Weight Loss: People who are overweight or obese and are suffering from back pain may not realize that their excess weight contributes to their back pain. It is a known fact that people who are overweight are at risk for back pain, joint pain and muscle strain. Not only is back pain an issue but other symptoms of obese or overweight people may include fatigue, difficulty breathing and/or shortness of breath during short periods of physical activity. When this happens people begin to avoid physical activity which in turn leads to not only pain but various other unhealthy conditions. Dr. Jimenez brings the PUSH-as-Rx ®™ System which is a program designed by a strength-agility coach and physiology doctor with a combined 40 years of experience. At its core, the program is the multidisciplinary study of reactive agility, body mechanics and extreme motion dynamics. Through continuous and detailed assessments of the clients in motion and while under direct supervised stress loads, a clear quantitative picture of body dynamics emerges. This system with continual dynamic adjustments has helped many of our patients in their weight loss. Plus they become faster and stronger. Results demonstrate clear improved agility and speed no matter the age. Along with physical training Dr. Jimenez and the trainers offer nutritional advice. For more information, please feel free to contact us at (915) 850-0900 or text to call Dr. Jimenez personally at (915) 540-8444.
If you are experiencing any of these situations, then try considering intermittent fasting.
Intermittent fasting is a dietary approach that has become increasingly popular in recent years. Humans have practiced this method of eating for centuries since the time of the hunter-gatherer societies. Studies have been shown that people used it historically for medicinal purposes by ancient Rome, Greek, and Chinese civilizations. Fasting has even been used for spiritual reasons in certain religions, including Buddhism, Islam, and Christianity.
What is Intermittent Fasting?
Fasting involves abstaining from calorie-containing food and beverage for at least twelve consecutive hours. This dietary party can be the result of several hormonal and metabolic changes in the body. Research shows that these changes may help promote specific health benefits, including weight loss, neuroprotective effects, decreased inflammation and can improve blood glucose and insulin levels.
Other methods involve abstaining from food for several days or even weeks, and intermittent fasting is one of the most common fasting methods that typically involves a shorter fasting period between 16 to 24 hours at regular intervals. Several types of intermittent fasting are determined by the duration of the “feeding window,” which is the timeframe of when the food is consumed, and the “fasting window,” which is the timeframe for the food to be avoided. Here are the other methods of fasting, which includes:
Time-restricted feeding (TRF): This type of fasting has a feeding window period from 4 to 12 hours every day, following by a fasting window for the remainder of the day when only water is permitted. The most common variation of time-restricted feeding is 16/8, which involves 16 consecutive hours of fasting per day.
Early time-restricted feeding (eTRF): This is a type of variation of time-restricted feeding that involves a 6-hour feeding window early in the day from 8 a.m. to 2 p.m., while the remainder of the day makes up for the fasting period.
Alternate day fasting (ADF): This type of fasting involves alternating one day of unrestricted eating with one day of complete fasting.
Period fasting (cycling fasting): This type involves fasting for one or two days per week with 5 or 6 days of eating as desired. The variations of periodic fasting include 5:2 and 6:1 fasting.
Modified fasting: This type of fasting has some methods of intermittent fasting like alternate day fasting. This fasting can be modified to include very-low-calorie consumption during the fasting window period.
How Does Intermittent Fasting Work?
Intermittent fasting is the result of changes in hormonal patterns and energy metabolism in the body. After consuming food, the contents are broken down into nutrients and are absorbed in the digestive tract. The carbohydrates are broken down, specifically, into glucose and absorb into the bloodstream, distributing it into the body’s tissue as the primary source of energy. The hormone insulin helps regulate the blood glucose levels by signaling the cells to uptake the glucose from the blood, where it provides fuel for the body to function.
With intermittent fasting, a person is done with a meal; the supply of glucose is depleted from the body. For the energy to meet its needs, the body will break down the glycogen, the storage form of glucose found in the liver and skeletal muscles. The body uses gluconeogenesis, which is a process where the liver produces glucose from non-carbohydrate sources.
Then after approximately 18 hours of intermittent fasting, the levels of insulin are low, and the process called lipolysis begins. During this process, the body starts to break down fat into free fatty acids. When there is an insufficient amount of glucose available to meet the body’s energy demand, the body itself will transition to using those fatty acids and fatty derived ketones for energy. This metabolic state is known as ketosis. Since liver cells are responsible for ketogenesis, which is the production of ketone bodies, the fatty acids start to break down in the mitochondria of cells by a process called beta-oxidation and start converting to ketones acetoacetate and beta-hydroxybutyrate.
The ketones are then used by muscle cells and neurons to generate ATP (adenosine triphosphate), which is the primary carrier of energy in cells. Research has stated that the availability and use of the fatty acids and ketone bodies for energy replace the use of glucose in other vital body tissues, including the heart, liver, pancreas, and brain.
Four metabolic states are induced by fasting are referred to as the fast-fed cycle, and they are:
The fed state
The post-absorptive state
The fasting state
The starvation state
The physiological effect of intermittent fasting can also be achieved by following a ketogenic diet, very high fat and low carbohydrate diet. This diet’s purpose is to shift the body’s metabolic state into ketosis.
Studies have been shown that several proposed mechanisms are responsible for these health effects of intermittent fasting and have proven to be beneficial to a person’s lifestyle.
Conclusion
Intermittent fasting has been practiced for centuries and has gain popularity in recent years. It involves abstaining from consuming foods for at least 12 consecutive hours by turning the fat cells into energy for the body to function. The health benefits that intermittent fasting provides is beneficial for an individual who is trying to maintain a healthy lifestyle. Some products help provide support to the gastrointestinal system as well as making sure that sugar metabolism is at a healthy level for the body.
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References:
Dhillon, Kiranjit K. “Biochemistry, Ketogenesis.” StatPearls [Internet]., U.S. National Library of Medicine, 21 Apr. 2019, www.ncbi.nlm.nih.gov/books/NBK493179/#article-36345.
Hue, Louis, and Heinrich Taegtmeyer. “The Randle Cycle Revisited: a New Head for an Old Hat.” American Journal of Physiology. Endocrinology and Metabolism, American Physiological Society, Sept. 2009, www.ncbi.nlm.nih.gov/pmc/articles/PMC2739696/.
Stockman, Mary-Catherine, et al. “Intermittent Fasting: Is the Wait Worth the Weight?” Current Obesity Reports, U.S. National Library of Medicine, June 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5959807/.
Zubrzycki, A, et al. “The Role of Low-Calorie Diets and Intermittent Fasting in the Treatment of Obesity and Type-2 Diabetes.” Journal of Physiology and Pharmacology: an Official Journal of the Polish Physiological Society, U.S. National Library of Medicine, Oct. 2018, www.ncbi.nlm.nih.gov/pubmed/30683819.
A large portion of the patients that seek out chiropractic care are suffering from some form of back pain. While chiropractic adjustments and associated therapies can do a lot to ease back pain symptoms and aid in healing, lifestyle changes are also quite important –, particularly weight loss. Excess weight puts increased pressure on the spine, especially the lower back. The more chiropractic patients can near their ideal weight, the easier it becomes to treat and often eliminate the back pain.
The Importance Of Weight Loss
Research shows that obesity makes back pain highly probable.
Research has shown that excess weight and obesity do increase the risk of suffering from low back pain. A meta-analysis of the research on obesity and low back pain found that overweight and obese individuals were most likely to seek care for low back pain, including chronic back pain.
The components of the spine can wear down.
The spine is strong, but it is also delicate. The vertebrae are linked and supported by soft tissues, like discs, ligaments, and tendons.
These soft tissues make it possible to move, flex, twist and turn in a variety of ways, allowing your body to be quite mobile. But these soft tissues are prone to wear and tear.
Even a healthy body will experience wear and tear as it ages. When you add extra weight, though, you increase the wear and tear – and become more susceptible to injuries.
Extra body weight increases damage.
If you have ever carried an object for an extended period of time, like a bag of groceries up and down stairs or a jug of liquid across a parking lot, you know how it can wear you down. While you may feel fine at first, the longer you go, the more tired you become.
Extra body weight is something you carry around with you everywhere you go.
Across the parking lot.
Up the stairs.
Even sitting in a chair.
The structural components of your body, including your joints and the muscles that support them, are constantly forced to handle the extra pressure.
All the extra pressure transfers force through your joints, including your spine. Over time, the force will do damage. Discs will wear out faster, which can lead to degenerative disc disease and back pain.
Injuries become more severe.
The extra weight makes every accident and injury more damaging. Slipping and catching yourself, which may have been okay before, could now pull or tear muscles and tendons. Every time you are in an accident, your body will have a harder time maintaining safe alignment.
Common Injuries Caused by Excess Weight
1. Herniation
A herniated disc occurs when the tough outer layer of the disc is torn, allowing the soft inner layer to protrude. The protrusion can put pressure on nerves in the spine.
2. Pulled tissues.
Excess weight makes it more likely that you will pull or tear muscles, tendons, and ligaments.
Every pound you lose is one less pound your body must carry. The closer you get to your optimal weight, the easier it will be for your body to support your spine. When you get chiropractic adjustments, they will be more likely to remain in place. A healthy weight makes chiropractic care more effective.
If you are suffering from back pain and excess weight, please contact us. Our chiropractic team can help you in your weight loss journey, and we can treat your pain in a way that is both effective and non-invasive.
Chronic pain is a common health issue which affects many people in the United States. While several medical conditions, such as fibromyalgia and myofascial pain syndrome, can cause chronic pain, it may also develop due to a variety of other health issues. Research studies have found that widespread inflammation is the leading cause of chronic pain. Inflammation is a natural defense mechanism to injury, illness, or infection. But, if the inflammatory process continues for too long, it can become problematic.
Inflammation signals the immune system to heal and repair damaged tissue as well as to protect itself against bacteria and viruses. As mentioned above, however, chronic inflammation can cause a variety of health issues, including chronic pain symptoms. Healthy lifestyle modifications can help manage chronic pain, but first, let’s understand the common causes of chronic pain.
What is Acute Inflammation?
Acute inflammation, by way of instance, occurs following an injury or something as simple as a sore throat. It is a natural response with adverse effects, meaning it works locally in the region where the health issue is found. The common signs of acute inflammation include swelling, redness, warmth, pain and loss of function, as stated by the National Library of Medicine. When acute inflammation develops, the blood vessels dilate causing blood flow to increase, and white blood cells in the injured region promote recovery.
During severe inflammation, compounds called cytokines are released by the damaged tissue. The cytokines act as “emergency signals” which bring on the human body’s own immune cells, as well as hormones and numerous nutrients to repair the health issue. Additionally, hormone-like substances, known as prostaglandins, cause blood clots to heal damaged tissue, and these may also trigger fever and pain as part of the inflammatory procedure. As the damage or injury recovers, the inflammation subsides.
What is Chronic Inflammation?
Unlike acute inflammation, chronic inflammation has long-term effects. Chronic inflammation, also known as persistent inflammation, produces low-levels of inflammation throughout the human body, as demonstrated by an increase in immune system markers located in blood and cell tissues. Chronic inflammation may also cause the progression of various diseases and conditions. Elevated levels of inflammation may sometimes trigger even if there is no injury, illness, or infection, which may also cause the immune system to react.
As a result, the human body’s immune system could begin attacking healthy cells, tissues, or organs. Researchers are still trying to understand the consequences of chronic inflammation in the human body and the mechanisms involved in this natural defense process. By way of instance, chronic inflammation has been associated with a variety of health issues, such as heart disease, and stroke.
One theory suggests that when inflammation remains in the blood vessels, it can encourage the accumulation of plaque. According to the American Heart Association, or the AHA, if the immune system identifies plaque as a foreign invader, the white blood cells can attempt to wall off the plaque found in the blood flowing through the arteries. This can create a blood clot which may block the blood flow to the heart or brain, causing it to become unstable and rupture. Cancer is another health issue associated with chronic inflammation. Furthermore, according to the National Cancer Institute, DNA damage can also be caused by chronic inflammation.
Persistent, low-grade inflammation frequently doesn’t have any symptoms, but healthcare professionals can check for a C-reactive protein, or CRP, known as lipoic acid, a marker for inflammation found in the blood. Elevated levels of CRP are associated with an increased risk of cardiovascular disease. Elevated CRP levels may be found in chronic disorders like lupus or rheumatoid arthritis.
In the case of other chronic conditions, such as fibromyalgia, the nervous system over-reacts to specific stimulation, however, it’s inflammation which causes chronic pain symptoms. Subjectively, it’s almost impossible to tell the difference between the chronic pain caused by an oversensitive nervous system and the chronic pain caused by widespread inflammation. Apart from searching for clues in the bloodstream, a person’s nutrition, lifestyle habits, and environmental exposures, can also promote chronic inflammation.
Inflammation is the immune system’s natural defense mechanism against injury, illness, or infection. While this inflammatory response can help heal and repair tissues, chronic, widespread inflammation can cause a variety of health issues, including chronic pain symptoms. A balanced nutrition, including a variety of diets and fasting, can help reduce inflammation. Fasting, also known as caloric restriction, promotes cell apoptosis and mitochondrial recovery. The fasting mimicking diet, which is a part of the longevity diet plan, is a dietary program which “tricks” the human body into a fasting state to experience the benefits of traditional fasting. Before following any of the diets described in this article, make sure to consult a doctor.
Dr. Alex Jimenez D.C., C.C.S.T. Insight
Nutrition, Diets, Fasting and Chronic Pain
Anti-inflammatory diets mainly consist of eating fresh fruits and vegetables, fish, and fats. The Mediterranean diet plan, by way of instance, is an anti-inflammatory diet which promotes eating moderate amounts of nuts, ingesting very little meat, and drinking wine. Anti-inflammatory food parts, such as omega-3 fatty acids, protect the human body against the damage brought on by inflammation.
An anti-inflammatory diet also involves staying away from foods which could promote inflammation. It is ideal to decrease the amount of foods you eat which are high in trans and saturated fats, such as meats. Additionally, an anti-inflammatory diet limits the consumption of refined carbohydrates and foods, such as bread and rice. These also promote cutting back on the utilization of margarine and oils that are packed with omega-6 fatty acids, such as sunflower, safflower and corn oils.
Fasting, or caloric restriction, has long been known to decrease oxidative stress and slow down the mechanisms of aging in various organisms. The effects of fasting involve programmed cell death, or apoptosis, transcription, mobile energy efficiency, mitochondrial biogenesis, antioxidant mechanisms, and circadian rhythm. Fasting also contributes to mitochondrial autophagy, known as mitophagy, where genes in the mitochondria are stimulated to undergo apoptosis, which promotes mitochondrial recovery.
Intermittent fasting can help you fight inflammation, improve digestion, and boost your longevity. The human body is designed to be able to survive for extended periods of time without food. Research studies have demonstrated that intermittent fasting can have positive changes in the overall composition of your gut microbiota. Moreover, intermittent fasting can reduce insulin resistance while increasing the immune system response. Finally, intermittent fasting can promote the production of a substance, known as β-hydroxybutyrate, that blocks a portion of the immune system involved in inflammatory ailments as well as substantially reducing the production of inflammatory markers, such as cytokines and the C-reactive protein, or CRP, previously mentioned above.
The Longevity Diet Plan, presented in the book by Dr. Valter Longo, eliminates the consumption of processed foods which can cause inflammation, promoting well-being and longevity. This unique dietary program, unlike most traditional diets, doesn’t promote weight loss. Although you may experience weight reduction, the emphasis of this unique dietary program is on eating healthier. The Longevity Diet Plan has been demonstrated to help activate stem cell-based renewal, reduce abdominal fat, and prevent age-related bone and muscle loss, as well as build resistance to developing cardiovascular disease, Alzheimer’s disease, diabetes, and cancer.
The fasting mimicking diet, or FMD, allows you to experience the benefits of traditional fasting without depriving your body of food. The main difference of the FMD is that instead of completely eliminating all food for several days or even weeks, you only restrict your calorie intake for five days out of the month. The FMD can be practiced once a month to help promote overall health and wellness.
While anyone can follow the FMD on their own, the ProLon® fasting mimicking diet offers a 5-day meal program which has been individually packed and labeled for each day, that serves the foods you need for the FMD in precise quantities and combinations. The meal program is made up of ready-to-eat or easy-to-prepare, plant-based foods, including bars, soups, snacks, supplements, a drink concentrate, and teas. Before starting the ProLon® fasting mimicking diet, 5-day meal program, or any of the lifestyle modifications described above, please make sure to talk to a healthcare professional to find out which chronic pain treatment is right for you.
The scope of our information is limited to chiropractic, spinal health issues, and functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Acute Back Pain
Back pain is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. Your spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
XYMOGEN’s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly, Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download
* All the above XYMOGEN policies remain strictly in force.
Adhering to a specific diet to maintain proper nutrition can sometimes make eating stressful. Natural lifestyle modifications are the key to changing your eating habits and this can help you live a longer, healthier life. The Longevity Diet Plan, created by Dr. Valter Longo, is a selection of practical eating guidelines which focuses on changing your eating patterns to achieve overall health and wellness.
The Rules of The Longevity Diet Plan
By merely following the nutritional tips below, you can overhaul your current diet plan and start eating healthier without all the stress of a traditional diet. The Longevity Diet Plan eliminates the consumption of processed foods that can cause a variety of health issues and boosts the consumption of nutrients that promote longevity. This unique dietary program shares the results of approximately 25 years of research studies all on a simple solution which can help people experience overall well-being through proper nutrition.
However, unlike most traditional diets, the Longevity Diet Plan doesn’t promote weight loss. Although you may experience weight reduction, the emphasis of this unique dietary program is on eating healthier. The Longevity Diet Plan has been demonstrated to help you activate stem cell-based renewal, lose weight and reduce abdominal fat, prevent age-related bone and muscle loss, build resistance to developing cardiovascular disease, Alzheimer’s disease, diabetes, and cancer, as well as extend longevity. Below, we will summarize the 8 most common nutritional tips of the Longevity Diet Plan which can ultimately help make your life longer and healthier.
The Longevity Diet Plan is a unique dietary program designed by Dr. Valter Longo to promote overall health, wellness, and longevity. Through simple lifestyle modifications, people can change their eating habits and take advantage of the many health benefits of this dietary program. By following a pescatarian diet and following the ProLon® Fasting Mimicking Diet, among the other nutritional tips described below, people can live longer and healthier lives. Traditional diets can often be difficult and stressful to follow, however, the Longevity Diet Plan is a practical and unique dietary program which can be suitable for many people.
Dr. Alex Jimenez D.C., C.C.S.T. Insight
8 Nutritional Tips of the Longevity Diet Plan
Follow a Pescatarian Diet
As a part of the Longevity Diet Plan, follow a pescatarian diet, which is almost 100 percent plant and fish-based. Also, make sure to limit fish consumption to two or three servings every week, avoiding fish with higher mercury content, such as tuna, swordfish, mackerel, and halibut. If you’re over 65 and you begin to experience reduced muscle mass, strength, and fat, add more fish into your diet alongside other animal-based foods, including eggs and specific cheeses, such as feta or pecorino, and yogurt made from goat’s milk.
Don’t Eat Too Much Protein
According to the Longevity Diet Plan, we should eat 0.31 to 0.36 grams of protein per pound of body fat every day. If you weigh 130lbs, you should eat about 40 to 47 grams of protein per day, or an equivalent of 1.5 filets of salmon, 1 cup of chickpeas or 2 1/2 cups of lentils, of which 30 grams should be consumed in one meal. If you weigh 200 to 220lbs, you should eat about 60 to 70 grams of protein per day, or an equivalent of two fillets of salmon, 3 1/2 cups of lentils or 1 1/2 cups of chickpeas. Protein consumption should be increased after age 65. For the majority of us, a 10 to 20 percent increase, or 5 to 10 grams more each day, is enough. Finally, the Longevity Diet is free of animal proteins like red meat, white meat, and poultry, with the exception of animal proteins in fish. This unique dietary program instead is comparatively high in vegetable proteins like legumes and nuts to optimize health and wellness.
Increase Good Fats and Complex Carbohydrates
As a part of the Longevity Diet Plan, you should eat higher amounts of polyunsaturated fats, such as those found in salmon, almonds, walnuts, and olive oil, while you should eat lower amounts of saturated, hydrogenated, and trans fats. Likewise, as a part of the Longevity Diet Plan, you should also eat complex carbohydrates, such as those found in whole wheat bread, legumes, and vegetables. Make sure to limit eating pasta, rice, bread, fruit, and fruit juices, which can be converted to sugars by the time they reach your gut.
Take Dietary Supplements
The human body needs proteins, essential fatty acids like omega-3 and omega-6, vitamins, minerals, and even sugars to function correctly. Whenever your intake of certain nutrients becomes too low, the repair, replacement, and defense methods of the human body can slow down or stop, allowing fungi, bacteria, and viruses to cause damage which can lead to a variety of health issues. Take vitamin and mineral dietary supplements, especially for omega-3, as recommended by your healthcare professional.
Eat Various Foods from your Ancestry
To take in all of the necessary nutrients you need, you have to eat a wide variety of foods, but it’s best to choose foods that were common on your parents’, grandparents’, and great-grandparents’ table. By way of instance, in many northern European countries where milk has been generally consumed, lactose intolerance is relatively rare, whereas lactose intolerance is quite common in southern European and Asian countries, where milk was not historically part of the conventional diet of adults. If a person of Japanese ancestry residing in the United States suddenly decides to begin drinking milk, which was probably rarely served in their grandparents’ dining table, they will probably start feeling sick. The most common problems in these cases are intolerances or autoimmunities, such as the response to gluten-rich foods like bread and pasta seen in people with celiac disease. Although further evidence is needed, it is possible that food intolerances could be related to many autoimmune disorders, including diabetes, colitis, and Crohn’s disease.
Eat Two Meals a Day and a Snack
According to the Longevity Diet Plan, it is ideal to eat breakfast and one major meal plus a nourishing low-calorie, low-sugar snack every day. While for some people it may be recommended to eat three meals and a snack every day. Many nutritional guidelines recommend that we should eat five to six meals every day. When people are advised to eat frequently, it can often become difficult for them to regulate their calorie intake. Over the last twenty years, approximately 70 percent of the population in the United States is considered to be overweight or obese. It’s much more difficult to overeat on the Longevity Diet Plan if you eat only two and a half meals every day. It would take massive portions of legumes, vegetables, and fish to reach the amount that would lead to weight gain. The high nourishment of the meals, plus the amount of the meal, sends a signal to your stomach and your brain that you have had enough food. This one major meal system may sometimes have to be broken down into two meals to avoid digestion issues. Adults and older people prone to weight loss should eat three meals a day. For people trying to lose weight as well as for people who are overweight or obese, the best nutritional advice would be to eat breakfast daily; have dinner or lunch, but not both, and substitute for the missed meal with one snack containing fewer than 100 calories and no more than 3 to 5 g of sugar. Which meal you skip depends upon your lifestyle, however, it’s not recommended to skip breakfast due to its adverse health issues. The benefit of skipping lunch is more free time and energy. But, there is a drawback for eating a large dinner, particularly for people who suffer from acid reflux or sleeping problems. The drawback for skipping dinner, however, is that it may eliminate the social meal of their day.
Eat Within a 12-Hour Window Every Day
Another common eating habit adopted by many centenarians is time-restricted eating or limiting all meals and snacks within a 12-hour window every day. The efficiency of this method was demonstrated in both human and animal research studies. Generally, you would eat breakfast at 8 a.m. and then eat dinner by 8 p.m.. A briefer eating window of ten hours or less can be even better for weight loss, but it’s considerably harder to maintain and it might increase the risk of developing side effects, such as gallstones and even potentially increasing the chance of developing cardiovascular disease. You should not eat three to four hours before sleeping.
Follow the ProLon® Fasting Mimicking Diet
Healthy people under the age of 65 should follow the ProLon® Fasting Mimicking Diet, 5-day meal program at least twice every year. The FMD is one of the key principles promoted by the Longevity Diet Plan. The fasting mimicking diet offers the same health benefits of fasting without actually fasting. By eating 800 to 1,100 calories in precise quantities and combinations of foods which have been individually packed and labeled for each day, you can “trick” the human body into a fasting state. Through various research studies, Dr. Valter Longo discovered that by depriving the body of food in this manner, our cells begin breaking down and regenerating our internal tissues, through a process known as autophagy, killing and replacing, or regenerating, damaged cells. Additionally, fasting can reverse various health issues, destroy cancer cells and significantly reduce the possibility of developing Alzheimer’s disease.
With the Longevity Diet Plan presented in the book by Dr. Valter Longo, you’ll eat better, feel better and, although it’s not designed as a weight loss plan, you may even shed a few pounds. You’re not going to have to consider complex food rules and make difficult choices with this unique dietary program. Once you get the hang of these lifestyle modifications, you’ll be able to improve your overall health and wellness as well as your longevity. The scope of our information is limited to chiropractic, spinal health issues, and functional medicine topics. To further discuss the subject matter, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Acute Back Pain
Back pain is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. Your spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
XYMOGEN’s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly, Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download
* All the above XYMOGEN policies remain strictly in force.
Ketosis is a natural procedure the human body goes through on a regular basis. This method provides the cells with energy from ketones if sugar isn’t readily available. A moderate degree of ketosis occurs when we skip a meal or two, do not consume many carbohydrates throughout the day or exercise for an extended amount of time. When there is an increased demand for energy and carbohydrates are not immediately available to meet that need, the human body will subsequently begin to raise its ketone levels.
If carbohydrates continue to be limited for a considerable amount of time, ketone levels may increase further. These deeper degrees of ketosis provide many favorable effects throughout the entire body. These benefits can be taken advantage of by following the ketogenic diet. However, the majority of people are seldom in ketosis since the human body prefers to utilize sugar, or glucose, as its principal fuel supply. Below, we will discuss ketosis, ketones, and how these procedures work together to keep the cells healthy.
How Nutrients are Converted into Energy
The human body processes several kinds of nutrients to produce the energy it requires. Carbohydrates, proteins, and fats can be converted to energy in order to fuel various metabolic processes. If you consume high-carbohydrate foods or excessive amounts of protein, your cells will break these down into a simple sugar called glucose. This occurs because sugar provides the cells with the fastest source of ATP, which one of the main energy molecules required to fuel virtually every system within the human body.
By way of instance, more ATP means more cell energy and more calories result in more ATP. As a matter of fact, each calorie consumed from carbohydrates, proteins, and fats may be utilized to maximize ATP levels. The human body consumes a lot of these nutrients to maintain the proper function of all its structures. If you consume more than sufficient food, nevertheless, there’ll be too much sugar which your system does not need. But, considering this, what does the human body do with all this excess sugar? Instead of eliminating excess calories which the body does not need, it will store them as fat where it can be used later once the cells require energy.
The human body stores energy in two ways:
Glycogenesis. Through this procedure, excess glucose is converted into glycogen, or the stored form of glucose, which is stored in the liver and muscles. Researchers estimate that the entire human body stores about 2000 calories in the shape of muscle and liver glycogen. This generally means that glycogen levels will be used within 6 to 24 hours if no additional calories are consumed. An alternate system of energy storage may help sustain the human body when glycogen levels are reduced: lipogenesis.
Lipogenesis. When there are sufficient amounts of glycogen in the muscles and liver, any excess glucose is converted into fats and stores through a procedure called lipogenesis. Compared to our limited glycogen stores, our fat stores are almost infinite. These supply us with the capability to sustain ourselves for weeks to even months without enough food being available.
When food is limited and the intake of nutrients like carbohydrates are restricted, glycogenesis and lipogenesis is no longer active. Rather, these procedures are replaced with glycogenolysis and lipolysis which free energy from glycogen and fat stores throughout the human body. However, something unexpected occurs when the cells no longer have stored sugar, fat or glycogen. Fat will continue to be used as fuel but an alternate fuel source known as ketones is produced as well. Because of this, the process of ketosis occurs.
Why Does Ketosis Occur?
When you don’t have any access to foods, such as when you’re sleeping, fasting, or following the ketogenic diet, then the human body will convert some of its stored fat into exceptionally efficient energy molecules known as ketones. Ketones are synthesized following the entire breakdown of fats into fatty acids and glycerol, where we can thank our cell’s capacity to change metabolic pathways for this. Although fatty acids and glycerol are turned into fuel throughout the entire body, they’re not utilized as energy by brain cells.
Because these nutrients are converted into energy too slowly to support the function of the brain, sugar is still considered to be the principal source of fuel for the brain. This process also helps us understand why we create ketones. Without an alternate energy supply, the brain would be exceedingly vulnerable if we don’t consume enough calories. Our muscles would be broken down instantly and converted into sugar to feed our hungry brains. Without ketones, the human race would have most probably been extinct.
Low-carbohydrate modified ketogenic diets have been demonstrated to have many health benefits, including weight loss and the increased ability to help fight diabetes. These type of diets have a remarkable way of providing energy for the brain. Research studies have discovered that entering ketosis has the ability to reduce insulin levels, freeing fat from fat cells. Researchers have also shown that the ketogenic diet can have a significant metabolic advantage, which leads to more calories burned than with any other diet. Dr. Alex Jimenez D.C., C.C.S.T. Insight
The Way Ketones are Produced
The human body breaks down fat into fatty acids and glycerol which may be utilized for fuel in the cells directly but not by the brain. To fulfill the requirements of the brain, the fatty acids from fats and glycerol go through the liver where they’re then converted into glucose, or sugar, and ketones. Glycerol undergoes a process called gluconeogenesis, which transforms it into glucose, where fatty acids are converted to ketone bodies through a procedure called ketogenesis. As a consequence of ketogenesis, a ketone body called acetoacetate is generated. Acetoacetate is then converted to two different types of ketone bodies:
Beta-hydroxybutyrate (BHB). After being keto-adapted for several weeks, the cells will start to convert acetoacetate into BHB because it’s a more efficient source of fuel where it destroys an extra chemical reaction which provides more energy to the cell compared to acetoacetate. Research studies have demonstrated that the human body and brain favor utilizing BHB and acetoacetate for energy because the cells can utilize it 70 percent better than they can sugar or glucose.
Acetone. This substance can occasionally be metabolized into glucose, however, it is largely eliminated as waste. This is what specifically provides the distinctly smelling breath which many ketogenic dieters have learned to understand.
Over time, the human body will release less surplus ketone bodies, or acetone, and, should you utilize keto sticks to monitor your degree of ketosis, you might believe it’s slowing down. As the brain burns off BHB as fuel, the cells attempt to present the brain with as much effective energy as they can. This is why long-term low-carbohydrate users won’t show profound levels of ketosis in their urine tests. As a matter of fact, long-term keto dieters can endure around 50 percent of their basal energy demands and 70 percent of their brain’s energy demands from ketones. Therefore, you shouldn’t allow the urine tests to fool you.
The Significance of Gluconeogenesis
Regardless of how keto-adapted the human body may become, the cells will still require glucose to function properly. To satisfy the energy demands of the human mind and body which can’t be fulfilled by ketones, the liver will initiate a process called gluconeogenesis. Amino acids in proteins and lactate in the muscles may also be transformed into glucose.
By converting amino acids, glycerol, and lactate into glucose, the liver can satisfy the glucose demands of the human body and brain during times of fasting and carbohydrate limitation. That is the reason why there’s not any crucial requirement for carbohydrates to be included in our diet. The liver will, generally, make sure to have sufficient sugar in the blood for your own cells to survive.
It’s important to remember, however, that certain variables, such as eating too much protein, may get in the way of ketosis and boost the demand for gluconeogenesis. Insulin levels and ketone production are closely connected. Protein sources, which are generally consumed on the ketogenic diet, can also increase insulin levels. In response to a rise in insulin levels, ketogenesis is downregulated, which raises the demand for gluconeogenesis to generate more sugar.
This is the reason why eating too much protein may impair your ability to enter ketosis. But this doesn’t necessarily mean you ought to limit your protein intake either. By restricting protein intake, your muscle cells will be employed to generate the sugar your body and brain demand for fuel. With proper guidance, you can consum the perfect quantity of protein your body needs to maintain muscle mass and fulfill your glucose needs when you’re on the road to ketosis.
Recognizing the Path to Ketosis
Almost all of our understanding behind ketosis originates from research studies on people who have fasted from all foods, not only from ketogenic dieters. However, we could make many inferences concerning the ketogenic diet out of what the researchers discovered from the research studies on fasting. First, let us look at the phases the body goes through during fasting:
Stage 1 – The glycogen depletion phase – 6 to 24 hours of fasting
In this phase, most energy is produced by glycogen. During this time, hormone levels begin to change, causing increases in gluconeogenesis and fat burning, however, ketone generation isn’t active yet.
Stage 2 – The gluconeogenic stage – 2 to 10 days of fasting
In this phase, glycogen is totally depleted and gluconeogenesis supplies the cells with energy. Ketones begin to be generated at reduced levels. You will notice you have keto breath and are urinating more frequently due to greater acetone levels in your blood. The timeframe for this phase is so extensive (two to ten days) since it is dependent upon who is fasting. By way of instance, healthy men and obese people have a tendency to remain in the gluconeogenic phase for extended periods of time compared to healthy women.
Stage 3 – The ketogenic stage – after 2 days of fasting or more
This phase is characterized by a decrease in protein breakdown for energy through an increase in fat and ketone usage. At this phase, you will surely be in ketosis. Every individual can enter this point at various rates based on lifestyle and genetic variables, their physical activity levels, and the number of times they fasted and/or restricted carbohydrates before. Whether you’re following the ketogenic diet or fasting, you may go through these phases, but this doesn’t guarantee the same benefits fasting as you do from the keto diet.
Ketogenic Diet Ketosis vs Starvation Ketosis
The ketosis which you experience on the ketogenic diet is considered to be a lot safer and healthier compared to the ketosis you get to when fasting. During the time you’re fasting, the human body doesn’t have any food resources, therefore it begins converting the protein from your muscles into sugar. This induces rapid muscle reduction.
The ketogenic diet, on the other hand, provides us with the healthiest and safest way to experience the advantages of ketosis. Limiting carbohydrates while keeping sufficient caloric intake from protein and fat permits the ketogenic procedure to sustain muscle tissue by employing ketosis and the ketone bodies we generate for fuel without having to utilize valuable muscle mass. Many research studies have discovered that ketones can also have an array of beneficial effects throughout the entire body too.
Ketoacidosis: The Bad Side of Ketosis
Ketoacidosis is a potentially lethal condition which occurs when excessive ketones accumulate in the blood. Some healthcare professionals may advise against increasing your ketone levels with the ketogenic diet because they fear you could enter ketoacidosis. The practice of ketosis is closely governed by the liver, and also the entire body infrequently generates more ketones then it requires for fuel. That is the reason why the ketogenic diet has been referred to as a safe and effective way to enter ketosis.
Ketoacidosis, on the other hand, is more likely to occur in type 1 and type 2 diabetics who don’t have their glucose under control. The mix of insulin deficiency and higher glucose levels, which are generally found in people with diabetes, produce a vicious cycle which causes ketones to build up in the blood. By limiting carbohydrates, nevertheless, healthy people and patients with diabetes may continue to keep their glucose under control and also experience the advantages of utilizing ketones for fuel.
Putting It All Together
Ketogenesis takes fatty acids from stored fat and transforms it into ketones. The ketones are subsequently released into the bloodstream. The procedure where the body burns off ketones for fuel is known as ketosis. However, not all cells can utilize ketones as fuel. Some cells will always utilize glucose to function accordingly. To satisfy the energy requirements which can’t be fulfilled by ketones, your liver utilizes a process called gluconeogenesis. Gluconeogenesis is the procedure where the liver converts glycerol from fatty acids, amino acids from proteins, and lactate from muscles, into glucose. Collectively, ketogenesis and gluconeogenesis produce the ketones and glucose which fulfill all the body’s energy demands when food is not available or when carbohydrates are limited.
Though ketones are well-known for being an alternate fuel supply, they supply us with several unique advantages too. The best and safest way to receive all the advantages of ketosis is by simply adhering to the ketogenic diet. In that way, you won’t encounter the chance of losing valuable muscle mass or inducing the potentially lethal condition of ketoacidosis. But, the ketogenic diet is somewhat more nuanced than a lot of men and women think. It is not just about restricting carbohydrates, it’s about making sure sufficient fat, protein, and overall calorie intake are consumed, which are ultimately vital. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Acute Back Pain
Back pain is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
Irrespective of a continuous surge in interest regarding the ketogenic diet, exactly why is it that individuals have been utilizing this dietary pendulum swing from the nutritional worries that have been spreading across the world? Many people appear to be obsessed with the latest diet fads and trends associated with achieving and maintaining a balanced weight and supporting overall health and wellness. Research studies have demonstrated evidence outcomes regarding the benefits of dieting.
The National Weight Control Registry has stored data about these types of ongoing research studies. More than half of subjects involved in these varieties of tests and evaluations had revealed that they were following some sort of diet or intended to become involved in programs or routines for weight loss. You often see annual reports listing the very best diets, including: the Top 5 Diets to Try in 2018, According to Experts, published by Time magazine. Moreover, the report claims that healthcare professionals have ranked the DASH Diet as the number one diet, followed by the Mediterranean Diet, Weight Watchers, the MIND diet, the TLC Diet and Volumetrics, as the top diets to try this year. The article, however, additionally discusses the ketogenic diet and ranks it as being among one of the lowest-ranked diets to try this year. No further details are given about this diet and the consensus appeared to be that it is challenging to follow.
However, the ketogenic diet is actually one of the most popular diets people generally talk about, subtly out-ranking paleolithic diet in most conversations. As a matter of fact, you may have already read or heard about the ketogenic diet from a variety of sources or perhaps you may even known a friend or a family member who has been trying it out themselves. A frequent concern about popular or fad diets, though, is that there doesn’t seem to be an exact guide on how to properly follow them, what kinds of problems they may cause, and/or even for whom these might be most appropriate. With eating habits like those described in the ketogenic diet, there are frequently risks or disadvantages, often involving nutrient deficiencies or lack of efficacy, especially if they’re truly hard to follow. But, how can this common issue regarding the proper diet be solved? Foremostly, it’s essential for individuals to weigh the advantages and disadvantages when choosing to attempt the ketogenic diet.
What is the Ketogenic Diet?
Let’s start with some history of what, where and when the ketogenic diet begain. There are various diets out there today which may have a lot in common with this well-known diet. Simply take a peek at a newstand, a bodybuilding website, or maybe the blogs of practicing healthcare professionals. First developed in 1921 by Dr. Russell Wilder of the Mayo Clinic as an alternative for children with intractable epilepsy, a classical ketogenic diet is supposed to alter the human body’s natural inclination to metabolize carbohydrates for energy. This can be achieved by adjusting an individual’s nutritional daily value to a particular macronutrient intake ratio of 4:1 fat-to-carbohydrates and protein diet. In this arrangement, fat comprises approximately 90 percent of daily calories, together with 7 percent of proteins and 3 percent of carbohydrates. Some alternatives for the ketogenic diet include a Medium Chain Triglyceride Diet consisting of 70 percent of fats, 10 percent of proteins and 20 percent of carbohydrates, or a Modified Atkins Diet with much more protein including 70 percent of fats, 25 percent of proteins, and 5 percent of carbohydrates, and a Low-Glycemic Index Treatment consisting of 45 percent of fats, 28 percent of proteins and 27 percent of carbohydrates.
The consequence of eating in this manner mimics what occurs when engaging in physical activities or exercise as well as what happens when fasting, a process referred to as ketosis. In ketosis, there is a depletion of glycogen reserves in the muscles and in the liver, which ultimately causes the liver to produce ketone bodies that can be used as fuel instead. Some healthcare professionals advise using either ketone strips or a sugar ketone meter to test the levels of ketosis in urine or blood. There is also a breath ketone analyzer available for purchase on Amazon. Don’t confuse ketosis with ketoacidosis, or the potentially deadly condition common to Type 1 diabetics when there are incredibly substantial levels of blood glucose and ketones.
Proof the Ketogenic Diet Works
It goes without saying, when a new dietary routine is useful for weight loss, nutrition experts understand they may also be used therapeutically for the treatment of many different diseases and ailments, among other health issues. The ketogenic diet has been used for decades to help with the treatment of epilepsy, and it has gained recent traction in its use for the treatment of obesity, type 2 diabetes, cardiovascular disease and neurological disorders. It has even been demonstrated to positively affect the gut microbiota.
Research studies regarding the use of a very-low carbohydrate, high fat diet for obesity, however, is in its initial stages. One research study, retrospectively in comparison to a non-carb/ketogenic-style diet, utilized a classic low-carb diet in bariatric patients, focusing on weight loss. The researchers found comparable weight-loss between both diets by 12 months post-intervention. Nonetheless, the ketogenic dieters that obtained follow-up guidance on a restricted carbohydrate routine had the best success following 24 months, indicating importance of care regarding an individual’s specific dietary habits.
One masterpiece post from 2008 clearly outlines the benefits of restricting carbohydrates to cause a unique metabolic state that favorably impacts atherogenic dyslipidemia, fatty acid partitioning and metabolic syndrome. The report clearly demonstrates that ketone bodies represent an efficient fuel for the body, about 25 percent more efficient at producing ATP than glucose or fatty acid, with curative potential towards numerous health issues. Following a carbohydrate-restrictive diet might also lead to a decrease in the release of pro-inflammatory chemicals, substances and compounds, which ultimately has positive implications for cardiovascular health.
On the reverse side, another research study found that the information on the effects of ketogenic diets on cardiovascular disease appeared to be contradictory in animal and human studies to produce an astounding recommendation. Recently presented in the 2018 American Diabetes Association seminar, a research study consisting of a 2-year randomized controlled trial, compared a high-carbohydrate diet to some very-low carbohydrate, like the ketogenic diet, with a reduced saturated fat diet in type 2 diabetic subjects. Both diets provided similar weight loss and reductions in HbA1c, whereas the very-low carbohydrate diet enabled participants to reduce their use of drugs/medications and improved their diurnal blood glucose equilibrium and blood lipids.
Missing Link in Keto Diet
One challenge that many healthcare professionals often face, however, is that sometimes, the ketogenic diet can make you feel sick. There is even a term for this: the Keto Flu. This is mostly because of a change in electrolyte conditioning together decreased insulin levels, resulting in a greater need for potassium, magnesium and sodium. If not properly managed, it can lead to nutrient deficiencies of those electrolytes, among different micronutrients, that may have consequences not completely elucidated as a result of the paucity of research on the long-term use of the ketogenic diet. Sodium is generally over-consumed in a typical diet, and a lot of high-sodium foods make their way into ketogenic diet cured meats, cheeses, and other foods that are processed. But most individuals in Western cultures today do not get enough potassium or magnesium, found mainly in fruits and vegetables, which may play a fundamental role in the pathology of chronic diseases like stroke and kidney stones.
A 2007 research study emphasized the risk factors for kidney stones after following the ketogenic diet. Approximately 6.7percent of the children who have been prescribed the ketogenic diet for intractable epilepsy were reported to have developed kidney stones. In these cases, utilizing potassium citrate significantly diminished the incidence of kidney stones and increased the expression time on the ketogenic diet. Potassium citrate solubilizes calcium, thus decreasing concentrations of free calcium readily available to crystallize. Additionally, it will also help to improve urine pH, helping to dissolve uric acid crystals. The research study concluded that “oral potassium citrate in clinical and prospective studies, using this treatment empirically was justified.”
Dr. Alex Jimenez’s Insight
The ketogenic diet, or the keto diet for short, is a low-carb, high-fat diet which has been previously described to offer many heath benefits. As a matter of fact, numerous research studies have demonstrated how this type of diet can help with weight loss as well as help improve overall health and wellness. The ketogenic diet may often be described as a “difficult to follow” diet because it involves drastically reducing carbohydrate intake to replace it with fat. However, its this reduction in carbs which allows the human body to enter a metabolic state known as ketosis. Once the human body enters ketosis, it becomes tremendously efficient in burning fat and turning it into energy, additionally turning fats into ketones in the liver, supplying energy directly to the brain. This, along with reductions in blood sugar and insulin levels, can have a variety of health benefits, making the ketogenic diet suitable for individuals with specific health issues.
Advice on the Keto Diet
If you would like to try the ketogenic diet or feel like it would benefit you in any sort of way, first make sure to check with your healthcare professional. There are a number of resources online and in texts that aren’t all peer-reviewed. Use the information with care and listen to your own body. Remember: this kind of diet requires additional understanding of biochemical processes, it may behard to follow due to its limitations and possible lack of palatability, and it has to be limited in length. Also, based on one’s genetics, the keto diet can yield quite different outcomes.
Nutrition is a fundamental part of overall health and wellness. Proper nutrition can ultimately affect the way an individual’s bodily system’s functions and without it, a variety of structures and functions can be affected. If you are seeking treatment for a specific health issue, nutrition becomes even more important. Chiropractic care focuses on the natural treatment of the spine, through the use of spinal adjustments and manual manipulations, as well as through the implementation of lifestyle modifications, to provide the human body with all the necessary components it needs to heal itself, without the use of drugs/medications and/or surgery. Many chiropractors often recommend the ketogenic diet, alongside chiropractic care, to improve well-being. Be sure to talk to your doctor of chiropractic, or DC, regarding any nutrition plan you want to follow and they can discuss the best options for your specific health issues and basic treatment needs.
That made clear, there are some smart recipes available on the marketplace to rival those which have observed from the fantastic Paleo popularity. One standout origin for the ketogenic diet is the Charlie Foundation website, which was put up to give dietary advice for caregivers of young children with uncontrolled epilepsy. Check out their site for ideas to feed your keto. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
There has been a lot in the media lately about alkalinity and acidity in the body, but finding solid, straightforward information isn’t always easy. In short, acidity can cause a number of health issues. There are many benefits of bringing your body into balance.
What Is High Acidity?
The term acidity describes a condition where the body is affected by the excess production of gastric acids. Under normal conditions, hydrochloric acid is secreted by the stomach, aiding in the digestion and breakdown of food.
However, when this normal process is triggered in such a way that it causes overproduction of the acid, it can result in health problems. Acidity can be caused by irregular eating patterns, fad diets, alcohol consumption, stress, smoking, an unhealthy diet, and a sedentary lifestyle. Symptoms can include:
Indigestion
Burning in the stomach
Belching
Sour taste
Burning in the throat
Constipation
Nausea
Restlessness
What Are The Dangers Of High Acidity In The Body?
When the body is acidic, it can affect everything from immunity to neurological function to bone health. The Japanese have linked acidity to degenerative diseases like arthritis, cancer, and osteoporosis.
An acidic body is also a very hospitable environment for bacteria and viruses to thrive meaning the person will often get sick more often. When the body is out of balance it becomes susceptible to conditions as simple as dandruff and as complex as diabetes. Interestingly, many people have reversed or gone into remission by simply bringing their body into balance.
What Is Alkalinity?
In order to understand alkalinity, you need to understand pH levels. This is the measure used to determine how alkaline or acid something is. A pH of 0 is at the acidic end of the scale and means the thing being measured is completely acidic. At the other end of the scale, a pH of 14 is totally alkaline. The neutral point is a pH of 7.
Different parts of the body have different pH levels, meaning that some parts are more acidic while others are more alkaline. For instance, blood typically has a pH that is between 7.35 and 7.45, making it slightly alkaline. The stomach, on the other hand, is highly acidic, registering a pH of 3.5 or lower. Making the body more alkaline is not about making it completely alkaline – you need some acidity, it is necessary for digestion and other processes – it is more about bringing the body into balance.
What Are The Benefits Of Alkalinity?
When the body has increased alkalinity, bringing it into better pH balance, it is healthier and has a decreased risk of chronic illness. There is also less likelihood of illness. When the body is in a better pH balance it can result in many benefits including:
More energy
Improved cognitive function
Slowed aging process
Weight loss
Lower cancer risk
Decreased risk of chronic illness
Increased immunity
How Can You Bring Your Body Into Balance?
The best way to bring your body into better pH balance is by modifying your diet. As a rule of thumb, animal based foods like meat, eggs, and dairy tend to be more acidic. A vegetarian diet rich in plant-based foods like vegetables and fruits tend to be more alkaline. While the body does need a diet that includes both acidic and alkaline foods, a diet of processed foods and foods high in fat and sugar can cause too much acidity. By adjusting the diet, eliminating processed foods, and maintaining a healthier, more vegetarian based diet, you can bring your body into balance and enjoy better health as a result.
Injury Medical Clinic: Elderly & Geriatric Fitness
Fitness Trackers: Exercise is usually a great compliment to chiropractic treatment. In fact, many chiropractors recommend regular exercise to their patients. It helps with pain management and speeds healing as well as give your mood a healthy, natural boost.
Fitness trackers are a popular workout tool that helps people set fitness goals, track their progress, and get healthier. How can they help chiropractic patients though? What can they offer that will patients get more out of their treatments? Find out what you need to know about chiropractic and fitness trackers.
Fitness Trackers
It Takes More Than The Tech To Get You Fit.
All the flashy, high tech bells and whistles in the world won’t roll you out of bed in the morning and place you on the treadmill. No fancy wristband will get you up and moving, getting exercise and getting fit. The tech is cool. It is fun and exciting, but it won’t get you fit. Only you can do that.
So if you are getting a fitness tracker with the belief that it is going to be some kind of fitness magic bullet, that just won’t happen. It is great as a fitness buddy, a tool, a nifty gadget that may help motivate you and help you achieve your fitness goals. In the end, though, you are the one driving that car. You are in control.
Is A Fitness Tracker For You?
There are so many fitness trackers on the market with an almost endless list of features. Finding the one that is right for you, or if you could even benefit from a fitness tracker takes a bit of research. Look for features that work for you and the activities you will be pursing.
For instance, if you enjoy water-based fitness activities you might want a waterproof model. There are also data limits, screen sizes (or no screen at all), heart rate tracking options, and whether you want a clip on tracker or one that straps on your wrist.
Before making your purchase, take some time to research all of the features that are available to you then decide what you like and what features would best help you meet your fitness goals.
How To Get The Most Out Of Your Fitness Tracker.
Once you have your fitness tracker you will want to make a plan to ensure that you get the most out of it. Try these tips to make your fitness tracker work its best for you.
Identify clear cut goals. When you begin your fitness quest, the first thing you need to do is know where you want to go with it. It is a good idea to record your stats at the beginning and then update them every month or so. This will let you see how many more steps you are taking, how much weight you’ve lost, or whatever else you wish to accomplish.
Set attainable benchmarks. Benchmarks help you along as you work toward your goal. The key is setting them so that they are attainable but still present a bit of a challenge. If weight loss is your key, you might set benchmarks for every two months. For fitness goals, you may set benchmarks for a certain number of steps in a given time or a certain number of workouts each week. When you reach a benchmark, celebrate a little.
Wear it on your non-dominant wrist. The Journal, Medical and Science in Sports and Exercise published a study that revealed participants who wore fitness trackers on their wrists throughout the day found that they were more accurate when worn on the non-dominant wrist. The theory is that the non-dominant wrist moves less, giving a more accurate reading.
Calibrate your tracker to match your stride. Not everyone has the same stride. You may be very tall or very short; you might take longer strides or time steps. Whatever the case, you’ll get the most out of your fitness tracker by calibrating your stride. Most trackers will provide instructions for doing the calibration. It is well worth taking the time to complete it.
Incorporate other apps to boost your fitness efforts. Many fitness trackers will recommend other apps that can help you meet your goals and you can sync them to your tracker. However, you can also look for apps on your own that can help. There are so many different fitness apps out there from food tracking to apps that use your phone’s GPS to provide more accurate measurements on your runs, walks, or bike rides.
The more fit you are the better your chiropractic treatments will typically work. Fitness trackers can help you reach your goals and get the most out of your chiropractic care.
Doctor 0f Chiropractic: Charlie Quiroga found the extra “push” she needed at PUSH Fitness so as to regain her fitness and get back in shape, as well as to improve her overall health and wellbeing. Charlie Quiroga is grateful to the coaches which helped keep her motivated to continue following a healthier lifestyle. Charlie Quiroga has heard the significance of “pushing” herself towards her goals and remaining positive. Charlie Quiroga urges PUSH as the fitness choice that is very best.
Weight Loss Doctor Of Chiropractic
Weight management techniques encircle long-term lifestyle plans that promote healthy eating and daily physical activity. Effective weight management programs consider not just weight reduction but also the maintenance of a healthy body weight with time. Moreover, weight control entails understanding of meaningful procedures to track weight over time and set perfect body weights for different individuals. Weight control doesn’t include things like fad diets that promote quick weight loss. It targets the results that are achieved through weight loss.
We are blessed to present to you El Paso’s Premier Wellness & Injury Care Clinic.
As El Paso’s Chiropractic Rehabilitation Clinic & Integrated Medicine Center, we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.
Bernadette Banda informs her compelling weight loss story while she clarifies how much her life has changed since she discovered the right fitness regimen with Dr. Alex Jimenez and Daniel “Danny” Alvarado in PUSH Fitness. PUSH became Bernadette Banda’s life philosophy, where she took it on herself never to give up and to always “push” herself towards any fitness goal she wished to attain. With tremendous gratitude, Bernadette Banda praises Danny’s and all the other coach’s efforts and support to help her become healthy.
Chiropractic Weight Loss Treatment
Intentional weight loss is the decrease in total body mass because of attempts to improve fitness and wellness. Weight loss in people who are overweight or obese can decrease health risks, increase health, and may delay the onset of diabetes. It may decrease pain and increase movement in people with osteoarthritis of the knee. Weight reduction may result in a drop in hypertension. Weight loss occurs when the body is expending more energy in metabolism than it’s swallowing from meals or additional nutrients. It is going to then use stored reserves from fat or muscle, slowly resulting in weight loss.
We are blessed to present to you El Paso’s Premier Wellness & Injury Care Clinic.
As El Paso’s Chiropractic Rehabilitation Clinic & Integrated Medicine Center, we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.
Effectiveness: We all know and understand the importance of maintaining a healthy weight. Some individuals do quite nicely at managing their pounds with seemingly little effort, while other struggle constantly.
A recent study by the Center for Disease Control and Prevention (CDC) reports that 78 million American adults suffer from obesity. A person who has sustained an injury or suffers from an illness that affects their back, hips, knees or ankles are especially susceptible to weight gain, because they must deal with limited mobility and the stress of daily pain.
Striving to stay in the ideal weight range for your body type and height provides a variety of health benefits such as adding less pressure on your back and joints, and increasing your range of motion. Patients who receive chiropractic care often enjoy the effectiveness of increased healing by pursuing weight loss.
Successfully fight the battle of the bulge with these four handy weight loss tips to:
Amplify The Effectiveness Of Chiropractic Care
First, Start Small
Replace a couple of negative behaviors with positive ones, and commit to making them stick. Great examples of these are substituting water for soft drinks, eating a high-protein breakfast, or changing out your nightly bowl of ice cream with yogurt.
Simply removing 100 calories a day adds up to a 10 pound weight loss over a year’s time. Small modifications offer the dual benefits of being easier to implement while still showing results.
Next, Keep A Journal
Write down every bite you eat along with the portion size. Listing your food intake provides accountability, which may keep you from noshing on that third slice of pizza or super-sizing those fries.
It also arms you with important intel that will be helpful throughout your weight loss journey. If you hit a plateau, read back through the journal to see what you may have changed over time that caused the scales to stall.
And speaking of scales….
Don’t Live And Cry By The Scales
Often, dieters weigh every day and are elated or depressed based on the number on the scales. That’s a roller coaster way to live, and those emotions can cause calorie laden binges!
Plus, daily weighing is not accurate, as fluctuations in water weight are common. Weigh once a week at the most, at roughly the same time each day. A weekly routine gives you a good idea of your success without the stressful up and down of daily weighing.
Decrease Your Sedentary Ways
Even if you are dealing with an injury or medical condition that limits the ability to exercise, you can still probably be less sedentary than you are now. Again, simplicity is the key.
Walk into the bank instead of using the drive through window, stand up to fold clothes instead of sitting down, and take periodic breaks at your desk to stand for a bit.
Ask your chiropractor about any limitations you need to follow, and request stretching exercises as your personal situation permits. Moving more on a daily basis will aid in shedding those extra pounds and keeping them off long-term.
It’s important for individuals to maintain a normal weight range in order to enjoy a healthy life. Chiropractic patients benefit even more from shedding those extra pounds.
By committing to a healthier lifestyle with fewer pounds to carry around, individuals with back and joint injuries will see greater positive impact from their chiropractic visits. Over time, the combination of a leaner body and chiropractic care will bring greater mobility, less pain, and a decreased chance for re-injury to the patient.
Shea Vaughn Talks “Targeting Obesity”
This article is copyrighted by Blogging Chiros LLC for its Doctor of Chiropractic members and may not be copied or duplicated in any manner including printed or electronic media, regardless of whether for a fee or gratis without the prior written permission of Blogging Chiros, LLC.
Losing Weight: Back pain is one of the most common and most troublesome problems that people experience. Eight out of 10 individuals will struggle with back pain during some point in their life, the US National Library of Medicine reports. Low and chronic back pain can be aggravated by many triggers. Mechanical stress, excessive strain, muscle weakness, poor sleeping position, lack of exercise and excessive weight could all contribute to making the situation worse.
The good news is that chiropractic ranks among the most popular and effective treatment options available today for back pain. Through the chiropractic adjustment, chiropractors not only help ease the pain but also work toward correcting the problem. According to chiropractors, spinal adjustments can deliver even better results when combined with weight loss.
In today’s article, we’ll exam the following:
How Obesity and Back Pain are Related
How Weight Loss Helps Reduce Back Pain
Improving Back Health through Chiropractic
How Obesity and Back Pain are Related
Individuals that are classified as overweight or obese are much more likely to experience back pain than people that aren’t according to the American Obesity Association.
Obesity prevents individuals from engaging in everyday physical activities, as well as healthy exercises. These are essential for strengthening the core muscles. A stronger core can take some of the burden away from the back, thus making back pain less likely.
In addition, the spinal cord becomes excessively burdened in the case of obese individuals. This is because it’s trying to compensate for the additional weight, which can cause tilting and uneven stress. Both of these can contribute to serious and chronic back pain. Thus the reason obesity is one of the most prominent aggravating factors in the case of lower back pain.
Losing Weight Helps Reduce Back Pain
According to weight loss experts and chiropractors, weight loss can contribute to partial or complete reduction in the back pain symptoms. The research on the connection between weight loss and back pain is still insufficient but numerous practitioners report that they’ve seen cases of patients experiencing serious reduction in pain after losing weight.
Obviously, this occurs because the extra weight is taken off the spine. As a result, the spine doesn’t experience further stress. Especially when a chiropractor realigns the vertebral column through multiple sessions of chiropractic adjustments.
According to the American Spine Society, individuals that stay within 10 pounds of their ideal weight are the ones least likely to experience spinal problems, particularly chronic lower back pain.
Improving Back Health through Chiropractic Care and Physical Activity
The combination of exercise and chiropractic care can produce noticeable, long-term improvements in spinal health.
Besides aiding in weight loss, exercise is also great for strengthening the core muscles and guaranteeing a proper distribution of the body’s weight throughout the spine. Stronger muscles, less weight and better posture will provide amazing long-term benefits for chiropractic patients that suffer from back pain.
If you need more pointers on how to incorporate weight loss and exercise in your daily routine, speak to your local chiropractor. He or she is more than competent to guide you along the way. If you aren’t currently seeing a chiropractor, give us a call. We’re here to help!
This article is copyrighted by Blogging Chiros LLC for its Doctor of Chiropractic members and may not be copied or duplicated in any manner including printed or electronic media, regardless of whether for a fee or gratis without the prior written permission of Blogging Chiros, LLC.
The increased prevalence of obesity and related comorbidities is a major public health problem. While genetic factors undoubtedly play a role in determining individual susceptibility to weight gain and obesity, the identified genetic variants only explain part of the variation. This has led to growing interest in understanding the potential role of epigenetics as a mediator of gene-environment interactions underlying the development of obesity and its associated comorbidities. Initial evidence in support of a role of epigenetics in obesity and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which reported epigenetic changes in key metabolically important tissues following high-fat feeding and epigenetic differences between lean and obese animals and by human studies which showed epigenetic changes in obesity and T2DM candidate genes in obese/diabetic individuals. More recently, advances in epigenetic methodologies and the reduced cost of epigenome-wide association studies (EWAS) have led to a rapid expansion of studies in human populations. These studies have also reported epigenetic differences between obese/T2DM adults and healthy controls and epigenetic changes in association with nutritional, weight loss, and exercise interventions. There is also increasing evidence from both human and animal studies that the relationship between perinatal nutritional exposures and later risk of obesity and T2DM may be mediated by epigenetic changes in the offspring. The aim of this review is to summarize the most recent developments in this rapidly moving field, with a particular focus on human EWAS and studies investigating the impact of nutritional and lifestyle factors (both pre- and postnatal) on the epigenome and their relationship to metabolic health outcomes. The difficulties in distinguishing consequence from causality in these studies and the critical role of animal models for testing causal relationships and providing insight into underlying mechanisms are also addressed. In summary, the area of epigenetics and metabolic health has seen rapid developments in a short space of time. While the outcomes to date are promising, studies are ongoing, and the next decade promises to be a time of productive research into the complex interactions between the genome, epigenome, and environment as they relate to metabolic disease.
Keywords: Epigenetics, DNA methylation, Obesity, Type 2 diabetes, Developmental programming
Introduction
Obesity is a complex, multifactorial disease, and better understanding of the mechanisms underlying the interactions between lifestyle, environment, and genetics is critical for developing effective strategies for prevention and treatment [1].
In a society where energy-dense food is plentiful and the need for physical activity is low, there is a wide variation in individuals’ susceptibility to develop obesity and metabolic health problems. Estimates of the role of heredity in this variation are in the range of 40–70 %, and while large genome-wide association studies (GWAS) have identified a number of genetic loci associated with obesity risk, the ~100 most common genetic variants only account for a few percent of variance in obesity [2, 3]. Genome-wide estimates are higher, accounting for ~20 % of the variation [3]; however, a large portion of the heritability remains unexplained.
Recently, attention has turned to investigating the role of epigenetic changes in the etiology of obesity. It has been argued that the epigenome may represent the mechanistic link between genetic variants and environmental factors in determining obesity risk and could help explain the “missing heritability.” The first human epigenetic studies were small and only investigated a limited number of loci. While this generally resulted in poor reproducibility, some of these early findings, for instance the relationship between PGC1A methylation and type 2 diabetes mellitus (T2DM) [4] and others as discussed in van Dijk et al. [5], have been replicated in later studies. Recent advances and increased affordability of high- throughput technologies now allow for large-scale epigenome wide association studies (EWAS) and integration of different layers of genomic information to explore the complex interactions between the genotype, epigenome, transcriptome, and the environment [6–9]. These studies are still in their infancy, but the results thus far have shown promise in helping to explain the variation in obesity susceptibility.
There is increasing evidence that obesity has develop mental origins, as exposure to a suboptimal nutrient supply before birth or in early infancy is associated with an increased risk of obesity and metabolic disease in later life [10–13]. Initially, animal studies demonstrated that a range of early life nutritional exposures, especially those experienced early in gestation, could induce epigenetic changes in key metabolic tissues of the offspring that persisted after birth and result in permanent alterations in gene function [13–17]. Evidence is emerging to support the existence of the same mechanism in humans. This has led to a search for epigenetic marks present early in life that predict later risk of metabolic disease, and studies to determine whether epigenetic programming of metabolic disease could be prevented or reversed in later life.
This review provides an update of our previous systematic review of studies on epigenetics and obesity in humans [5]. Our previous review showcased the promising outcomes of initial studies, including the first potential epigenetic marks for obesity that could be detected at birth (e.g., RXRA) [18]. However, it also highlighted the limited reproducibility of the findings and the lack of larger scale longitudinal investigations. The current review focuses on recent developments in this rapidly moving field and, in particular, on human EWAS and studies investigating the impact of (pre- and postnatal) nutritional and lifestyle factors on the epigenome and the emerging role of epigenetics in the pathology of obesity. We also address the difficulties in identifying causality in these studies and the importance of animal models in providing insight into mechanisms.
Review
Epigenetic Changes In Animal Models Of Obesity
Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.
Animal studies have played a critical role in our current understanding of the role of epigenetics in the developmental origins of obesity and T2DM. Both increased and decreased maternal nutrition during pregnancy have been associated with increased fat deposition in offspring of most mammalian species studied to date (reviewed in [11, 13–15, 19]). Maternal nutrition during pregnancy not only has potential for direct effects on the fetus, it also may directly impact the developing oocytes of female fetuses and primordial germ cells of male fetuses and therefore could impact both the off- spring and grand-offspring. Hence, multigenerational data are usually required to differentiate between maternal intergenerational and trans-generational transmission mechanisms.
Table 1 summarizes a variety of animal models that have been used to provide evidence of metabolic and epigenetic changes in offspring associated with the parental plane of nutrition. It also contains information pertaining to studies identifying altered epigenetic marks in adult individuals who undergo direct nutritional challenges. The table is structured by suggested risk transmission type.
(i) Epigenetic Changes In Offspring Associated With Maternal Nutrition During Gestation
Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13–15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes, especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20–30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic “memory” response that precedes development of the altered phenotype in offspring.
(ii)Effects Of Paternal Nutrition On Offspring Epigenetic Marks
Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31–34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling [35]. Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.
(iii)Potential Trans-generational Epigenetic Changes Promoting Fat Deposition In Offspring
Stable transmission of epigenetic information across multiple generations is well described in plant systems and C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species [31]. The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse [38]. In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color [41]. One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 [42]; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.
(iv) Direct Exposure Of Individuals To Excess Nutrition In Postnatal Life
While many studies have identified diet-associated epigenetic changes in animal models using candidate site-specific regions, there have been few genome-wide analyses undertaken. A recent study focussed on determining the direct epigenetic impact of high-fat diets/ diet-induced obesity in adult mice using genome-wide gene expression and DNA methylation analyses [43]. This study identified 232 differentially methylated regions (DMRs) in adipocytes from control and high-fat fed mice. Importantly, the corresponding human regions for the murine DMRs were also differentially methylated in adipose tissue from a population of obese and lean humans, thereby highlighting the remarkable evolutionary conservation of these regions. This result emphasizes the likely importance of the identified DMRs in regulating energy homeostasis in mammals.
Human Studies
Drawing on the evidence from animal studies and with the increasing availability of affordable tools for genome- wide analysis, there has been a rapid expansion of epigenome studies in humans. These studies have mostly focused on the identification of site-specific differences in DNA methylation that are associated with metabolic phenotypes.
A key question is the extent to which epigenetic modifications contribute to the development of the metabolic phenotype, rather than simply being a con- sequence of it (Fig. 1). Epigenetic programming could contribute to obesity development, as well as playing a role in consequent risk of cardiovascular and metabolic problems. In human studies, it is difficult to prove causality [44], but inferences can be made from a number of lines of evidence:
(i) Genetic association studies. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46–48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation [49].
(ii)Timing of epigenetic changes. The presence of an epigenetic mark prior to development of a phenotype is an essential feature associated with causality. Conversely, the presence of a mark in association with obesity, but not before its development, can be used to exclude causality but would not exclude a possible role in subsequent obesity-related pathology.
(iii)Plausible inference of mechanism. This refers to epigenetic changes that are associated with altered expression of genes with an established role in regulating the phenotype of interest. One such example is the association of methylation at two CpG sites at the CPT1A gene with circulating triglyceride levels [50]. CPT1A encodes carnitine palmitoyltransferase 1A, an enzyme with a central role in fatty acid metabolism, and this is strongly indicative that differential methylation of this gene may be causally related to the alterations in plasma triglyceride concentrations.
Epigenome-Wide Association Studies: Identifying Epigenetic Biomarkers Of Metabolic Health
A number of recent investigations have focused on exploring associations between obesity/metabolic diseases and DNA methylation across the genome (Table 2). The largest published EWAS so far, including a total of 5465 individuals, identified 37 methylation sites in blood that were associated with body mass index (BMI), including sites in CPT1A, ABCG1, and SREBF1 [51]. Another large-scale study showed consistent associations between BMI and methylation in HIF3A in whole blood and adipose tissue [52], a finding which was also partially replicated in other studies [9, 51]. Other recently reported associations between obesity-related measures and DNA methylation include (i) DNA methylation differences between lean and obese individuals in LY86 in blood leukocytes [53]; (ii) associations between PGC1A promoter methylation in whole blood of children and adiposity 5 years later [54]; (iii) associations between waist-hip ratio and ADRB3 methylation in blood [55]; and (iv) associations between BMI, body fat distribution measures, and multiple DNA methylation sites in adipose tissue [9, 56]. EWAS have also shown associations between DNA methylation sites and blood lipids [55, 57–59], serum metabolites [60], insulin resistance [9, 61], and T2DM [48, 62, 63] (Table 2).
From these studies, altered methylation of PGC1A, HIF3A, ABCG1, and CPT1A and the previously described RXRA [18] have emerged as biomarkers associated with, or perhaps predictive of, metabolic health that are also plausible candidates for a role in development of metabolic disease.
Interaction Between Genotype And The Epigenome
Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20–40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 [8]. Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice [43] and weight loss in humans [64]. These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.
The Impact Of The Prenatal And Postnatal Environment On The Epigenome
Prenatal environment: Two recently published studies made use of human populations that experienced “natural” variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants [69]. The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood [68]. The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.
Other recent studies have provided evidence that prenatal over-nutrition and an obese or diabetic maternal environment are also associated with DNA methylation changes in genes related to embryonic development, growth, and metabolic disease in the offspring [70–73].
While human data are scarce, there are indications that paternal obesity can lead to altered methylation of imprinted genes in the newborn [74], an effect thought to be mediated via epigenetic changes acquired during spermatogenesis.
Postnatal environment: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the “mature” epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells [77], and muscle tissue [78] in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver [79] and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat [64]. Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80–82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport [83]. Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss [84].
Collectively, the evidence in support of the capacity to modulate the epigenome in adults suggests that there may be the potential to intervene in postnatal life to modulate or reverse adverse epigenetic programming.
Effect Sizes And Differences Between Tissue Types
DNA methylation changes associated with obesity or induced by diet or lifestyle interventions and weight loss are generally modest (<15 %), although this varies depending on the phenotype and tissue studied. For instance, changes greater than 20 % have been reported in adipose tissue after weight loss [64] and associations between HIF3A methylation and BMI in adipose tissue were more pronounced than in blood [52].
The biological relevance of relatively small methylation changes has been questioned. However, in tissues consisting of a mixture of cell types, a small change in DNA methylation may actually reflect a significant change in a specific cell fraction. Integration of epigenome data with transcriptome and other epigenetic data, such as histone modifications, is important, since small DNA methylation changes might reflect larger changes in chromatin structure and could be associated with broader changes in gene expression. The genomic context should also be considered; small changes within a regulatory element such as a promotor, enhancer, or insulator may have functional significance. In this regard, DMRs for obesity, as well as regions affected by prenatal famine exposure and meQTL for metabolic trait loci have been observed to overlap enhancer elements [8, 43, 68]. There is evidence that DNA methylation in famine-associated regions could indeed affect enhancer activity [68], supporting a role of nutrition-induced methylation changes in gene regulation.
A major limitation in many human studies is that epigenetic marks are often assessed in peripheral blood, rather than in metabolically relevant tissues (Fig. 2). The heterogeneity of blood is an issue, since different cell populations have distinct epigenetic signatures, but algorithms have been developed to estimate the cellular composition to overcome this problem [86]. Perhaps more importantly, epigenetic marks in blood cells may not necessarily report the status of the tissues of primary interest. Despite this, recent studies have provided clear evidence of a relationship between epigenetic marks in blood cells and BMI. In the case of HIF3A for which the level of methylation (beta-value) in the study population ranged from 0.14–0.52, a 10 % increase in methylation was associated with a BMI increase of 7.8 % [52]. Likewise, a 10 % difference in PGC1A methylation may predict up to 12 % difference in fat mass [54].
Conclusions
The study of the role of epigenetics in obesity and metabolic disease has expanded rapidly in recent years, and evidence is accumulating of a link between epigenetic modifications and metabolic health outcomes in humans. Potential epigenetic biomarkers associated with obesity and metabolic health have also emerged from recent studies. The validation of epigenetic marks in multiple cohorts, the fact that several marks are found in genes with a plausible function in obesity and T2DM development, as well as the overlap of epigenetic marks with known obesity and T2DM genetic loci strengthens the evidence that these associations are real. Causality has so far been difficult to establish; however, regardless of whether the associations are causal, the identified epigenetic marks may still be relevant as biomarkers for obesity and metabolic disease risk.
Effect sizes in easily accessible tissues such as blood are small but do seem reproducible despite variation in ethnicity, tissue type, and analysis methods [51]. Also, even small DNA methylation changes may have biological significance. An integrative “omics” approach will be crucial in further unraveling the complex interactions between the epigenome, transcriptome, genome, and metabolic health. Longitudinal studies, ideally spanning multiple generations, are essential to establishing causal relationships. We can expect more such studies in the future, but this will take time.
While animal studies continue to demonstrate an effect of early life nutritional exposure on the epigenome and metabolic health of the offspring, human data are still limited. However, recent studies have provided clear evidence that exposure to suboptimal nutrition during specific periods of prenatal development is associated with methylation changes in the offspring and therefore have the potential to influence adult phenotype. Animal studies will be important to verify human findings in a more controlled setting, help determine whether the identified methylation changes have any impact on metabolic health, and unravel the mechanisms underlying this intergenerational/transgenerational epigenetic regulation. The identification of causal mechanisms underlying metabolic memory responses, the mode of transmission of the phenotypic effects into successive generations, the degree of impact and stability of the transmitted trait, and the identification of an overarching and unifying evolutionary context also remain important questions to be addressed. The latter is often encapsulated by the predictive adaptive response hypothesis, i.e., a response to a future anticipated environment that increases fitness of the population. However, this hypothesis has increasingly been questioned as there is limited evidence for increased fitness later in life [87].
In summary, outcomes are promising, as the epigenetic changes are linked with adult metabolic health and they act as a mediator between altered prenatal nutrition and subsequent increased risk of poor metabolic health outcomes. New epigenetic marks have been identified that are associated with measures of metabolic health. Integration of different layers of genomic information has added further support to causal relationships, and there have been further studies showing effects of pre- and postnatal environment on the epigenome and health. While many important questions remain, recent methodological advances have enabled the types of large-scale population-based studies that will be required to address the knowledge gaps. The next decade promises to be a period of major activity in this important research area.
Susan J. van Dijk1, Ross L. Tellam2, Janna L. Morrison3, Beverly S. Muhlhausler4,5† and Peter L. Molloy1*†
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
All authors contributed to the drafting and critical revision of the manuscript, and all authors read and approved the final manuscript.
Authors’ information
Beverly S. Muhlhausler and Peter L. Molloy are joint last authors.
Acknowledgements
This work has been supported by a grant from the Science and Industry Endowment Fund (Grant RP03-064). JLM and BSM are supported by the National Health and Medical Research Council Career Development Fellowships (JLM, APP1066916; BSM, APP1004211). We thank Lance Macaulay and Sue Mitchell for critical reading and comments on the manuscript.
Author details
1CSIRO Food and Nutrition Flagship, PO Box 52, North Ryde, NSW 1670, Australia. 2CSIRO Agriculture Flagship, 306 Carmody Road, St Lucia, QLD 4067, Australia. 3Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, GPO Box 2471, Adelaide, SA 5001, Australia 4FOODplus Research Centre, Waite Campus, The University of Adelaide, PMB 1, Glen Osmond, SA 5064, Australia. 5Women’s and Children’s Health Research Institute, 72 King William Road, North Adelaide, SA 5006, Australia.
Blank
References:
1. WHO. WHO | Overweight and obesity. http://www.who.int/gho/ncd/
risk_factors/overweight/en/index.html. Accessed 29 January 2015.
2. Visscher PM, Brown MA, McCarthy MI, Yang J. Five years of GWAS discovery.
Am J Hum Genet. 2012;90:7–24.
3. Locke AE, Kahali B, Berndt SI, Justice AE, Pers TH, Day FR, et al. Genetic
studies of body mass index yield new insights for obesity biology. Nature.
2015;518:197–206.
4. Ling C, Del Guerra S, Lupi R, Rönn T, Granhall C, Luthman H, et al.
Epigenetic regulation of PPARGC1A in human type 2 diabetic islets and
effect on insulin secretion. Diabetologia. 2008;51:615–22.
5. Van Dijk SJ, Molloy PL, Varinli H, Morrison JL, Muhlhausler BS. Epigenetics
and human obesity. Int J Obes (Lond). 2015;39:85–97.
6. Teh AL, Pan H, Chen L, Ong M-L, Dogra S, Wong J, et al. The effect of
genotype and in utero environment on interindividual variation in neonate
DNA methylomes. Genome Res. 2014;24:1064–74.
7. Olsson AH, Volkov P, Bacos K, Dayeh T, Hall E, Nilsson EA, et al. Genomewide
associations between genetic and epigenetic variation influence
mRNA expression and insulin secretion in human pancreatic islets. PLoS
Genet. 2014;10:e1004735.
8. Grundberg E, Meduri E, Sandling JK, Hedman AK, Keildson S, Buil A, et al.
Global analysis of DNA methylation variation in adipose tissue from twins
reveals links to disease-associated variants in distal regulatory elements.
Am J Hum Genet. 2013;93:876–90.
9. Ronn T, Volkov P, Gillberg L, Kokosar M, Perfilyev A, Jacobsen AL, et al.
Impact of age, BMI and HbA1c levels on the genome-wide DNA
methylation and mRNA expression patterns in human adipose tissue
and identification of epigenetic biomarkers in blood. Hum Mol Genet.
2015;24:3792–813.
10. Waterland RA, Michels KB. Epigenetic epidemiology of the developmental
origins hypothesis. Annu Rev Nutr. 2007;27:363–88.
11. McMillen IC, Rattanatray L, Duffield JA, Morrison JL, MacLaughlin SM, Gentili
S, et al. The early origins of later obesity: pathways and mechanisms. Adv
Exp Med Biol. 2009;646:71–81.
12. Ravelli A, van der Meulen J, Michels R, Osmond C, Barker D, Hales C, et al.
Glucose tolerance in adults after prenatal exposure to famine. Lancet.
1998;351:173–7.
13. McMillen IC, MacLaughlin SM, Muhlhausler BS, Gentili S, Duffield JL,
Morrison JL. Developmental origins of adult health and disease: the role of
periconceptional and foetal nutrition. Basic Clin Pharmacol Toxicol.
2008;102:82–9.
14. Zhang S, Rattanatray L, McMillen IC, Suter CM, Morrison JL. Periconceptional
nutrition and the early programming of a life of obesity or adversity. Prog
Biophys Mol Biol. 2011;106:307–14.
15. Bouret S, Levin BE, Ozanne SE. Gene-environment interactions controlling
energy and glucose homeostasis and the developmental origins of obesity.
Physiol Rev. 2015;95:47–82.
16. Borengasser SJ, Zhong Y, Kang P, Lindsey F, Ronis MJ, Badger TM, et al.
Maternal obesity enhances white adipose tissue differentiation and alters
genome-scale DNA methylation in male rat offspring. Endocrinology.
2013;154:4113–25.
17. Gluckman PD, Lillycrop KA, Vickers MH, Pleasants AB, Phillips ES, Beedle AS,
et al. Metabolic plasticity during mammalian development is directionally
dependent on early nutritional status. Proc Natl Acad Sci U S A.
2007;104:12796–800.
18. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C,
et al. Epigenetic gene promoter methylation at birth is associated with
child’s later adiposity. Diabetes. 2011;60:1528–34.
19. McMillen IC, Adam CL, Muhlhausler BS. Early origins of obesity:
programming the appetite regulatory system. J Physiol. 2005;565(Pt 1):9–17.
20. Begum G, Stevens A, Smith EB, Connor K, Challis JR, Bloomfield F, et al.
Epigenetic changes in fetal hypothalamic energy regulating pathways are
associated with maternal undernutrition and twinning. FASEB J.
2012;26:1694–703.
21. Ge ZJ, Liang QX, Hou Y, Han ZM, Schatten H, Sun QY, et al. Maternal obesity
and diabetes may cause DNA methylation alteration in the spermatozoa of
offspring in mice. Reprod Biol Endocrinol. 2014;12:29.
22. Jousse C, Parry L, Lambert-Langlais S, Maurin AC, Averous J, Bruhat A, et al.
Perinatal undernutrition affects the methylation and expression of the leptin
gene in adults: implication for the understanding of metabolic syndrome.
FASEB J. 2011;25:3271–8.
23. Lan X, Cretney EC, Kropp J, Khateeb K, Berg MA, Penagaricano F, et al.
Maternal diet during pregnancy induces gene expression and DNA
methylation changes in fetal tissues in sheep. Front Genet. 2013;4:49.
24. Li CC, Young PE, Maloney CA, Eaton SA, Cowley MJ, Buckland ME, et al.
Maternal obesity and diabetes induces latent metabolic defects and
widespread epigenetic changes in isogenic mice. Epigenetics. 2013;8:602–11.
25. Lillycrop KA, Phillips ES, Jackson AA, Hanson MA, Burdge GC. Dietary protein
restriction of pregnant rats induces and folic acid supplementation prevents
epigenetic modification of hepatic gene expression in the offspring. J Nutr.
2005;135:1382–6.
26. Radford EJ, Ito M, Shi H, Corish JA, Yamazawa K, Isganaitis E, et al. In utero
effects. In utero undernourishment perturbs the adult sperm methylome
and intergenerational metabolism. Science. 2014;345(80):1255903.
27. Suter M, Bocock P, Showalter L, Hu M, Shope C, McKnight R, et al.
Epigenomics: maternal high-fat diet exposure in utero disrupts
peripheral circadian gene expression in nonhuman primates. FASEB J.
2011;25:714–26.
28. Suter MA, Ma J, Vuguin PM, Hartil K, Fiallo A, Harris RA, et al. In utero
exposure to a maternal high-fat diet alters the epigenetic histone code in a
murine model. Am J Obs Gynecol. 2014;210:463 e1–463 e11.
29. Tosh DN, Fu Q, Callaway CW, McKnight RA, McMillen IC, Ross MG, et al.
Epigenetics of programmed obesity: alteration in IUGR rat hepatic IGF1
mRNA expression and histone structure in rapid vs. delayed postnatal
catch-up growth. Am J Physiol Gastrointest Liver Physiol.
2010;299:G1023–9.
30. Sandovici I, Smith NH, Nitert MD, Ackers-Johnson M, Uribe-Lewis S, Ito Y,
et al. Maternal diet and aging alter the epigenetic control of a promoterenhancer
interaction at the Hnf4a gene in rat pancreatic islets. Proc Natl
Acad Sci U S A. 2011;108:5449–54.
31. Braunschweig M, Jagannathan V, Gutzwiller A, Bee G. Investigations on
transgenerational epigenetic response down the male line in F2 pigs. PLoS
One. 2012;7, e30583.
32. Carone BR, Fauquier L, Habib N, Shea JM, Hart CE, Li R, et al. Paternally
induced transgenerational environmental reprogramming of metabolic
gene expression in mammals. Cell. 2010;143:1084–96.
33. Ost A, Lempradl A, Casas E, Weigert M, Tiko T, Deniz M, et al. Paternal diet
defines offspring chromatin state and intergenerational obesity. Cell.
2014;159:1352–64.
34. Martínez D, Pentinat T, Ribó S, Daviaud C, Bloks VW, Cebrià J, et al. In utero
undernutrition in male mice programs liver lipid metabolism in the secondgeneration
offspring involving altered Lxra DNA methylation. Cell Metab.
2014;19:941–51.
35. Wei Y, Yang C-R, Wei Y-P, Zhao Z-A, Hou Y, Schatten H, et al. Paternally
induced transgenerational inheritance of susceptibility to diabetes in
mammals. Proc Natl Acad Sci U S A. 2014;111:1873–8.
36. Grossniklaus U, Kelly WG, Kelly B, Ferguson-Smith AC, Pembrey M, Lindquist
S. Transgenerational epigenetic inheritance: how important is it? Nat Rev
Genet. 2013;14:228–35.
37. Pembrey M, Saffery R, Bygren LO. Human transgenerational responses to
early-life experience: potential impact on development, health and
biomedical research. J Med Genet. 2014;51:563–72.
38. Wolff GL, Kodell RL, Moore SR, Cooney CA. Maternal epigenetics and methyl
supplements affect agouti gene expression in Avy/a mice. FASEB J.
1998;12:949–57.
39. Jirtle RL, Skinner MK. Environmental epigenomics and disease susceptibility.
Nat Rev Genet. 2007;8:253–62.
40. Morgan HD, Sutherland HG, Martin DI, Whitelaw E. Epigenetic inheritance at
the agouti locus in the mouse. Nat Genet. 1999;23:314–8.
41. Cropley JE, Suter CM, Beckman KB, Martin DI. Germ-line epigenetic
modification of the murine A vy allele by nutritional supplementation. Proc
Natl Acad Sci U S A. 2006;103:17308–12.
42. Hoile SP, Lillycrop KA, Thomas NA, Hanson MA, Burdge GC. Dietary protein
restriction during F0 pregnancy in rats induces transgenerational changes in
the hepatic transcriptome in female offspring. PLoS One. 2011;6, e21668.
43. Multhaup ML, Seldin MM, Jaffe AE, Lei X, Kirchner H, Mondal P, et al. Mousehuman
experimental epigenetic analysis unmasks dietary targets and
genetic liability for diabetic phenotypes. Cell Metab. 2015;21:138–49.
44. Michels KB, Binder AM, Dedeurwaerder S, Epstein CB, Greally JM, Gut I, et al.
Recommendations for the design and analysis of epigenome-wide
association studies. Nat Methods. 2013;10:949–55.
45. Dayeh TA, Olsson AH, Volkov P, Almgren P, Rönn T, Ling C. Identification of
CpG-SNPs associated with type 2 diabetes and differential DNA methylation
in human pancreatic islets. Diabetologia. 2013;56:1036–46.
46. Relton CL, Davey Smith G. Two-step epigenetic Mendelian randomization: a
strategy for establishing the causal role of epigenetic processes in pathways
to disease. Int J Epidemiol. 2012;41:161–76.
47. Liu Y, Aryee MJ, Padyukov L, Fallin MD, Hesselberg E, Runarsson A, et al.
Epigenome-wide association data implicate DNA methylation as an
intermediary of genetic risk in rheumatoid arthritis. Nat Biotechnol.
2013;31:142–7.
48. Yuan W, Xia Y, Bell CG, Yet I, Ferreira T, Ward KJ, et al. An integrated
epigenomic analysis for type 2 diabetes susceptibility loci in monozygotic
twins. Nat Commun. 2014;5:5719.
49. Nitert MD, Dayeh T, Volkov P, Elgzyri T, Hall E, Nilsson E, et al. Impact of an
exercise intervention on DNA methylation in skeletal muscle from firstdegree
relatives of patients with type 2 diabetes. Diabetes. 2012;61:3322–32.
50. Gagnon F, Aïssi D, Carrié A, Morange P-E, Trégouët D-A. Robust validation of
methylation levels association at CPT1A locus with lipid plasma levels.
J Lipid Res. 2014;55:1189–91.
51. Demerath EW, Guan W, Grove ML, Aslibekyan S, Mendelson M, Zhou Y-H,
et al. Epigenome-wide association atudy (EWAS) of BMI, BMI change, and
waist circumference in African American adults identifies multiple replicated
loci. Hum Mol Genet. 2015:ddv161–.
52. Dick KJ, Nelson CP, Tsaprouni L, Sandling JK, Aïssi D, Wahl S, et al. DNA
methylation and body-mass index: a genome-wide analysis. Lancet.
2014;6736:1–9.
53. Su S, Zhu H, Xu X, Wang X, Dong Y, Kapuku G, et al. DNA methylation of
the LY86 gene is associated with obesity, insulin resistance, and
inflammation. Twin Res Hum Genet. 2014;17:183–91.
54. Clarke-Harris R, Wilkin TJ, Hosking J, Pinkney J, Jeffery AN, Metcalf BS, et al.
PGC1α promoter methylation in blood at 5–7 years predicts adiposity from
9 to 14 years (EarlyBird 50). Diabetes. 2014;63:2528–37.
55. Guay S-P, Brisson D, Lamarche B, Biron S, Lescelleur O, Biertho L, et al.
ADRB3 gene promoter DNA methylation in blood and visceral adipose
tissue is associated with metabolic disturbances in men. Epigenomics.
2014;6:33–43.
56. Agha G, Houseman EA, Kelsey KT, Eaton CB, Buka SL, Loucks EB. Adiposity is
associated with DNA methylation profile in adipose tissue. Int J Epidemiol.
2014:1–11.
57. Irvin MR, Zhi D, Joehanes R, Mendelson M, Aslibekyan S, Claas SA, et al.
Epigenome-wide association study of fasting blood lipids in the genetics of
lipid-lowering drugs and diet network study. Circulation. 2014;130:565–72.
58. Frazier-Wood AC, Aslibekyan S, Absher DM, Hopkins PN, Sha J, Tsai MY, et al.
Methylation at CPT1A locus is associated with lipoprotein subfraction
profiles. J Lipid Res. 2014;55:1324–30.
59. Pfeifferm L, Wahl S, Pilling LC, Reischl E, Sandling JK, Kunze S, et al. DNA
methylation of lipid-related genes affects blood lipid levels. Circ Cardiovasc
Genet. 2015.
60. Petersen A-K, Zeilinger S, Kastenmüller G, Römisch-Margl W, Brugger M, Peters
A, et al. Epigenetics meets metabolomics: an epigenome-wide association
study with blood serum metabolic traits. Hum Mol Genet. 2014;23:534–45.
61. Hidalgo B, Irvin MR, Sha J, Zhi D, Aslibekyan S, Absher D, et al. Epigenomewide
association study of fasting measures of glucose, insulin, and HOMA-IR
in the genetics of lipid lowering drugs and diet network study. Diabetes.
2014;63:801–7.
62. Dayeh T, Volkov P, Salö S, Hall E, Nilsson E, Olsson AH, et al. Genome-wide
DNA methylation analysis of human pancreatic islets from type 2 diabetic
and non-diabetic donors identifies candidate genes that influence insulin
secretion. PLoS Genet. 2014;10, e1004160.
63. Nilsson E, Jansson PA, Perfilyev A, Volkov P, Pedersen M, Svensson MK, et al.
Altered DNA methylation and differential expression of genes influencing
metabolism and inflammation in adipose tissue from subjects with type 2
diabetes. Diabetes. 2014;63:2962–76.
64. Benton MC, Johnstone A, Eccles D, Harmon B, Hayes MT, Lea RA, et al. An analysis of DNA methylation in human adipose tissue reveals differential modification of obesity genes before and after gastric bypass and weight
loss. Gene. 2015;16:1–21.
65. Bateson P, Gluckman P. Plasticity and robustness in development and
evolution. Int J Epidemiol. 2012;41:219–23.
66. Feinberg AP, Irizarry RA, Feinberg AP, Irizarry RA. Evolution in health and
medicine Sackler colloquium: stochastic epigenetic variation as a driving
force of development, evolutionary adaptation, and disease. Proc Natl Acad
Sci U S A. 2010;107(Suppl):1757–64.
67. Martino D, Loke YJ, Gordon L, Ollikainen M, Cruickshank MN, Saffery R, et al.
Longitudinal, genome-scale analysis of DNA methylation in twins from birth
to 18 months of age reveals rapid epigenetic change in early life and pairspecific
effects of discordance. Genome Biol. 2013;14:R42.
68. Tobi EW, Goeman JJ, Monajemi R, Gu H, Putter H, Zhang Y, et al. DNA
methylation signatures link prenatal famine exposure to growth and
metabolism. Nat Commun. 2014;5:5592.
69. Dominguez-Salas P, Moore SE, Baker MS, Bergen AW, Cox SE, Dyer RA, et al.
Maternal nutrition at conception modulates DNA methylation of human
metastable epialleles. Nat Commun. 2014;5:3746.
70. Quilter CR, Cooper WN, Cliffe KM, Skinner BM, Prentice PM, Nelson L, et al.
Impact on offspring methylation patterns of maternal gestational diabetes
mellitus and intrauterine growth restraint suggest common genes and
pathways linked to subsequent type 2 diabetes risk. FASEB J. 2014:1–12.
71. Morales E, Groom A, Lawlor DA, Relton CL. DNA methylation signatures in
cord blood associated with maternal gestational weight gain: results from
the ALSPAC cohort. BMC Res Notes. 2014;7:278.
72. Ruchat SM, Houde AA, Voisin G, St-Pierre J, Perron P, Baillargeon JP, et al.
Gestational diabetes mellitus epigenetically affects genes predominantly
involved in metabolic diseases. Epigenetics. 2013;8:935–43.
73. Liu X, Chen Q, Tsai H-J, Wang G, Hong X, Zhou Y, et al. Maternal
preconception body mass index and offspring cord blood DNA
methylation: exploration of early life origins of disease. Environ Mol
Mutagen. 2014;55:223–30.
74. Soubry A, Murphy SK, Wang F, Huang Z, Vidal AC, Fuemmeler BF, et al.
Newborns of obese parents have altered DNA methylation patterns at
imprinted genes. Int J Obes (Lond). 2015;39:650–7.
75. Jacobsen SC, Brøns C, Bork-Jensen J, Ribel-Madsen R, Yang B, Lara E, et al.
Effects of short-term high-fat overfeeding on genome-wide DNA
methylation in the skeletal muscle of healthy young men. Diabetologia.
2012;55:3341–9.
76. Gillberg L, Jacobsen SC, Rönn T, Brøns C, Vaag A. PPARGC1A DNA
methylation in subcutaneous adipose tissue in low birth weight subjects–
impact of 5 days of high-fat overfeeding. Metabolism. 2014;63:263–71.
77. Huang Y-T, Maccani JZJ, Hawley NL, Wing RR, Kelsey KT, McCaffery JM.
Epigenetic patterns in successful weight loss maintainers: a pilot study. Int J
Obes (Lond). 2015;39:865–8.
78. Barres R, Kirchner H, Rasmussen M, Yan J, Kantor FR, Krook A, Näslund E,
Zierath JR. Weight loss after gastric bypass surgery in human obesity
remodels promoter methylation. Cell Rep. 2013:1–8.
79. Ahrens M, Ammerpohl O, von Schönfels W, Kolarova J, Bens S, Itzel T, et al.
DNA methylation analysis in nonalcoholic fatty liver disease suggests
distinct disease-specific and remodeling signatures after bariatric surgery.
Cell Metab. 2013;18:296–302.
80. Voisin S, Eynon N, Yan X, Bishop DJ. Exercise training and DNA methylation
in humans. Acta Physiol (Oxf). 2014;213:39–59.
81. Lindholm ME, Marabita F, Gomez-Cabrero D, Rundqvist H, Ekström TJ,
Tegnér J, et al. An integrative analysis reveals coordinated reprogramming
of the epigenome and the transcriptome in human skeletal muscle after
training. Epigenetics. 2014;9:1557–69.
82. Denham J, O’Brien BJ, Marques FZ, Charchar FJ. Changes in the leukocyte
methylome and its effect on cardiovascular related genes after exercise.
J Appl Physiol. 2014:jap.00878.2014.
83. Rowlands DS, Page RA, Sukala WR, Giri M, Ghimbovschi SD, Hayat I, et al.
Multi-omic integrated networks connect DNA methylation and miRNA with
skeletal muscle plasticity to chronic exercise in type 2 diabetic obesity.
Physiol Genomics. 2014;46:747–65.
84. Horvath S, Erhart W, Brosch M, Ammerpohl O, von Schonfels W, Ahrens M,
et al. Obesity accelerates epigenetic aging of human liver. Proc Natl Acad
Sci. 2014;111:15538–43.
85. Almén MS, Nilsson EK, Jacobsson JA, Kalnina I, Klovins J, Fredriksson R, et al.
Genome-wide analysis reveals DNA methylation markers that vary with
both age and obesity. Gene. 2014.;548:61–7
86. Houseman EA, Molitor J, Marsit CJ. Reference-free cell mixture adjustments
in analysis of DNA methylation data. Bioinformatics. 2014;30:1431–9.
87. Wells JC. A critical appraisal of the predictive adaptive response hypothesis.
Int J Epidemiol. 2012;41:229–35.
88. Williams-Wyss O, Zhang S, MacLaughlin SM, Kleemann D, Walker SK, Suter
CM, et al. Embryo number and periconceptional undernutrition in the
sheep have differential effects on adrenal epigenotype, growth, and
development. Am J Physiol Endocrinol Metab. 2014;307:E141–50.
89. Zhang S, Rattanatray L, Morrison JL, Nicholas LM, Lie S, McMillen IC.
Maternal obesity and the early origins of childhood obesity: weighing up
the benefits and costs of maternal weight loss in the periconceptional
period for the offspring. Exp Diabetes Res. 2011;2011:585749.
90. Zhang S, Williams-Wyss O, MacLaughlin SM, Walker SK, Kleemann DO, Suter
CM, et al. Maternal undernutrition during the first week after conception
results in decreased expression of glucocorticoid receptor mRNA in the
absence of GR exon 17 hypermethylation in the fetal pituitary in late
gestation. J Dev Orig Heal Dis. 2013;4:391–401.
91. Lie S, Morrison JL, Williams-Wyss O, Suter CM, Humphreys DT, Ozanne SE,
et al. Periconceptional undernutrition programs changes in insulin-signaling
molecules and microRNAs in skeletal muscle in singleton and twin fetal
sheep. Biol Reprod. 2014;90:5.
92. Van Straten EM, van Meer H, Huijkman NC, van Dijk TH, Baller JF, Verkade
HJ, et al. Fetal liver X receptor activation acutely induces lipogenesis but
does not affect plasma lipid response to a high-fat diet in adult mice. Am J
Physiol Endocrinol Metab. 2009;297:E1171–8.
93. Fernandez-Twinn DS, Alfaradhi MZ, Martin-Gronert MS, Duque-Guimaraes
DE, Piekarz A, Ferland-McCollough D, et al. Downregulation of IRS-1 in
adipose tissue of offspring of obese mice is programmed cellautonomously
through post-transcriptional mechanisms. Mol Metab.
2014;3:325–33.
94. Waterland RA, Travisano M, Tahiliani KG. Diet-induced hypermethylation at
agouti viable yellow is not inherited transgenerationally through the female.
FASEB J. 2007;21:3380–5.
95. Ge ZJ, Luo SM, Lin F, Liang QX, Huang L, Wei YC, et al. DNA methylation in
oocytes and liver of female mice and their offspring: effects of high-fat-dietinduced
obesity. Env Heal Perspect. 2014;122:159–64.
96. Ollikainen M, Ismail K, Gervin K, Kyllönen A, Hakkarainen A, Lundbom J, et al.
Genome-wide blood DNA methylation alterations at regulatory elements
and heterochromatic regions in monozygotic twins discordant for obesity
and liver fat. Clin Epigenetics. 2015;7:1–13.
Even though the effects of overweight and obesity on diabetes, cardiovascular disease, all-cause mortality, and other health outcomes are widely known, there is less awareness that overweight, obesity, and weight gain are associated with an increased risk of certain cancers. A recent review of more than 1000 studies concluded that sufficient evidence existed to link weight gain, overweight, and obesity with 13 cancers, including adenocarcinoma of the esophagus; cancers of the gastric cardia, colon and rectum, liver, gallbladder, pancreas, corpus uteri, ovary, kidney, and thyroid; postmenopausal female breast cancer; meningioma; and multiple myeloma.1 An 18-year follow-up of almost 93 000 women in the Nurses’ Health Study revealed a dose-response association of weight gain and obesity with several cancers.2
Obesity Increase
The prevalence of obesity in the United States has been increasing for almost 50 years. Currently, more than two-thirds of adults and almost one-third of children and adolescents are overweight or obese. Youths who are obese are more likely to be obese as adults, compounding their risk for health consequences such as cardiovascular disease, diabetes, and cancer. Trends in many of the health consequences of overweight and obesity (such as type 2 diabetes and coronary heart disease) also are increasing, coinciding with prior trends in rates of obesity. Furthermore, the sequelae of these diseases are related to the severity of obesity in a dose-response fashion.2 It is therefore not surprising that obesity accounts for a significant portion of health care costs.
Cancers
A report released on October 3, 2017, by the US Centers for Disease Control and Prevention assessed the incidence of the 13 cancers associated with overweight and obesity in 2014 and the trends in these cancers over the 10-year period from 2005 to 2014.3 In 2014, more than 630 000 people were diagnosed as having a cancer associated with overweight and obesity, comprising more than 55% of all cancers diagnosed among women and 24% of cancers among men. Most notable was the finding that cancers related to overweight and obesity were increasingly diagnosed among younger people.
From 2005 to 2014, there was a 1.4% annual increase in cancers related to overweight and obesity among individuals aged 20 to 49 years and a 0.4% increase in these cancers among individuals aged 50 to 64 years. For example, if cancer rates had stayed the same in 2014 as they were in 2005, there would have been 43 000 fewer cases of colorectal cancer but 33 000 more cases of other cancers related to overweight and obesity. Nearly half of all cancers in people younger than 65 years were associated with overweight and obesity. Overweight and obesity among younger people may exact a toll on individuals’ health earlier in their lifetimes.2 Given the time lag between exposure to cancer risk factors and cancer diagnosis, the high prevalence of overweight and obesity among adults, children, and adolescents may forecast additional increases in the incidence of cancers related to overweight and obesity.
Clinical Intervention
Since the release of the landmark 1964 surgeon general’s report on the health consequences of smoking, clinicians have counseled their patients to avoid tobacco and on methods to quit and provided referrals to effective programs to reduce their risk of chronic diseases including cancer. These efforts, coupled with comprehensive public health and policy approaches to reduce tobacco use, have been effective—cigarette smoking is at an all-time low. Similar efforts are warranted to prevent excessive weight gain and treat children, adolescents, and adults who are overweight or obese. Clinician referral to intense, multicomponent behavioral intervention programs to help patients with obesity lose weight can be an important starting point in improving a patient’s health and preventing diseases associatedwith obesity. The benefits of maintaining a healthy weight throughout life include improvements in a wide variety of health outcomes, including cancer. There is emerging but very preliminary data that some of these cancer benefits may be achieved following weight loss among people with overweight or obesity.4
The US Preventive Services Task Force (USPSTF)
The US Preventive Services Task Force (USPSTF) recommends screening for obesity and intensive behavioral interventions delivered over 12 to 16 visits for adults and 26 or more visits for children and adolescents with obesity.5,6 Measuring patients’ weight, height, and body mass index (BMI), consistent with USPSTF recommendations, and counseling patients about maintaining a healthy weight can establish a foundation for preventive care in clinical care settings. Scientific data continue to emerge about the negative health effects of weight gain, including an increased risk of cancer.1 Tracking patients’ weight over time can identify those who could benefit from counseling and referral early and help them avoid additional weight gain. Yet less than half of primary care physicians regularly assess the BMI of their adult, child, and adolescent patients. Encouraging discussions about weight management in multiple health care settings, including physicians’ offices, clinics, emergency departments, and hospitals, can provide multiple opportunities for patients and reinforce messages across contexts and care environments.
Weight Loss Programs
Implementation of clinical interventions, including screening, counseling, and referral, has major challenges. Since 2011, Medicare has covered behavioral counseling sessions for weight loss in primary care settings. However, the benefit has not been widely utilized.7 Whether the lack of utilization is a consequence of lack of clinician or patient knowledge or for other reasons remains uncertain. Few medical schools and residency programs provide adequate training in prevention and management of obesity or in understanding how to make referrals to such services. Obesity is a highly stigmatized condition; many clinicians find it difficult to initiate a conversation about obesity with patients, and some may inadvertently use alienating language when they do. Studies indicate that patients with obesity prefer the use of terms such as unhealthy weight or increased BMI rather than overweight or obesity and improved nutrition and physical activity rather than diet and exercise.8 However, it is unknown if switching to these terms will lead to more effective behavioral counseling. Effective clinical decision support tools to measure BMI and guide physicians through referral and counseling interventions can provide clinicians needed support within the patient-clinician encounter. Inclusion of recently developed competencies for prevention and management of obesity into the curricula of health care professionals may improve their ability to deliver effective care. Because few primary care clinicians are trained in behavior change strategies like cognitive behavioral therapy or motivational interviewing, other trained health care professionals, such as nurses, pharmacists, psychologists, and dietitians could assist by providing counseling and appropriate referrals and help people manage their own health.
Achieving sustainable weight loss requires comprehensive strategies that support patients’ efforts to make significant lifestyle changes. The availability of clinical and community programs and services to which to refer patients is critically important. Although such programs are available in some communities, there are gaps in availability. Furthermore, even when these programs are available, enhancing linkages between clinical and community care could improve patients’ access. Linking community obesity prevention, weight management, and physical activity programs with clinical services can connect people to valuable prevention and intervention resources in the communities where they live, work, and play. Such linkages can give individuals the encouragement they need for the lifestyle changes that maintain or improve their health.
The high prevalence of overweight and obesity in the United States will continue to contribute to increases in health consequences related to obesity, including cancer. Nonetheless, cancer is not inevitable; it is possible that many cancers related to overweight and obesity could be prevented, and physicians have an important responsibility in educating patients and supporting patients’ efforts to lead healthy lifestyles. It is important for all health care professionals to emphasize that along with quitting or avoiding tobacco, achieving and maintaining a healthy weight are also important for reducing the risk of cancer.
Corresponding Author: Greta M. Massetti, PhD, Centers for Disease Control and Prevention, 4770 Buford Hwy NE, Atlanta, GA 30341 ([email protected]).
Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflict of Interest. Dr Dietz reports receipt of scientific advisory board fees from Weight Watchers and consulting fees from RTI. No other disclosures were reported.
Disclaimer: The findings and conclusions in this report are those of the authors and not necessarily the official position of the Centers for Disease Control and Prevention.
References
1. Lauby-Secretan B, Scoccianti C, Loomis D, Grosse Y, Bianchini F, Straif K; International Agency for Research on Cancer Handbook Working Group. Body fatness and cancer—viewpoint of the IARC Working Group. N Engl J Med. 2016;375(8):794-798. PubMedArticle
2. Zheng Y, Manson JE, Yuan C, et al. Associations of weight gain from early to middle adulthood with major health outcomes later in life. JAMA. 2017;318(3):255-269. PubMedArticle
4. Byers T, Sedjo RL. Does intentional weight loss reduce cancer risk? Diabetes Obes Metab. 2011;13(12):1063-1072. PubMedArticle
5. Grossman DC, Bibbins-Domingo K, Curry SJ, et al; US Preventive Services Task Force. Screening for obesity in children and adolescents: US Preventive Services Task Force recommendation statement. JAMA. 2017;317(23):2417-2426. PubMedArticle
7. Batsis JA, Bynum JPW. Uptake of the centers for Medicare and Medicaid obesity benefit: 2012-2013. Obesity (Silver Spring). 2016;24(9):1983-1988. PubMedArticle
8. Puhl R, Peterson JL, Luedicke J. Motivating or stigmatizing? public perceptions of weight-related language used by health providers. Int J Obes (Lond). 2013;37(4):612-619. PubMedArticle
Ketosis is a metabolic state where the liver takes proteins and fat and produces molecules to use for energy. Ketosis allows a starving person to survive for days (or even months). Some athletes see improvements while others feel miserable whenever they are in a condition that is ketogenic. Is a ketogenic diet right for you?
Ketogenic Diet and the Brain
Your brain is about 2 percent of your body mass, even though it requires approximately 20 percent of your basal metabolic rate, more if you are a thinker. Various parts of your brain use different amounts of glucose, and almost twice as much in the morning. You will need to fuel your mind more if you are using your mind working hard through the day and solving problems. If you’re working more on engine control, (state a skill involving precision or equilibrium), then you will use less glucose. Many people can attest to how much energy is used by the brain when challenged.
Although sugar is run off by our brains rather than fat, they are also able to run off of ketones as an alternate fuel source. People who market diets tend to be aware the simple fact that an increase in ketones improves repair and the healing of neurons and increases the neurotransmitter GABA. (GABA makes it possible to sleep. It’s also the main neurotransmitter that sleep drugs and antipsychotic drugs influence.) Due to the impact of ketones on the brain, a ketogenic diet can really help those with seizures. Of course, ketosis means you’re burning far more fat, (in the form of ketones), for energy compared to glucose, and also, for the most part, that’s usually great thing.
You won’t venture to some harmful diabetic ketosis amount as long as you are generating even only a tiny amount of insulin. So as long as you are not Type 2 or a Type 1, there is nothing to immediately worry about. However, to stay in a state of ketosis, you typically need to eat less than 50g of carbs per day if not less than that. In this state, the body’s functions are based on fat rather than glycogen, and the brain is based on ketones instead of glucose.
People wishing to achieve ketosis can not consume an excessive amount of protein. This means no more than 150g per day. Protein could be converted into glycogen and as it may have been mentioned before by professionals, this protein can also be used to make glucose and you would throw the body out of ketosis.
Ketones vs Glucose
So, should you attempt to achieve this ketogenic state? For many people, they need to do it at least to change their body from insulin resistance. Again, like most things, it is very individualized. If you’re severely resistant this might be your way out of it and about the road to health again.
Overall, most people could do much better, (significance become more fit and more healthy), eating less carbs. But when they don’t need to, some people have a tendency to go to the stress and extreme carbs. Many people also fear insulin because everything we read about obesity, cancer, and pretty much any disorder talks about insulin and inflammation. But remember it is all about making just the right amount. Insulin is not a bad guy, just too much of it is. If you don’t make insulin when you ought to be you’re really in a more dire situation than becoming insulin resistant.
It typically takes two to three weeks to really shift your body over to fat from using glucose as a main fuel source, which is with an extremely low carb, high fat diet plan. Merely tweaking your diet a little bit won’t do the job. You have to go to the more extreme for a few weeks, and after that you can add in some carbohydrates and determine how you react to them, mentally and physically. The nice thing about changing your body from sugar burning is that you also won’t convert back to being a sugar-burner if you consume too many carbs for a brief period of time.
Whether your want to be in ketosis or not is your choice, but you should be able to go days with no carbs (other than veggies) in your diet plan. Carbohydrates should generally only be consumed when you only want to eat them, like pizza, or anything you are into, or once you are training hard or extended.
Remember, even if you’re only eating about 2,000 calories per day then 100g of carbohydrates is only 20 percent of your diet plan. You’re getting the identical amount of protein and the fat is left by that around 60 percent, which is grams of fat. (Fat is 9 calories per gram; protein and carbohydrates are every 4 cals.) You are going to want some more carbs, if you are training hard. You’ll need some carbohydrates. If you’re trying to select a diet , training difficult or in any medium to high intensity for a period. Therefore, if you are going to try a diet do it in the off season when you are building a strong base or when you’re in a recovery interval in racing or training hard.
On a clinical note, many individuals perform well staying in ketosis for more than a month or two months, max. Health disorders and pain have been a result of being in a ketogenic condition for such a long time. The diet helps people progress mentally and physically, but it can turn on them, without proper understanding. Therefore, if you’re going to go keto, have a rest every few months or so, and see how you operate and feel in and out of ketosis.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Don’t Live And Cry By The Scales
Obesity is a complex, multifactorial disease, and better understanding of the mechanisms underlying the interactions between lifestyle, environment, and genetics is critical for developing effective strategies for prevention and treatment [1].
Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.
(i) Epigenetic Changes In Offspring Associated With Maternal Nutrition During Gestation
Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13–15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes, especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20–30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic “memory” response that precedes development of the altered phenotype in offspring.
Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31–34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling [35]. Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.
Stable transmission of epigenetic information across multiple generations is well described in plant systems and C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species [31]. The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse [38]. In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color [41]. One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 [42]; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.
While many studies have identified diet-associated epigenetic changes in animal models using candidate site-specific regions, there have been few genome-wide analyses undertaken. A recent study focussed on determining the direct epigenetic impact of high-fat diets/ diet-induced obesity in adult mice using genome-wide gene expression and DNA methylation analyses [43]. This study identified 232 differentially methylated regions (DMRs) in adipocytes from control and high-fat fed mice. Importantly, the corresponding human regions for the murine DMRs were also differentially methylated in adipose tissue from a population of obese and lean humans, thereby highlighting the remarkable evolutionary conservation of these regions. This result emphasizes the likely importance of the identified DMRs in regulating energy homeostasis in mammals.
(i) Genetic association studies. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46–48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation [49].
From these studies, altered methylation of PGC1A, HIF3A, ABCG1, and CPT1A and the previously described RXRA [18] have emerged as biomarkers associated with, or perhaps predictive of, metabolic health that are also plausible candidates for a role in development of metabolic disease.
Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20–40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 [8]. Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice [43] and weight loss in humans [64]. These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.
Prenatal environment: Two recently published studies made use of human populations that experienced “natural” variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants [69]. The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood [68]. The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.
Postnatal environment: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the “mature” epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells [77], and muscle tissue [78] in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver [79] and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat [64]. Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80–82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport [83]. Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss [84].
DNA methylation changes associated with obesity or induced by diet or lifestyle interventions and weight loss are generally modest (<15 %), although this varies depending on the phenotype and tissue studied. For instance, changes greater than 20 % have been reported in adipose tissue after weight loss [64] and associations between HIF3A methylation and BMI in adipose tissue were more pronounced than in blood [52].
Conclusions
The prevalence of obesity in the United States has been increasing for almost 50 years. Currently, more than two-thirds of adults and almost one-third of children and adolescents are 
From 2005 to 2014, there was a 1.4% annual increase in cancers related to overweight and obesity among individuals aged 20 to 49 years and a 0.4% increase in these cancers among individuals aged 50 to 64 years. For example, if cancer rates had stayed the same in 2014 as they were in 2005, there would have been 43 000 fewer cases of colorectal cancer but 33 000 more cases of other cancers related to overweight and obesity. Nearly half of all cancers in people younger than 65 years were associated with overweight and obesity. Overweight and obesity among younger people may exact a toll on individuals’ health earlier in their lifetimes.
The 
Implementation of clinical interventions, including screening, counseling, and referral, has major challenges. Since 2011, Medicare has covered behavioral counseling sessions for weight loss in primary care settings. However, the benefit has not been widely utilized.
Achieving sustainable weight loss requires comprehensive strategies that support patients’ efforts to make significant lifestyle changes. The availability of clinical and community programs and services to which to refer patients is critically important. Although such programs are available in some communities, there are gaps in availability. Furthermore, even when these programs are available, enhancing linkages between clinical and community care could improve patients’ access. Linking community obesity prevention, weight management, and physical activity programs with clinical services can connect people to valuable prevention and intervention resources in the communities where they live, work, and play. Such linkages can give individuals the encouragement they need for the lifestyle changes that maintain or improve their health.
The high prevalence of overweight and obesity in the United States will continue to contribute to increases in health consequences related to obesity, including cancer. Nonetheless, cancer is not inevitable; it is possible that many cancers related to overweight and obesity could be prevented, and physicians have an important responsibility in educating patients and supporting patients’ efforts to lead healthy lifestyles. It is important for all health care professionals to emphasize that along with quitting or avoiding tobacco, achieving and maintaining a healthy weight are also important for reducing the risk of cancer.
