Myostatins myotonic dystrophy and bodybuilding

Protein is a vital part of your diet. Consisting of a variety of amino acids, proteins compound and fuse to regulate virtually every aspect of your body. Genetics play an important part in how and where those proteins are used – and how long they endure. Different proteins aid muscle development and use. They also help cellular growth. Over the last decade, researchers have isolated some proteins that can hinder and harm muscles and cells. Some may occur in birth others occur in your life span. Myostatin is a probable protein compound that does both. It is part of the roots of muscle diseases from dystrophies to recent diseases like DDX3X that affect many lives. Isolation of myostatin as having a role is a small part of a huge puzzle thwarting treatments and cures.

Myostatins are a group of micronutrients that bodybuilders use to control muscle growth. Most people have them naturally but, through aging process, there is muscle loss. Myostatins have this strange side-effect. They aid in the eventual wasting of muscle growth.

Myostatin inhibitors have been a rage in muscular and fitness. Some competitive athletes were disqualified for using supplements or gene-doping to produce enhanced performance effects. There are many muscle issues with natural aging and an entire list of neurological and muscle wasting diseases. Is it worth the excitement?

Myostatin is a secreted protein that acts as a negative regulator of skeletal muscle mass. During embryo-genesis (within the womb), myostatin is expressed by cells in the myotome (group of muscles that a single spinal nerve innervates) and in developing skeletal muscle and acts to regulate the final number of muscle fibers that are formed. The MSTN gene provides instructions for making a protein called myostatin. Myostatin is found almost exclusively in muscles used for movement (skeletal muscles), where it is active both before and after birth. This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

The general theories to stop this myostatin-based muscle wasting is to inhibit this protein from infecting those muscles. Myostatin inhibitors are found in foods as phytonutrients – naturally occurring micronutrients:

Green tea
Chocolate (especially dark chocolate and raw cocoa powder)
Blackberries
Pomegranates
Broad beans (e.g. Fava Beans)

In the body, Myostatin is produced by the muscle tissue of the heart, and damage to the heart causes it to be released into the bloodstream. It is associated with potential muscle loss of heart tissue in people with heart disease. This may also be associated with producing naturally high LDL cholesterol levels within that group. It may also trigger low HDL and high triglyceride measurements within a cardiac lipid panel in repeated serum tests.

High myostatin levels are associated with muscle wasting and may be associated with many diseases. Research on animals indicate that Myostatin levels may be significantly higher in patients with diseases like amyotrophic lateral sclerosis (ALS), Duchenne muscular dystrophy, myotonic dystrophy and multiple sclerosis, among other neurological and muscle diseases. Disease diagnosis usually demonstrates a genetic cause. Those myostatin levels and muscular atrophy may be the result of this genetic impulse. Myostatin levels may show why drugs for Duchenne Muscular Dystrophy do not work.

So…it seems that myostatin inhibition might lead to helping people with muscle weakness but it isn’t easy. It’s very complicated. There are other proteins that have been influenced over time. For example, BP3 is a protein that may be involved in eliminating obesity. These proteins need co-factors to allow certain effects. Myostatin inhibition has to coincide with BP3 to trigger fat loss and muscle re-development.

One possible concern, according to Dr. Markus Schuelke, the pediatric neurologist at Charite University Medical Center in Berlin who discovered the myostatin mutation in the baby, is that blocking myostatin could interfere with satellite cells that help replace injured or dead muscle cells. It’s thought that myostatin helps keep the satellite cells at rest until they’re needed, and it’s possible that without myostatin the satellite cells could become depleted.

There are many conflicting opinions that myostatin blockers may be too targeted to boost muscle growth, as there are a variety of proteins similar to myostatin that also limit muscle growth.

There are several potential downsides to be aware of when using myostatin inhibitors for athletic enhancement.

One potential concern is that increased muscle growth will lead to an increased risk of injury due to increased stress on the muscle fibers. This is especially true for individuals using myostatin inhibitors as workout supplements instead of as part of a medical treatment for muscular dystrophy or other disorders. Muscle stress is linked with increased muscle atrophy among the various dystrophy illnesses.

It has been noted that drugs that induce myostatin inhibition may lead to higher probable risks of injury.

Other possible side effects of myostatin inhibitors include increased the chance of tendon rupture, heart failure due to inflamed cardiac muscle, and rhabdomyolysis, a breakdown of muscle fibers that often leads to kidney failure.

Meanwhile, vitamin supplement shelves have many products offering myostatin inhibitors in a bottle. They have many ingredients. Neither of these have been thoroughly tested by the FDA or European health organizations.

If myostatins and concordant protein compound interactions of the weaknesses of myotonia bring clues, treatments and cures are even more sophisticated as transport pathways may differ. Are transport pathways different because age or disease exist? Or were those pathways results from genetic instructions? Anyway, key muscles just do not work properly. That is myotonia.

Myostatin is a statin compound. Statins may irritate and amplify the effects of muscular dystrophy. Those with muscular dystrophies heart disease are told to avoid statins. The misuse of statins can produce some very insidious muscle effects without muscular dystrophy incidence.

According to WebMD, possible statin side effects among average people may be:
Headache
Difficulty sleeping
Flushing of the skin
Headache
Difficulty sleeping
Flushing of the skin
Muscle aches, tenderness, or weakness (myalgia)
Drowsiness
Dizziness
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
Diarrhea
Constipation
Rash
Drowsiness
Dizziness
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
Diarrhea
Constipation
Rash
Memory Loss

If muscle aches and weakness occur in people without muscular dystrophy, you might imagine how myostatin may effect those with muscular dystrophies.

The problems lie in the etiology or source among what makes muscles weak. For those with muscle wasting diseases – congenital and adult – the fantasy that myostatin inhibitors may work brings glimmers of hope. But will it heal the damages already done? There are research studies and results that are still clinically inconclusive. It may still be a long process ahead with many pathways. How myostatin works, how inhibitors work, and how dystrophic muscles vary are just a few of many questions that need thorough answers.

As I wrote this article, new DMD1 research is coming from UK using Tideglusib, as a pharmacological approach:

AMO-02 (tideglusib) is in development for the treatment of congenital myotonic dystrophy and has potential for use in additional CNS, neuromuscular and oncology indications. AM0-02 is positioned to enter clinical stage development for the treatment of the severe form of congenital myotonic dystrophy known as DM1 or Steinert disease. In cellular and animal models of DM1 and Duchenne muscular dystrophy, as well as in muscle biopsies from patients, activity of glycogen synthase kinase 3 beta (GSK3ß) has been shown to increase. Inhibitors of GSK3ß have been shown to correct the activity of regulatory proteins, such as CUGBP1 in animal models of DM1. AMO-02 is an inhibitor of GSK3ß that has demonstrated pre-clinical efficacy in transgenic models and reversal of muscle cell deficits in ex vivo tissue samples in patients with DM1.

I will follow this and see how it develops.

Sarcopenia muscle loss with aging

Is it possible to maintain muscle strength and integrity through the duration of life? Sarcopenia may be against you. Can you battle against sarcopenia? Maybe. If not today, perhaps soon.

There’s an old Grimm fable that when living things asked God about longevity, God like the number 30 years.With a little negotiating, humans got 70 years but at a price. Sometimes these fairy tales are true. At age 30, lean muscle tissue decreases and is replaced by fat. This decrease is partly caused by a loss of muscle tissue (atrophy). The speed and amount of skeletal muscle changes seem to be caused by genes. This muscle loss happens very slowly yet gradually – usually noticed un 10 year differences. The process is Sarcopenia that, thus far, is an untestable condition.

Barring genetic diseases such as Muscular Dystrophy and DDNX3, sarcopenia is a normal process of aging. Body builders have been using a pseudo-genetic chemical called Myostatin, that some believe may help slow sarcopenia muscle loss with aging.

Myostatin (also known as growth differentiation factor 8, abbreviated GDF-8) is a myokine, a protein produced and released by myocytes that acts on muscle cells’ function to inhibit myogenesis: muscle cell growth and differentiation. In humans it is encoded by the MSTN gene. Myogenesis is a form of regeneration as the process by which damaged skeletal, smooth or cardiac muscle undergoes biological repair and formation of new muscle when other muscle fibers waste or die due to disease. This process may slow with aging and hormonal changes.

When discussing sarcopenia and myostatin, there are two sides of a coin. Muscle atrophy is a decrease in muscle mass; muscle hypertrophy is an increase in muscle mass due to an increase in muscle cell size. Hypertrophy is a very rare condition and sarcopenia is more associated with aging and conditions like muscular dystrophies. As a possible method at treating sarcopenia, myostatin inhibitors are being explored by doctors albeit at mouse level experiments.

The potential side effects of using myostatin inhibitors provoke heated debates in research communities. With few studies, there are some negative side effects reported:

One potential concern is that increased muscle growth will lead to an increased risk of injury due to increased stress on the muscle fibers. This is especially true for individuals using myostatin inhibitors as workout supplements instead of as part of a medical treatment for muscular dystrophy or other disorders.

Other possible side effects of myostatin inhibitors include increased the chance of tendon rupture, heart failure due to inflamed cardiac muscle, and rhabdomyolysis, a breakdown of muscle fibers that often leads to kidney failure

Despite few thorough clinical trials, Myostatin has become a main target for the development of drugs for cachexia and muscle wasting diseases. While sarcopenia behaves at wasting skeletal muscles, The cachectic state is observed in many pathological conditions such as cancer, chronic obstructive pulmonary disease (COPD), sepsis, or chronic heart failure. These are also muscles. The other problem associated with Myostatin is it is not targeted for research by the US Food and Drug Administration for testing and approval. It is available as a supplement.

In the United Kingdom, use of a myostatin inhibitor is targeted for experimentation for Duchenne Muscular Dystrophy, one of many muscular dystrophy diseases.

While muscle wasting is associated with muscular dystrophies and other emerging genetic conditions, including sarcopenia, there is no certainty whether myostatin might reverse muscle wasting that has already happened. Among small and possibly skewed studies it is generally accepted that age-related changes in skeletal muscle structure and function are inevitable, whether these deleterious effects on skeletal muscle can be stopped or reversed is debatable.Some studies support myostatin inhibitor supplementation, most studies agree that more research is needed. In 2017, a reasonably thorough German study of myostatin inhibitors as treatment for muscle wasting concluded with interest but for further experimentation required.

The general wisdom is that muscle integrity within normal sarcopenia is activity – virtually any activity – may reduce muscle wasting over time. Activity may also benefit hippocampus growth for cognitive support. Unused muscles can waste away if you are not active. Even after it begins, this type of atrophy can often be reversed with exercise and improved nutrition. Muscle atrophy can also happen if you are bedridden or unable to move certain body parts due to a medical condition.

Muscle wasting with age varies but sarcopenia may not be considered a leading cause of death in aging. There are some foods that include flavonoids that dietitians believe may work as myostatin inhibitors. They are: green tea, chocolate (especially dark chocolate and raw cocoa powder),
blackberries, pomegranates, and broad beans, broccoli, cauliflower, and spinach.

There are genetic tests to evaluate your myostatin levels. Discuss with your doctor to determine whether you need one.

Aging well seems to many a fantasy as new diseases and conditions creep in unrelenting succession. Living is an activity. Damned genetic muscle wasting diseases may one day be curbed. Will it be myostatin related? There seem to be many promises but all we can do is wait. Might as well go for a walk while waiting. Wisdom points that activity may be helpful. Sarcopenia and many other neuromuscular disease treatments is definitely worth researching as the aging population increases.

As you battle with the bulges and size upgrades as you grow older, sarcopenia might be the cause behind the results.

Normal to age and get fat with sarcopenia

Believe it or not, if you’re over 50 and are disconcerted with that tire growing around your waist, it is normal to age and get fat. There are things you can do.

There’s a crisis at getting fat as you age. Suddenly fat begins showing where it never appeared before. Sizes rise and appearance seems to enlarge in all the wrong places. The human body is made up of fat, lean tissue (muscles and organs), bones, and water. After age 30, people tend to lose lean tissue. Your muscles, liver, kidney, and other organs may lose some of their cells. This process of muscle loss is called atrophy. These changes result in changes in function and in appearance. It is normal to age and get fat but it’s very difficult or impossible to prevent. Diets may only help marginally. Atrophy has an enemy. It is activity. All those cell losses reduce your energy levels as your body gets fat.

The bulk of the population have a common disease where it is normal to age and get fat. It is called Sarcopenia and is a condition that is virtually impossible to cure. Sarcopenia affects millions of people who gradually become weak and frail as they age due to loss of muscle mass.

While not everyone has Sarcopenia, research does show that it is closely associated with the process that is normal to age and get fat. In Sarcopenia, it is the severity.

Starting and following through with an exercise program might help control the progression of fat and Sarcopenia but it won’t cure it. Sarcopenia develops rapidly with a lack of physical activity, especially the lack of overload to the muscle, as in resistance exercise. The amount of physical activity generally declines with age. Physically inactive adults will see a faster and greater loss of muscle mass than physically active adults. The problem is that the loss of muscle mass reduces the metabolic production of energy. The results include developed intolerance of exercise that is all too real. It is not fear. It is a form of myopathy.

In most myopathies, weakness occurs primarily in the muscles of the shoulders, upper arms, thighs, and pelvis (proximal muscles). The symptoms are capped by general fatigue because muscles and energy production efficiency are closely associated. Other symptoms may include aching, cramping, stiffness, tenderness, tightness, and pain.

Sarcopenia and myopathies ARE NOT always present as people get fat with age. It is normal to age and get fat and Sarcopenia or myopathy may be fundamentally associated with symptoms. That is why exercise is extremely important over age 30 for those who not have chronic diseases. such as muscular dystrophy, multiple sclerosis, and myasthenia gravis, among others.

There are other subtle conditions associated with weight gain. These include an underactive thyroid gland (which can also cause weight gain despite eating less, intolerance to cold, constipation and dry skin) and diabetes (other symptoms include needing to pass water more often, feeling thirsty and recurrent minor infections like boils and thrush). Several medications can also lead to tiredness – beta-blocker tablets for heart conditions and antidepressant tablets are top of the average doctor’s list. Stress often leads to tiredness, but so too can symptoms of depression. Believe it or not, among aging individuals, weight gain is a cause for depression. Depressing generally reduces activity.

In the case of coping with the symptoms of normal muscle loss, changing habits from inactive to active is extremely difficult. For most, walking can help a lot. As you get older, your metabolic rate – the rate at which your body burns energy – will probably slow. Adjust your meal size and make a resolution to do a brisk daily walk of 20-30 minutes – just a 10% loss in weight will reduce the fat inside your tummy up to 30%! That means, if you are 200 pounds, you will lose about 30% of belly fat if you reach 180. If you’re 150, you may lose 30% belly fat when you reach 135 pounds. Doing so, however, requires a persistent, gradual habits that may be contrary to your known lifestyle.

Once you get over the “work effort” associated with exercise, you will find that you feel better because the body releases endorphins that help pick you up. For most normal people, exercise makes you feel better, perform physical tasks better and reduce the risk of disability due to arthritis. It now appears that exercise – specifically, resistance training – actually rejuvenates muscle tissue in healthy senior citizens. Resistance training doesn’t necessarily mean joining a gym and hoisting weights. There are rubber stretch bands. They are normally called Therabands and are used by many physical therapists. Like walking, these exercises must be approached in graduated steps.

As you evolve, Yoga and Seniors is a gaining partnership for overall conditioning and stretching. There are many community centers that offer free classes. It is recommended that you work towards 3 classes per week.

Of course, the process that is normal to age and get fat leaves muscles tense, stiff, and painful. Senior citizens should seek out massage therapy from a certified therapist or acupuncture. None near you? Try to find a nearby school that teaches massage and acupuncture.

According to WebMD, People who are physically inactive can lose as much as 3% to 5% of their muscle mass per decade after age 30. Even if you are active, you will still experience some muscle loss. If you are 60, you may have lost about 15% of lean muscle because it is normal to age and get fat. The lean muscle you lost helped make you look trim because muscle fibers kept your fat from showing.

If you are aging and reminisce about times when you were thin and strong, remember how normal it is to age and get fat. Lifestyle changes help but it’s all in the routine. That’s the most difficult thing. The hardest part is starting. After a few repetitions, it does get easier and your body will be trimmer. Just give it time. It took years to grow.

Obesity Surgery improves brain functioning

Some people call it excessively fat. Others call it overweight. Doctors may call it obese. For politicians and statisticians, obesity is a broad problem, though perhaps, too broad. In the past 40 years, weight-loss surgeries have greatly expanded as a medical specialization to help reduce obesity. They are costly interventions and very profitable. It is surprising that research has been published demonstrating that Obesity Surgery improves brain functioning. Some of the researchers were bariatric surgeons. In a culture where obesity and diseases are threatening longevity, is surgery a viable quick-fix solution?

Is being overweight a result of age, genetics, or lifestyle? Studies show some life-threatening diseases are associated with being overweight. According to the Center for Disease Control, a USA government agency, degrees of being overweight and obesity is more pervasive. Obesity is definitely not merely age related. Invasive surgical techniques (bariatric) are being advertised as treatments. Insurances cover procedures for certain obese levels. Obesity has been linked as possible causes for many diseases. On August 26 2014, a new study examining bariatric surgery was published inferring that obesity Surgery improves brain functioning. It may reduce the likelihood of Alzheimer Disease symptoms. Many of the diseases, purportedly tied to weight and obesity, may be sourced from other origins.

Obesity has been associated to diabetes and circulatory diseases. A new endocrinology study shows Changes in Neuropsychological Tests and Brain Metabolism After Bariatric Surgery may reduce brain circulation problems that associate with heart, organ, and brain conditions, including Alzheimer Disease symptoms.

There may be over 78 million people classified as obese or very overweight in the USA, according to a report in the Journal of the American Medical Association. That’s near one-third of the country’s population.

The most common way to find out whether you’re overweight or obese is to figure out your body mass index (BMI). BMI is an estimate of body fat, and it’s a good gauge of your risk for diseases that occur with more body fat. Few physicians rely on BMI but use weight on scales to diagnose obesity and the BMI debate seems to question the diagnosis. BMI may not be accurate as a reliable diagnostic tool.

One mode of measurement has been gaining popularity to determine obesity is waist circumference measurements. Men with a waist circumference of more than 40 inches and women with a circumference of more than 35 inches are at a higher risk for developing obesity-related conditions like type 2 diabetes, high blood pressure and high cholesterol.

I often comment about how many men use pants with sizes less than 40″ beneath their belly, that might actually be substantially over 40 inches. The maximum waist size of most standard pants sold is up to 42 inches. Beyond that, men must buy “big-size” pants from a specialty source. Women must resort to Plus-size clothing for sizes beyond extra-large parameters. Many squeeze into standard sizes resulting in pain and (possibly) organic problems.

Measuring obesity in women may also require waist and hip sizes but, often, Waist Hip Ratio (WHR) may be a poor obesity marker. Unlike waist circumference, WHR is not necessarily a measure of absolute abdominal fat mass. It is, however, a measure of abdominal fat relative to lower body mass. As such, a relatively lean individual could theoretically have the same WHR as an obese individual.

Two imaging techniques are now considered to be the most accurate methods for measuring tissue, organ, and whole-body fat mass as well as lean muscle mass and bone mass. These help indicate how obesity is affecting your body. While obesity is impacting radiology departments throughout the country, many overweight peopl3e do not fit into these machines.

Yet statisticians set the standards for obesity and how many people are actually very fat. When it comes to overweight, the numbers are staggering high.

Exercise, diet, and lifestyle changes are being weighed to discuss obesity control. A surgical procedure called Bariatric Surgery is becoming more popular for those people who are very obese. It is an invasive surgery geared for people who have tried other ways of losing weight and size to help move out of the clinical obesity ranges. Few studies have examined long-term efficiency of surgical methods and obesity. Yet, the large initial weight loss is associated with reducing risks on related diseases. The researchers of the recent obesity study and brain association are affiliated with a bariatric surgery group. More people are electing bariatric surgery as a means of weight control and image improvement. Does it work?

Weight loss surgery is not even close to the solution for obesity. Whether it is liposuction that vacuums the fat from certain areas, or bariatric surgery that reduces the capacity to eat, neither guarantees permanent weight loss. Many regain any weight lost and several still are threatened with diabetes and circulatory diseases. Obesity, however, is not always linked to high blood levels of cholesterol that may contribute to plaque in arteries and veins that might cause heart and brain diseases. As for incidence of neurocognitive conditions like Alzheimer’s Disease, there’s very little conclusive evidence that directly relate obesity to the incidence of memory disorders. Basically, weight loss surgery is a tool but not a clear solution to solving obesity.

Bariatric surgery can help a 300 pound person become 200 pounds. Prospective patients should not anticipate moving from a size 26 to a size 8 for social and psychological reasons. Those that do, are far from average. They are highly motivated at maintaining long-term lifestyle changes post-surgically. Most do not experience radical differences in appearance. It may be those changes that help improve certain fat-related conditions. Bariatric surgery may help by reducing food storage capacity. Sticking to strict diets will help prevent and reduce problems like vomiting and nausea by exceeding capacity.

Typically, Bariatric Surgery costs are around $20,000 to $30,000. This may not include hospital and anesthesia fees. Many health insurance companies will pay some costs if obesity is directly linked to heart disease, hypertension, hyperlipidemia, and a few others. In a world where loss of memory is a great fear, it is obvious that bariatric surgeons research and conclude that results may dramatically reduce incidence of memory loss. That, too, may be insurable.

Numerous conditions, diseases, and ailments may lead to weight gain and, possibly, obesity. Aging means loss of lean muscle and gain of fat, as a natural progression. Some say longevity may be related to fat among older people. Also, hypothyroidism, Cushing Syndrome, and mood disorders may be medical reasons for obesity. Common arthritis and fibromyalgia may result in obesity due to experiential pain with movement. Any disorder affecting mobility may add pounds.

Statistics also don’t take consideration of varieties of height, bone sizes, and muscular width as possible reasons that define obesity. A man at 77 inches tall may naturally have a 40″ waist and not be obese. Standards for men show 40″ waist as borderline obese.

Barring disease, natural size variations, and statistical errors, lifestyles following conscient9ious diets and active lifestyles may, over years, help people stay trimmer.

TV is part of a sedentary activity that thwarts any diet. Children eat more snacks when watching TV. Watching action shows may promote mindless snacking. A small study at Cornell University binds TV content with snacking. Streams of Binge watching TV may also promote snacking appetites. Long terms of TV watching may be one leading cause of weight gain.

Sitting in offices or working on computers for extended lengths may increase weight and hip sizes. The condition is Sitting Disease and it may contribute to larger hip sizes throughout years of seated work. This may contribute to an obese appearance. The cure is more standing, walking, and stretching throughout the day.

A common misconception among those people in normally acceptable weight ranges is that weight gain is quick. It isn’t. It’s a gradual process where aging, genetics, and lifestyles form a complex network. Other than laundry shrinkage, your clothes are getting tighter because muscles are becoming less lean with age. It is referred as Sarcopenia but is relatively normal and effects vary among individuals. According to an article in WebMD:

People who are physically inactive can lose as much as 3% to 5% of their muscle mass per decade after age 30. Even if you are active, you will still experience some muscle loss.

The causes of Sarcopenia process are varied and some research points to calibrations in homeostasis that are normal in the aging body. More research is targeting this area. Yet small studies among seniors demonstrate that lean muscle may be gained with routine daily activity.

Weight gain is a normal aging process and vigilant activity may slow it down. No activity over decades beyond age 30 could lead to obesity and all those partner symptoms that reduce longevity. Ironically, at some ages, weight loss at older ages can contribute to higher mortality rates.

Obesity has existed throughout history. In art, many images from centuries ago depict fatter people. There are few remnants to predict or trace their longevity. Fat is normal. Obesity was common.

Of all the wisdom and variances, moderate diet and moderate activity (walking at brisk pace 30 minutes per day) is likely to stave off obesity among people over 45. Whether it improves brain function or longevity is in need of further examination.

For the majority of the population, more sedentary times and availability/marketing of snack foods help accelerate the fat accumulation associated with Sarcopenia and poor habits. Fighting obesity within a normal population is a painfully slow process. There are no quick-fix solutions. Bariatric surgeries and plastic surgeries are valuable but only tools. Reversing the habits we’ve acquired in the modern and digital ages is as difficult and impossible as smokers and alcoholics succeed in fighting their addictions. Successes are very small.

Barring medical reasons, the growth rates associated with obesity is the end-product of 70 years of snacking and technology that are integral parts of living. Learning to add exercise and food management routines early in life may likely curb obesity levels. Whether one can follow through these skills and habits throughout life’s stresses, adversities, and progressions is a big question mark. We may never look like fashion models. Obesity rates are natural and (theoretically) can be controlled easily. For most, however, starting and following-through may be a Herculean task in a society that stresses snacks and seated activities as a comforting lifestyle.

It takes very little effort each day to battle obesity and possibly suppress any life-threatening conditions that obesity may be linked with. There is no quick fix. Barring genetics, there is no turning back the clock of age. As a long term goal, balancing obesity and health is a habit to target at ages when most don’t think about it.

Gaining weight is as natural as gravity. Gravity is a constant. As we seek to conquer gravity, the perpetual efforts to battle the influences of obesity and weight gain are within the grasp of most people at any age. In this case, memory and remembering are important factors. Weight loss surgeries don’t necessarily help in the long run.