the effects that weight loss may have on BMD.

“In general, weight loss has been associated with bone loss and fractures, but this study suggests the type of weight loss — lean vs. fat mass — may be important in determining if or how much bone loss occurs,” Jain said.

Deleting genes could boost lifespan by 60 per cent, say scientists

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DNA
Switching off parts of the genetic code could help people live longer, scientists believe

The secret of extending life by decades may lie in switching off certain genes, scientists believe, after showing that small genetic tweaks can make organisms live 60 per cent longer.

Ten years of research by the Buck Institute for Research on Ageing and the University of Washington has identified 238 genes that, when silenced, increase the lifespan of yeast cells.

Many of the genes are present in mammals, including humans, suggesting that switching them off could dramatically increase lifespan.

“This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is,” said lead author Dr Brian Kennedy.

“Almost half of the genes we found that affect aging are conserved in mammals.

“In theory, any of these factors could be therapeutic targets to extend healthspan. What we have to do now is figure out which ones are amenable to targeting.”

To determine which genes were responsible for ageing, researchers examined 4,698 strains of yeast, each with a single gene deletion and then monitored how long cells lived for before they stopped dividing.

They found that deleting a gene called LOS1 produced particularly impressive results, extending life by 60 per cent. LOS1 is linked to a genetic master switch which has long been associated with calorie restriction through fasting and increased lifespan.

“Calorie restriction has been known to extend lifespan for a long time,” added Dr. Kennedy.

Co-author Dr Mark McCormick, of the Buck Institute said: “Our best results were single gene deletions that increased lifespan by around 60 per cent compared to normal yeast.”

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Switching off the gene LOS1 appears to mimic fasting 

Earlier this year academics from the University of Southern California found that a five day diet which mimics fasting can slow down ageing, add years to life, boost the immune system and cut the risk of heart disease and cancer.

The plan restricts calories to between one third and a half of normal intake.

Last year the same team discovered that fasting can regenerate the entire immune system, bringing a host of long-term health benefits.

When humans tested out the regimen, within three months they had reduced biomarkers linked to ageing, diabetes, cancer and heart disease as well as cutting overall body fat.

The researchers think it works by slashing a hormone which encourages growth, and has been linked to cancer susceptibility. Essentially it tricks the body into ageing more slowly.

This Kind of Body Fat Burns Calories More Quickly

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The good news is that you can turn your body fat into a super-burner that’s better at melting away calories and lowering blood sugar. But it takes a lot to make the switch

For years researchers have been tantalizing us with news of amysterious type of fat that can burn through calories and keep blood sugar levels in check. Unlike white fat that tends to sit in deposits where we least want them, this other kind of fat—called brown fat—is scant inside the human body. While newborns tend to have more brown fat, the average adult harbors barely two ounces of the stuff.

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As little of it as we have, recent studies have suggested that brown fat can be triggered under the right conditions. And now, in a new paper, scientists report for the first time that it’s possible to turn white fat into brown fat — or at least something that acts like brown fat and burns up more calories.

Researchers had accomplished the feat in animals, but the latest study, published in the journal Cell Metabolism, is the first to describe the phenomenon in people. The research was conducted by Ladros Sidossis from the University of Texas Medical Branch at Galveston and his colleagues.

While previous studies showed that cold temperatures could activate brown fat in healthy people, none demonstrated that the stress of the frigid exposure could transform white fat into brown fat. Speculating that it would take an extreme and continued stress on the body for that to happen, Sidossis decided to study brown fat stores in burn patients; as director of the metabolism unit at Shriners Hospitals for Children, he knew that burn injuries that cover more than 30% of the body caused the body’s stress response to remain high for weeks.

Indeed, when he compared white fat samples taken from the patients soon after their injury to those of healthy controls, he found markedly higher signs of a revved-up energy process in these cells that showed the white fat was acting more like brown fat. Confirming the finding further, when he compared the burn patients’ white fat cells soon after their injury and then a month later, he found signs that the white fat had reverted back to its original state again as the patients began recovering and their stress response waned.
 Of course, Sidossis is in no way suggesting that burns are a strategy for enhancing brown fat stores. What’s important is the fact that the study showed it’s possible to make white fat burn more calories, something that could be the start of a new way of addressing obesity and diabetes. “The next step is to find the mechanism of how this is happening,” he says. “Then we can find drugs that mimic this effect to turn white fat into a more metabolically active form to help normalize weight and blood sugar.”

Scientists working with animals are already heading down that path; they’ve identified some 40 agents that might be useful in convincing white fat to work more efficiently. Now that there’s evidence that the process does occur in people — albeit under extreme conditions — studying those substances further to see if they can accomplish the same transformation of white fat, without the stress, seems worthwhile.