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The terms Paleolithic diet, paleo diet, caveman diet, and stone-age diet[1] describe modern fad diets requiring the sole or predominant consumption of foods presumed to have been the only foods available to or consumed by humans during the Paleolithic era.[2]

The digestive abilities of anatomically modern humans, however, are different from those of Paleolithic humans, which undermines the diet's core premise.[3] During the 2.6-million-year-long Paleolithic era, the highly variable climate and worldwide spread of human populations meant that humans were, by necessity, nutritionally adaptable. Supporters of the diet mistakenly presuppose that human digestion has remained essentially unchanged over time.[3][4]

While there is wide variability in the way the paleo diet is interpreted,[5] the diet typically includes vegetables, fruits, nuts, roots, and meat and typically excludes foods such as dairy products, grains, sugar, legumes, processed oils, salt, alcohol or coffee.[1][additional citation(s) needed] The diet is based on avoiding not just processed foods, but rather the foods that humans began eating after the Neolithic Revolution when humans transitioned from hunter-gatherer lifestyles to settled agriculture.[2] The ideas behind the diet can be traced to Walter Voegtlin,[6]:41 and were popularized in the best-selling books of Loren Cordain.[7]

Like other fad diets, the Paleo diet is promoted as a way of improving health.[8] There is some evidence that following this diet may lead to improvements in terms of body composition and metabolic effects compared with the typical Western diet[5] or compared with diets recommended by national nutritional guidelines.[9] There is no good evidence, however, that the diet helps with weight loss, other than through the normal mechanisms of calorie restriction.[10] Following the Paleo diet can lead to an inadequate calcium intake, and side effects can include weakness, diarrhea, and headaches.[2][10]

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According to Adrienne Rose Johnson, the idea that the primitive diet was superior to current dietary habits dates back to the 1890s with such writers as Dr.Emmet Densmore and Dr.John Harvey Kellogg. Densmore proclaimed that "bread is the staff of death," while Kellogg supported a diet of starchy and grain-based foods.[11] The idea of a Paleolithic diet can be traced to a 1975 book by gastroenterologist Walter Voegtlin,[6]:41 which in 1985 was further developed by Stanley Boyd Eaton and Melvin Konner, and popularized by Loren Cordain in his 2002 book The Paleo Diet.[7] The terms caveman diet and stone-age diet are also used,[12] as is Paleo Diet, trademarked by Cordain.[13]

In 2012 the Paleolithic diet was described as being one of the "latest trends" in diets, based on the popularity of diet books about it;[14] in 2013 the diet was Google's most searched-for weight-loss method.[15]

Like other fad diets, the paleo diet is marketed with an appeal to nature and a narrative of conspiracy theories about how nutritional research, which does not support the supposed benefits of the paleo diet, is controlled by a malign food industry.[8][16] A Paleo lifestyle and ideology have developed around the diet.[17][18]

The diet advises eating only foods presumed to be available to Paleolithic humans, but there is wide variability in people's understanding of what foods these were, and an accompanying ongoing debate.[2]

In the original description of the paleo diet in Cordain's 2002 book, he advocated eating as much like Paleolithic people as possible, which meant:[19]

The diet is based on avoiding not just modern processed foods, but also the foods that humans began eating after the Neolithic Revolution.[2]

The scientific literature generally uses the term "Paleo nutrition pattern", which has been variously described as:

The aspects of the Paleo diet that advise eating fewer processed foods and less sugar and salt are consistent with mainstream advice about diet.[1] Diets with a paleo nutrition pattern have some similarities to traditional ethnic diets such as the Mediterranean diet that have been found to be healthier than the Western diet.[2][5] Following the Paleo diet, however, can lead to nutritional deficiencies such as those of vitaminD and calcium, which in turn could lead to compromised bone health;[1][20] it can also lead to an increased risk of ingesting toxins from high fish consumption.[2]

Research into the weight loss effects of the paleolithic diet has generally been of poor quality.[10] One trial of obese postmenopausal women found improvements in weight and fat loss after six months, but the benefits had ceased by 24 months; side effects among participants included "weakness, diarrhea, and headaches".[10] In general, any weight loss caused by the diet is merely the result of calorie restriction, rather than a special feature of the diet itself.[10]

As of 2016 there are limited data on the metabolic effects on humans eating a Paleo diet, but the data are based on clinical trials that have been too small to have a statistical significance sufficient to allow the drawing of generalizations.[2][5][20][not in citation given] These preliminary trials have found that participants eating a paleo nutrition pattern had better measures of cardiovascular and metabolic health than people eating a standard diet,[2][9] though the evidence is not strong enough to recommend the Paleo diet for treatment of metabolic syndrome.[9] As of 2014 there was no evidence the paleo diet is effective in treating inflammatory bowel disease.[21]

The rationale for the Paleolithic diet derives from proponents' claims relating to evolutionary medicine.[22] Advocates of the diet state that humans were genetically adapted to eating specifically those foods that were readily available to them in their local environments. These foods therefore shaped the nutritional needs of Paleolithic humans. They argue that the physiology and metabolism of modern humans have changed little since the Paleolithic era.[23] Natural selection is a long process, and the cultural and lifestyle changes introduced by western culture have occurred quickly. The argument is that modern humans have therefore not been able to adapt to the new circumstances.[24] The agricultural revolution brought the addition of grains and dairy to the diet.[25]

According to the model from the evolutionary discordance hypothesis, "[M]any chronic diseases and degenerative conditions evident in modern Western populations have arisen because of a mismatch between Stone Age genes and modern lifestyles."[26] Advocates of the modern Paleo diet have formed their dietary recommendations based on this hypothesis. They argue that modern humans should follow a diet that is nutritionally closer to that of their Paleolithic ancestors.

The evolutionary discordance is incomplete, since it is based mainly on the genetic understanding of the human diet and a unique model of human ancestral diets, without taking into account the flexibility and variability of the human dietary behaviors over time.[27] Studies of a variety of populations around the world show that humans can live healthily with a wide variety of diets, and that in fact, humans have evolved to be flexible eaters.[28] Lactose tolerance is an example of how some humans have adapted to the introduction of dairy into their diet. While the introduction of grains, dairy, and legumes during the Neolithic revolution may have had some adverse effects on modern humans, if humans had not been nutritionally adaptable, these technological developments would have been dropped.[29]

Evolutionary biologist Marlene Zuk writes that the idea that our genetic makeup today matches that of our ancestors is misconceived, and that in debate Cordain was "taken aback" when told that 10,000 years was "plenty of time" for an evolutionary change in human digestive abilities to have taken place.[3]:114 On this basis Zuk dismisses Cordain's claim that the paleo diet is "the one and only diet that fits our genetic makeup".[3]

Advocates of the diet argue that the increase in diseases of affluence after the dawn of agriculture was caused by changes in diet, but others have countered that it may be that pre-agricultural hunter-gatherers did not suffer from the diseases of affluence because they did not live long enough to develop them.[30] Based on the data from hunter-gatherer populations still in existence, it is estimated that at age15, life expectancy was an additional 39 years, for a total age of 54.[31] At age 45, it is estimated that average life expectancy was an additional 19 years, for a total age of 64 years.[32][33] That is to say, in such societies, most deaths occurred in childhood or young adulthood; thus, the population of elderlyand the prevalence of diseases of affluencewas much reduced. Excessive food energy intake relative to energy expended, rather than the consumption of specific foods, is more likely to underlie the diseases of affluence. "The health concerns of the industrial world, where calorie-packed foods are readily available, stem not from deviations from a specific diet but from an imbalance between the energy humans consume and the energy humans spend."[34]

Adoption of the Paleolithic diet assumes that modern humans can reproduce the hunter-gatherer diet. Molecular biologist Marion Nestle argues that "knowledge of the relative proportions of animal and plant foods in the diets of early humans is circumstantial, incomplete, and debatable and that there are insufficient data to identify the composition of a genetically determined optimal diet. The evidence related to Paleolithic diets is best interpreted as supporting the idea that diets based largely on plant foods promote health and longevity, at least under conditions of food abundance and physical activity."[35] Ideas about Paleolithic diet and nutrition are at best hypothetical.[36]

The data for Cordain's book only came from six contemporary hunter-gatherer groups, mainly living in marginal habitats.[37] One of the studies was on the !Kung, whose diet was recorded for a single month, and one was on the Inuit.[37][38][39] Due to these limitations, the book has been criticized as painting an incomplete picture of the diets of Paleolithic humans.[37] It has been noted that the rationale for the diet does not adequately account for the fact that, due to the pressures of artificial selection, most modern domesticated plants and animals differ drastically from their Paleolithic ancestors; likewise, their nutritional profiles are very different from their ancient counterparts. For example, wild almonds produce potentially fatal levels of cyanide, but this trait has been bred out of domesticated varieties using artificial selection. Many vegetables, such as broccoli, did not exist in the Paleolithic period; broccoli, cabbage, cauliflower, and kale are modern cultivars of the ancient species Brassica oleracea.[29]

Trying to devise an ideal diet by studying contemporary hunter-gatherers is difficult because of the great disparities that exist; for example, the animal-derived calorie percentage ranges from 25% for the Gwi people of southern Africa to 99% for the Alaskan Nunamiut.[40]

Researchers have proposed that cooked starches met the energy demands of an increasing brain size, based on variations in the copy number of genes encoding for amylase.[41][42]

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Chronic Obstructive Pulmonary Disease (COPD) is by definition an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, refractory (non-reversible) asthma, and some forms of bronchiectasis. This disease is characterized by increasing breathlessness.

Many people mistake their increased breathlessness and coughing as a normal part of aging. In the early stages of the disease, you may not notice the symptoms. COPD can develop for years without noticeable shortness of breath. You begin to see the symptoms in the more developed stages of the disease.

Damage to the lung tissue over time causes physical changes in the tissues of the lungs and clogging of the airways with thick mucus. The tissue damage in the lungs leads to poor compliance (the elasticity, or ability of the lung tissue to expand).

 

The decrease in elasticity of the lungs means that oxygen in the air cannot get by obstructions (for example, thick mucus plugs) to reach air spaces (alveoli) where oxygen and carbon dioxide exchange occurs in the lung. Consequently, the person exhibits a progressive difficulty, first coughing to remove obstructions like mucus, and then in breathing, especially with exertion.

Chronic Obstructive Pulmonary Disease Symptoms

 

People with COPD can often mistake their symptoms for other respiratory problems, such as exercise induced asthma or a bad cold. If you have any of the following symptoms, you should see your doctor as soon as possible:

• Wheezing
• Tightness in the chest
• Fatigue
• Multiple respiratory infections
• Shortness of breath (dyspnea) that gets worse with mild activity
• Having to clear your throat first thing in the morning, due to excess mucus in your lungs
• A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or greenish
• Blueness of the lips or fingernail beds (cyanosis)
• Frequent respiratory infections
• Unintended weight loss (in later stages)
• Swelling in ankles, feet or legs

 

If left untreated, COPD can lead to hospitalization and even death. Be proactive if you are showing signs of the disease and be evaluated by your physician promptly.

What Causes COPD?

The main cause of COPD in developed countries is tobacco smoking. In the developing world, COPD often occurs in people exposed to fumes from burning fuel for cooking and heating in poorly ventilated homes.

 

Only about 20 to 30 percent of chronic smokers may develop clinically apparent COPD, although many smokers with long smoking histories may develop reduced lung function. Some smokers develop less common lung conditions. They may be misdiagnosed as having COPD until a more thorough evaluation is performed.

Exposure to certain gases or fumes in the workplace, exposure to heavy amounts of secondhand smoke and pollution, frequent use of a cooking fire without proper ventilation, and genetic problems like Alpha-1 Antitrypsin Deficiency are also causes of COPD.

Stages of COPD

 

One way to establish stages for chronic obstructive pulmonary disease is the Global Initiative for Chronic Obstructive Lung Disease program (GOLD).

 

The staging is based on the results of a pulmonary function test. Specifically, the forced expiratory volume (how much air one can exhale forcibly) in one second (FEV1) of a standard predicted value is measured, based on the individual patient's physical parameters.

 

The stages are as follows:

• Stage I is FEV1 of equal or more than 80% of the predicted value
• Stage II is FEV1 of 50% to 79% of the predicted value
• Stage III is FEV1 of 30% to 49% of the predicted value
• Stage IV is FEV1 of less than 30% of predicted value or an FEV1 less than 50% of predicted value plus respiratory failure

Other staging methods are similar but are based on severity of the shortness of breath symptom.

COPD Treatment

 

Medical treatments of chronic obstructive pulmonary disease include bronchodilators, steroids, mucolytic agents, oxygen therapy, and surgical procedures such as bullectomy, lung volume reduction surgery, and lung transplantation.

The treatments are often based on the stage of chronic obstructive pulmonary disease, for example:

• Stage I - short-acting bronchodilator as needed
• Stage II - short-acting bronchodilator as needed and long-acting bronchodilators plus cardiopulmonary rehabilitation
• Stage III - short-acting bronchodilator as needed, long-acting bronchodilators, cardiopulmonary rehabilitation, and inhaled glucocorticoids for repeated exacerbations
• Stage IV - as needed, long-acting bronchodilators, cardiopulmonary rehabilitation, inhaled glucocorticoids, long-term oxygen therapy, possible lung volume reduction surgery, and possible lung transplantation (stage IV has been termed "end-stage" chronic obstructive pulmonary disease)

The three major goals of the comprehensive treatment and management of chronic obstructive pulmonary disease are to reduce airflow limitation, prevent and treat secondary medical complications, decrease respiratory symptoms, and improve quality of life.

The patient may need to be hospitalized if they develop severe respiratory dysfunction, if the disease progresses, or if they have other serious respiratory diseases. The purpose of hospitalization is to treat symptoms and to prevent further deterioration.

 

The patient may be admitted to an intensive care unit (ICU) if they require invasive or noninvasive mechanical ventilation or if they have the following symptoms:

• Confusion
• Lethargy
• Respiratory muscle fatigue
• Worsening hypoxemia (not enough oxygen in the blood)
• Respiratory acidosis (retention of carbon dioxide in the blood)

Treatment of Moderate to Severe COPD

 

Doctors often use these additional therapies for people with moderate or severe COPD:

 

• Oxygen therapy - Some people with COPD use oxygen only during activities or while sleeping. Others use oxygen all the time. Oxygen therapy can improve quality of life and is the only COPD therapy proven to extend life.

 

• Pulmonary rehabilitation program. These programs generally combine education, exercise training, nutrition advice and counseling. You'll work with a variety of specialists, who can tailor your rehabilitation program to meet your needs.

Even with ongoing treatment, you may experience times when symptoms become worse for days or weeks. This is called an acute exacerbation, and it may lead to lung failure if you don't receive quick and appropriate treatment.

Exacerbations may be caused by a respiratory infection, air pollution, or other triggers of inflammation. Whatever the cause, it's important to seek prompt medical help if you notice a sustained increase in coughing, a change in your mucus or if you have a harder time breathing.

 

When exacerbations occur, you may need additional medications, supplemental oxygen, or treatment in the hospital. Once symptoms improve, your doctor will talk with you about measures to prevent future exacerbations.

 

Surgical Procedures

Surgery is an option for some people with some forms of severe emphysema who aren't helped sufficiently by medications alone. Surgical options include:

• Lung volume reduction surgery. In this surgery, your surgeon removes small wedges of damaged lung tissue from the upper lungs. This creates extra space in your chest cavity so that the remaining healthier lung tissue can expand, and the diaphragm can work more efficiently.

 

• Lung transplant. Lung transplantation may be an option for certain people who meet specific criteria. Transplantation can improve your ability to breathe and to be active. However, it's a major operation that has significant risks, such as organ rejection, and it requires taking lifelong immune-suppressing medications.

 

• Bullectomy. Large air spaces (bullae) form in the lungs when the walls of the air sacs are destroyed. These bullae can become very large and cause breathing problems. In a bullectomy, doctors remove bullae from the lungs to help improve air flow.

Can You Live Well With COPD?

 

There are many things you can do at home to stay as healthy as you can.

• Avoid things that can irritate your lungs, such as smoke and air pollution.
• Use an air filter in your home.
• Get regular exercise to stay as strong as you can.
• Eat well so you can keep up your strength. If you are losing weight, ask your doctor or dietitian about ways to make it easier to get the calories you need.

As COPD progresses, you may have flare-ups when your symptoms quickly get worse and stay worse. It is important to know what to do if this happens. Many doctors will give you an action plan and medicines to help you breathe if you have a flare-up. But if the attack is severe, you may need to go to the emergency room.

Knowing that you have a disease that gets worse over time can be hard. It's common to feel sad or hopeless sometimes. Having trouble breathing can also make you feel very anxious. If these feelings last, be sure to tell your doctor. Counseling, medicine, and support groups can help you cope.

 

Source: LifePolicyShopper.com

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How was Muhammad Ali able to float like a butterfly and sting like a bee? How did Jordan take off from the free throw line? Have you seen that one handed catch by Odell Beckham Jr.? Crazy.

 

Athletes dedicate their entire lives to becoming the absolute best at what they do. They wake up before the sun, spend every available minute learning and perfecting their craft, and when everyone else has gone to bed, they’re still awake, practicing under the streetlights.

 

It’s this level of dedication that has got them to where they are.

But, there is something else that helps them achieve success and push them over the edge - supplements. While this may not necessarily be the case for Jordan, Ali or Beckham, most of the worlds greatest athletes include supplements in their daily routines.

No, there isn’t a supplement you can take that will give you the dedication these athletes have, but there are plenty of supplements on the market that can help you achieve our own athletic goals. Your goals may not be the same as the world's top performing athletes, but you can still benefit from the supplements they use.

What supplements should athletes take for improved performance?

 

First things first. What supplements do the world’s best athletes take on a regular basis?

 

The overwhelming majority of athletes are taking supplements to aid in there performance. There are many legal supplements available today that can help athletes gain an extra edge in their respective sports. But what vitamin supplements for athletes are the most important?

 

Omega 3 fatty acids are one of the most well known and most used supplements on the market. Omega 3’s may improve cardiovascular health and function, improve lipid profiles, improve brain function and mental acuity, and have powerful anti-inflammatory properties. When taken correctly, Omega 3’s can provide you with the biggest bang for your buck.

 

B-Vitamins are another popular supplement that can increase your energy production, improve your mood, and help your body detoxify. If you’re doing heavy workouts that may damage your muscles, it is a good idea to take B-Vitamins to help your body in the rebuilding process.  

 

Magnesium is one of the most recommended supplement for athletes because it’s essential to our biological systems and most athletes are likely deficient. A recent study suggested that up to 80% of Americans are deficient in magnesium, and that number is likely higher among athletes. Magnesium is important to athletes because it regulates heart rhythm, allows muscles to contract and relax properly, and reduces blood pressure. Every athlete should be taking magnesium.

Vitamin D is more like a hormone than a drug. Your body produces vitamin D when you’re exposed to the sun, which means you’re probably not producing enough. Unless you’re walking around naked in the sun for a few hours a day, you probably aren’t getting enough Vitamin D.  

 

Vitamin D can help reduce inflammation, improves mood and upper respiratory health and allows the brain to release melatonin so you can fall asleep easier. If for nothing else, vitamin D is important so you can get a good night's sleep after a long day in the gym.

 

Protein is probably the most popular and well known supplement for athletes. It’s almost second nature for people starting to train and workout to look up what protein shake they need to be drinking. If taken within 10 minutes of training, protein will reduce the amount of stress hormones released.

 

Protein should be eaten from animal sources throughout the day for best results. Too much protein can cause problems in the body, but the right amount repairs tissues and reduces muscle soreness.

 

Vitamin C is used by most people to help them get over a sickness. And while vitamin C can help protect the immune system, it also helps athletes recover from intense workouts. Vitamin C is found in most fruits and is nearly impossible to overdose on.  Take vitamin C during your post workout to help your body start repairing your muscles immediately.

 

Coenzyme Q10 may not be well-known, but it’s essential. CoQ10 is the only antioxidant found within cells, and it gets rid of lactic acid and other wastes. CoQ10 should be more widely known because of what it does for your heart.

There have been a number of young, healthy distance runners that have died of cardiac arrest recently, and it’s been found that there was a lack of CoQ10 in their hearts. This in turn caused scarring and damage from years of training. If you’re doing any kind of serious training, you should take CoQ10. The most usable form of CoQ10 is ubiquinone and delivered in oil. Just be sure not to take it at the same time as your fish oils because that could inhibit the absorption rate.

 

Branched Chain Amino Acids are said to be the best recovery supplement to take for athletes. Sipping on BCAAs during your workouts is shown to speed up the recovery and repair process. Research suggests that participants who ingest BCAAs experience significantly less muscle soreness and damage following a high-volume workout.  

 

Creatine Monohydrate is a muscle-building, power-enhancing supplement.  It’s one of the best supplements for strength and size, and one of the best supplements for strength gains.  If you’re looking to lose weight, creatine may not be what you’re looking for, at least initially, because creatine helps build muscle which makes the number on the scale go up.  Creatine also helps maintain energy during workouts, helps speed up your recovery, and enhances the quality of your weight training.

 

The best recovery drink after any workout is a protein shake. Whey protein is a very popular option, but whey protein doesn’t sit well on some people's stomachs. Because of that, vegan protein shakes are becoming more and more popular. If you’re looking for something to eat after your workout to compliment your supplements, there’s nothing better than some grilled chicken and roasted vegetables.  

 

Best Supplements Specifically For Runners

 

Probably the most widely used workout technique is running. Every athlete uses cardio in their workouts in some form or fashion, and there's no better cardio workout than a good old fashioned run. If running is a part of your routine, there are some specific supplements you can take to aid in your progression.

 

First, take the supplements mentioned above. Fish oil, magnesium, vitamin C are all essential supplements for runners, and magnesium carries extra benefits because it helps with endurance, energy, and muscle contraction.  

 

But there are a few others that are recommended specifically for runners.

 

Caffeine is actually one of the best supplements for endurance athletes like runners. It’s one of the best ways for runners to increase their stamina. Caffeine's ability to reduce perception of effort and help delay fatigue can make those longer runs more bearable.  As an added bonus, caffeine can increase fat oxidation, which can help with weight management.

 

Celadrin helps cushion bones and joints and improve flexibility. You can understand why this would be important to runners given the constant pounding on the joints. It's made from a blend of essential fatty acids and is fast acting and long lasting. It also benefits muscles, tendons and deep tissue.

 

L-Glutamine is good for runners because glutamine is depleted in the body when it undergoes physical stress. As an amino acid, l-glutamine helps fuel muscles and can stop them from becoming sore during exercise.

 

Zinc is another supplement that can help us maintain energy. Runners lose zinc during exercise, so it's important to supplement to build levels back up. Zinc also helps maintain a healthy immune system.

 

When thinking about creatine, most people don’t associate it with running. When you think creatine, you think of heavy lifting and building muscle, not running. However,  Creatine supplements can boost the quality of high intensity training, an essential part of a training routine for runners.

 

None of these supplements will magically turn you into an elite sprinter, but if you take them all as directed, you should begin to see improvements.  

 

Are PEDs and Supplements The Same Thing?

 

Don’t get supplements confused with performancing enhancing drugs. When talking about PEDs, most people are talking about various types of steroids. These PEDs are in a category all alone, and shouldn’t be confused with natural supplements.  

 

Performance enhancing drugs come with a laundry list of side effects. Depending on what you’re taking, you could develop acne, lose your hair, have severe headaches, increase your risk of stroke, and become much more aggressive and easily agitated.

 

Even though most PEDs aren’t legal and are extremely frowned upon in professional sports, they are still used, and sometimes more than you’d would think. If you are a baseball fan, you know all about the use of PEDs that rocked the MLB a few years back.  

 

One of America's most beloved athletes, Lance Armstrong, even had his reputation stained when he was caught “doping” for the Tour de France.  Every major sport has a program in place to test it’s athletes to be sure they aren't using any banned substances.

 

The most important thing to remember about PEDs is that they can cover a very broad spectrum of drugs and supplements. Caffeine, creatine and other very good and legal supplements we’ve talked about can all be considered legal performance enhancing drugs, but they are nothing like the illegal steroids people are usually referencing when they are talking about PEDs.

 

Conclusion

Supplementing your diet and workout routines might not get you to perform “like Mike,” but they do provide multiple benefits that people like me and you should take full advantage of. Whether your goal is to drop a few pounds, train for a marathon, or make the high school football team, adding supplements can do wonders for your workouts and recovery.

 

Source: DoublewoodSupplements

 

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You probably know that testosterone is important for men. After all, it’s responsible for things like sex drive, sperm count, fat distribution, red blood cell count, and muscle strength.

When you have low levels of testosterone, there are significant negative side effects, including:

Diminished sex drive
Muscle loss
Increased breast size
Erectile dysfunction or impotence
Depression, irritability, and the inability to concentrate
Loss of hair
Shrunken testes
Low energy
Decreased physical endurance
Increased chance of bone fractures

It’s absolutely essential for you to maintain healthy levels of testosterone in order to function effectively.

This raises an important question: how can you increase testosterone levels?

After all, it’s one thing to know that you have low testosterone levels; it’s something else altogether to increase them.

Consider this article a primer on increasing your testosterone levels. We’re going to break down the what, why, and how so that you are able to make informed decisions about your health.

What Is Testosterone?

Before we discuss how to increase your testosterone levels, it’s essential to understand what exactly what testosterone is.

Testosterone is a male sex hormone that’s essential for both reproductive development and sexual health. It’s part of a class of hormones called androgens (also known as “steroids” or “anabolic steroids”). While women do have testosterone in their bodies, their levels are around one-tenth to one-twentieth what’s found in men.

Testosterone is primarily created in the testes, although a small amount is also produced from the adrenal glands. The hypothalamus and the pituitary gland work together to control a man’s testosterone production, with the hypothalamus instructing the pituitary gland and those instructions being passed on to the testes.

The hormone is also responsible for the initial development of male sex organs before birth, as well as the changes that happen at puberty like increased penis and testes size, increased facial and body hair, and a deeper voice.

EMBED: https://youtu.be/sGCp4fXf4R0

Causes Of Low Testosterone

Normal levels of testosterone fall anywhere between 300-1000 nanograms per deciliter (ng/dl), with free testosterone levels usually being between 3-9 ng/dl.

There are a number of causes of low testosterone levels, including:

Aging
Pituitary gland problems
Toxin or heavy metal exposure
Stroke
Surgery
Anabolic steroid use
And many others…

Dr. Robert Kominiarek notes:

Most commonly, I find some history of neurologic insult as the cause — a traumatic brain injury with or without loss of consciousness, stroke, surgery, medical imaging with iodinated contrast, medication, illegal drug use, excessive alcohol [consumption], toxin or heavy metal exposure, prior anabolic steroid use, penetrating or blunt trauma, radiation, chemotherapy, [arrhythmia], motorcycle accident, rollercoaster rides, boxing, martial arts, football, and the list goes on.

The point is that while there are numerous reasons for low testosterone, the cause may not be immediately apparent. And while identifying the underlying cause is crucial, it’s even more important to know how to bring testosterone levels back to normal levels.

If you think you have low testosterone levels, the easiest way to confirm your suspicion is to have your doctor perform a simple blood test.

If your levels fall below the “normal” range, then you have a problem that, thankfully, can be corrected.

How To Raise Testosterone Levels

If testing reveals that you have low testosterone levels, there are some relatively simple, yet powerful ways to increase them.

Improved Diet

The simplest, most natural place to start is with your diet. Saturated and monounsaturated fats have both been to shown to increase testosterone levels. As a study in the Journal of Applied Physiology notes:

Individuals consuming a diet containing ?20% fat compared with a diet containing ?40% fat have significantly lower concentrations of T. Also, replacement of dietary carbohydrate with protein has been shown to decrease T concentrations. These studies indicate that the energy supplied by the different macronutrients has a significant influence on T concentrations.

In other words, if your diet is high in healthy fat, there’s a greater chance that your overall testosterone levels will be higher.

Some outstanding, high-fat foods to incorporate into your diet are:

Red meat
Cheese
Eggs
Olive and coconut oil
Avocado
Peanut butter

Two things to remember, however, as you bring these foods into your diet. First, if you’re not carefully monitoring your calorie intake, you can put on weight, which is not good for your health. Second, it’s important to not cut your carbohydrate intake when you add high-fat foods to your diet. Consuming low amounts of carbs can increase cortisol, which then decreases testosterone. It’s essential to balance your intake of carbs and fats.

Supplements

In addition to improving your diet, taking supplements can also be an effective, natural way to maintain your overall testosterone levels. One thing to note: the only supplements that seems to have a connection with raising testosterone levels are vitamin D3 and omega-3 fish oil. All other supplements help in maintaining optimal health levels.

So what supplements should you be taking?

Zinc gluconate - low levels of zinc can lead to lower testosterone levels.

Magnesium - magnesium is essential for muscle health, sleep, and energy. When you’re low on magnesium you may have lower testosterone levels as well.

Exercise

There are numerous studies that have demonstrated the testosterone boosting power of High Intensity Interval Training (HIIT). As William Kraemer notes:

Resistance exercise has been shown to elicit a significant acute hormonal response. It appears that this acute response is more critical to tissue growth and remodelling than chronic changes in resting hormonal concentrations, as many studies have not shown a significant change during resistance training despite increases in muscle strength and hypertrophy. Anabolic hormones such as testosterone and the superfamily of growth hormones (GH) have been shown to be elevated during 15-30 minutes of post-resistance exercise providing an adequate stimulus is present. [emphasis added]

HIIT involves doing exercises at a high intensity for short periods interspersed with periods of rest.

The best type of HIIT exercises are those which involve and stimulate as many muscles as possible. Some outstanding exercises include:

Kettlebell exercises. Doing kettlebell swings, deadlifts, curls, snatches, and squats can get your body into a prime testosterone producing state.

Sprints. Flying down the track at top speed pushes your body to the max and encourages it to produce more testosterone.

Don’t Cut Calories Too Often

There’s a fine line between trying to lose weight and keeping your testosterone levels high. When you diet for long periods of time, your body reduces testosterone levels. Returning to normal calories level will bring your levels back up to normal.

If you’re going to diet, don’t overdo it. Balance your calorie cuts with your standard diet.

Go To Sleep

Most production of testosterone happens when you sleep. In fact, if you don’t wake up with a morning erection, you might have low testosterone levels.

If you sleep fewer than five hours per night, it can reduce your testosterone levels by up to 15%. Additionally, low sleep typically increases cortisol levels, which also diminishes the amount of testosterone in your body.

To keep your testosterone levels high, be sure to get a solid night’s sleep.

Conclusion

Testosterone is one of things you take for granted while it’s there. But low testosterone can be seriously problematic and dramatically reduce the quality of your life. A decreased sex life can hurt your relationships, reduced energy can lower the quality of your work, and extra weight can take a strain on your body. Testosterone is essential for a good life.

Thankfully, if you have low levels, you can take steps to repair your body. Most of these steps are simple, like exercising, sleeping well, and eating a healthy diet. These natural solutions are much better than medical alternatives like hormone therapy or testosterone patches.

If you think your deficient in testosterone, take action. It doesn’t usually fix itself. Take steps in the right direction today.

Source: Vitamonk

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In this article we have given in-detailed explanation on : What is HCG diet? How to start HCG diet? What are HCG diet phases? History of HCG Diet, HCG Diet phase 1 foods with recipes, HCG Diet phase 2 with recipes and HCG Diet phase 3 with recipes. Almost we have covered everything about HCG diet program and its diet plan. You need not have to browse any other website looking for information on HCG Diet. Just keep reading till the end of this page.

Note: If you have landed over this page in search of the best hcg drops, then it is recommended to visit our HCG drops comparison page where we have discussed worlds best HCG drops based on Amazon, Ebay and Walmart ratings.After purchasing HCG drops, you need to come back to this page to follow the low calorie diet.There is a famous saying, Weight loss without HCG diet is No weight loss..

Synopsis of the article:

hcg diet falls in the category of very low calorie diet, restricting the calorie intake to 500 calories per day. The hcg diet plan was formulated by Dr. Simeons. The VLCD HCG dietary regime has four phases. Food lists and recipes are different for each phase. The first two phases of the hcg diet plan is accompanied by the administration of hcg drop shots. The hcg drops help in shedding the excess weight faster as well as remedying the hypothalamus gland.

HCG diet is the unique contribution of the famous British endocrinologist Dr. Albert Theodore William Simeons. The world came to know about this dietary regime, Very Low Calorie Diet HCG or VLCD HCG, through his book Pounds & Inches in the year 1954. Human Chorionic Gonadotropin (HCG) is a human hormone, found aplenty in the urine of the pregnant women. It was observed that, when the pregnancy hormone diet is administered in small amounts, it helps in burning the abnormal fats and reduces weight fast.

There is apprehension, does HCG diet work?. Due to its strict dietary plan the FDA even banned this diet plan.

Dr. Oz HCG diet, however, is slightly modified from VLCD HCG. In the article you will know what is the HCG diet plan?

HCG diet program has four phases. The first phase is called Loading Phase. The daily doses of HCG diet shots start in this phase. No restriction is imposed on the dieter. On the other hand the dieter is encouraged to eat oily and fatty foods which are high in calories. You will get to know about the various recipes for phase 1.

The second phase is called Working Phase. The HCG doses continue. The calorie intake is restricted to 500 calorie per day. There are restrictions in foods. You can know about the list of foods and various recipes for phase 2.

The third phase is called Stabilization Phase. From phase 3, HCG drops are stopped. Calorie intake is still restricted to 500 calories per day. Some addition in food varieties is allowed. You will know about foods and recipes for phase 3.

The fourth phase is called Maintenance Phase. Calorie intake is increased to 1500 calories. More food choices are permitted. You will get to know about the food recipes for phase 4. In this phase you get accustomed to the optimum calorie intake, exercises and positive living styles. This serves as the gate way for your future life. You get stabilized in living without HCG drops and without any increase in weights, happily, energetically and in high spirits.

How much the HCG weight loss diet cost?The cost varies from $30 to $60 per bottle.

HCG diet and pregnant women:The pregnant and lactating women need to consult doctor before starting HCG diet.

At the end of the article you will know, how to lose weight faster on the HCG diet. When you are through the plan you will feel energetic and be in high spirit with reduced weight. By now you have endeared positive and meaningful lifestyle. It is expected to follow this newly acquired living style for retaining the benefits accrued from the dietary regime.

For some extreme cases, needing shedding of excessive weights, the diet plan may require to be repeated. In such cases you have to give a break of some weeks after which you may again repeat the VLCD HCG dietary regime. This article gives lots of hopes and encouragements for the obese and overweight people of the world.

When armed with proper and detailed instructions, you minimize the risk of failure and thats true for anything in life, hCG diet included. By strictly following the original hCG diet protocol created by Dr. Simeons and the specific recommendations provided by the manufacturer of your hCG oral drops, youll be staying on the path of effective and durable weight-loss.

In this article, you will find a detailed description of the hCG diet in general and of each phase specifically, receive valuable recommendations and info on many tricks that will help you follow through every crucial aspect of your diet. Weve tried to keep it as simple and as informative as possible, but if youre still left with unresolved questions of any kind feel free to contact us for more information. Lets get started!

This particular weight-loss regime was designed by Dr. Albert Theodore William Simeons, a British endocrinologist. After years of studying the problem of excess weight and obesity, in 1954 he proposed an innovative dietary model that became later known as the hCG VLCD diet (human chorionic gonadotropin very low calorie diet) in his book Pounds and Inches. A New Approach to Obesity. And moreover, this strict diet is being followed by top celebrities around the world.

Read full article on What is HCG before going to HCG Diet >

Doctor Simeons came up with the idea of using hCG for weight reduction while studying the effects of the said hormone both present naturally (in pregnant women) and taken from the outside (for pituitary disorders treatment). The result was basically the same: under guidance of hCG, the human body burns body fat more actively under conditions of calorie and fat deficiency. This is thought to be one of hCGs main benefits during pregnancy and serves to protect the developing fetus from possible malnutrition. In other words, when the mother hasnt the possibility to eat well, the hCG resent in your body will gently break up the excess fat present in her body in order to provide her baby with the nutrients and energy necessary.

The diet itself is a complex of recommendations that, when followed strictly (this is the reason why FDA banned HCG products in the market), reveal the hCGs potential to its maximum. We will cover in details every aspect of the diet, so you can understand the underlying processes, but in any case always double check with the instructions and details provided by your manufacturer.

Read full article on Who is Dr Simeons and What did he said about HCG Diet >

Traditionally, the classic hCG diet is divided into four separate stages: loading, diet (weight-loss), stabilization and maintenance. This segregation is explained by the fact that your body needs several consecutive steps when adapting to something new boy weight included. Its impossible to cut off 40 pounds off yourself in a couple of days without going under the surgeons knife. If you want it done naturally and sustainable in the long run, its crucial to give your body the necessary time and resources to get used to the process of weight loss and to your new weight as well and the 4 phases of the hCG diet ensure that just right.

Also known as the gorging or bingeing days, this phase is somewhat paradoxical: in order to lose weight in the following stages, you must first stuff yourself for a couple of days. Eat up to the point of nauseating mostly with the help of fatty high-calorie products and dishes.

What is the goal of this phase? To load your body with enough energy substrate that will be used up later in the following stages. This is of particular need in the beginning of phase two, while your body still has not adapted to its fullest. Any given hCG product needs a couple of days to start burning your fat reserves. Meanwhile, you need to receive plenty of energy from any other source available so the food you intake during the loading phase will do just fine.

Keep in mind that people that neglect the meaning of this stage usually feel a lot more hungry and tired on the following weeks, while those who follow it and eat plenty of fatty food usually feet energetic and ready to keep on dieting.

To summarize: on the phase 1 (loading) you start taking your hCG oral drops and eat as much high-calorie and high-fat food as you physically can (without traumatizing yourself, of course) in order to give your hypothalamus the time it needs to tune your metabolism into burning excess fat. This phase usually takes 1-2 days (3-4 days if youre going out of a previous different diet).

Here is a list of products particularly recommended to eat during phase 1:

This is the stage in which the magic starts. Lasting from 15 to 40 days (depending on multiple factors, including the peculiar properties of the specific hCG oral drops youve chosen), the main goal of this diet is to get rid of your abnormal fat for good.

This is done through a strict following of a 500 calorie per day diet. The effect is astonishing because the normal calorie intake for an adult male is about 2500 calories per day, while females should intake at least 2000 calories. The difference between these two numbers will be the amount of fatty tissue your body will be burning in order to receive the energy necessary. For example, if your usual calorie intake is 2500 and you receive just 500 with your food 2000 calories will be received by means of breaking up your body fat.

One may ask what is the point in taking hCG here, if I can just follow the VLCD diet itself? Of course, if you dont take any hCG and still stick to your 500 calories per day diet, youll lose weight just right. But:

Besides that, as strange as it may sound, your body is more inclined towards building fat during the hungry times than burning it for energy. And thats explained simply: your body will do its best to store every single calorie left just in case this hunger will last on. hCG helps you to prevent and break that mechanism, adjusting your inner processes towards fat burning. Other components of popular modern hCG formulas aid you in muscle building too, so youre not just losing excess weight: youre giving your organism the resources necessary to be stronger and healthier by increasing muscle mass.

Therefore, take your hCG oral drops according to the official instructions that come with your oral drops and stick to the following diet: 2 servings of identical proteins per day (lean meat or fish), 2 identical vegetables per day, 2 identical fruits per day, 2 pieces of one type of bread from the allowed (breadsticks or melba toasts) per day, 2-3 liters of allowed liquids (water, mineral water, sugar-free tea, sugar-free coffee) daily.

Main principles of the second phase of the hCG diet:

A viable example of the menu suited for phase 2:

Breakfast: unlimited coffee without sugar (but with 1 tablespoon of milk), half a grapefruit.

Lunch: 100 g of fat-free grilled chicken breast, a tomato, a melba toast.

Afternoon snack: half a grapefruit, unlimited tea with stevia.

Dinner: same choices as for lunch.

You can make your meal the way you like it, as long as you follow the main principles listed above. Also, it is recommended to always have at hand a table with the caloric value of everything youre eating in order to be sure that youre not eating more than 500 calories per day.

By this stage youll be already feeling like a hero, a winner, a triumphant achiever of your goals. If youd followed the recommendations for phases 1 and 2 of the hCG diet, the weight lost will be easily noticed with the naked eye no need to measure anything at all. But you know thats not the end. Not yet. And thats the reason why theres a third stage in the hCG diet protocol. The goal of this phase is to carve in stone the results you managed to achieve, because were aiming for long-term results here, not just a fleeting experience, a fading image of something healthy. Were seizing real well-being; therefore your weight needs to be stabilized.

During the stabilization phase, you should stop taking your hCG drops and start eating some new foods, previously forbidden during phase 2. Be sure to still follow the 500 calories per day restriction and carefully count the caloric value of everything you eat! Wouldnt want to destroy everything youve fulfilled, right?

Heres a list of some the new vegetables allowed during phase 3: broccoli, eggplant, pumpkin, pickles, sauerkraut, zucchini, mushrooms, jalapeno peppers or red chili peppers, kohlrabi, bamboo shoots.

Or, maybe, you were craving for a couple of new fruits? Check these ones out: cranberries, papaya, pears, plums, watermelon, kiwi, guava, pineapples. Just be sure to check their calorie content and adjust the portion accordingly. Especially, be aware of those fruit that taste sweeter than the others the slightest error in counting their weight or value may cost you enormous amounts of efforts put previously into your diet.

New approved sources of proteins: nuts, tofu, soy, bacon, elk, turkey, duck, ham, lamb, liver, eel, herring, mussles, oysters, salmon, sardines, trout, pork chops, Vienna sausages, ground beef. Be sure to weight your protein servings before preparing them 100 g for one serving is just the right amount to go. Also, its preferred to prepare your proteins without adding extra fat just like you did during the previous phase of this diet.

Main principles of the third phase of the hCG diet:

This is the grand finale, so to speak. On this stage, you gradually increase your calorie intake level up to 1500 calories per day. Its important that the things you eat are still healthy, but now youre not restricted as violently as on the previous stages. During maintenance phase, you can slowly re-introduce sugars (hooray!) and starches into your diet. Main point here: re-introduce them SLOWLY, bit by bit. By now, you shouldnt have much of a craving for them, due to the long period of abstinence. Yet still, dont be over hesitated on the matter and stay on the healthy lane.

One more important point: as in the previous phase, if on any given day you find your weight 2 pounds (or more than that) greater than the one you saw on your last hCG assisted day, give yourself a steak day. Just like on phase 3, skip breakfast and lunch and savor an enormous steak with one vegetable or fruit of your liking. Dont forget to drink plenty during steak days.

Main principles of the fourth stage of the hCG diet:

But remember that every single hCG product has something that makes it different from the other ones. Therefore, the diet regimes can slightly vary, and thats understandable. Weve disclosed you in details the general scheme of the traditional hCG VLCD diet, but in order to achieve the best results and discover for yourself the true power of hCG stick to the official instructions provided by your hCG product manufacturer. Also, if any questions arise at any phase of your diet never hesitate to ask for help either somebody from the community or your authorized manufacturer and seller.

If you had a lot of excess weight and you couldnt get rid of it in one single hCG diet session give yourself a break of a couple of weeks and repeat the diet at will.

But, in general now youre free! Free of your fatty burden, ready to engage in all sorts of healthy exciting activities. Do your best to stay on the right path and always strive to keep your well-being a top priority. With the help of the hCG diet, youd seen how great a life without excess weight can be. The best you can do after that is to keep up with the good work! Well, and maybe share the word with a friend that needs help with dealing with his excess weight too.

Remember that the hCG diet is not a dead soulless alimentary regime. Its the base for a community of happy people that became passionate about healthy lifestyle thanks to the effects of hCG! Join the crowd, share your experience and help newbies with their diet. Together with hCG, we can make the world a better place, thats for sure!

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What Is HCG Diet?, How Does HCG Diet Works? and How Safe ...

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Dr. Albert T.W. Simeons , born in 1900, was a British endocrinologist who is responsible for multiple advancements in research of many diseases.

When researching boys with low testosterone levels, Simeons began giving them HCG and discovered that they began losing abnormal belly fat and slimmed down.

In 1967, Simeons published Pounds and Inches: A New Approach to Obesity, which would help summarize and deliver his weight loss findings to the world.

The stage of gain before loss. This is a period of anywhere from 3 days, to one week before treatment, where patients are asked toforce feed to maximum capacity.

The HCG injection phase is the bulk of the treatment. Each meal includes 100g of meat, 3.5 ounces of vegetables, a fruit and slice of bread.

In this phase, patients have completed their injections or drops and follow the 500 calorie diet for 3 more days as they finish out the program.

First Time Dieter Steps & Tricks

Take HCG drops 3 times per daydo this before breakfast, lunch, and dinner

Begin taking HCG drops, eat fatty, calorie-rich foods to stock your body up

Continue taking HCG drops 3 times per day, follow 500-calorie protocol

Stop taking HCG drops, begin increasing calories slowly, adding proteins and fats

Step 1:Remove blue cap that covers the tip.

Step 2:Make sure plunger is pushed to the bottom of the syringes barrel.

Step 3:Place syringe into the open bottle of HCG so the tip is touching the bottom of the HCG bottle.

Step 4:Pull plunger up so that the HCG diet drops fills the syringe barrel

Step 5: Keep syringe tip over the mouth of the open HCG bottle and push the plunger down the barrel. This will release the excess HCG liquid from the syringe back into the HCG bottle.

Step 6:Push the plunger down. The entire black stopper of the plunger should be below the .38ml line mark on the syringe. Extracting the right amount of HCG diet drops with every dose.

Step 7:Place the tip of the syringe under your tongue and pish the plunger all the way down making sure all the HCG diet drops are dispersed under your tongue. Hold for at least 15 seconds then swallow.

Step 8:Clean syringe. Rinse with room temperature water.

HCG Triumph customers have lost an average of 20-25 pounds while on the HCG 26-day kit. If you have more to lose, you can do multiple rounds of 26-day (with a maintenance phase between), or try our 40-day kit. If you have any questions we encourage you to call us at:1-877-485-1030. Free shipping Continental United States Only.

Beginning of HCG hormone and 500 calorie diet

First Days of Phase 2

Ending the HCG hormone and beginning to increase calories

Phase 3 Basics

Two Common Post-Diet Problems

HCG Cautions and Warnings

1. The HCG is not simply something you can take-up without research and that any patient who thinks he can reduce by taking a few shots and eating less is not only sure to be disappointed but may beheading for serious trouble.

2. While the hormone can provide incredible benefits and results in just a few weeks, the way in which it should be done is strict, but easy to follow.

3. The most important thing, is to follow a physicians instructions when thinking about joining the HCG diet.

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At Family Medicine of Federal Way we strive to accommodate your health needs today, not next week. New Patients please call and ask for Courtney

Testosterone Replacement Therapy Serving Federal Way Seattle Tacoma Bellevue Olympia CovingtonAll treatment is not equal. At Family Medicine Clinic of Federal Way we strive to provide the highest quality care available. This is especially true for our patients suffering from testosterone deficiency, aka Androgen Deficiency or Low T. Hormone replacement is not without potential risks. Thorough evaluations are required to ensure some underlying health condition isn't being missed as the cause of low testosterone. This requires more than a simple testosterone test. Additionally, if you find yourself a candidate for therapy, effective and safe management requires additional regularly scheduled lab testing. This means a few visits a year, which are usually covered by insurance, to make sure your therapy is customized and managed in a responsible manner Read More

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Dr. Fox and Dr. Leng base their success on our patients' long-term good health.

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Family Medicine Clinic of Federal Way

Dr. Scott Fox & Dr. Vuthy Leng

Federal Way Office

34618 11th Place South, Federal Way, WA, United States

+1.253-336-4462

We accept most private insurance plans. We also offer special pricing for cash-paying patients for most procedures.

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Hormonal and metabolic imbalances or even prescription medicine can interfere with your body's ability to lose weight. Our personalized approach to weight loss begins with a complete evaluation, where we review your health, diet history, body composition, blood panel and EKG to better understand your total health profile. We also consult with your primary care provider as needed to assure optimal overall health.

From there, we tailor a personalized weight loss plan that will work for your body. Unlike rapid weight loss and fad diets that help you lose weight fast - only to regain it later - our safe weight loss program takes a multidisciplinary, holistic approach to set you up for long-term success. You'll have frequent follow-ups that provide support, motivation and education, addressing the medical, emotional and physical aspects of your weight loss journey.

You can expect a positive, encouraging environment where we celebrate your successes and support you through any setbacks.

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Fat-burners are over-the-counter supplements that typically blend different kinds of herbs and stimulants to raise your core temperature, which can help you burn more calories at rest and during exercise, and suppress appetite. Common ingredients include green tea extract, caffeine, synephrine, capsicum, raspberry ketones, and garcinia cambogia.

Synephrine is a substance found in a variety of citrus foods, such as mandarin and clementines. Recent research suggests its safe for the heart and may increase resting metabolic rate. Capsicum, the chemical that makes hot peppers taste spicy, is generally used for pain relief, and a 2011 Chemical Senses review suggests capsicum consumption may benefit weight loss. Caffeine and garcinia cambogia act as appetite suppressants, which help you keep portions small and junk-food cravings at bay.

Fat-burners can increase your metabolism, give you more energy, suppress hunger, and increase your core temperature so you indirectly burn more calories. However, watch out for side effects of these ingredients and be sure to not combine them with other stimulants or medications. Here are 10 of the best supplements for weight loss.

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Abstract

Objective To investigate whether improving adherence to healthy dietary patterns interacts with the genetic predisposition to obesity in relation to long term changes in body mass index and body weight.

Design Prospective cohort study.

Setting Health professionals in the United States.

Participants 8828 women from the Nurses Health Study and 5218 men from the Health Professionals Follow-up Study.

Exposure Genetic predisposition score was calculated on the basis of 77 variants associated with body mass index. Dietary patterns were assessed by the Alternate Healthy Eating Index 2010 (AHEI-2010), Dietary Approach to Stop Hypertension (DASH), and Alternate Mediterranean Diet (AMED).

Main outcome measures Five repeated measurements of four year changes in body mass index and body weight over follow-up (1986 to 2006).

Results During a 20 year follow-up, genetic association with change in body mass index was significantly attenuated with increasing adherence to the AHEI-2010 in the Nurses Health Study (P=0.001 for interaction) and Health Professionals Follow-up Study (P=0.005 for interaction). In the combined cohorts, four year changes in body mass index per 10 risk allele increment were 0.07 (SE 0.02) among participants with decreased AHEI-2010 score and 0.01 (0.02) among those with increased AHEI-2010 score, corresponding to 0.16 (0.05) kg versus 0.02 (0.05) kg weight change every four years (P<0.001 for interaction). Viewed differently, changes in body mass index per 1 SD increment of AHEI-2010 score were 0.12 (0.01), 0.14 (0.01), and 0.18 (0.01) (weight change: 0.35 (0.03), 0.36 (0.04), and 0.50 (0.04) kg) among participants with low, intermediate, and high genetic risk, respectively. Similar interaction was also found for DASH but not for AMED.

Conclusions These data indicate that improving adherence to healthy dietary patterns could attenuate the genetic association with weight gain. Moreover, the beneficial effect of improved diet quality on weight management was particularly pronounced in people at high genetic risk for obesity.

Obesity is a multifactorial disorder that has a genetic predisposition but requires environmental influences for it to manifest.12 In the US, the past decades witnessed considerable transition of habitual dietary habits from a traditional pattern high in complex carbohydrates and fiber toward one high in sugar, fat, and animal products, which has played a key role in triggering the surge of obesity.34 Compelling evidence has shown that certain dietary factors such as sugar sweetened drinks, fried foods, and coffee might modify the genetic susceptibility to elevated body mass index, supporting potential interactions between genetic predisposition and overall dietary patterns on the risk of obesity.567

On the basis of scientific evidence and dietary recommendations, several diet quality scores have been developed to evaluate the healthfulness of dietary patterns.8910 One such score is the Alternate Healthy Eating Index 2010 (AHEI-2010), which has been consistently associated with lower risk of chronic disease in clinical and epidemiological investigations.8 The other two commonly studied scores are the Dietary Approach to Stop Hypertension (DASH), which represents the DASH-style diet aimed at reducing blood pressure,9 and the Alternate Mediterranean Diet (AMED), which focuses on a Mediterranean dietary pattern.10 Improving adherence to healthy dietary patterns, as assessed by these three diet quality scores, has been associated with less weight gain in previous studies.111213 However, no study has assessed the interactions between changes in adherence to healthy dietary patterns over time and genetic susceptibility to obesity on long term weight gain.

In this study, we prospectively examined the interactions of changes in the AHEI-2010, DASH, and AMED over up to 20 years with genetic predisposition to obesity, as evaluated by a genetic risk score based on 77 genetic variants associated with body mass index, on long term changes in body mass index and body weight in US men and women from two independent, prospective cohorts: the Nurses Health Study and the Health Professionals Follow-up Study.

The Nurses Health Study is a cohort of 121701 female registered nurses aged 30-55 years at enrollment in 1976.14 The Health Professionals Follow-up Study is a cohort of 51529 male health professionals aged 40-75 years at enrollment in 1986.15 Participants were followed with application of biennial validated questionnaires about medical history and lifestyle. For this study, the baseline year in both studies was 1986, when detailed information of diet and lifestyle was available. Between 1989 and 1990, 32826 women in the Nurses Health Study provided blood samples; likewise, between 1993 and 1995, a blood sample was obtained from 18225 men in the Health Professionals Follow-up Study. This analysis included 8828 women and 5218 men of European ancestry who had complete baseline information and available genotype data based on genome-wide association studies1617181920 and were free from diabetes, cancer, or cardiovascular at baseline.

Height was assessed by questionnaires administered at enrollment, and body weight was requested by questionnaires administered at enrollment and at each follow-up. Weights reported in questionnaires and measured by technicians were highly correlated (r=0.97 in both studies) in a validation subsample.21 Body mass index was calculated as weight in kilograms divided by the square of height in meters. Changes in body mass index and weight were evaluated every four years as the differences in body mass index and weight between the beginning and the end of each four year interval, with positive differences representing weight gain and negative differences weight loss.

Dietary intake information was collected by a validated 131 item semiquantitative food frequency questionnaire, administered in 1986 and every four years thereafter.22 Participants were asked how often on average they had consumed each food of a standard portion size over the previous 12 months. The responses had nine frequency categories ranging from never or less than once per month to six or more times per day. The reproducibility and validity of the food frequency questionnaire showed good correlation of food intake with that measured by multiple diet records.2324 Diet quality scores were calculated from the food frequency questionnaires every four years. Criteria for computation of each diet quality score are given in supplementary table A.

The AHEI-2010 score was based on 11 foods and nutrients predictive of chronic disease risk,8 emphasizing higher intake of vegetables (excluding potatoes), fruits, whole grains, nuts and legumes, long chain (n-3) fats, and polyunsaturated fatty acids; moderate intake of alcohol; and lower intake of sugar sweetened drinks and fruit juice, red and processed meats, trans fat, and sodium. Each component was scored from 0 (unhealthiest) to 10 (healthiest) points, with intermediate values scored proportionally. All component scores were summed to obtain a total score ranging from 0 (non-adherence) to 110 (best adherence) points.

The DASH score was based on eight foods and nutrients that were either emphasized or de-emphasized in the DASH-style diet.9 Each component was scored from 1 to 5 points according to fifths of intake, with 5 being the best score for higher intake of vegetables, fruits, nuts and legumes, whole grains, and low fat dairy products and for lower intake of sugar sweetened drinks, red and processed meats, and sodium. The total score ranged from 8 to 40 points.

The AMED score was modified and adapted to a Mediterranean diet in a Greek population.25 This score included nine components and awarded 1 point for an intake equal to or above the cohort specific median for vegetables, fruits, whole grains, nuts, legumes, fish, and ratio of monounsaturated to saturated fat and 1 point for an intake below the cohort specific median for red and processed meat and for alcohol intake 5-15 g/d for women and 10-25 g/d for men.10 The total score ranged from 0 to 9 points, with a higher score representing higher resemblance to the Mediterranean diet.

Changes in the diet quality scores were calculated as their differences between the beginning and the end of each four year interval. Therefore, positive differences represented increased adherence to a high quality diet and negative differences decreased adherence to a high quality diet.

We selected 77 single nucleotide polymorphisms (SNPs) that represent all 77 loci associated with body mass index identified in people of European descent (supplementary table B).26 The detailed information on SNP genotyping and imputation have been described previously.1617181920 Most of the SNPs were genotyped or had a high imputation quality score (r20.8), as assessed with the use of MACH software, version 1.0.16. No proxy SNPs were used.

Consistent with our previous study,27 we used a weighted method to calculate the genetic risk score on the basis of the 77 SNPs. Each SNP was recoded as 0, 1, or 2 according to the number of risk alleles (body mass index increasing alleles), and each SNP was weighted by its relative effect size ( coefficient) on body mass index obtained from the previous genome-wide association study.26 We calculated the genetic risk score by using the equation: GRS=(1SNP1+2SNP2++77SNP77) (77/sum of the coefficients), where SNPi is the risk allele number of each SNP. The genetic risk score ranges from 0 to 154, with each unit corresponding to one risk allele and higher scores indicating a higher genetic predisposition to obesity.

Information on demographics, lifestyle, and medical history came from the biennial questionnaires. We converted leisure time physical activity to metabolic equivalent hours (METs) per week.28 The reproducibility and validity of physical activity have been described previously.29 Alcohol intake was updated on the food frequency questionnaires every four years, and total energy intake was derived from these questionnaires.

In the Nurses Health Study and Health Professionals Follow-up Study, data were analyzed within five intervals of four years during a follow-up of 20 years from 1986 to 2006.27 We used multivariable generalized linear models with repeated measures analyses to assess the main associations of the genetic risk score and changes in the AHEI-2010, DASH, and AMED scores with change in body mass index within each four year interval, the associations between each additional 10 risk allele and change in body mass index according to thirds of changes in the three diet quality scores, and the associations between each 1 SD increase in diet scores and change in body mass index according to genetic risk subgroups. We classified genetic risk as low risk, intermediate risk, and high risk on the basis of thirds of the genetic risk score. We tested interactions of the genetic risk score with changes in the three diet quality scores and each dietary components on change in body mass index by including the respective interaction terms in the models (for example, change in the AHEI-2010genetic risk score), with the main effects included in the models as well. We also examined the genetic associations and interactions on weight change. We used multivariable models to adjust for age, genotyping source, baseline levels of body mass index, respective diet quality scores, physical activity, and other dietary and lifestyle factors at the beginning of each four year interval, as well as concurrent changes in these dietary and lifestyle factors within each four year interval. Missing values for diet, body mass index, and body weight were carried forward only once, and after that the follow-up was censored; for other variables, we coded missing data during any follow-up period as a missing indicator category for categorical variables (for example, smoking status) or used carried forward values for continuous variables.

In sensitivity analyses, considering potential confounding caused by age related or smoking related weight change, we assessed the genetic associations and interactions in participants younger than 65 years by censoring participants who were aged 65 years and in participants who had never smoked throughout the follow-up period. Moreover, we repeated the analyses of genetic association and interactions by using an extensive genetic risk score based on 97 SNPs comprising the 77 SNPs identified in people of European descent and 20 more SNPs identified in a combination of people of European and non-European descent (supplementary table B).26 We pooled the findings across the two cohorts by means of inverse variance weighted fixed effects meta-analysis. All reported P values are nominal and two sided. We used SAS software, version 9.4, for statistical analyses.

No patients were involved in setting the research question or the outcome measures, nor were they involved in recruitment or the design and implementation of the study. No patients were asked to advice on interpretation or writing up of results. There are no plans to disseminate the results of the research to study participants or the relevant patient community.

Table 1 shows characteristics at baseline and the first four year changes in characteristics of women in the Nurses Health Study and men in the Health Professionals Follow-up Study. Compared with participants with relatively stable adherence to diet quality scores, participants with the greatest increases in diet quality scores seemed to have lower diet quality scores at baseline and increased physical activity and less weight gain during the first four year period. The mean genetic risk score was 69.5 (SD 5.5) in the Nurses Health Study and 69.3 (SD 5.6) in the Health Professionals Follow-up Study; the genetic risk score was significantly correlated with body mass index and showed normal distributions across the two cohorts (supplementary figure A).

Characteristics according to first four year changes in three diet quality scores in thirds among 14046 US men and women in Nurses Health Study and Health Professional Follow-up Study

In general, the genetic risk score was associated with increases in body mass index and body weight every four years: in the two cohorts combined, each additional 10 risk allele was associated with 0.02 (SE 0.01) increase in body mass index and 0.05 (SE 0.03) kg increase in body weight (supplementary tables C and D). The difference in body mass index change between people at high genetic risk and those at low genetic risk was more prominent among participants with decreased adherence to the AHEI-2010 (0.12) than those with increased adherence to the AHEI-2010 (0.03); a similar pattern was observed for DASH but not for AMED (fig 1). When viewed jointly, the genetic associations with change in body mass index attenuated in participants who increased adherence to the AHEI-2010 and DASH; from another perspective, the inverse associations of increased adherence to the AHEI-2010 and DASH with change in body mass index were more prominent in participants at high genetic risk. Similar results were observed for weight change (supplementary figure B).

Pooled, multivariable adjusted means of change in body mass index (BMI) every four years, according to categories of genetic risk and changes in diet quality scores in thirds. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension. Histograms and bars are means and SEs. Decreased, stable, and increased adherence to each diet quality score refers to third 1, 2, and 3 of each score, respectively. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

The genetic associations with change in body mass index were significantly attenuated with increased AHEI-2010 score in the Nurses Health Study (P=0.001 for interaction) and Health Professionals Follow-up Study (P=0.005 for interaction) (table 2). In the combined cohorts, changes in body mass index per 10 risk allele increment were 0.07 (SE 0.02) among participants in the lowest third with decreased AHEI-2010 score and 0.01 (0.02) among those in the highest third with increased AHEI-2010 score (P<0.001 for interaction), corresponding to a weight change of 0.16 (0.05) kg versus 0.02 (0.05) kg (supplementary table E). Similarly, changes in body mass index per 10 risk allele increment were 0.04 (0.02) among participants with decreased DASH score and 0.01 (0.02) among those with increased DASH score (P=0.01 for interaction); corresponding weight change was 0.07 (0.06) kg versus 0.01 (0.06) kg. No clear interaction pattern was observed for AMED (P=0.33 for interaction).

Body mass index change every four years per 10 risk allele increment, according changes in diet quality scores in thirds*

Increase in each diet quality score was associated with decreases in body mass index and body weight every four years in total participants (supplementary tables C and D), and such association seemed to be more prominent in participants at high genetic risk (fig 2). Changes in body mass index per 1 SD increase in AHEI-2010 score were 0.12 (SE 0.01), 0.14 (0.01), and 0.18 (0.01) among participants at low, intermediate, and high genetic risk, respectively, corresponding to weight changes of 0.35 (0.03), 0.36 (0.04), and 0.50 (0.04) kg, respectively (supplementary figure C). Similarly, changes in body mass index per 1 SD increase in DASH score were 0.14 (0.01), 0.16 (0.01), and 0.19 (0.02) across these genetic risk subgroups. Differences in body mass index changes associated with change in the AMED across these subgroups were not evident. Similar results were observed for weight changes (supplementary figure C).

Pooled, multivariable adjusted body mass index (BMI) change every four years per 1 SD increment of each diet quality score, according to genetic risk. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension. Histograms and bars are coefficients and SEs. Value of 1 SD: AHEI-2010: 8.38; DASH: 3.71; AMED: 1.72. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

In the combined cohorts, increases in AHEI-2010 and DASH scores significantly attenuated the genetic association with change in body mass index: each 1 SD increase in the AHEI-2010 and DASH score was associated with 0.05 (95% confidence interval 0.08 to 0.03; P<0.001 for interaction) and 0.04 (0.07 to 0.01; P=0.005 for interaction) change in body mass index attributed to each additional 10 risk allele, respectively (fig 3). Such interaction effect was not statistically significant for AMED. For individual dietary components, each 1 SD increases in fruits ( 0.05, 0.08 to 0.02; P=0.001 for interaction), vegetables (0.04, 0.07 to 0.02; P=0.002 for interaction), long chain (n-3) fats (0.02, 0.04 to 0.001; P=0.037 for interaction), and trans fat (0.04, 0.01 to 0.07; P=0.015 for interaction) showed nominally significant interactions with the genetic risk score per additional 10 risk allele on change in body mass index. Similar interactions for weight change are shown in supplementary figure D.

Interaction of genetic risk score with changes in diet quality scores and dietary components on change in body mass index (BMI) every four years. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension; NHS=Nurses Health Study; HPFS=Health Professionals Follow-up Study. Histograms and bars are coefficients and 95% CIs for interactions between genetic risk score (per 10 risk allele) and changes in diet quality scores and dietary components (per 1 SD increment) on BMI change. Value of 1 SD: AHEI-2010: 8.38; DASH: 3.71; AMED: 1.72; fruits (servings/d): 1.12; vegetables (servings/d): 2.06; long chain (n-3) fats (mg/d): 300.7; whole grains (g/d): 17.34; low fat dairy (servings/d): 0.88; legumes (servings/d): 0.27; fish (servings/d): 0.38; alcohol (drinks/d): 0.70; sodium (mg/d): 3.10; red and processed meats (servings/d): 0.26; nuts (servings/d): 0.52; ratio of monounsaturated to saturated fat: 0.21; polyunsaturated fatty acids (% of energy): 1.68; sugar sweetened drinks and fruit juice (servings/d): 0.92; trans fat (% of energy): 0.01. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

In participants younger than 65 years and in those who had never smoked throughout the follow-up period, we observed similar but weaker results for genetic associations and interactions between the genetic risk score and changes in diet quality scores on change in body mass index (supplementary tables F and G). Moreover, analyses using the genetic risk score comprising 97 SNPs yielded consistent results (supplementary table H).

In this study, we found consistent interactions between changes in diet quality scores and genetic predisposition related to long term changes in body mass index and body weight in two independent prospective cohorts of US women and men. Our findings show that improving adherence to healthy dietary patterns assessed according to the AHEI-2010 and DASH could significantly attenuate the genetic association with increases in body mass index and body weight. Viewed differently, improving diet quality over time was associated with decreases in body mass index and body weight, and such favorable effect was more prominent in people at high genetic risk for obesity than in those with low genetic risk.

The dramatic alternations in dietary patterns over the past decades have paralleled the rapid rise in the prevalence of obesity in the US.34 Emerging evidence supports a protective effect of improved adherence to healthy dietary patterns on weight gain and other health outcomes such as cardiovascular disease and total and cardiovascular disease mortality.1112133031 In previous studies, we have shown that dietary factors such as sugar sweetened drinks and fried foods could amplify the genetic associations with elevated body mass index.56 Similar interactions have also been reported by another group.32 Our findings in this study are consistent with these previous reports and for the first time indicate that improving adherence to healthy dietary patterns might diminish the genetic association with weight gain. Here, we evaluated healthy dietary patterns by diet quality scores. Instead of considering individual diets in isolation, diet quality scores provide comprehensive measures of diets incorporating nutrients and foods and therefore represent a broader picture of dietary intake.3334 In this study, the AHEI-2010 showed the most significant interaction with genetic predisposition to obesity on changes in body mass index and body weight, and we also found a similar interaction pattern for DASH but not for AMED. When evaluating changes over time, the continuous scale and wider range of the AHEI-2010 may allow for greater sensitivity to differentiate dietary changes; in contrast, the wider scale and narrower range of AMED may limit its ability to detect the differences in dietary changes. Additionally, the AHEI-2010 captured all four dietary components (fruits, vegetables, long chain (n-3) fats, and trans fat) that contributed to significant interactions with the genetic risk score at a nominal significance threshold, whereas DASH and AMED each captured two, which might also account for the observed differences between the three diet quality scores.

From another point of view, our findings indicate that people with a greater genetic predisposition seem to be more susceptible to the favorable effect of improving diet quality on weight management. Our results are in line with the findings of a meta-analysis (including 6951 participants from 10 studies) showing that people carrying the homozygous FTO allele predisposing to obesity may lose more weight than non-carriers through diet and lifestyle interventions.35 In a more recent meta-analysis of 9563 participants from eight randomized controlled trials, each copy of the FTO obesity predisposing allele was associated with non-significant reductions in body mass index (0.02, 95% confidence interval 0.13 to 0.09) and body weight (0.04, 0.34 to 0.26, kg) (indicative of gene by treatment interactions) after weight loss intervention in the treatment versus control arm.36 Of note, the effect sizes of gene by treatment (dietary, physical activity, or drug based intervention) interaction in this meta-analysis are in similar ranges to the effect sizes of gene by dietary patterns interaction shown in our study, supporting the generalization of the effect sizes yielded by our study.

The precise mechanisms underlying the observed interactions remain unclear. The beneficial bioactivities of healthy dietary patterns, such as balancing energy intake, regulating metabolism, and reducing cardiometabolic risk,3738 may partly explain their modifying effect on genetic predisposition to weight gain. In addition, several genes associated with body mass index have been shown to be involved in central appetite regulation and energy homeostasis,26 which may also be responsible for the observed interactions. However, we cannot exclude the involvement of other biological pathways, and future functional studies are needed to provide biological insights into the gene by diet interactions on weight change.

The strengths of our study include the cross validation from two independent prospective cohorts of men and women, the well validated measures of dietary factors and body weight within five repeated four year periods of a 20 year follow-up, and the reliable findings improved by several sensitivity analyses. Notably, we evaluated changes in diet quality scores and changes in body mass index and body weight during the same four year intervals in discrete periods, because this change-on-change analytic approach has been shown to generate more robust, consistent, and biologically plausible relations between diet and long term weight change than the approaches of prevalent diet with weight change (prevalent analysis) or change in diet with weight change in the subsequent four years (lagged changes analysis).39

Our study also has several potential limitations. Firstly, although we have carefully controlled for baseline and concurrent changes of lifestyle and dietary factors in the analyses, unmeasured or unknown confounders may also exist. Secondly, because adherence to healthy dietary patterns was not randomized, the association between dietary factors and weight change may not imply a causal relation. Thirdly, the results could be underestimated by potential reverse causality; for example, people who gained weight might tend to adopt healthier eating patterns to lose weight. Fourthly, our study was restricted to health professionals of European descent in the US, and the generalizability of our findings should be tested in other demographic and racial/ethnic populations.

Our results suggest that weight gain associated with genetic predisposition can be at least partly counteracted by improving adherence to healthy dietary patterns. Importantly, for people who are genetically predisposed to obesity, improving adherence to a healthy diet is more likely to lead to greater weight loss. Our findings support recommendation of adherence to healthy dietary patterns,37 particularly for people at high genetic risk of obesity. The observed genetic effects were modest in magnitude, compared with lifestyle risk factors. Of note, the changes in body mass index and body weight reported in our study were changes per four years. Because changes in body mass index and body weight are essentially cumulative during the life course, the long term effect size would be substantial. Furthermore, long term, dramatic weight loss is difficult to achieve, even in the context of weight loss interventions. Therefore, even modest weight loss or simply maintaining weight from adulthood onward, compared with gaining weight, may have a substantial effect on population health.

Our study provides reproducible evidence from two prospective cohorts of US men and women that improving adherence to healthy dietary patterns could attenuate the genetic association with body mass index increment and weight gain, and the beneficial effect of improving diet quality on weight management was more prominent in people at high genetic risk. Our findings highlight the importance of improving adherence to a healthy diet in the prevention of weight gain, particularly in people genetically predisposed to obesity.

Improving adherence to healthy dietary patterns, as assessed by various diet scores, has been associated with weight loss in several studies

No study has assessed the interactions between changes in these diet quality scores and genetic predisposition to obesity in relation to long term changes in body mass index and body weight

Improving adherence to healthy dietary patterns as assessed by the Alternate Healthy Eating Index 2010 and Dietary Approach to Stop Hypertension can counteract part of gene related, long term weight gain

People at high genetic risk for obesity are more susceptible to the beneficial effect of improving diet quality on weight loss

This underlines the importance of improving adherence to healthy dietary patterns in the prevention of weight gain, especially in people with greater genetic predisposition to obesity

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