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:
Chocolate (especially dark chocolate and raw cocoa powder)
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.
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:
Flushing of the skin
Flushing of the skin
Muscle aches, tenderness, or weakness (myalgia)
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
Nausea or vomiting
Abdominal cramping or pain
Bloating or gas
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.
One would favor how many countries seem to be somewhat more conscious about tourists with mobile disabilities. They treat them as invalids – not valid. But they try. Overcoming mobile disability travel challenges are difficult both in the USA and internationally. It is virtually impossible for those without disabilities to conceive all the details people with wheels, crutches, and canes require to smoothly go from point-a to point-b. Current statistics show about 10% of the world’s population (650 million) have some form of disability.
Part of the statistical problem is that most people who need mobility aids don’t want to use them. It took me years to realize I needed a cane to walk better. Another 6 months that I needed AFO braces. Based on data from the 2002 US Census Bureau, 96 percent of people who live with an illness live with an invisible one, and 73 percent of people who live with a severe disability do not use devices like a wheelchair. So, counting invisible mobile disability and mental disability, about 15 percent of the world’s population — some 785 million people — has a significant physical or mental disability, including about 5 percent of children, based on the World Health Organization in 2011.
Mobility handicaps meant no challenges if you sat comfortably on the inside looking out. For most of history that seemed fine. Mobile disability travel challenges happen when you want to go somewhere. Devices and scooters help you move. Traveling between points and having the comforts and necessities you need require considerable study. Yes, when going to supermarkets to parks or on vacations, even visiting friends and relatives, mobile disabilities uncover some hidden travel challenges.
It can be very disconcerting for those with mobile disabilities to navigate into certain stores, houses of worship, and other public spaces. There are disability travel challenges whether you are young and old. United States, over the past 30 years, has been implementing standards to help enable those that require mobility aid. Passed by Congress in 1990, the Americans with Disabilities Act (ADA) is the nation’s first comprehensive civil rights law addressing the needs of people with disabilities. Of course many buildings, subways, and other areas built prior to 1990 still have poor access for disability travel.
I use AFO braces as a mobile compromise for walking. To others I am walking relatively well, albeit slowly. What many do not know is, while I can walk on smoothly paved paths, I really can’t walk stairs, on grass, on sand, cobblestones, and rough surfaces. Somehow, when it comes to mobile disability travel challenges, manufacturers are designing more mobility scooters for travel.
Thinking of accessibility, parts of New York City are working towards removal of 19th-century cobblestones so that disability travel on those streets could be more accessible. This is causing many debates from travelers and local residents who see the removal as damage to historic infrastructures. In countries all around the world, different cobblestones have remained for centuries. Some countries replace old cobblestones with new ones.
For people using AFO braces, canes, and walkers, these surfaces may be impossible to travel. For those in wheelchairs or mobility scooters, this can be a very bumpy ride, even a dangerous ride if the scooter isn’t stable. For tourists, these rough surfaces make public plazas and churches historically attractive. After all, when these were built, disabled people weren’t supposed to travel anywhere.
Many of these countries barely have accessible accessories (high toilets with bars or shower bars) available in hotel rooms. There aren’t any ADA standards there. They barely have sidewalks and most still maintain bricked streets.
Rough and rugged US National Parks also provide facilities for wheelchairs and some trails that accept human-pushed wheelchairs. They are not accommodating for powered mobility scooters and virtually impossible for AFO-brace users.
First introduced in the 1960’s, Mobility scooters offer freedom and independence, leading to improved quality of life for a growing number of people. Manufacturers are continually investing in research and development to enhance existing products and introduce new models and features. Even electric car research has trickled to mobility scooters by introducing longer-lasting and lighter lithium-ion batteries to extend power and range abilities. More companies are introducing folding scooters that may be stored in the boot of many cars. Some of these are called travel scooters. But are they easy to fold and unfold?
What’s Required to Transport a Typical Travel Mobility Scooter:
Remove the seat by lifting it off of the scooter
Remove the battery pack by lifting it off of the scooter
Undo the retaining clips that connect the front and rear halves of the scooter, separating the frame into 2 compact pieces
Fold the tiller (steering column)
Place the scooter component into vehicle
Basically, any person with the need for convenient disability travel would require a competent aid. There are new design revolutions that simplify the processes, if you aren’t very tall or big.
Yet the largest challenges that disability travel encounter are the many roads, hotels, dining areas, and recreation areas that define accessible within narrow definitions. For example, Disney parks are accessible – bathrooms and paths. The rides and shows are probably not. Some restaurants there may have some stairs.
I have spoken to people using mobility scooters and their realities are they wish they could use AFO or K-AFO instead. Ultimately, all these disability travel accessories are compromises and out-of-the-box compromises. They allow mobility challenged individuals some control to move around environments.
Many technologies are being explored to allow people with mobility challenges more independence. Some scooters have elevating seats so you can have eye-contact with people. There are also more heavy-duty models with solid suspensions to tackle rough and rugged terrains, while remaining comfortable and easy to maneuver. Advances in battery technology mean you can now cover substantial distances on a single charge too, offering greater freedom. In deed, greater hope exists for overcoming disability travel challenges. The world wasn’t really designed for us.
Among all the challenges that people with motion disabilities encounter is that handicap accessible usually does not follow ADA standards. People without these challenges, as in many things, can only view things through their constructions of reality. After accidents, they might be sharing your perspectives. They get better but you don’t. Thankfully physiatrists, orthodists, and manufacturers strive for better mobility devices to give those with disability travel challenges better solutions that promote movement.
As far as international traveling, much care and attention is still required. On an AFO, I found it impossible. Some people with scooters find it challenging. We, unfortunately, can’t expect the world to adapt to our conditions. Thankfully, in the USA, the Congress passed the ADA act. Since passing that act, people with all forms of disabilities may get accessibility options that were never considered before.
In the aging baby-boomer generation, deeper studies isolate issues of disability as a stigma. Having a disability is seen as socially inferior. There is a sense of discrimination toward those with physical or mental disabilities. Some disabled people try to adapt to the world around them, if they can. As one of the most overlooked minorities of the world, disabilities are by ways of genetics and environment. No one wants a disability.
When travelling to other countries, the stigma is probably unintentional. Mobile disability travel challenges are to try to overcome the many staircases, cobblestones, and other features that make areas tourist destinations. From bathrooms, hotel rooms, and many public spaces, one actually sees those features that are not adaptable.
For fear of falling or injury, while physically disabled people do attempt to adapt toward experiencing many of the world’s wonders, those remain from a chair staring at images on a tablet or computer. Mobile disability travel challenges will likely remain one of those perilous things that require extensive research for superior disability awareness.
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.
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.
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.
Tuna, salmon, sardines have been popular sandwich-stuffers and salad toppers for decades. Shifted to the side, virtually ignored, was another fish – mackerel. Holy mackerel! Why?
Mackerel is the common name for members of the family Scombridae, which includes many species of open-sea fishes, including the bonito and tuna. Mackerel is loaded with omega-3 fatty acids; some varieties have a stronger, oilier flavor than other fish, as saturated, monounsaturated, and polyunsaturated fat from about 5 grams per 3-ounce serving.
Mackerels are pelagic fish. Examples of species include forage fish such as anchovies, sardines, shad, and menhaden and the predatory fish that feed on them. Oceanic pelagic fish typically inhabit waters below the continental shelf. Pelagic fishes are those that spend much of their lives swimming in open water away from the bottom. These areas are highly productive and supply nutrients for the growth of plankton which forms the food for the smaller pelagic species. A mackerel is typically less than 2 feet in length. Fourteen-inch fish weigh about 1 pound in the spring and about 1¼ pounds in the fall when they are fat; 18-inch fish weigh about 2 to 2½ pounds; a 22-inch mackerel will likely weigh 4 pounds. Examples of pelagic fish include larger fish such as swordfish, tuna, mackerel, and even sharks. Of these, the mackerel is the smallest. They are found in the Atlantic and Pacific ocean regions.
Typically, a mackerel has fins, gills, and they are considered kosher. Popular kosher fish are bass, carp, cod, flounder, halibut, herring, sardines, mackerel, trout and salmon.
Mackerel is an oily fish, a rich source of healthy omega-3 fatty acids. The flesh of mackerel spoils quickly, especially in the tropics, and can cause scombroid, a type of food poisoning. Mackerel should be eaten on the day of capture, unless properly refrigerated or cured. Mackerel preservation is not simple. In the USA, you can find canned and smoked mackerel that’s perfectly safe. While salmon and tuna are caught in colder climates, they are also vulnerable to the bacteria that may result in food poisoning. So why is mackerel segregated from other canned fish products?
A serving 3 ounces of cooked Boston mackerel contains 1.1 grams of omega-3 fatty acids. Like tuna, mackerel is also an important source of protein and B vitamins, particularly vitamin B12. A 3-ounce serving provides nearly 700 percent of the recommended daily amount of the vitamin. Canned mackerel provides comparable nutritional values.
It should be noted that (if you are monitoring cholesterol) there is about 79.0 mg amount of Cholesterol in 100 grams (3-ounces) portion amount of Fish, mackerel, canned food, drained solids. It is similar to salmon, a little bit more than tuna, or sardines. Although fish will not help to lower cholesterol, it has lots of benefits for your heart. Omega-3 fats, which are found in oil-rich fish such as salmon, trout, mackerel, herring and sardines, are very beneficial for your heart. It is also believed that eating fatty fish several times per week may help increase HDL cholesterol levels (good cholesterol). These fish may also reduce triglycerides.
Oily fish such as salmon, mackerel and sardines are said to help against cardiovascular disease, prostate cancer, age-related vision loss and dementia. It’s a good source of vitamin D, protein, some B vitamins and selenium. It’s also a rich source of omega-3 fatty acids, a type of fat that is good for health and digestion. Why do few restaurants serve Mackerel in the USA?
Among the two-dozen species of Mackerel found around the world, some have a fishy odor. People in many Asian countries may like it. People in European and USA consider that type of mackerel as a pet food ingredient. In the USA, mackerel tastes like a cross between Hake and Swai and is part of normal diets, as a mild tasting fish. Atlantic mackerel or jack mackerel are popular and safe in the USA. Jack mackerel is sourced from the Pacific, along the California coast. Jack mackerel usually is sold canned.
Most people hate to eat mackerel because they don’t know how to cook them. Broil or bake the mackerel (remove fat from the flesh, don’t add more fat/oil). Some people like to bake them with a little anchovy paste/butter – try it. Bar-b-queued mackerel is fairly good and smoked mackerel is even better. But no, it will never be the same as eating halibut but halibut often sells at 3-4 times the price as mackerel.
Mackerel may be pan fried if placed on a grill. For example:
Heat a roasting pan with rack in the oven at around 400 degrees.
Clean the fish, pad dry, and covered it in olive oil, salt, and pepper. …
Stuff slices of lemon into the cavity.
Place the fish on the hot rack.
Cook for about 20 minutes on each side, or until they are crispy.
Mackerel is a relatively inexpensive fish. Fresh Mackerel often sells for less than $5.00 per pound. Canned mackerel sells for about $2.00 per 15-ounce can. As such, more people can access mackerel and its nutrients in a healthy diet, as salads, fish cakes, and stews.
Why is mackerel so holy? Many agree that the phrase is a euphemism for Holy Mary. Blurting “Holy Mackerel” instead of taking the Madonna’s name in vain. Holy mackerel is phrase having no direct relationship to the fish? Originally, Catholics were told to have fish on Fridays. Mackerel were relatively easy to catch and, thus, became very popular Friday foods.
Mackerel is a big, oily fish, similar to tuna, but it has lower levels of mercury per serving, and is less at risk of overfishing. It’s high in both omega-3 and -6 fatty acids and a good source of protein, and has been found to lower blood pressure in men. Pregnant? King mackerel contains too much mercury to be considered safe during pregnancy.
USA Government dietary guidelines recommend that people eat fish twice a week. It offers significant protein and nutrients, and we know that fish are full of omega-3 fatty acids—which can benefit both heart and brain. While most use 3 ounces as a serving, a portion is around 140g (4.9oz). Compared to tuna and wild salmon, mackerel has lower Mercury levels.
Just as you would make tuna, salmon, shrimp or sardine salad sandwiches, mackerel may be another alternative. Mash it with dressing, onions, shredded carrots, and diced celery, I doubt any eater would know the difference.
There really isn’t anything holy about mackerel. It is a reasonable, inexpensive, and healthy alternative to tuna, salmon, and sardines. These days, when budgets seem tight, mackerel is a great, cheap addition for you and your family to get the nutrition and protein they need.
19th-century writer and speaker, Edward Brooks is quoted as saying in 1882 The desire of activity is designed by nature to promote our physical well-being. Physical activity is the law of physical health. But how much exercise is necessary? Well…many centuries earlier Socrates wrote Moderate exercise is indispensable; exercise till the mind feels delight in reposing from the fatigue. Yet, in this heyday run-quick, digital world. people want quick results and shift from still to hardcore exercise. Hardcore exercise may be toxic to your health.
Almost any health condition may be helped by activity and diet. When it comes to controlling activity levels, mind over body usually is a losing battle. The rage of hardcore exercise to lose weight, control cholesterol, or bring down hyperactivity is popular in a competitive society seeking speedy results. We tend to shift into hardcore modes instead of regulating our habits over time. Hardcore exercise not only causes physical pain but may also result in kidney failure. Can you learn to moderate your hardcore exercise regimen?
For many, the very thought of exercise is profane. Exercise is a dirty word. Every time I hear it, I wash my mouth out with chocolate. Yet, the inevitable results are weight gain, loss of muscle plasticity, and diabetes. The answer isn’t a hardcore exercise regimen. For most people, it can result with serious health issues.
The goal of exercising to active extremes follows the “No Pain No Gain” approach. But exercise mavens caution moderation. Don’t practice for a marathon or a great body if you don’t realize stamina and endurance must teach your metabolism that activity is normal. Exercising too much to feel muscular pain may deliver reverse results and also damage your kidneys. Rhabdomyolysis is a condition dealing with muscle breakdown that releases the enzyme myoglobin—along with creatine kinase—into the bloodstream. The result, over a long term, may be severe kidney impairment.
Now as hardcore exercise may result in degrees of kidney problems, treating Rhabdomyolysis equally requires certain avenues. It usually does not require hospitalization. The goals of at-home treatment include resting the body so muscles can recover and hydration to help prevent further kidney damage. When you’re feeling fatigued, recline in a comfortable position and try to relax. Essentially hardcore exercise is nixed.
How do you know if you are at risk? Do your muscles ache for longer than usual? Diagnosing Rhabdomyolosis requires a doctor of sports medicine that is experienced with hardcore exercise issues. It requires a blood test.
Hardcore exercise isn’t the only cause. Rhabdomyolysis may occur as a result of several conditions that disrupt body balance.
Trauma or crush injuries
Use of drugs such as cocaine, amphetamines, statins, heroin, or PCP
Genetic muscle diseases
Extremes of body temperature
Ischemia or death of muscle tissue
Low phosphate levels
Seizures or muscle tremors
Severe exertion, such as marathon running or calisthenics
Lengthy surgical procedures
Fundamentally, many conditions taken to a chronic level may cause Rhabdomyolosis to emerge. The issue is how long and pain severity. If you wait for dark urine then it’s likely you are damaging kidney function. Some pharmaceutical medications may also result in hormonal harm. A popular class are Statins, used to control cholesterol and blood lipid levels.
The hardcore exercise adage of “No Pain, No Gain”, us something that newly active people must take lightly. The ceiling of pain is relatively low, even if not felt during exercise itself. Yet, hours later your muscles stiffen and you feel immobilizing pain. Yes, you will add muscle tone when you recover but the cost may crmp your lifestyle by causing un-needed trauma.
By being inactive over most of your lifetime, hardcore exercise is relatively dangerous. Appropriate exercises may actually be positively therapeutic.
I have myotonic dystrophy, a genetic disease that results in muscle loss and immobility. Prior to symptom onset I was very active. In my condition, if I exercise to pain, I accelerate muscle loss. Moderation is a tough lesson. With no cure and no treatment, exercise is low impact and brief. Myotonic dystrophy, one of many muscular dystrophy diseases, makes one conscious that those who begin hardcore exercise without professional training, may cause severe muscle trauma. The idea is not to over-exercise. The secret is learning endurance when exercising.
While there are many people that market hardcore exercise for, let’s say, cardiovascular strength, improper training may result in heart, kidney, and other hormonal failures. It can result in physical and emotional pain.
The burden of hardcore exercise is that no one will ever attain or keep the perfect body appearance. Genetics, age, diet, and other conditions will interfere. Establishing and developing active body habits over a lifestyle will be less traumatic to your kidneys and other vital organs. Hardcore exercise may seem sensible. Yet, it can make you sick. Exercise for health.
Unfortunately, I can’t do these anymore. But you can benefit from these low-impact routines. Don’t do more than you can. Exercise and diet are the keys to finding strength and energy without provoking disease. Hardcore exercise benefits the precious few. You are aiming for the healthier roads.
Socrates also wrote, All things in moderation, including moderation.. It is wise. Not everyone could appear as an Amazon goddess or an Athenian god. Hardcore exercise may cause kidney failure. Your body wants balance and will rebel if you push it too hard.
Are you eating right or wrong? Are you eating what you need for proper nutrition? The Unites States Department of Agriculture (USDA) has a food pyramid that helps you make choices. Is it helpful? There are supporters and critics. Let’s study the USDA food pyramid and their more recent MyPlate plan.
The USDA Pyramid, developed in 1992, emphasized eating more vegetables and fruits, less meat, salt, sugary foods, bad fat, and additive-rich factory foods. There has been quite a but if research in nutrition and dietary plans since then. Also, obesity, diet-based diabetes and other health issues arose since then. No-fat diets were proven as a suspicious way to diet. In 2015, the USDA revised the pyramid approach with Choose MyPlate. The new guidelines add whole grains and varied protein sources as the correct diets for Americans to eat from 2015 to 2020:
MyPlate plan is designed to help you eat food from the 5 basic food groups
Vegetables and legumes/beans.
Grain (cereal) foods, mostly wholegrain and/or high cereal fibre varieties.
Lean meats and poultry, fish, eggs, tofu, nuts and seeds and legumes/beans.
Milk, yogurt cheese and/or alternatives, mostly reduced fat.
Make half your plate fruits and vegetables. Focus on whole fruits. Vary your veggies.
Make half your grains whole grains.
Move to low-fat and fat-free dairy.
Vary your protein routine.
Eat and drink the right amount for you.
Yet, the food pyramid has been around for so long. The abstract notions of the food pyramid seemed biblical but difficult to follow with reason.
The USDA food pyramid was a widely recognized nutrition education tool that translated nutritional recommendations into the kinds and amounts of food to eat each day. The Pyramid is based on USDA’s research on what foods Americans eat, nutrition, and quantity. While the USDA food pyramid has been fine all these years, the USDA updated the program to What’s On My Plate for the present and future.
The U.S. Department of Agriculture (USDA) created MyPlate, an easy-to-follow food guide, to help parents to figure out how to feed their kids nutritious, balanced meals. The colorful divided plate includes sections for vegetables, fruits, grains, and foods high in protein. MyPlate helps you eat on the basis of a 1600 calorie diet plan, while maintaining fullness from one meal to another. Using MyPlate approaches, variance is the key to help make meals interesting. Besides, kids (and adults) are picky (and irresponsible) consumers of food.
The USDA targets the USA diet and the bluegrass roots for outlining good meals as the core of the healthy USA eating lifestyle. It isn’t about starving. It’s about diversifying the food groups and understanding what constitutes a serving. Does this mean that those 16-ounce sirloin steaks are gone? Well….not as a habit. The My Plate theme is habit of most meals. USDA Choose MyPlate seems to make more sense than the Pyramid but is it realistic?
The Choose My Plate method helps organize meals according to the USDA dietary guidelines for basic health. It’s a more focused approach, especially if you eat at home.
While the Cover MyPlate food choices don’t account for cakes, cookies, and fried snacks, the USDA makes sure that people – young and old – can access the wholesome nutrition these meals provide. USDA Cover MyPlate meals are distributed to schools, summer camps, seniors, and depressed areas.
The Commodity Supplemental Food Program (CSFP) works to improve the health of low-income elderly persons at least 60 years of age by supplementing their diets with nutritious USDA Foods. These include hot breakfasts and lunches at day senior centers and food distribution directly to elderly with severe mobility problems. The latter usually requires registering with a neighborhood senior program for direct distribution to your door.
Since the 1960’s, under President Lyndon Baines Johnson, USA made a pledge that no USA resident should ever go hungry. While there are many fancy diets available these days targeting weight and health management, the USDA helps overwhelmingly (often incognito) to aid healthy food to the needy of the USA.
Yet, most physicians were poorly trained in nutrition. Few medical schools offered more than 25 hours of nutrition studies. Many…zero.
Nutrition has also been associated with moods, including depression and anxiety disorders.
While the USDA MyPlate Pyramid diet plan may be basic and not exactly mouth watering, MyPlate helps provide nutrition through food to many needy individuals. While research hasn’t been vast enough to support MyPlate as an overall route to health and longevity, it’s a basis for all to begin eating healthier. Smoking, alcohol, and richer foods might be confounding variables in any study. Then there are genetic and activity issues – many undiscovered.
USDA MyPlate is a budget minded entrance to getting healthy nutrition directly from small servings of whole foods. The USDA offers many resources to help you choose whether MyPlate is suitable for you. They also provide a list of informative videos.
The USDA MyPlate diet plan wasn’t intended to help everyone reduce obesity. MyPlate was designed to provide healthy nutrition to the young, old, poor and devastated. Yet, for those seeking a healthier lifestyle, choosing a USDA MyPlate flexible diet plan may be one benefit to help bring your health to normal levels.
With USDA MyPlate plan dieting isn’t a matter of right or wrong. Like anything of value, it’s a lifestyle choice.
Hormones are chemicals manufactured by your body organs and cells. Raging hormones excite children and teens through the adventures to young adults. Declining hormones are found among those over 50, with a few at 35. Estrogen dominance becomes an issue when ovulating stops. At that point, progesterone – an associative hormone – level drops. There are numerous emotional and physical consequences with hormonal balance. It is not just women, hormone balance also affects men. Aging people can still have wonderful living opportunities. How do you keep hormones balanced?
There is life. There is living. Life is a solid state of being, like a cell. Living is a complex network of interactions that require sophistication and control. Among the many are a group of bio-tropic chemicals produced by glands that naturally occur and are essentials parts within our bodies. A dysfunction of one or more glands (by inheritance, environment, lifestyle, development) poses threats to delicate balances that living requires. Estrogen is a human hormone that exists in women and in men. Estrogen dominance, as part of aging, is a developing process that has taken scientists and people’s attention as the population life expectancy gets longer. Some of those new conditions that seem to crop-up after age 50 may actually be dependent in the levels of hormones, such as estrogen, progesterone, and several others.
There are many hormones throughout the body that act as regulators to maintain balance. Certain key hormones are monitored in blood tests taken at a routine medical exam. Each has a normal range, plus high or low. Beyond normal, a form of dominance shows up defining special conditions. Under variances, two specific hormones – estrogen and progesterone – change levels dramatically as women age. This process was recently identified with aging men. Neurotransmitters, endorphins, epinephrines, are also among hormones that vary with age. Estrogen dominance, excessive estrogen hormone, may lie as a key to many complaints through our aging bodies.
There are about 50 known hormones in your body as part of network that stimulate and inhibit hormone production.
In many senses, living makes use of a vast array of chemicals that may help make living possible – living better or worse. The next few pages list these hormones, although our discussion focuses on estrogen dominance and associations with aging:
Melatonin – Think of melatonin as your biological clock. This hormone is responsible for the way you feel throughout the day as far as alertness is concerned. All those drowsy feelings? Blame the melatonin.
Serotonin – This is the one you can blame for PMS and your moody teenager. Serotonin controls your mood, appetite, and your sleep cycles.
Thyroxin – A form of thyroid hormone, thyroxin increases the rate of your metabolism and also affects protein synthesis, which is the process that cells go through to build protein.
Epinephrine – This is one that you have most likely heard of; it’s also called adrenaline. Among a whole list of other things, epinephrine is responsible for what is known as the, “fight or flight” response. This is the hormone that tells you when to fight and when it’s best to run. Some of the bodily responses demonstrated when this hormone kicks in are dilated pupils, increased heart rate, and tensing of the muscles.
Norepinephrine – Also called noradrenaline, this hormone controls the heart and blood pressure. Norepinephrine also contributes to the control of sleep, arousal, and emotions. Obvious effects take place when there is too much or too little of this hormone. Too much gives you an anxious feeling while too little can leave you feeling depressed or sedated.
Dopamine – This controls the heart rate and also assists in perception; deciphering what is real and what is not.
Antimullerian Hormone – An inhibitor for the release of prolactin, the protein responsible mainly for lactation.
Adiponectin – This is a protein hormone, it regulates metabolic processes such as the regulation of glucose.
Adrenocorticotropic Hormone – This assists in synthesizing corticosteroids, which are responsible for stress response, blood electrolyte levels, and other physiologic systems.
Angiotensinogen – Responsible for the narrowing of blood vessels; a process known as vasoconstriction.
Antidiuretic Hormone – This hormone is also known by other names, but it is mainly responsible for retaining water within the kidneys.
Atrial Natriuretic Peptide – A peptide hormone secreted by the cells of the heart and other muscles, it’s mostly involved with the control of water, sodium, potassium, and fat within the body.
Calcitonin – Aids in constructing bone and reducing blood calcium.
Cholecystokinin – Aids in the release of digestive enzymes for the pancreas and acts as an appetite suppressant.
Corticotrophin-Releasing Hormone – Releases cortisol in response to stress.
Erythropoietin – Stimulates the production of erythrocytes, which are blood cells responsible for delivering oxygen.
Follicle-Stimulating Hormone – Stimulates the follicles within the sex organs of both males and females.
Gastrin – Secretes gastric acid.
Ghrelin – Hunger stimulant as well as aiding in the secretion of the growth hormone.
Glucagon – Helps to increase the blood glucose level.
Growth Hormone-Releasing Hormone – As its name clearly implies, this hormone releases the growth hormone.
Human Chorionic Gonadotropin – Keeps the immune system from attacking a forming embryo during pregnancy.
Growth Hormone – Helps to stimulate growth and the reproduction of cells.
Insulin – Responsible for several anabolic effects, primarily glucose intake.
Insulin-Like Growth Factor – Has the same effects as insulin while also regulating the growth and development of cells.
Leptin – Slows down the appetite while simultaneously speeding up metabolism.
Luteinizing Hormone – Aids ovulation in women and testosterone production in men.
Melanocyte Stimulating Hormone – Produce melanocytes, which are responsible for the pigment in skin and hair.
Orexin – Increases the appetite while also increasing your alertness and energy levels.
Oxytocin – A hormone that plays a major role in reproduction, it aids in orgasm and is also responsible for the release of breast milk.
Parathyroid Hormone – Among other functions, this hormone is mainly responsible for the activation of Vitamin D.
Prolactin – A major contributor in sexual satisfaction and the production of breast milk.
Secretin – Inhibits gastric acid production.
Aldosterone – Mainly responsible for absorbing sodium in the kidneys to increase the volume of blood within the body.
Testosterone – The major male hormone, testosterone is responsible for sex drive, development of the sex organs, and the changes that take place during puberty.
Androstenedione – Essentially estrogen.
Estradiol – In males, this hormone is responsible for preventing what is basically known as cell death of the germ cells. In females, this hormone is in overdrive. Among other things, estradiol accelerates height and metabolism, maintains the blood vessels and skin, aids in water retention, and even aids in hormone-sensitive cancers.
Progesterone – A major contributor to the body’s support of pregnancy.
Lipotropin – Stimulates the production of pigment by aiding in melanin production.
Brain natriuretic peptide – Aids in reducing blood pressure.
Histamine – A hormone based in the stomach, histamine aids in the secreting of gastric acid.
Endothelin – Controls muscle contractions within the stomach.
Enkephalin – Simply a pain regulator.
These are only examples of some of the 600 known hormones within the body; there are more complex hormones whose functions are not easily understood.
As people age, they often see their bodies change. Whether they eat responsibly and, regardless of activity, fat seems to accumulate and energy seems to drop. In a sense, it is your body’s way of alerting a possible imbalance as part of homeostasis. It’s a hormonal imbalance that comes at menopause. While estrogen may increase in women, progesterone levels may drop up to 70%.
In men and pre-menopausal women, too much estrogen — a condition called estrogen dominance — causes toxic fat gain, water retention, bloating, and a host of other health and wellness issues. As women age, there is a natural decline in testosterone and progesterone levels, leaving a relative excess of estrogen. This imbalance, this excess ratio of estrogen to progesterone makes dieting seem impossible as your sizes increase. The distribution of fat in women goes from young appearances to matronly, from a little overweight to obese. While genes may be involved, estrogen dominance over decreasing levels of progesterone may make normal dieting regimens impractical. Some might say estrogen is confusing because it is an essential
Decreased sex drive
Irregular or otherwise abnormal menstrual periods
Bloating (water retention)
Breast swelling and tenderness
Headaches (especially premenstrually)
Mood swings (most often irritability and depression)
Weight and/or fat gain (particularly around the abdomen and hips)
Cold hands and feet (a symptom of thyroid dysfunction)
Foggy thinking, memory loss
Symptoms of low progesterone for women who aren’t pregnant include:
headaches or migraines.
mood changes, including anxiety or depression.
irregular menstrual cycle.
Hormonal imbalances and aging aren’t just secluded for women. Men, in recent years, seem to also pass a menopause-like phase. It is called Andropause. Age-related decline in testosterone levels is also called testosterone deficiency, androgen decline in the aging male (ADAM) or late onset hypogonadism (LOH). Andropause is different from the menopause women experience. In menopause, the production of female hormone drops suddenly.Men may experience a more gradual loss.
According to Healthline, Male menopause can cause physical, sexual, and psychological problems. They typically worsen as you get older. They can include:
depression or sadness
insomnia or difficulty sleeping
increased body fat
reduced muscle mass and feelings of physical weakness
gynecomastia, or development of breasts
decreased bone density
It’s kind of neat that these symptoms are often diagnosed in response to individual complaints and treated as such. Yet, estrogen dominance and the changes of mood, energy, and blood changes with new alarming indicators may actually be a part of modulating estrogen dominance in your body.
One of the problems in dealing with estrogen dominance and other hormonal issues are treatments. While you may deal with each symptom as it appears, those treatments may still be counter-productive within the entire context of male and female menopause. It is suggested that frequent, routine treatments and testing be done with either a urologist or an OB/GYN. An estrogen test measures the level of the most important estrogen hormones in a blood or urine sample.
Generally, after menopause, once the menstrual cycle stops, the ovaries no longer produce progesterone. However, the body still needs progesterone and does continue producing it in the adrenal glands and nerve cells. Is it enough?
So…at a point to mediate estrogen during menopause, physicians began prescribing lab-produced estrogen – estradiol and Premarin. Premarin was produced by Pfizer. Responsibly, over the years, Pfizer has been adding cautions on Premarin, this drug designed to only reduce hot flashes gave many women causes of concern:
Using estrogen-alone may increase your chance of getting cancer of the uterus (womb). Report any unusual vaginal bleeding right away while you are using PREMARIN. Vaginal bleeding after menopause may be a warning sign of cancer of the uterus (womb). Your healthcare provider should check any unusual vaginal bleeding to find out the cause.
Do not use estrogens with or without progestins to prevent heart disease, heart attacks, strokes or dementia (decline in brain function).
Using estrogen-alone may increase your chances of getting strokes or blood clots. Using estrogens with progestins may increase your chances of getting heart attacks, strokes, breast cancer, or blood clots.
According to Healthline, sponsored by the USA government, using Premarin may help develop some common side effects that might include:
breast changes and pain
depression or mood changes
high blood pressure
increased heart rate
Taking Premarin may cause these additional common side effects:
partial or complete vision loss
Risks and interactions
Use of either estradiol or Premarin may also increase your risk of:
But at postmenopausal years, when hot flashes subside, and the symptoms of estrogen dominance prevail, you wonder how to increase progesterone. Prometrium is another prescription drug for that. That sounded great when it was introduced over a decade ago. Are there side effects?
Common Side Effects of Progesterone
Painful or tender breasts
Greater risk for viral infections
Serious Side Effects of Progesterone
Dementia in post-menopausal women who are more than 65 years of age
Swelling in the feet, ankles, and lower legs
Heart attack, stroke, or blood clots in the lungs
Missed periods or breakthrough bleeding
Breast cancer (most common in women between ages 50 and 79)
Rare Side Effects of Progesterone
Some patients may notice mood swings and feel tired or nauseated while taking progesterone.
Progesterone Interactions – If you are taking any of the following, ask your doctor about other possible options before taking progesterone:
Cancer drugs like Gilotrif (afatinib), Zydelig (idelasalib), and Tafinlar (dabrafenib)
HIV/AIDS medications like Stribild (eltivagravir/cobicistat/emtricitabine/tenofovir)
Afrezza (inhaled insulin)
Of course many drugs have side effects because they tend to mimic our natural chemicals but are not specific clones. They do not interact fully in opening and closing the body’s many doors and windows well.
So…as with many articles on Lifedoc Lifetime, we discuss how acts of living – diet, activity, nutrition, and other natural ways might just help make living easier under an umbrella of wellness.
Perhaps one of the more predominant gripes of entering the mid-fifties may be noticeable size changes from Medium to Extra Large (or plus sizes) may be life and living threatening to many.
To achieve weight loss or to prevent weight gain during menopause, stay active and eat a healthy diet. If your lifestyle begins to change as you age, try to keep physical activity and portion control at the top of your priority list. Here estrogen dominance is not a clear issue. There may be dietary components along with reduction of activities that increase depression. So, though, estrogen dominance may not be present, certain foods may reduce estrogen’s role in your metabolic rate to use foods. Lack of estrogen may also cause the body to use starches and blood sugar less effectively, which would increase fat storage and make it harder to lose.
Weight loss diets of postmenopausal people are not really fat-dependent. The consensus of most physicians seems to negate low-fat diets with hormonal balance. Reducing sugars and starches and focusing on healthy fats may be a route to weight loss. Fat-free or reduced-fat foods are bad news for postmenopausal women for a few reasons. One, they keep you from eating the healthy fats your body needs to combat heart disease, which postmenopausal women may be at increased risk of due to a combination of , poor diet, and lack of exercise.
Part of the real culprit of weight gain in women is age and muscle loss. Women generally become less physically active as they pass through their 40s, 50s, and 60s. At any age, burning fewer calories because we are less active increases weight and fat mass. With decreased activity, muscle mass decreases.
Hormonal imbalances are multi-factorial disorders, meaning they are caused by a combination of factors such as your diet, medical history, genetics, stress levels and exposure to toxins from your environment. For example, most food storage containers are BPA-Free. BPA stands for bisphenol A. BPA is an industrial chemical that has been used to make certain plastics and resins since the 1960s. They are thought to cause endocrine disruption (of hormone activities). Continued exposure to BPA has been linked to estrogen dominance. While many containers and plastic cans may be BPA-Free, do you think those take-out plastic containers are BPA-Free?
Basically, once you get your hormone levels checked, you may want to add the help of a licensed, competent nutritionist. A nutritionist professional can help guide you through supplements (not approved by FDA) and dietary choices. Supplements and foods use ingredients that may mimic hormones like estrogen and progesterone. Xenoestrogens are a type of xenohormone that imitates estrogen. They can be either synthetic or natural chemical compounds. Because the primary route of exposure to these compounds is by consumption of phytoestrogenic plants, they are sometimes called “dietary estrogens”.
Herbal supplements for controlling menopause symptoms are very available. They may have ancient roots in alchemy and may be used as treatments around the world. They are not considered traditional medicine in the USA. Effectiveness and proper dosing have not been tested for use. Popular supplements include:
Black Cohosh – Studies on the benefits of black cohosh are mixed, but there have been some encouraging findings about the herb’s ability to decrease hot flashes, sweating, insomnia, and depression. A 2010 review by researchers found that black cohosh provided a 26% reduction in hot flashes and night sweats. According to WebMD, “It is used to treat women’s hormone-related symptoms, including premenstrual syndrome (PMS), menstrual cramps, and menopausal symptoms”. Not FDA approved in USA.
Dong Quai is an ancient Chinese remedy for menopausal and postmenopausal primary and secondary symptoms. Nutritionists claim Dong Quai is very beneficial. Again, though sold alone or in menopause supplement formulas in the USA, it is not FDA approved.
Another popular ingredient added to these supplements goes on the brand name Vitex. Vitex (chasteberry) is the most popular herbal remedy for premenstrual syndrome (PMS). It does not supply hormones but acts directly on the hypothalamus and pituitary glands. Vitex increases luteinizing hormone (LH) and modulates prolactin, resulting in a balance of estrogen and progesterone levels. This supplement has no FDA approval. There are also scientific questions how this herb functions and whether it is effective for all claims West coast health guru Dr. Axe disusses Vitex and cites some studies that claim both male and female symptom relief.
Supplements really should be discussed with a certified nutritionist. They are chemicals and may interact with areas that aren’t related but somehow have a secondary effect on hormone balancing. What may go well in Europe and Asia may not apply in the United States.
Controlling hormones isn’t dietary exclusively. Activity – walking, running or cycling – help restore hormone balance as well. While routine diet and activity are, by many, a word that is often censored, they help you create health holistically. Creating health and wellness is a bit different than the traditional medical problem that deals with a diagnosis of a specific problem, Dr. Eric Berg outlines why creating health through diet and activity as aids to balance hormones through the aging process:
Subsequently, traditional medicine and routine exams (at least once per year) are very effective methods that help isolate hormonal imbalances or, rather, conditions that arise when the symbiosis of those hundreds of hormones are changing.
Life has value but living is priceless. Estrogen dominance and progesterone deficiency partner with many symptoms that occur with aging. The key to understanding a quest for wellness and longevity is that hormonal balance is important, even though our endocrine system also deteriorates with age. Trying to escape those symptoms means diet, activity, and recovery by controlling stress and other values.
Recent research at Columbia University expresses that neurons continue to grow among older individuals. Barring chronic, disabling illnesses, they observed that (based on protein markers such as BDNF – Brain Derived Neurotropic Factors) within the hippocampus, neuron development did not yield neuronal network development. These protein factors are derived from hormones. Able social and physical activity, with aging, may offer potential development of neuronal networks. “It does appear to be the case that neurogenesis in the hippocampus is remarkably preserved in human beings,” says one of the researchers.
Life or living well. Are they choices? Well, you can sit, eat what you want, and minimize movement, other than taking racks of prescribed pills. Or you can use responsible methods of dieting and (social,physical) activities to grow better with age and aiding hormone balance.. Perhaps the best ways to mediate and control estrogen dominance and hormone imbalances is to become dominant yourself. Establish new wellness habits. Is it a gamble? Everything has side effects. It depends on who and what you want to bet. Living is an activity and, with awareness, you can control your hormone balances to help get rid of the symptoms derived from possible hormone imbalances.
Alzheimer’s disease is attributed to a slow breakdown of neuronal networks throughout the brain. It may begin in the mid-brain level in an area called the hippocampus. A neuronal network may be dedicated to a scene (person, animal, place), sound, taste, smell, touch. In conjunction with other neuronal networks, these help form your reality. Alzheimer disease interferes and destroys these networks. There are several hypotheses as to why and how this happens. A group of researchers at the University of California San Francisco have detected a gene variant among Alzheimer brains and are studying its use to find causes and a cure of Alzheimer disease.
Alzheimer disease apoE4 genetic cure? Studies published in April 2018 show positive indicators that a gene variant of APOE4 may be associated with beta-amyloid fragments and plaque found in those diagnosed as dementia/Alzheimer disease.. There are many kinds of memory loss coming from many sources. Alzheimer is seemingly over-diagnosed and is not limited to an older population. This APOE4 genetic variant may be only a piece of a very large puzzle. Alzheimer disease is not a game. It’s very serious. Yet, inferences of causality and treatment of those are ethereal – like gases.
The APOE gene set provides instructions for making a protein called apolipoprotein E. This protein combines with fats (lipids) in the body to form molecules called lipoproteins. Lipoproteins are responsible for packaging cholesterol and other fats and carrying them through the bloodstream. One of these APOE4 genes might lead to a pathway to cure Alzheimer’s disease, a cognitive memory disorder.
Alzheimer disease is a diagnosis within the category of dementia. Alzheimer is usually found on brain examinations after death. New tests, such as MRI, PET, and Tau help physicians study potential possibilities to infer exact causes. Complicating an Alzheimer disease diagnosis is that both dementia and Alzheimer is a neurodegenerative disease, which means there is progressive brain cell death that happens over time. In a person with Alzheimer’s, the tissue has fewer and fewer nerve cells and connections.
For example, I was part a study on REM-Dream Sleep and cerebral memory storage. During REM, there is a switch among 2 neurotransmitters – acetylcholine and nor-epinephrine. Dreaming helps store long-term memories and associations. REM dreaming involves bringing acetylcholine up to the cortex to help store these memories. Theory was that if normal REM did not occur, long term memories would not be stored. This remains one of a dozen possible theories of a possible inference of dementia toward Alzheimer.
A more current hypothesis are the development of beta-amyloid plaques and tangles to (and within) the brain. These could disassociate memory linkages. These are found in results of MRI and PET scans. The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. By disrupting neuronal network interaction, formation of these beta-amyloid proteins and peptides (over time) may result on Alzheimer disease symptoms.
Beta-amyloid is an important peptide, an amino acid chain from a host protein.. It does leave fragments between neurons that can form plaques. A normal brain, however, can eliminate beta-amyloid fragments before they disrupt neuron transmissions. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically “sticky” and gradually builds up into plaques.
Based on the beta-amyloid hypothesis and APOE44 variants, there are tests available to determine if you have these APOE4 gene variants. It is not FDA approved and is not concise at determining whether or not you may get Alzheimer disease. It may cause more worry than calm. APOE4 has been behind diagnoses such as high-cholesterol, coronary artery diseases, and obesity. Can APOE4 variants be used to treat, cure, or detect Alzheimer disease with some accuracy?
Could something as nasty as APOE4 variations help treat dementia and aging? Who knows? Potentially there may be other genes and other proteins? Nutritionists believe that diets rich in these foods may help reduce beta-amyloid build-up:
Foods That Reduce Your Alzheimer’s Risk
Walnuts (and almonds, pecans, hazelnuts) Walnuts might be small in size, but they pack a big nutritional punch.
Salmon (and mackerel, sardines, other fatty fish) …
Spinach (and kale, other leafy greens)
In March 2018, the president signed into law a $414 million increase for Alzheimer’s and dementia research funding at the National Institutes of Health (NIH) and Kevin and Avonte’s Law, important legislation to protect those who wander. Alzheimer disease is getting everyone’s attention.
The dilemma is how valid this Beta-Amyloid hypothesis is, and how solid the apoE4 genetic cure for Alzheimer disease might be. As most early studies indicate, further research is necessary.
The food and mood relationship keeps coming up in research. Does that mean you should drop your medications? The answer is No. Depression and other mood disorders may very well be chemically related. It is associated with hormones and fluids in the brain and elsewhere, heavily supported by comprehensive studies. Eating certain foods may augment those chemicals but not necessarily change their bio-availability. The food and mood relationship is further exacerbated by what foods help and what food don’t help. The professionals are so conflicted about the foods that, for affective effectiveness, you might just as well stick to the pill.
For more than 30 years, books on food and mood have lined shelves and online searches filled with twists of what may work.
Columbia University’s Mailman institute seems to be focused on food and mood by delivering interesting studies about childhood anxiety and food allergies. CBS news has produced a story how researchers are trying to tie-in numerous and large studies to explore and reveal the food and mood connection.
digestive system parts are linked to the brain by the vagus nerve.
The vagus nerve, when stimulated, sends mild signals to the brain to indicate that the gut is hungry. At this point all sorts of hormones are triggered, insulin is -preparing for food but none is coming. That might have something to do with brain fog that develops a couple hours after a routine meal. Brain fog occurs when the symptoms of low blood sugar are experienced a few hours after a meal even though blood glucose levels remain normal. This is also known as postprandial (“after eating”) hypoglycemia or postprandial dip. Performance a few hours after eating can fade and lead to anxiety.
There are some unique clinical aspects that are discussed because the relationships of food and mood seem like a simple way of treating depression. Is it? And do we really know what they are and how they work?
Then there are many other possible causes of depression mood disorder, not associated with food. The exact cause of depression disorders are not clearly known. However, there are several factors that can increase the risk of developing the condition. The APA might suggest that there are combinations of genes and stress that can influence changes in brain chemistry and reduce the ability to maintain mood stability. Yet, the American Psychiatric Association (APA) does stress depression’s alarming statistics:
Depression affects an estimated one in 15 adults (6.7%) in any given year. And one in six people (16.6%) will experience depression at some time in their life.
Yet the diagnosis is more involved with the symptoms than lifestyle causes of depression. It is very unlikely to indicate food and mood.
Per APA, symptoms are:
(Depression symptoms can vary from mild to severe and can include:)
Feeling sad or having a depressed mood
Loss of interest or pleasure in activities once enjoyed
Changes in appetite — weight loss or gain unrelated to dieting
Trouble sleeping or sleeping too much
Loss of energy or increased fatigue
Increase in purposeless physical activity (e.g., hand-wringing or pacing) or slowed movements and speech (actions observable by others)
Feeling worthless or guilty
Difficulty thinking, concentrating or making decisions
Thoughts of death or suicide
Of course, other possibilities may have an influence over any of these symptoms.
Food and mood may be associated with adding certain Omega 3 fats with slow absorbing carbohydrates. Low glycemic foods, chocolate, and food that has high levels of omega-3 fatty acids, magnesium, tryptophan, folate and other B vitamins, have all been studied to evaluate their impact on mood. Results vary from study to study, but there usually appears to be an association between these foods and improved mood. Fundamentally, a good, healthy meal, with a vitamin supplement, might suggest an elevation in mood.
Beyond food, the importance of adequate hydration is often neglected. Your body needs water above any other liquid refreshment. General recommendations indicate that you drink 2 liters of water each day. Studies seem to indicate that moods change as your hydration drops. Water is the most overlooked nutrient. Many active people use skin sensing hydration monitors to assure that they are adequately hydrated. Drinking water also helps reduce that brain fog that may occur when meals are spaced too far apart – or beyond habituation. Think of water as a filling snack. Just keep it clear. No sweet drinks, sodas, juices, or coffee. Just cool, clear water.
Considering food and mood routinely is noble. There are subtle nuances in wither with differing benefits and consequences. Prescription anti-depressants are probably the best bet if your mood is blue for over a few months. Anti-depressants also have side effects that may continue to affect your moods negatively.
Severe or abrupt diets or intermittent fasting may be more depressing unless you really believe that you can and will transition for long term results. Food, processed or whole, have calories, carbohydrates, fats, cholesterol (and other things that people need to control) may be significant confounding variables. Eating tuna and salmon daily can bring Mercury poisoning. That alone is something to get depressed over.
Barring any unique illnesses or conditions, following USDA dietary guidelines would provide a healthy diet plan that could be satisfying in many ways, including your mood.
Chronic mood disorders may really require competent psychotherapists to prescribe those medications that work best and that you can tolerate.
Pardon my political incorrectness! This is my entry for Black History Month, February 1018, about a unique part of African-American history yn New York City at the 19th Century – the 1800’s.
In the 18th and 19th centuries, the city of New York used outer areas to house orphans, sick, and unwanted. It kept the peace stable. Most people lived in what is now the financial center and Tribeca. Farms gave way to establishing a city in lower Manhattan. One key question, how were “Negro” orphans treated in the segregated 19th century?
Orphans are and have been a reality for centuries. Churches have tried to camouflage it but there were orphanages in most western civilized societies. If you were black, Afro-American, or Negro in New York City’s 19th-century, and an orphan, you had a safe place to stay. The NY Colored Orphan Asylum was a secure, racist-free orphanage on Fifth Avenue, between 42nd and 43rd Streets. The Colored Orphan Asylum provided home services for about 233 children.
The New York City Colored Orphan Asylum was at this location from 1836 to 1863. Actually, the idea began in 1834 when three Quakers decided to create a safe haven for negro orphans. In 1836 they purchased a house on 12th Street between Fifth and Sixth Avenues. The purchase was necessary because no property owner would lease to a group housing black children. With the house ready to receive orphans, three Quaker women headed to the almshouse. They rescued 11 children who were being housed in the cellar there.
In 1836, New York City barely resembled how it appears today. Most New York City residents lived south of 14th Street. Actually, south pf Canal Street. The infamous 5-Points neighborhood wasn’t built yet toward the now trendy lower east-side.
42nd Street and Fifth Avenue was undeveloped land and a socially acceptable area to build asylums, particularly a Colored Orphan Asylum. People didn’t need to see, hear, or think about the wayward, the sick, and the orphans. As a matter, one main reservoir from the original Croton Reservoir (1843) was on 42nd Street, where Bryant Park is today. That’s how remote the current midtown hub was in 1836. It remained there until 1863 when it was destroyed and burned.
White racism among the poor and immigrant people reacted to the Civil War military draft imposed by President Abraham Lincoln. A key problem focused that the advantaged wealthy were able to pay for exemption. The poor and new immigrants from Germany and Ireland would be drafted.
The poor Irish and German immigrants had a particular focal point at targeting the African-Americans of New York as scapegoats. The Irish usually had to compete with the “Negroes” for jobs and grunt labor, particularly in building tunnels, such as the water tunnels and sewage tunnels. In addition, “Negroes” were pretty much exempt from being drafted due to a lack of military opportunities.
The riots were a three-day orgy of violence towards Afro-American owned businesses, Afro-Americans, and Native Americans. They marched upwards to the shanty areas where those “minorities” lived. And, by the third day, the Colored Orphan Asylum was burned to the ground. Most of the children were rescued by the Fire and Police department.
The asylum would relocate to 144th Street and Amsterdam Avenue, in the new village of Harlem, at Sugar Hill. Later it moved to Riverdale in the Bronx. Though attractive, the Riverdale site was the most upper, out-of-the-way area of the Bronx, on West 261 Street bordering Yonkers. It was larger and considered one of the best orphanages in New York City. In the 1960’s, the site was sold to the Hebrew Home for the Aged.
Dr. James McCune Smith, an African-American physician, provided medical services for about 20 years to the orphans at Colored Orphan Asylum in New York. As there were absolutely no opportunities for Africans to enter medical schools in the United States, Dr. McCune received his medical education at the University of Glasgow in Scotland. In addition, he was the founder of the American Geographic Society.
It is difficult to put yourself in the shoes of those who are not seen as being on par with tour status. Many minorities are viewed under different scopes. This included blacks and the poor. The conceptualization of race (or gender) moved from the biological to the sociological sphere with the march of science. The atmosphere created by racial inferiority theories and stereotypes, 246 years of black chattel slavery, along with biased educational processes, almost inevitably led to medical and scientific abuse, unethical experimentation, and over-utilization of African-Americans as subjects for teaching and training purposes. Stricter ethical controls became issues only in the late 1970’s.
With no acceptance to the American Medical Society, most 19th-century African medical doctors received training in Africa, Europe, or very segregated schools in the Americas. Thus it is important to understand how influential the Quakers were in providing medical care to those residing at the New York City Colored Orphan Asylum.
In contrast to what happened in Manhattan in 1863, There was a Home for Colored Aged in Crown Heights in 1863, supported by many philanthropists of that area. These African Americans had lived in a Brooklyn area called Weeksville. This area had one of the largest (one of three) “Colored” communities.
Unwanted or orphaned children continues to be a society-wide dilemma, often debated. Fortunately, segregation is no longer legally valid. Despite strides toward the American Dream of equal opportunity, people are still separated by race, ethnic, religious and gender issues. As Senator Patrick Moynihan may have said, New York (and the USA) is less of a melting pot but more like a tossed salad. There are still many strides and challenges to overcome.