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Stubborn Weight: Genetics or Diet?

Stubborn Weight: Genetics or Diet?

Today, there can be a lot of confusion when it comes to diet. The information received can be contradicting, confusing, and leave individuals feeling lost. This can often result in giving up on the diet and being left with joint pain, inflammation, discomfort, headaches and more.

The reason why there is more than one diet out there is because the research is always advancing. We have come to realize that everyone’s body reacts to different food sources and diets differently.

Genetic Code

As more and more research is being done, the more we are realizing how the genetic factor of individual cells directly correlate to a patient’s weight, diet, and changes as they age. For years, as one would get older and start gaining weight, we would attribute it to age. Although age is a factor, what we are finding now is that the genes are actually changing as we age and that is what creates this weight gain.

Sure enough, there are also genes that will tell us if you are susceptible to snacking. These genes can detect if you have a predisposition for heightened snacking or satiety. Satiety is the feeling of fullness after a meal. If you have reduced satiety, you tend to snack more because you do not feel as full after the meals you eat.

Getting your genes tested will allow the treatment plans created to be more personal and more geared to see results! Believe it or not, your genes can tell us if you are genetically prone to obesity,� if you have weight loss resistance when it comes to carbohydrates, and how your body responds to exercise! Using the genes, we can see how many hours per week you will need for weight loss or to maintain your current weight.

Proven Methods

The best option is to know your genes so the diet plan can be geared more towards you directly. However, if that is not a possibility right away, there has been one diet that has been proven time and time again to work for almost everyone. This diet is referred to as the Ketogenic Diet.

In simple terms, the ketogenic diet is a low carb, high-fat diet. This diet works by sending the body into a state of ketosis which burns fat as fuel.

Research shows that those using a ketogenic diet demonstrated a higher percentage of weight loss and kept the weight off longer when compared to those who did a low-fat diet.

Available Resources

Considering the fact that there is misinformation about diets out there, proper education is going to be the key. As someone who has gone through dietary changes myself and figuring out what works best with my body with type 1 diabetes for optimal health, the right team is what made me successful.

Surround yourself with those who are continuously educating themselves and have a system in place. For example, we make sure our patients get one on one time with the doctor and a health coach. From here, the health coach and patient become connected through a virtual database allowing the patient’s food, weight, supplements, hydration, BMI, BIA, and activity to be tracked by the health coach. The health coach can then instant message or video chat the patient throughout the week to ensure they are staying on track, staying motivated, and answer any questions they may have!

Do not be left confused over diets anymore! Remember that your genetic code holds the key to the right diet for you.

The right diet has the ability to make individuals see the results they have been waiting for. It all comes down to the genes. As mentioned, genes change over time but they hold the code. If you are someone who has struggled with diets, feeling good, or are stuck at a certain weight, I highly recommend getting tested! The information you gain from this is so beneficial! I have seen the results first hand, and they are eye-opening. They let you know if you have the genetics that will hold onto fat. This knowledge can help us prevent health issues such as metabolic syndrome! – Kenna Vaughn, Senior Health Coach�

Dr. Alex Jimenez�s Blog Post DisclaimerThe scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.


Bueno, Nassib Bezerra, et al. �Very-Low-Carbohydrate Ketogenic Diet v. Low-Fat Diet for Long-Term Weight Loss: a Meta-Analysis of Randomised Controlled Trials.� British Journal of Nutrition, vol. 110, no. 7, 2013, pp. 1178�1187., doi:10.1017/s0007114513000548.


Ketogenic Diet for Metabolic Syndrome

Ketogenic Diet for Metabolic Syndrome

The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.


What is the Ketogenic Diet?

As previously mentioned, the keto diet is a low-carb, high-fat diet similar to the Atkins diet, as well as other low-carbohydrate diets. The primary goal of the ketogenic diet is to considerably decrease the consumption of carbohydrates and replace them with “good” fats. Reducing carb intake will allow the body to enter a metabolic state, known as ketosis. During ketosis, the body becomes tremendously efficient at burning fat in order to turn it into energy for fuel. It will also produce ketones in the liver to be used as energy by the brain. The ketogenic diet can greatly improve high blood sugar levels and insulin resistance.


Metabolic syndrome is commonly characterized by 5 risk factors. People with 3 our of 5 risk factors may have metabolic syndrome, including:


  • Excess waist fat (> 40 inches in men, and > 35 inches in women)
  • High blood pressure (130/85 mm Hg)
  • Hight blood sugar or glucose levels (100 mg/dL or greater)
  • High triglyceride levels (150 mg/dL or greater)
  • Low HDL cholesterol (< 40 mg/dL in men or < 50 mg/dL in women)


Metabolic syndrome can increase the risk of a variety of health issues, including diabetes, stroke, and heart disease. Fortunately, the keto diet can help improve the risk factors associated with metabolic syndrome, such as increased HDL cholesterol as well as decreased blood pressure and blood sugar levels. In a controlled 12-week research study, people with metabolic syndrome following a calorie-restricted ketogenic diet lost 14 percent of their body fat. The research study also found that the participants had decreased triglycerides by more than 50 percent and experienced several other health benefits.


How the Keto Diet Helps Improve Metabolic Syndrome

The ketogenic diet has been demonstrated to help improve the risk factors associated with metabolic syndrome. As a low-carbohydrate, high- fat diet, the keto diet is effective in decreasing high blood sugar levels and improving insulin resistance by having the body break down body fat into ketones for energy. Metabolic syndrome is a cluster of signs that are associated with various health issues, including diabetes, stroke, and heart disease. The signs of metabolic syndrome include excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL or “good” cholesterol.


A research study conducted by researchers at Bethel University, Minnesota, USA, compared the health of three groups of adults with metabolic syndrome. The first group followed the ketogenic diet without exercise, the second group followed the standard American diet without exercise, and the third group followed the standard American diet with 30 minutes of exercise or physical activity for three to five days per week. The findings showed that the ketogenic diet without exercise was much more effective than the other groups at promoting weight loss, decreasing body fat and reducing HbA1c.


According to a variety of other research studies like the one above, the ketogenic diet may help improve a variety of other health issues, including:�


Type 2 Diabetes

Although there’s a variety of research studies on what is the best type of diet for people with type 2 diabetes to promote weight loss and improve insulin resistance, healthcare professionals recommend following the keto diet. The keto diet lowers carb intake which causes high blood glucose levels to drop, producing less insulin, burning fat, and potentially improving insulin sensitivity. Research studies suggest that the keto diet may be helpful for people with type 2 diabetes. Several hospitals have comprehensive programs dedicated to using the nutritional approach to help treat type 2 diabetes.



Excess weight and obesity increase the risk of developing type 2 diabetes. A small research study published in December 2016 in the journal Endocrine involved 45 obese participants either on a very-low-calorie ketogenic diet or a standard low-calorie diet. After two years, the participants following the keto diet lost approximately 27 pounds on average compared with less than 10 pounds in the low-calorie participants. The participants following the keto diet also lost more belly fat. The ketogenic diet also helped keep lean body mass during weight loss which prevented a metabolic slowdown.


Metabolic Syndrome


Metabolic syndrome is a collection of risk factors, including excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL cholesterol, according to the American Heart Association. Improving insulin resistance may also reduce the risk of developing metabolic syndrome. One small research study on 30 adults found that adults with metabolic syndrome who followed the ketogenic diet for 10 weeks lost more weight and body fat as well as lowered their A1C levels compared with participants who followed a standard American diet, even with or without exercise.


Dr. Alex Jimenez Insights Image

About 23 percent of adults in the United States have metabolic syndrome. Although the risk factors for developing the collection of signs are significant, there are good news. Many of the risk factors associated with metabolic syndrome can be addressed through diet and lifestyle modifications, such as the ketogenic diet as well as exercise and physical activity. By making these changes, people can considerably reduce their risks of developing a variety of other health issues, including diabetes, stroke, and heart disease. Although metabolic syndrome can be a serious health issue, people can reduce their risks by reducing their weight; increasing exercise and physical activity; eating a heart-healthy diet that’s rich in fruits, vegetables, whole grains, and fish; as well as working with a healthcare professional to regulate blood pressure, blood sugar, blood cholesterol. In the following article, we will discuss how the ketogenic diet can help improve metabolic syndrome and its risk factors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight


The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.


The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. 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



  1. Mawer, Rudy. �The Ketogenic Diet: A Detailed Beginner’s Guide to Keto.� Healthline, Healthline Media, 30 July 2018,
  2. Spritzler, Franziska. �15 Health Conditions That May Benefit From a Ketogenic Diet.� Healthline, Healthline , 12 Sept. 2016,
  3. Editor. �Ketogenic Diet Improves Metabolic Syndrome in Multiple Ways.� Diabetes, Diabetes Media, 18 Dec. 2017,
  4. Migala, Jessica. �Can Keto Cure You? 11 Conditions It May Help and 6 It Won’t: Everyday Health.� Everyday Health, Everyday Health Media, 28 Dec. 2018,


Dr. Alex Jimenez Podcast: Metabolic Syndrome


Metabolic syndrome is a cluster of risk factors that can ultimately increase the risk of developing a variety of health issues, including heart disease, stroke, and diabetes, among other problems. Central obesity, high blood pressure, high blood sugar, high triglycerides, and low HDL or good cholesterol levels are the 5 risk factors associated with metabolic syndrome. Having at least three of the five risk factors may suggest the presence of metabolic syndrome. Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas explain the 5 risk factors associated with metabolic syndrome, in further detail, as they recommend diet and lifestyle modification advice and guidelines, such as the ketogenic diet or the keto diet, as well as demonstrate the biochemical and chemical pathways that the body goes through during ketosis to help people with metabolic syndrome improve their overall health and wellness. From eating good fats and staying hydrated to exercise and better sleep, Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas discuss how diet and lifestyle modifications, such as the ketogenic diet or keto diet, can help improve the 5 risk factors associated with metabolic syndrome to prevent the risk of developing a variety of other health issues, including heart disease, stroke, and diabetes. – Podcast Insight



Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor


Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.


Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor


Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with a variety of food sensitivities and intolerances. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs.


Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Gut Zoomer | El Paso, TX Chiropractor


Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders.


Dunwoody Labs: Comprehensive Stool with Parasitology | El Paso, TX Chiropractor

GI-MAP: GI Microbial Assay Plus | El Paso, TX Chiropractor


Formulas for Methylation Support

Xymogen Formulas - El Paso, TX


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.

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For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download


* All of the above XYMOGEN policies remain strictly in force.





Modern Integrated Medicine

The National University of Health Sciences is an institution that offers a variety of rewarding professions to attendees. Students can practice their passion for helping other people achieve overall health and wellness through the institution’s mission. The National University of Health Sciences prepares students to become leaders in the forefront of modern integrated medicine, including chiropractic care. Students have an opportunity to gain unparalleled experience at the National University of Health Sciences to help restore the natural integrity of the patient and define the future of modern integrated medicine.



What Is Metabolic Syndrome?

What Is Metabolic Syndrome?

Metabolic syndrome is caused by having more than one condition. Metabolic syndrome often leaves individuals with headaches, joint pain, fatigue, and more! Metabolic syndrome is an epidemic all over the world, but in the US, we are seeing this condition all too often.


Metabolic Syndrome can be defined as having two or more of the conditions listed below:


  • Women with abdominal fat or a waistline greater than 35
  • Men with abdominal fat or a waistline greater than 40
  • Individuals with high blood pressure ( 130/85 or higher)
  • Patients with triglycerides higher than 150
  • A fasting glucose of 100 or greater
  • Low HDL ( good cholesterol ) less than 40 in men and 50 for women


These symptoms are often associated with inflammation. Many people believe inflammation is just something that occurs in the joints and on the skin, but inflammation can occur to the organs inside the body and create havoc.


Metabolic syndrome does not target a specific population but can affect anyone who has an overlap of the factors listed above. Those who have an “apple” or “pear” body shape, are likely to have higher abdominal fat, and therefore are more at risk.


apple and pear body shape


As individuals age, their chances of developing metabolic syndrome increases. On top of age, previously having or having a history of diabetes in one’s family also increases their risk of developing metabolic syndrome.


Speaking from personal experience, and having Type 1 Diabetes myself, I can say that metabolic syndrome really takes a toll on one’s body. With experiencing these symptoms first hand, it can leave your body feeling exhausted. When the blood glucose level in the body rises, it causes the blood to become thick due to the excess sugar in the blood. This then causes the heart to work harder and raise the body’s blood pressure due to the effort needed to pump. From here, the body responds with a hard and heavy headache, nausea, occasional vomiting, increased thirst, increased urination, and blurred vision. Recovering from a day of high blood sugars can leave you feeling defeated and similar to feeling like you are recovering from the flu.


One of the things that occur within the body when an individual has metabolic syndrome is their insulin sensitivity decreases. Insulin is the hormone produced that helps to turn the food you eat into fuel for the body or store it as fat. When the insulin sensitivity becomes decreased, it means not enough glucose in the body is being absorbed.� Leading to high blood glucose levels and increases the risk for Type 2 Diabetes.


For those who are suffering from metabolic syndrome, or have one or more of the above risk factors there are ways to take charge. The benefits of taking charge and preventing metabolic syndrome from getting worse or returning means getting back the energy you thought was lost. By decreasing your symptoms and increasing your energy, you could be feeling better than you remembered.


The best diet to quickly gain control of blood sugars and raise HDL is the ketogenic diet. This diet works by eating low carb, high-fat foods. In turn, this makes the body burn fat as fuel rather than carbohydrates. It starts by burning the fat around the pancreas and liver and then starts to burn the intramuscular fat ( excess abdominal weight ). By eliminating most carbs and increasing water intake, individuals can see a decrease in depression, brain fog, their risk of stroke, and blood pressure. All while seeing an increase in sleep and energy.


One of the best ways to reach your goals and stay healthy is to work with a team who understands them and is willing to educate you. We provide 1:1 coaching, scales to track weight that also reports the water weight and BMI of the individual, wrist bands to track caloric activity, and education. The education will help you understand why you are following a specific diet or food guidelines, how that food is breaking down to help you, and what foods to avoid. We will never leave a patient confused or with unanswered questions.


Speaking from personal experience, it is best to get a handle on these symptoms before they cause permanent damage. There are ways and things to do to help reduce your risk. I highly recommend seeing us, or a local doctor to start to build your plan. We can create personalized plans that will help you reach your goals, lower your risk, and work with your lifestyle. Take it from me, you do not want to be stuck feeling the side effects metabolic syndrome comes with.� -Kenna Vaughn, Senior Health Coach


The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.


Mayo Clinic Staff. �Metabolic Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 14 Mar. 2019,
Sherling, Dawn Harris, et al. �Metabolic Syndrome.� Journal of Cardiovascular Pharmacology and Therapeutics, vol. 22, no. 4, 2017, pp. 365�367., doi:10.1177/1074248416686187.

Ketogenic Diet and Intermittent Fasting

Ketogenic Diet and Intermittent Fasting

Why is it that the ketogenic diet and intermittent fasting always seem to fall within the same topic of conversation? This is simply because intermittent fasting may be utilized as an instrument to achieve ketosis, the metabolic state associated with the keto diet. During intermittent fasting, the human body is depleted of glycogen stores. Once these glycogen stores are eliminated, fat stores are then released into the bloodstream in order to be converted into energy molecules, known as ketones, from the liver.

What is Ketosis?

Ketosis is a metabolic state which uses ketone bodies, or ketones, as fuel for energy. On a normal carbohydrate-based diet, the human body burns glucose as its main fuel source, where excess glucose is subsequently stored as glycogen. If the human body cannot utilize sugar as fuel for energy, it will utilize glycogen as fuel for energy. Once glycogen is depleted, you begin to burn fat. The ketogenic diet generates a metabolic state which enables you to break down fat into ketones, or ketone bodies, in the liver for energy.

There are 3 major types ketone bodies found in the blood, urine, and breath, including:

  • Acetoacetate: The type of ketone which is created first. It may be converted to beta-hydroxybutyrate or flipped into acetone.
  • Acetone: Made spontaneously in the breakdown of acetoacetate. It is a very volatile ketone and it is frequently detectable on the breath once an individual first enters ketosis.
  • Beta-hydroxybutyrate (BHB): The type of ketone which is utilized for energy and is most abundant on the bloodstream as soon as you’re completely into ketosis. It is the kind that is located in exogenous ketones and what blood tests quantify.

Intermittent Fasting in the Keto Diet

Intermittent fasting is composed of eating within a specific feeding window rather than eating throughout the day. Each individual, whether they are conscious of it or not, fasts intermittently from dinner to breakfast. There are lots of methods to intermittent fasting. A few individuals fast for 16-20 hours intervals on alternate days while others follow a 24-hour day fast. The most common intermittent fasting variety is the 16/8 method, in which you eat in an 8-hour window followed by a 16-hour fasting window.

Other fasting programs incorporate the 20/4 or even 14/10 methods. Other people follow 24-hour fasts one or two times each week. Intermittent fasting can get you in ketosis quicker because your cells will immediately absorb your glycogen stores and begin burning fat. However, what about once you get into ketosis? Is intermittent fasting worth following consistently? Following the ketogenic diet and intermittent fasting can be a great addition towards an individual’s overall health and wellness, providing various health benefits.

The keto diet and intermittent fasting can provide the following health benefits, including:

  • Healthy weight-loss
  • Fat reduction, not muscle reduction
  • Balancing cholesterol levels
  • Enhancing insulin sensitivity
  • Maintaining blood glucose levels steady

Health Benefits of the Ketogenic Diet

The ketogenic diet dramatically reduces your caloric intake, forcing your body to burn fat instead of sugar, which makes it a powerful tool for weight reduction. While individual results vary, the keto diet has always resulted in a decrease in body fat in a selection of situations. Within a 2017 study, subjects who followed a very low carbohydrate keto meal program significantly decreased body fat percentage and body fat mass, losing an average of 7.6 lbs and 2.6 percent body fat while preserving lean muscle mass.

Likewise, a 2004 research detecting the long-term consequences of a ketogenic diet in overweight patients discovered that the weight and body mass of those patients diminished dramatically over the span of two decades. Individuals who radically reduced their carb intake saw a substantial decline in LDL (bad) cholesterol, triglycerides, and enhanced insulin sensitivity. In 2012, researchers compared a ketogenic diet to eating fewer calories for overweight kids and adults. The results showed kids after the keto diet lost significantly more body fat. They also revealed a dramatic decline in insulin levels, a biomarker of Type 2 diabetes.

Health Benefits of Intermittent Fasting

Studies have shown that intermittent fasting may be an effective weight loss tool, more powerful than just cutting calories. In one analysis, intermittent fasting has been proven to be as successful as constant calorie restriction in combating obesity. In studies done by the NIH, there was reported weight reduction with over 84 percent of participants, regardless of which fasting program they picked.

Much like ketosis, intermittent fasting increases fat loss while preserving lean muscle mass. In one study, researchers reasoned that fasting led to greater weight loss compared to a low-carb diet, though the overall caloric consumption was exactly the same. If you are attempting to lose weight, then a keto diet or intermittent fasting can be a massive help. But that is not where the rewards stop.

Intermittent Fasting and the Keto Diet for Mental Health

Both intermittent fasting and the ketogenic diet can provide various mental health advantages. Both have been clinically shown to boost memory, improve mental clarity and focus, as well as prevent the development of neurological disorders like Alzheimer’s and epilepsy. On a carb-based diet, changes in glucose can cause changes in energy levels. During ketosis, your brain employs a more consistent supply of fuel: ketones from the fat stores, leading to better productivity and psychological performance.

Whenever you’ve got a consistent and clean energy source from ketones, the brain works better. In addition to this, ketones are better at protecting your brain. Studies reveal that ketone bodies might have antioxidant properties which protect your brain cells from free radicals and oxidative stress. In one study conducted on adults with diminished memory, the growth of BHB ketones in their own blood helped enhance cognition. Also, when you’ve got difficulty staying focused, your hormones can be to blame.

Your brain has two chief neurotransmitters: glutamate and GABA. Glutamate will help you form new memories, and get your brain cells to communicate with one another. GABA is what helps restrain glutamate. If there is too much glutamate, it can cause brain cells to quit working and finally perish. GABA is there to control and slow down glutamate. If GABA levels are reduced, glutamate reigns free and you experience mental fog. Ketones stop damage to cells by processing surplus glutamate into GABA. Considering that ketones raise GABA and lessen glutamate, they assist in preventing cell damage, preventing cell death and enhancing mental focus.

Researchers believe that intermittent fasting enhances memory, decreases oxidative stress, and conserves learning abilities. Since your cells are under moderate strain whilst fasting, the top cells adapt to the stress by improving their particular ability to deal with these circumstances while the weakest tissues die. This is much like the strain that your body gets when you reach the gym.

Exercise is a kind of stress that your body adjusts to improve and get more powerful. This also applies for intermittent fasting: so long as you are still alternate between routine eating habits and fasting, it is going to continue to benefit you. Implying equally that ketosis and intermittent fasting will help improve your cognitive functioning because of the synergistic and protective effects of ketones.

Dr Jimenez White Coat
The ketogenic diet and intermittent fasting are two different nutritional strategies which provide many common health benefits. According to various research studies, both the keto diet and intermittent fasting can help boost ketones, helping the body burn fat more efficiently than any other nutritional strategy. And when these are utilized together, they definitely form a powerful dietary program. The article above discusses the differences between the ketogenic diet and intermittent fasting as well as demonstrates the health benefits of both of these dietary programs and how they can help improve overall health and wellness. Dr. Alex Jimenez D.C., C.C.S.T. Insight

The Perks of Intermittent Fasting and the Keto Diet

The ketogenic diet and intermittent fasting possess similar health benefits because both approaches involve ketosis. Ketosis has lots of physical and mental advantages, from weight loss to enhanced brain function. People following a ketogenic diet may use intermittent fasting as a tool to achieve ketosis and enhance their general well-being. 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

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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. �

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EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


Keto Diet Health Benefits

Keto Diet Health Benefits

If you are currently thinking about the ketogenic diet, then you might be asking yourself, is the keto diet right for you? While you may have already heard about the benefits of the ketogenic diet, you might still be wondering about whether if it is worth it to completely change your diet to take advantage of these benefits.

The keto diet has many benefits, from weight loss and improved physical health to mental clarity and enhanced physical performance. In the following article, we will dive into the details of some of the ketogenic diet health benefits. These benefits can help with the particular health goal you may be attempting to attain.

Ketogenic Diet and Weight Loss

In comparison to low-fat dieting, a low-carb diet can deliver superior results within a shorter time period in terms of weight loss, and the management of cholesterol, and blood pressure. If you want to shed weight, the ketogenic diet plan provides the following benefits and will get you closer to attaining your objective. There can be many reasons for this, including:

  • Low-carb and ketogenic diets are more satisfying with their low carb content and higher quantities of fats and protein.
  • Going onto a low-carb diet usually makes you lose extra water weight.
  • Most individuals can undergo weight loss fairly quickly, especially within the first week�of beginning a ketogenic diet.

Increased HDL Cholesterol

Together with the high consumption of saturated fats and other healthy fats, the ketogenic diet may help raise HDL cholesterol and enhance triglycerides levels. Both of these are�considerably significant towards promoting heart health.

Ketogenic Diet and Physical Health


Following the ketogenic diet has been demonstrated to also be able to help reduce inflammation and lesions of the skin like those found in acne. This is believed to occur due to the effects of ketosis, or the state in which the cells use ketones instead of glucose for energy.

IBS Support

Moreover, several research studies have also associated a link between the reduced consumption of glucose, or sugar, and an improvement in symptoms of irritable bowel syndrome, or IBS. As a matter of fact, one research study demonstrated that following a ketogenic diet may improve bowel movement habits and help reduce abdominal pain, improving quality of life in people with IBS.

Ketogenic Diet and Physical Performance

Balanced Energy Levels

Do not be surprised if you’re ready to stop drinking coffee every day after adapting to the keto diet. Achieving and maintaining ketosis involves benefits like no day slumps, no mood swings, and reducing changes in energy levels that you might experience otherwise.

In addition, you’ll likely find it much easier to remain longer periods of time without feeling hungry. This is what ultimately helps with weight loss, steady blood sugar levels, and extended periods of fasting, which is one of the best ways to get into ketosis.

Enhanced Workouts

Adjusting to the ketogenic diet may take time, however, once your body gets used to burning fat for fuel rather than sugar, or glucose, from carbohydrates, you will likely notice a difference in your physical performance and endurance, such as more energy and focus for workouts. This makes sense because being in ketosis “instructs” the entire human body to burn fat for fuel more efficiently.

The most important first step in case you start the ketogenic diet and notice limitations in your physical performance is to give your body some time to adapt from utilizing carbohydrates as its primary fuel to utilizing ketones as a source of energy. For individuals who participate in a lot of physical activities and exercise as well as athletes may benefit from a cyclical or targeted ketogenic diet.

Fat Loss / Muscle Gain

The amount of protein intake on a ketogenic diet makes it excellent for building muscle mass. Results might seem to come more gradually than for someone fueling their workouts but that is usually because you’re building lean mass together with fat reduction. By way of instance, when documenting a keto fast for four days, the individual gained 2.4 lbs of muscle with 1.1 lbs of fat reduction.

Ketogenic Diet and Mental Clarity

Several research�studies have demonstrated that a ketogenic diet may have the ability to support mental clariy as well as help boost productivity, support better memory, and also, have positive effects in regard to moderate cognitive impairment.

Neurological Support

Early usage of the ketogenic diet has been used as a treatment for reducing seizures in people with epilepsy, especially children. Additionally, it has been shown to benefit people with Parkinson’s disease, Alzheimer’s disease, and other neurodegenerative disorders. This is likely because ketone bodies created through the keto diet can have neuroprotective effects.

Dr Jimenez White Coat
Weight loss is one of the most well-known advantages of the ketogenic diet, however, this nutritional plan can have many other health benefits. By reducing the consumption of carbohydrates, the cells will go into a state of ketosis and instead utilize ketones created from fats, providing a steadier supply of energy than that of glucose, or sugar. Furthermore, research studies have also demonstrated the ketogenic diet’s possible role in disease prevention, such as for people with epilepsy. Dr. Alex Jimenez D.C., C.C.S.T. Insight

The benefits of the ketogenic diet are essential, not just for weight loss, but for overall health and wellness. When you are eating more fats and proteins with fewer carbohydrates, you are more likely to end up eating fewer calories. With this, you also don’t experience a change of energy levels but instead maintain a level of energy that lets you remain focused on your everyday tasks.

Regardless of the health goal you have in mind, the ketogenic, or keto, offers many benefits to improve your quality of life. Being aware of the proper foods you should eat on the keto diet is also important. 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

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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. �

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EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


Essential Fats on the Ketogenic Diet

Essential Fats on the Ketogenic Diet

Have you started following the ketogenic diet? Are you confused with what type of fats you should eat to achieve and maintain ketosis? In the following article, we will list the different types of essential fats which are vital in the ketogenic diet.

Fats are crucial in the ketogenic diet. To promote the breaking down of fat rather than protein or carbohydrates, you need to consume fat, a process known as ketosis. However, the value of the healthy fats you eat is fundamental.�Fat is satiating and it tastes good. Simply, be sure to eat the ideal kind of fat. There are four categories of fat permitted on the ketogenic, or keto, diet:

  • Polyunsaturated fats
  • Monounsaturated fats (MUFAs)
  • Polyunsaturated fats (PUFAs), which comprises omega 3
  • Only naturally-occurring trans fats

Remember that a balance of omega-3s and omega-6s can help maintain overall health and wellness, improving brain and nerve function and decreasing the risk of cardiovascular disease, Alzheimer’s disease,�and type-2 diabetes. While omega-6 is vital, however, too much of it can cause inflammation in the human body, therefore, avoid eating high amounts of omega-6 from sources like peanuts and vegetable oils, such as corn oil or sunflower oil.

Instead, focus largely on the intake of omega-3s from fish sources like trout, salmon, tuna, and mackerel or take a high-quality fish oil supplement. Additionally, be cautious of seeds and nuts since they do include some carbohydrates, particularly pistachios and almonds. Make certain that the fat you eat�is currently coming out of nutrient-dense foods, such as fatty cuts of meat. Below is a food listing of the major types of fat in the ketogenic diet.

Dr Jimenez White Coat
Fats are the basis of the ketogenic diet. The high fat intake and the low fat intake helps achieve and maintain ketosis, or the creation of ketones. Utilizing ketones for fuel, the human body can burn fat instead of sugar or glucose from carbohydrates. Getting and keeping your body in the state of ketosis can provide many health benefits, including weight loss and overall health and wellness. The quality of fats you consume while on the keto diet is essential towards reaching ketosis. The following article discusses the different types of fats you can eat while on the ketogenic diet and which ones you should avoid. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Fats and Oils in the Ketogenic Diet

The value of your dietary fat on keto creates a massive difference in the results that you’ll see. If you are taking an unhealthy approach for your new low-carb diet program, then you will quickly discover reverse health consequences. That is why it’s vital to understand which sources of fat are actually considered safe and healthy to consume on while on the ketogenic diet.

The very first sort of healthy fat to begin including on your keto diet plan is saturated fat. Saturated fat was analyzed and proven to enhance HDL and LDL cholesterol levels, both good and bad cholesterol markers, and it may also strengthen bone density and improve the function of your immune system as well as promote the production of important hormones in the human body.

Saturated fats include:

  • Grass-fed and organic red meats
  • High fat dairy like ghee, grass-fed butter, and heavy cream
  • Lard, tallow, and eggs

These are animal-based saturated fats but there are also plant-based selections like olive oil and MCT oil that could provide you with the wholesome dose of saturated fats that you need to maintain your�well-being. Branching out of healthy unsaturated fats, both monounsaturated fatty acids and polyunsaturated fatty acids can help you accomplish your ketosis objectives. Take a look at the graph below to get a visual of these wholesome oils and fats to focus on if following a ketogenic diet.

Monounsaturated fats include:

  • Virgin olive oil, avocado oil, and macadamia nut oil (eating avocados and olives also helps you reap these healthy fats)
  • Certain nuts and seeds

Polyunsaturated fats include:

  • Nuts and seeds such as walnuts, flaxseeds, chia seeds, sunflower, and pumpkin seeds
  • Flaxseed oil, sesame oil, fish oil, avocado oil, and krill oil
  • Fatty fish like trout, mackerel, salmon, and tuna

Fats and Oils to Avoid in the Keto Diet

You will also have to learn that some dietary fats should be avoided altogether. Simply because you are after a high-fat ketogenic diet does not mean that you ought to indulge in each fat you encounter. All fats aren’t created equal. Stay away from unhealthy fats like:

Hydrogenated and partially hydrogenated oils. These fats can be present in packaged foods. They may also increase your risk of developing higher cholesterol, cancer, obesity, and heart disease along with inflammation. If you are relying on packaged foods to get you through the ketogenic diet, check the tag and ditch any foods with them.

Highly processed vegetable oils. Peanut oil, corn oil, canola oil, soybean oil, sunflower oil, and grapeseed oil are fats which seem healthier than they are. These fats are generally created with genetically modified seeds which are possible allergens. Extreme heat can also make these oils go rancid. Additionally, they may leave fatty deposits on your body that may result in heart attacks and premature death. Finally, these oils contain higher levels of omega 6 fatty acids which can lead to chronic inflammation.

Nuts and Seeds in the Ketogenic Diet

Another simple and gratifying way to sneak healthy fats into the ketogenic diet would be to reach for uncooked seeds and nuts. These nutrient powerhouses are packed with essential nutrients, such as magnesium, selenium, and manganese. Seeds and nuts may enhance brain health, fortify your immune system, and assist with digestion and blood sugar control.

They are also high in healthy fats, have a moderate quantity of protein, and are usually low carb, based on the kind you select. Nuts and seeds are also simple to�carry, which makes them among the best snacks when on a keto diet. Some nuts and seeds, however, are better than others. In keto, this implies that they have more fat and less carbohydrates.

The five best nuts in the ketogenic diet include:

  • Macadamia nuts
  • Pecans
  • Brazil nuts
  • Walnuts
  • Hazelnuts

Pine nuts, almonds, cashews, and pistachios are also great nuts to include into the ketogenic diet. However, because they have more carbohydrates compared to the top five, they need to be consumed in moderation so that you don’t accidentally tip on your carbohydrate count daily. Consuming one or more one of these nuts as nut butter is a handy way to receive a spoonful of nourishment during snack time. However, you are going to want to practice portion control too since the serving size is really small.

The following best seeds in the ketogenic diet include:�

  • Pumpkin seeds
  • Sesame seeds
  • Sunflower seeds and sunflower seed butter
  • Tahini (sesame seed paste)
  • Chia seeds
  • Flaxseeds

Nuts and Seeds to Avoid in the Keto Diet

Are you wondering why peanuts and peanut butter is not part of the list of ketogenic diet foods? The majority of us have grown up eating and snacking on peanut butter. But a lot of us don’t recognize that peanut butter isn’t really made out of nuts; peanuts are a legume, which is part of the exact same family as peas, soybeans, and lentils. While the macro dysfunction and low-fat level of a serving of peanuts might be like other nuts, that is where their healthy comparison stops.

Peanuts and peanut butter are:

  • Packed with unnecessary added sugars
  • Loaded with hydrogenated oils (essentially harmful trans fats)
  • Low in fat and filled with junk as a replacement
  • Hard to digest
  • Covered in pesticides
  • High in oxalates (which prevent proper nutrient absorption and can lead to kidney stones)
  • High in inflammatory omega-6 fatty acids

Dairy in the Ketogenic Diet

Most dairy products fit into the “fat” and “protein” category but they are accepted as part of the ketogenic diet as long as you’re not lactose intolerant. Simply make sure you eat the full-fat version and preferably choose organic and raw options, if possible. Dairy is not an extremely important element of a keto�diet. If you are lactose intolerant, you may safely omit it.

For people with dairy sensitivities:

  • Find hard and long-aged dairy
  • Use ghee, a butter alternative without the irritating milk solids
  • Get checked for a casein sensitivity to rule out the other common irritant found in dairy

Other dairy choices can include:

  • Unflavored greek yogurt, fermented yogurt, and kefir
  • Hard cheeses like blue cheese, gouda, and parmesan
  • Semi-hard cheese such as Colby, provolone, and swiss cheese
  • Softer cheeses like mozzarella, brie, muenster, and Monterey Jack
  • Cream cheese, mascarpone, creme fraiche, and cottage cheese, which are also okay on a high-fat diet

Dairy to Avoid in the Keto Diet

Very similar to healthy versus unhealthy fats, these dairy things are packed using the wrong ingredients and aren’t good if you are trying to achieve and maintain ketosis. To reach ketosis, avoid these 3 dairy products on the ketogenic diet.

Low fat, reduced fat, and fat-free milk. When fat is removed from dairy, sugar is added to fill in the gaps and make these taste much better. The sugar in these products will prevent you from going into ketosis. Whole milk is not much better, however, with 12.8 grams of carbohydrates per glass, you’re much better off enjoying low carb cheese over a glass of milk.

Half and half. Do not go with this particular half milk/half cream mix either. You are still getting a dose of sugar and less fat, two of which is not ideal for a keto diet. Reach for heavy whipping cream and you won’t hav carbohydrates or sugar to contend with.

Evaporated and condensed milk. Before incorporating these canned milk choices for your next recipe, you need to know these are essentially a cooked down variation of milk syrup and sugar in disguise. Luckily, it is simple to substitute this cooking staple with unsweetened, full-fat, canned coconut milk. Plus, as it is made from coconuts, you also receive healthy saturated fats.

Fats are ultimately essential in the ketogenic diet. Recognizing the different types of fats you can eat while on the keto diet is important in order to help you achieve and maintain ketosis. 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

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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. �

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EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


What Fats To Eat On The Ketogenic Diet

What Fats To Eat On The Ketogenic Diet

Fats are an essential�part of the ketogenic diet since they constitute approximately 70 percent of your dietary calories. However, the type of fat you eat on the ketogenic diet is also important and there may be some confusion regarding good fats and bad fats. The following article discusses exactly what fats you need to include and what fats you must avoid while on the keto diet.

Good Fats on the Ketogenic Diet

The type of “good” fats included while on the ketogenic diet are divided into four groups: saturated fats, monounsaturated fats (MUFAs), polyunsaturated fats (PUFAs), and naturally-occurring trans fats. All fats can be classified into more than one group, however, we classify them according to the most dominant of these mixtures. It’s essential to be able to recognize what type of fat you are eating on the ketogenic diet. Below, we will describe each group of good fat so you can properly implement them into your own food choices.

Saturated Fats

For many years, saturated fats were considered to be detrimental for heart health and we were advised to�limit their�consumption as much as possible. However, recent research studies have demonstrated no substantial connection between saturated fats and the increased risk of cardiovascular disease. As a matter of fact, including healthy saturated fats into your diet can have many benefits.

One type of saturated fat contains medium-chain triglycerides (MCTs), which can be largely found in coconut oil, or in small quantities in butter and palm oil, and it may be digested quite easily by the human body. Medium-chain triglycerides pass through the liver for immediate use as energy when consumed. MCTs are beneficial towards promoting weight loss and improving athletic performance.

Health benefits of saturated fats on the keto diet can include:

  • Improved HDL and LDL cholesterol levels
  • Maintenance of bone density
  • Boosting of immune system health
  • Support in creation of important hormones like cortisol and testosterone
  • Raising of HDL (good) cholesterol in the blood to prevent buildup of LDL in the arteries
  • Improved HDL to LDL ratio

Recommended types of saturated fats while on the ketogenic diet include:

  • Butter
  • Red meat
  • Cream
  • Lard
  • Coconut oil
  • Eggs
  • Palm oil
  • Cocoa butter

Monounsaturated Fats

Unlike saturated fats, monounsaturated fats, also referred to as monounsaturated fatty acids or MUFAs,�have been approved as a healthy source of fat for several years. A variety of research studies have connected them to numerous health benefits associated with improved levels of “good” cholesterol and better insulin resistance, among other health benefits, as described below.

Health benefits of MUFAs on the keto diet can include:

  • Increased HDL cholesterol
  • Lowered blood pressure
  • Lowered risk for heart disease
  • Reduced belly fat
  • Reduced insulin resistance

Recommended types of MUFAs while on the ketogenic diet include:

  • Extra virgin olive oil
  • Avocados and avocado oil
  • Macadamia nut oil
  • Goose fat
  • Lard and bacon fat

Healthy Polyunsaturated Fats

The most important point to keep in mind about eating polyunsaturated fats, also referred to as polyunsaturated fatty acids or PUFAs, on the ketogenic diet is that the specific type you consume actually matters. When heated, some polyunsaturated fats may produce substances that can cause inflammation in the human body, increasing the risk of cardiovascular disease and even cancer.

Many PUFAs must be consumed cold and they should never be utilized for cooking. PUFAs can be found both in very processed oils and in very healthy sources. The right types can additionally provide many health benefits on the ketogenic diet, particularly because several of these include omega 3s and omega 6s, both of which are essential nutrients in a healthy and balanced diet.

Health benefits of PUFAs on the keto diet can include:

  • Reduced risk of heart disease
  • Reduced risk of stroke
  • Lowered risk of autoimmune disorders and other inflammatory diseases
  • Improved symptoms of depression
  • Improved symptoms of ADHD

Recommended types of PUFAs while on the ketogenic diet include:

  • Extra virgin olive oil
  • Flaxseeds and flaxseed oil
  • Walnuts
  • Fatty fish and fish oil
  • Sesame oil
  • Chia seeds
  • Nut oils
  • Avocado oil

Naturally-Occurring Trans Fats

Many people might be confused to see trans fats classified as “good” fats. While most trans fats are considered to be extremely unhealthy and even harmful, one type of trans fat, known as vaccenic acid, can be found naturally in various kinds of food, such as in grass-fed animal products and dairy fats. These naturally-occurring trans fats also provide several health benefits on the keto diet.

Health benefits of naturally-occurring trans fats on the keto diet include:

  • Reduced risk of heart disease
  • Reduced risk of diabetes and obesity
  • Possible protection against cancer risk

Recommended types of naturally-occurring trans fats while on the ketogenic diet include:

  • Grass-fed animal products
  • Dairy fats like butter and yogurt
Dr Jimenez White Coat
When following a ketogenic diet, or any other low carb diet, eating the right type of fat is essential, especially since these make up about 70 percent of your daily caloric intake. The type of fat you eat is classified into various groups depending on the dominant amount found in the mixture. Extra Virgin Olive Oil, for example, is approximately 73 percent monounsaturated fat, therefore, it is considered a monounsaturated fat. Butter is about 65 percent saturated fat and thus, is a saturated fat.�It’s essential to be able to recognize what type of fat you are eating on the ketogenic diet in order to enjoy its health benefits. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Bad Fats on the Ketogenic Diet

One of the greatest advantages of the ketogenic diet is the capacity to eat lots of satisfying dietary fats such as those mentioned previously. However, we have to also cover the kinds of fats that you should reduce or eliminate from your diet in order to prevent damaging your�well-being. On the keto diet, the quality of food you eat is especially important to achieve ketosis.

Unhealthy Polyunsaturated Fats and Processed Trans Fats

Processed trans fats are the group of fat which most people as the “bad” fats and the truth is, they can actually be quite damaging to your overall health and wellness.� Artificial trans fats are made during food production via the processing of polyunsaturated fats. That is the reason why it’s very important to choose PUFAs which are unprocessed and not overheated or modified. The consumption of unhealthy PUFAs can create harmful free radicals where processed trans fats often contain genetically modified seeds.

Health risks of unhealthy polyunsaturated fats and processed trans fats include:

  • Increased risk of heart disease
  • Increased risk of cancer
  • Reduced HDL cholesterol and increased LDL cholesterol
  • Pro-inflammatory
  • Bad for the health of your gut

Examples of unhealthy polyunsaturated fats and processed trans fats to avoid include:

  • Hydrogenated and partially hydrogenated oils found in processed products like cookies, crackers, margarine, and fast food
  • Processed vegetable oils like cottonseed, sunflower, safflower, soybean, and canola oils

In conclusion, it’s essential to recognize what type of fat you are eating while on the ketogenic diet. In the end, the function of the ketogenic diet will always be to enhance your health, which includes eating the appropriate amount of fat, protein, and carbohydrate ratio as well as picking food resources which promote health and wellness. 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

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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. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


What Are Exogenous Ketones?

What Are Exogenous Ketones?

Ketones serve as a source of energy for the mitochondria found inside the cells of the human body. These are an alternative fuel to sugar. Ketones are basic substances with a simple molecular structure. Ketones are natural,�or carbon-based, chemicals made up of a central carbon atom double-bonded into an oxygen atom and two carbon-containing substituents, denoted by”R”.

Genetic Ketone Structure

In humans, there are 3 distinct ketones created by the mitochondria. These are referred to as ketone bodies. The 3 ketones are:

  1. Acetone
  2. Acetoacetate, also known as Acetoacetic Acid
  3. Beta-Hydroxybutyric Acid, also known as Beta Hydroxybutyrate or BHB. Additional compound names include 3-hydroxybutyric acid or 3-hydroxybutyrate.

BHB isn’t particularly considered a ketone because it comprises a reactive OH-group rather than a double-bonded oxygen which would generally function as demonstrated in the diagram below. However, BHB continues to function much like a ketone because it transforms into energy, such as acetone and acetoacetate. The following is demonstrated in the diagram below.

Structures of Ketone Bodies

Ketogenesis is the metabolism of fatty acids through ?-oxidation. This procedure provides acetyl CoA which converts to ?-hydroxy-?-methyglutaryl-CoA, or HMG-CoA, as shown below. HMG-CoA turns into Acetoacetone which may change back-and-forth to BHB. The conversion of Acetoacetate into Acetone is irreversible (as seen on the bottom left). Acetoacetate and BHB, through acetoacetate, are utilized to make energy when converted into acetyl-CoA in the cell’s mitochondria whilst Acetone is excreted in the breath and urine.

Formation of Ketone Bodies from Acetyl-CoA2

Understanding Exogenous Ketone Bodies

Exogenous ketone bodies are simply ketone bodies which are consumed via a nutritional supplement. Ketone bodies created in the liver are more correctly referred to as endogenous ketone bodies. The following is described below.

Most nutritional supplements depend�on BHB as the origin of the exogenous ketone bodies. BHB transforms into acetoacetic acid where a small amount is turned into acetone via an acetoacetate decarboxylase waste pathway. A percentage of that acetoacetic acid may enter the energy pathway utilizing beta-ketothialase, which transforms acetoacetic acid into 2 Acetyl-CoA molecules.

Ketosis Pathway Before Entering the Krebs (Energy) Pathway

The Acetyl-CoA will then enter the Krebs cycle and creates ATP. Exogenous ketone body nutritional supplements provide an instantaneous supply of ketones to consumers. Even when you’re not in the state of ketosis before eating, such as when ingesting a higher-carb diet. These also increase blood ketones even in the presence of insulin, which inhibits ketogenesis.

Researchers do not completely comprehend what the long-term ramifications of combining a non-ketogenic diet with exogenous ketone bodies nutritional supplements really are. Research studies are at their first phases and much more information is required. A standard issue involves why BHB is the ketone body to receive exogenous ketone nutritional supplements. The explanation is a mixture in the simplicity of its formula and its conversion to energy. it is simpler to devise BHB into a nutritional supplement.

Are “Raspberry Ketones” Similar to “Ketone Bodies”?

Raspberry ketones are a�common ingredient used in weight-loss nutritional supplements. However, despite their title, they don’t have any connection. This has generated some confusion for individuals considering ketone nutritional supplements that are exogenous.

Raspberry ketones are in reality phenolic compounds that provide raspberries their pleasant odor. They are similar to the stimulant synephrine. Regardless of the research studies, raspberry ketones don’t seem to have much impact on weight loss.

Ketone Salts vs. Ketone Esters

Exogenous ketones of all beta-hydroxybutyrate can be found in two kinds:

  1. Ketone Salts are naturally-derived chemicals which blend sodium as well as potassium and/or calcium with BHB to boost absorption. Commercially available nutritional supplements are all created from ketone salts now (contains KetoForce, KetoCaNa and Keto OS). These are also occasionally called “Ketone Mineral Salts” or “BHB Mineral Salts”.
  2. Ketone Esters are Synthetically-made chemicals that connect an alcohol to a ketone body, where this can be metabolized in the liver as a ketone. Ketone esters are used primarily in search for testing their effectiveness on improving ketone body levels. Below is a standard arrangement of a BHB ester. The very first Ketone Ester beverage is currently accessible by HVMN. Research esters are very unpleasant tasting, something which HVMN expects to modify soon.
Structure of a Beta-Hydroxybutyrate Ester

Ketone Esters increase blood levels of beta-hydroxybutyrate to greater levels compared to Ketone Salts. There’s strong evidence supporting that esters are more powerful than Ketone Salts, so much as their advantages proceed. It’s not apparent why this occurs, but it might be from the gastrointestinal, or GI, tract due to a gap in the absorption rate.

However, esters are normally somewhat tougher to endure because of gut distress after intake and they do not have the most agreeable taste, as stated previously in the article. Figure 1 below demonstrates the difference between eating equivalent quantities of BHB in the kind of a Ketone ester and Ketone salts on bloo BHB. The supplements contained are:

  • BMS (Beta-hydroxybutyrate Mineral Salt) — sodium/ potassium established (KetoForce)
  • KE (Ketone Ester) — (R- 3-hydroxybutyl-R-1,3-hydroxybutyrate) (HVMN)
Figure 1: Blood BHB level after consuming a ketone ester vs a ketone salt drink.

What are the Benefits of Exogenous Ketones?

Exogenous ketone nutritional supplements can offer a great number of benefits. These include more effective weight reduction, athletic performance improvement, cancer prevention, cognitive advancement,�and anti-inflammatory properties.

Weight Loss Goals

  • Appetite suppression: Appetite was quantified in 10 males and 5 females after taking a ketone ester, abbreviated as KE, or a dextrose, abbreviated as DEXT, beverage. The wish to consume and perception of appetite dropped after both supplements, however, the KE was 50 percent more successful for 1.5 to 4 hours. Insulin levels rose with both supplements but were 3 times lower with the KE beverage after 30 minutes, according to Figure 2. The desire hormone, ghrelin, was considerably lower between 2 to 4 hours after ingesting the KE, as seen on Figure 2. Ketone esters lower the urge and delays appetite.
Figure 2: Perceived hunger, fullness, and satiety after consuming a dextrose or ketone ester drink over time. Effects of ketone ester or dextrose drink on plasma insulin and ghrelin levels over time.
  • Extra ketones: In case someone has an inordinate number of ketones in the bloodstream, the human body, especially the kidneys, will function as swiftly as possible to filter out ketones via urine instead of converting them into adipose tissue. This isn’t to say you can not gain fat with�exogenous ketones, however, they are not as inclined to be converted into fat than other nourishment.
  • More tolerable compared to MCT oil: MCT oil was known to cause gastrointestinal distress in consumers, particularly when taken in high quantities. Exogenous ketones as ketone salts are well-tolerated. They prevent adverse GI events while supplying similar kinds of benefits. Figure 2 demonstrates how Ketone esters may be capable of reducing hunger. A combo of exogenous ketones and MCT oil can help with weight loss and permit a loading of nutritional supplements, with no GI distress.

Athletic Performance Goals

  • Athletic enhancem: The development of energy and�fuel pairing mechanisms. Exogenous ketone supplementation may boost these components of athletic performance. There’s a promising prognosis in this area for many different motives:
  1. Exogenous ketones induce severe ketosis, lasting for many hours. This is without having to possess depleted muscle glycogen stores. Low muscle nourishment is well-known to inhibit sustained physical functionality.
  2. The “carb-sparing” impact from BHB inhibits the breakdown of muscle glycogen. This contributes to reduced lactate levels. When raising exercise intensity, fat oxidation, or burning, reaches a limit. Carbohydrates are then burned�for energy.�But when swallowing Ketone esters, the body doesn’t make this change. This implies ketones are used instead.
  3. Exogenous ketones induce your system to rely on fat as fuel, as seen in Figure 3. Fat takes longer to metabolize compared to muscle glycogen for vitality. That is because fatty acids aren’t the fuel that is favored by the human body under exercise. This might be useful for athletes performing resistance training or cardiovascular exercises. This is especially helpful for�athletes that would like to experience cardiovascular or resistance training.
  4. Ketone esters boost free carnitine whilst exercising which appears to enhance physical performance.
  5. Exogenous ketones decrease the usage of Branched-chain amino acids, or BCAAs, as�energy, a process known as deamination. The growth was decreased by consumption of a ester beverage by 50 percent during exercise in muscle BCAAs.
Figure 3: Plasma free fatty acid (FFA) and glycerol concentrations after consuming high fat, carbohydrate, or ketone ester drink.
  • Increased cognition: Elevated plasma ketone concentrations divert the brain to use ketone bodies for the synthesis of phospholipids, which drives growth and myelination. Sugar is often the preferred�fuel for this process, which is not as efficient. BHB appears to work as a signal for pathways. These improve cognition, plasticity and stress immunity. In rat research studies, ingestion of a ketone ester for 5 days enhanced memory and their learning.

Health & Longevity

  • Anti-carcinogenic properties: Statistics appears to imply that exogenous ketones are a powerful anti-carcinogen. The motive for this is that cancer cells cannot utilize ketone bodies efficiently. In fact ketone supplementation was demonstrated to improve survival rates of mice with cancer.
  • Neuroprotection: As people age, the brain becomes more prone to neurodegeneration and following conditions like Alzheimer’s and Parkinson’s disease. Ketone supplementation seems to ameliorate the decline. The mechanism is that ketone bodies decrease hyperexcitability and the redness that’s ordinarily shown as sugar metabolism declines from the brain.
  • Anti-Inflammatory attributes: There’s proof that ketone bodies play an essential part in reducing inflammation by inhibiting a particular class of proteins known as inflammasones.
  • Gene regulation profile alterations: There’s proof that gene sets could be regulated with an alteration in mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase, or mHS, as see in rats on a ketogenic diet.
Dr Jimenez White Coat
Ketones are a source of energy which is produced when there is not enough sugar or glucose for the human body to burn as fuel. They serve as an alternative fuel source to glucose. Ketogenesis, the metabolism of fatty acids through ketosis, can have a variety of health benefits. Many people achieve these benefits by following the ketogenic diet, however, these advantages can be achieved without the keto diet as well. Exogenous ketone bodies are simply ketones which are consumed through a nutritional supplement. Although the over-consumption of any supplement can have risks, exogenous ketone bodies can provide similar benefits to ketosis. Dr. Alex Jimenez D.C., C.C.S.T. Insight

How Exogenous Ketones Function

Exogenous ketones possess many different physiological effects soon after ingestion:

  • For starters, ingesting ketones, particularly ketone esters, is an effective approach to Boost BHB from the bloodstream above 2 mMol for almost 8 hours. Ketone salts do not seem to elevate BHB from the bloodstream as efficiently or significantly where ketone esters do, however.
  • Exogenous ketone supplementation induces blood sugar to reduce significantly, likely as a result of an intense increase in insulin sensitivity. Exogenous ketones may pose a possible treatment.
  • Exogenous ketones additionally improve oxygen use, particularly in the central nervous system, or CNS. This effect reduces the odds of oxygen reaching potentially hazardous levels in the CNS, which then has a variety of additional favorable health effects like the ones discussed in the prior section.

Potential Downsides to Ketone Supplementation

Like any other nutritional supplement, side effects and drawbacks are possible after consuming exogenous ketones. As ketone supplementation becomes more notable, they are generally quite benign and will improve. The most frequent side effects to know about when using exogenous ketones consist of:

  • Electrolyte Imbalance: The physiological rationale supporting electrolytes during a state of ketosis is a result of the absence of water retention and frequent urination. The frequency of urination will�increase when supplementing exogenous ketones, but it will not deplete glycogen stores. It could be handy after taking ketones if you’re urinating a lot to drink an electrolyte solution, but it is dependent upon the way you are feeling.
  • Halitosis or bad breath: If you are on a ketogenic diet, you’re most likely aware that since the body begins to metabolize fat, ketones may cause bad breath. There is little one can do about this. This may arise when utilizing exogenous ketones, but it is not quite as durable as when on the ketogenic diet. If it turns into a problem, chewing gum or mints is the best choice. This issue may occur due to the over-consumption of this nutritional supplement, tailoring extra BHB.
  • Potential GI distress (flatulence) at exceptionally substantial doses: Exogenous ketones taken in massive doses sometimes lead to GI distress, particularly flatulence. On the other hand, this cause can be hypothesized to be a result of how ketones were blended in a fluid which was palatable. If you are taking a balanced dose of ketones GI distress can be avoided. If some GI distress is widespread, it must improve as you become accustomed to carrying ketones.
  • Hypoglycemia: Accepting exogenous ketones can induce blood sugar levels to become very low, but you’re unlikely to feel the normal signs of hypoglycemia. That is because if levels are large enough, they control energy in the brain; despite having low blood sugar, therefore, you may feel just fine. A research by George Cahill, discovered that if they had been administered insulin to induce hypoglycemia, ketone levels can protect fasted participants.

Future Research Studies

Research studies on exogenous ketones concentrates on the advantages of their use. Research studies will also concentrate more on their therapeutic use. The information on all those applications is currently limited. 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

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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. �

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EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


Ketogenic Diet in Cancer Treatment

Ketogenic Diet in Cancer Treatment

Cancer is the second leading cause of death in the United States. Research studies have estimated that approximately 595,690 Americans die from cancer every year, that’s about 1,600 deaths every day, on average. Cancer is frequently treated utilizing a combination of surgery, chemotherapy, and radiation. Recent research studies have analyzed a variety of nutritional strategies for cancer treatment. Early research studies suggest�that the ketogenic diet may help treat cancer.

What is the Ketogenic Diet?

The ketogenic diet is a very low-carb, high-fat diet which is often compared with the Atkins diet and other low carb diets. Also commonly known as the keto diet, this nutritional strategy entails drastically reducing your consumption of carbohydrates and instead substituting them with fat. This dietary shift is what causes the human body to enter a state of ketosis, the well-known metabolic state associated with the keto�diet. Ketosis utilizes fat as the cell’s main source of energy, rather than sugar or glucose.

Ketosis causes a considerable increase in the levels of ketones. In general, a ketogenic diet used for weight loss consists of about 60 to 75 percent of calories from fat, with 15 to 30 percent of calories from protein and 5 to 10 percent of calories from carbohydrates. However, when a ketogenic diet is used therapeutically to treat cancer, the fat content might be significantly higher, up to 90 percent of calories from fat, and the protein content will also be considerably lower, up to 5 percent of calories from protein.


The Role of Blood Sugar in Cancer

Many cancer treatments are designed to target the biological differences between cancer cells and normal cells. Nearly all cancer cells share one common characteristic: they feed off of blood sugar or glucose in order to grow and multiply. During the ketogenic diet, several conventional metabolic processes are modified and blood sugar levels decrease, “starving” cancer cells. As a result, cancer cells have been demonstrated to grow much slower, often decreasing in size or even dying.

This nutritional strategy as a form of cancer treatment was first proposed by Otto Heinrich Warburg,�a leading cell biologist. Otto Warburg led to the discovery that cancer cells are unable to flourish using energy produced from cellular respiration but instead from glucose fermentation. The Warburg effect developed from the role of glycolysis and lactic acid fermentation to transfer energy, compensating for lower dependence on oxidative phosphorylation and limited mitochondrial respiration.

Benefits of the Keto�Diet for Cancer

The ketogenic diet provides other benefits in cancer treatment. Primarily, reducing carbohydrates from your diet can quickly lower calorie intake, reducing the energy available to the cells. In turn, this may slow down tumor development and the progression of cancer. Additionally, the ketogenic diet may help lower insulin levels. Insulin is an anabolic hormone which promotes cell growth, including cancerous cells. Therefore, lower insulin may help slow down tumor development.

The Ketogenic Diet and Cancer in Animals

Researchers have analyzed the ketogenic diet as an alternative cancer treatment for many decades. Until recently, most research studies�were performed in animals. A big number of these animal research studies have demonstrated that the ketogenic diet can reduce tumor growth and improve survival levels in mice.

One research study in mice reviewed the cancer-fighting effects of the ketogenic diet along with other diets. Strikingly, the researchers found that 60 percent of mice following the ketogenic diet survived. This increased to 100 percent in mice that received a ketone supplement while on the keto�diet. None lived on a standard diet.

The Ketogenic Diet and Cancer in Humans

Despite the promising evidence of the benefits of the ketogenic diet as a form of cancer treatment in animals, research studies in humans have only just started. At present, the limited research studies does seem to demonstrate that a ketogenic diet may decrease tumor size and decrease the progression�of certain cancers. One of the few documented cases was conducted on a 65-year-old woman with brain cancer. Following surgery, she followed a ketogenic diet and the tumor’s progression decreased.

However, 10 weeks after returning to a normal diet, she experienced a substantial increase in tumor growth. Similar case reports analyzed the reactions to a ketogenic diet in two women who were undergoing therapy for advanced brain cancer. Researchers discovered that glucose uptake was decreased from the tumors of both patients. One of the women reported improved quality of life and stayed on the diet for 12 weeks. During that time her disease showed no further progression.

One research study tracked tumor growth in response to a high-carbohydrate diet versus a ketogenic diet in 27 patients with gastrointestinal cancer. Tumor growth increased by 32.2 percent in patients who received the high-carb diet while tumor growth decreased by 24.3 percent in patients on the ketogenic diet. In a different research study, three out of five patients on a ketogenic diet combined with radiation or chemotherapy experienced complete remission.

Can the Ketogenic Diet Help Prevent Cancer?

A variety of research studies have also demonstrated that the ketogenic diet can help prevent cancer in the first place. Primarily, it can help reduce several risk factors for cancer. The keto diet may help decrease IGF-1 levels. Insulin-like growth factor 1, or IGF-1, is a hormone that’s essential for cell growth while reducing programmed cell death. This hormone can play a part in the evolution and progression of cancer. The ketogenic diet is thought to decrease IGF-1 levels, thereby decreasing the effects insulin has on cell growth, reducing the risk of cancer.

The ketogenic diet can also help lower blood sugar levels and decrease the risk of diabetes. Other evidence indicates that people with elevated glucose and diabetes have an increased risk of developing cancer. Research studies show that a ketogenic diet can be extremely effective at lowering blood sugar levels and handling diabetes. The keto diet can reduce obesity. Obesity can be a risk factor for cancer. Since the ketogenic diet is a powerful weight loss tool, it may also help reduce the chance of cancer by fighting obesity.

Dr Jimenez White Coat
Emerging research studies continue to demonstrate that sugar or glucose is the main source of fuel for cancer. Researchers have attempted to demonstrate that regulating the metabolic functions within the human body is the real solution towards treating cancer. The ketogenic diet can help treat cancer because it limits the amount of sugar in the body and instead replaces it with ketones, “starving” cancer cells and decreasing cell growth and cancer progression. Dr. Alex Jimenez D.C., C.C.S.T. Insight


A ketogenic diet offers many health advantages. Based on animal and early research studies in humans, it may also serve as a cancer treatment. However, it’s important to keep in mind that further research studies are still required to conclude the effects of the ketogenic diet on cancer. You shouldn’t avoid conventional cancer therapy in favor of an alternative treatment option like the keto�diet.�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

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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. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


Multi-Dimensional Roles of Ketone Bodies

Multi-Dimensional Roles of Ketone Bodies

Ketone bodies are created by the liver and utilized as an energy source when glucose is not readily available in the human body. The two main ketone bodies are acetoacetate (AcAc) and 3-beta-hydroxybutyrate (3HB), while acetone is the third and least abundant, ketone body. Ketones are always present in the blood and their levels increase during fasting and prolonged exercise.�Ketogenesis is the biochemical process by which organisms produce ketone bodies through the breakdown of fatty acids and ketogenic amino acids.

Ketone bodies are mainly generated in the mitochondria of liver cells. Ketogenesis occurs when there are low glucose levels in the blood, particularly after other cellular carbohydrate stores, such as glycogen, have been exhausted. This mechanism can also occur when there is insufficient amounts of insulin. The production of ketone bodies is ultimately initiated to make available energy which is stored in the human body as fatty acids. Ketogenesis occurs in the mitochondria where it is independently regulated.


Ketone body metabolism is a central node in physiological homeostasis. In this review, we discuss how ketones serve discrete fine-tuning metabolic roles that optimize organ and organism performance in varying nutrient remains and protect from inflammation and injury in multiple organ systems. Traditionally viewed as metabolic substrates enlisted only in carbohydrate restriction, recent observations underscore the importance of ketone bodies as vital metabolic and signaling mediators when carbohydrates are abundant. Complementing a repertoire of known therapeutic options for diseases of the nervous system, prospective roles for ketone bodies in cancer have arisen, as have intriguing protective roles in heart and liver, opening therapeutic options in obesity-related and cardiovascular disease. Controversies in ketone metabolism and signaling are discussed to reconcile classical dogma with contemporary observations.


Ketone bodies are a vital alternative metabolic fuel source for all the domains of life, eukarya, bacteria, and archaea (Aneja et al., 2002; Cahill GF Jr, 2006; Krishnakumar et al., 2008). Ketone body metabolism in humans has been leveraged to fuel the brain during episodic periods of nutrient deprivation. Ketone bodies are interwoven with crucial mammalian metabolic pathways such as ?-oxidation (FAO), the tricarboxylic acid cycle (TCA), gluconeogenesis, de novo lipogenesis (DNL), and biosynthesis of sterols. In mammals, ketone bodies are produced predominantly in the liver from FAO-derived acetyl-CoA, and they are transported to extrahepatic tissues for terminal oxidation. This physiology provides an alternative fuel that is augmented by relatively brief periods of fasting, which increases fatty acid availability and diminishes carbohydrate availability (Cahill GF Jr, 2006; McGarry and Foster, 1980; Robinson and Williamson, 1980). Ketone body oxidation becomes a significant contributor to overall energy mammalian metabolism within extrahepatic tissues in a myriad of physiological states, including fasting, starvation, the neonatal period, post-exercise, pregnancy, and adherence to low carbohydrate diets. Circulating total ketone body concentrations in healthy adult humans normally exhibit circadian oscillations between approximately 100�250 �M, rise to ~1 mM after prolonged exercise or 24h of fasting, and can accumulate to as high as 20 mM in pathological states like diabetic ketoacidosis (Cahill GF Jr, 2006; Johnson et al., 1969b; Koeslag et al., 1980; Robinson and Williamson, 1980; Wildenhoff et al., 1974). The human liver produces up to 300 g of ketone bodies per day (Balasse and Fery, 1989), which contribute between 5�20% of total energy expenditure in fed, fasted, and starved states (Balasse et al., 1978; Cox et al., 2016).

Recent studies now highlight imperative roles for ketone bodies in mammalian cell metabolism, homeostasis, and signaling under a wide variety of physiological and pathological states. Apart from serving as energy fuels for extrahepatic tissues like brain, heart, or skeletal muscle, ketone bodies play pivotal roles as signaling mediators, drivers of protein post-translational modification (PTM), and modulators of inflammation and oxidative stress. In this review, we provide both classical and modern views of the pleiotropic roles of ketone bodies and their metabolism.

Overview of Ketone Body Metabolism

The rate of hepatic ketogenesis is governed by an orchestrated series of physiological and biochemical transformations of fat. Primary regulators include lipolysis of fatty acids from triacylglycerols, transport to and across the hepatocyte plasma membrane, transport into mitochondria via carnitine palmitoyltransferase 1 (CPT1), the ?-oxidation spiral, TCA cycle activity and intermediate concentrations, redox potential, and the hormonal regulators of these processes, predominantly glucagon and insulin [reviewed in (Arias et al., 1995; Ayte et al., 1993; Ehara et al., 2015; Ferre et al., 1983; Kahn et al., 2005; McGarry and Foster, 1980; Williamson et al., 1969)]. Classically ketogenesis is viewed as a spillover pathway, in which ?-oxidation-derived acetyl-CoA exceeds citrate synthase activity and/or oxaloacetate availability for condensation to form citrate. Three-carbon intermediates exhibit anti-ketogenic activity, presumably due to their ability to expand the oxaloacetate pool for acetyl-CoA consumption, but hepatic acetyl-CoA concentration alone does not determine ketogenic rate (Foster, 1967; Rawat and Menahan, 1975; Williamson et al., 1969). The regulation of ketogenesis by hormonal, transcriptional, and post-translational events together support the notion that the molecular mechanisms that fine-tune ketogenic rate remain incompletely understood (see Regulation of HMGCS2 and SCOT/OXCT1).

Ketogenesis occurs primarily in hepatic mitochondrial matrix at rates proportional to total fat oxidation. After transport of acyl chains across the mitochondrial membranes and ?-oxidation, the mitochondrial isoform of 3-hydroxymethylglutaryl-CoA synthase (HMGCS2) catalyzes the fate committing condensation of acetoacetyl-CoA (AcAc-CoA) and acetyl-CoA to generate HMG-CoA (Fig. 1A). HMG-CoA lyase (HMGCL) cleaves HMG-CoA to liberate acetyl-CoA and acetoacetate (AcAc), and the latter is reduced to d-?-hydroxybutyrate (d-?OHB) by phosphatidylcholine-dependent mitochondrial d-?OHB dehydrogenase (BDH1) in a NAD+/NADH-coupled near-equilibrium reaction (Bock and Fleischer, 1975; LEHNINGER et al., 1960). The BDH1 equilibrium constant favors d-?OHB production, but the ratio of AcAc/d-?OHB ketone bodies is directly proportional to mitochondrial NAD+/NADH ratio, and thus BDH1 oxidoreductase activity modulates mitochondrial redox potential (Krebs et al., 1969; Williamson et al., 1967). AcAc can also spontaneously decarboxylate to acetone (Pedersen, 1929), the source of sweet odor in humans suffering ketoacidosis (i.e., total serum ketone bodies > ~7 mM; AcAc pKa 3.6, ?OHB pKa 4.7). The mechanisms through which ketone bodies are transported across the mitochondrial inner membrane are not known, but AcAc/d-?OHB are released from cells via monocarboxylate transporters (in mammals, MCT 1 and 2, also known as solute carrier 16A family members 1 and 7) and transported in the circulation to extrahepatic tissues for terminal oxidation (Cotter et al., 2011; Halestrap and Wilson, 2012; Halestrap, 2012; Hugo et al., 2012). Concentrations of circulating ketone bodies are higher than those in the extrahepatic tissues (Harrison and Long, 1940) indicating ketone bodies are transported down a concentration gradient. Loss-of-function mutations in MCT1 are associated with spontaneous bouts of ketoacidosis, suggesting a critical role in ketone body import.

� With the exception of potential diversion of ketone bodies into non-oxidative fates (see Non-oxidative metabolic fates of ketone bodies), hepatocytes lack the ability to metabolize the ketone bodies they produce. Ketone bodies synthesized de novo by liver are (i) catabolized in mitochondria of extrahepatic tissues to acetyl-CoA, which is available to the TCA cycle for terminal oxidation (Fig. 1A), (ii) diverted to the lipogenesis or sterol synthesis pathways (Fig. 1B), or (iii) excreted in the urine. As an alternative energetic fuel, ketone bodies are avidly oxidized in heart, skeletal muscle, and brain (Balasse and Fery, 1989; Bentourkia et al., 2009; Owen et al., 1967; Reichard et al., 1974; Sultan, 1988). Extrahepatic mitochondrial BDH1 catalyzes the first reaction of ?OHB oxidation, converting it to back AcAc (LEHNINGER et al., 1960; Sandermann et al., 1986). A cytoplasmic d-?OHB-dehydrogenase (BDH2) with only 20% sequence identity to BDH1 has a high Km for ketone bodies, and also plays a role in iron homeostasis (Davuluri et al., 2016; Guo et al., 2006). In extrahepatic mitochondrial matrix, AcAc is activated to AcAc-CoA through exchange of a CoA-moiety from succinyl-CoA in a reaction catalyzed by a unique mammalian CoA transferase, succinyl-CoA:3-oxoacid-CoA transferase (SCOT, CoA transferase; encoded by OXCT1), through a near equilibrium reaction. The free energy released by hydrolysis of AcAc-CoA is greater than that of succinyl-CoA, favoring AcAc formation. Thus ketone body oxidative flux occurs due to mass action: an abundant supply of AcAc and rapid consumption of acetyl-CoA through citrate synthase favors AcAc-CoA (+ succinate) formation by SCOT. Notably, in contrast to glucose (hexokinase) and fatty acids (acyl-CoA synthetases), the activation of ketone bodies (SCOT) into an oxidizable form does not require the investment of ATP. A reversible AcAc-CoA thiolase reaction [catalyzed by any of the four mitochondrial thiolases encoded by either ACAA2 (encoding an enzyme known as T1 or CT), ACAT1 (encoding T2), HADHA, or HADHB] yields two molecules of acetyl-CoA, which enter the TCA cycle (Hersh and Jencks, 1967; Stern et al., 1956; Williamson et al., 1971). During ketotic states (i.e., total serum ketones > 500 �M), ketone bodies become significant contributors to energy expenditure�and are utilized in tissues rapidly until uptake or saturation of oxidation occurs (Balasse et al., 1978; Balasse and Fery, 1989; Edmond et al., 1987). A very small fraction of liver-derived ketone bodies can be readily measured in the urine, and utilization and reabsorption rates by the kidney are proportionate to circulating concentration (Goldstein, 1987; Robinson and Williamson, 1980). During highly ketotic states (> 1 mM in plasma), ketonuria serves as a semi-quantitative reporter of ketosis, although most clinical assays of urine ketone bodies detect AcAc but not ?OHB (Klocker et al., 2013).

Ketogenic Substrates and their Impact on Hepatocyte Metabolism

Ketogenic substrates include fatty acids and amino acids (Fig. 1B). The catabolism of amino acids, especially leucine, generates about 4% of ketone bodies in post-absorptive state (Thomas et al., 1982). Thus the acetyl-CoA substrate pool to generate ketone bodies mainly derives from fatty acids, because during states of diminished carbohydrate supply, pyruvate enters the hepatic TCA cycle primarily via anaplerosis, i.e., ATP-dependent carboxylation to oxaloacetate (OAA), or to malate (MAL), and not oxidative decarboxylation to acetyl-CoA (Jeoung et al., 2012; Magnusson et al., 1991; Merritt et al., 2011). In liver, glucose and pyruvate contribute negligibly to ketogenesis, even when pyruvate decarboxylation to acetyl-CoA is maximal (Jeoung et al., 2012).

Acetyl-CoA subsumes several roles integral to hepatic intermediary metabolism beyond ATP generation via terminal oxidation (also see The integration of ketone body metabolism, post-translational modification, and cell physiology). Acetyl-CoA allosterically activates (i) pyruvate carboxylase (PC), thereby activating a metabolic control mechanism that augments anaplerotic entry of metabolites into the TCA cycle (Owen et al., 2002; Scrutton and Utter, 1967) and (ii) pyruvate dehydrogenase kinase, which phosphorylates and inhibits pyruvate dehydrogenase (PDH) (Cooper et al., 1975), thereby further enhancing flow of pyruvate into the TCA cycle via anaplerosis. Furthermore, cytoplasmic acetyl-CoA, whose pool is augmented by mechanisms that convert mitochondrial acetyl-CoA to transportable metabolites, inhibits fatty acid oxidation: acetyl-CoA carboxylase (ACC) catalyzes the conversion of acetyl-CoA to malonyl-CoA, the lipogenic substrate and allosteric inhibitor of mitochondrial CPT1 [reviewed in (Kahn et al., 2005; McGarry and Foster, 1980)]. Thus, the mitochondrial acetyl-CoA pool both regulates and is regulated by the spillover pathway of ketogenesis, which orchestrates key aspects of hepatic intermediary metabolism.

Non-Oxidative Metabolic Fates of Ketone Bodies

The predominant fate of liver-derived ketones is SCOT-dependent extrahepatic oxidation. However, AcAc can be exported from mitochondria and utilized in anabolic pathways via conversion to AcAc-CoA by an ATP-dependent reaction catalyzed by cytoplasmic acetoacetyl-CoA synthetase (AACS, Fig. 1B). This pathway is active during brain development and in lactating mammary gland (Morris, 2005; Robinson and Williamson, 1978; Ohgami et al., 2003). AACS is also highly expressed in adipose tissue, and activated osteoclasts (Aguilo et al., 2010; Yamasaki et al., 2016). Cytoplasmic AcAc-CoA can be either directed by cytosolic HMGCS1 toward sterol biosynthesis, or cleaved by either of two cytoplasmic thiolases to acetyl-CoA (ACAA1 and ACAT2), carboxylated to malonyl-CoA, and contribute to the synthesis of fatty acids (Bergstrom et al., 1984; Edmond, 1974; Endemann et al., 1982; Geelen et al., 1983; Webber and Edmond, 1977).

While the physiological significance is yet to be established, ketones can serve as anabolic substrates even in the liver. In artificial experimental contexts, AcAc can contribute to as much as half of newly synthesized lipid, and up to 75% of new synthesized cholesterol (Endemann et al., 1982; Geelen et al., 1983; Freed et al., 1988). Because AcAc is derived from incomplete hepatic fat oxidation, the ability of AcAc to contribute to lipogenesis in vivo would imply hepatic futile cycling, where fat-derived ketones can be utilized for lipid production, a notion whose physiological significance requires experimental validation, but could serve adaptive or maladaptive roles (Solinas et al., 2015). AcAc avidly supplies cholesterogenesis, with a low AACS Km-AcAc (~50 �M) favoring AcAc activation even in the fed state (Bergstrom et al., 1984). The dynamic role of cytoplasmic ketone metabolism has been suggested in primary mouse embryonic neurons and in 3T3-L1 derived-adipocytes, as AACS knockdown impaired differentiation of each cell type (Hasegawa et al., 2012a; Hasegawa et al., 2012b). Knockdown of AACS in mice in vivo decreased serum cholesterol (Hasegawa et al., 2012c). SREBP-2, a master transcriptional regulator of cholesterol biosynthesis, and peroxisome proliferator activated receptor (PPAR)-? are AACS transcriptional activators, and regulate its transcription during neurite development and in the liver (Aguilo et al., 2010; Hasegawa et al., 2012c). Taken together, cytoplasmic ketone body metabolism may be important in select conditions or disease natural histories, but are inadequate to dispose of liver-derived ketone bodies, as massive hyperketonemia occurs in the setting of selective impairment of the primary oxidative fate via loss of function mutations to SCOT (Berry et al., 2001; Cotter et al., 2011).

Regulation of HMGCS2 and SCOT/OXCT1

The divergence of a mitochondrial from the gene encoding cytosolic HMGCS occurred early in vertebrate evolution due to the need to support hepatic ketogenesis in species with higher brain to body weight ratios (Boukaftane et al., 1994; Cunnane and Crawford, 2003). Naturally occurring loss-of-function HMGCS2 mutations in humans cause bouts of hypoketotic hypoglycemia (Pitt et al., 2015; Thompson et al., 1997). Robust HMGCS2 expression is restricted to hepatocytes and colonic epithelium, and its expression and enzymatic activity are coordinated through diverse mechanisms (Mascaro et al., 1995; McGarry and Foster, 1980; Robinson and Williamson, 1980). While the full scope of physiological states that influence HMGCS2 requires further elucidation, its expression and/or activity is regulated during the early postnatal period, aging, diabetes, starvation or ingestion of ketogenic diet (Balasse and Fery, 1989; Cahill GF Jr, 2006; Girard et al., 1992; Hegardt, 1999; Satapati et al., 2012; Sengupta et al., 2010). In the fetus, methylation of 5� flanking region of Hmgcs2 gene inversely correlates with its transcription, and is partially reversed after birth (Arias et al., 1995; Ayte et al., 1993; Ehara et al., 2015; Ferre et al., 1983). Similarly, hepatic Bdh1 exhibits a developmental expression pattern, increasing from birth to weaning, and is also induced by ketogenic diet in a fibroblast growth factor (FGF)-21-dependent manner (Badman et al., 2007; Zhang et al., 1989). Ketogenesis in mammals is highly responsive to both insulin and glucagon, being suppressed and stimulated, respectively (McGarry and Foster, 1977). Insulin suppresses adipose tissue lipolysis, thus depriving ketogenesis of its substrate, while glucagon increases ketogenic flux through a direct effect on the liver (Hegardt, 1999). Hmgcs2 transcription is stimulated by forkhead transcriptional factor FOXA2, which is inhibited via insulin-phosphatidylinositol-3-kinase/Akt, and is induced by glucagon-cAMP-p300 signaling (Arias et al., 1995; Hegardt, 1999; Quant et al., 1990; Thumelin et al., 1993; von Meyenn et al., 2013; Wolfrum et al., 2004; Wolfrum et al., 2003). PPAR? (Rodriguez et al., 1994) together with its target, FGF21 (Badman et al., 2007) also induce Hmgcs2 transcription in the liver during starvation or administration of ketogenic diet (Badman et al., 2007; Inagaki et al., 2007). Induction of PPAR? may occur before the transition from fetal to neonatal physiology, while FGF21 activation may be favored in the early neonatal period via ?OHB-mediated inhibition of histone deacetylase (HDAC)-3 (Rando et al., 2016). mTORC1 (mammalian target of rapamycin complex 1) dependent inhibition of PPAR? transcriptional activity is also a key regulator of Hmgcs2 gene expression (Sengupta et al., 2010), and liver PER2, a master circadian oscillator, indirectly regulates Hmgcs2 expression (Chavan et al., 2016). Recent observations indicate that extrahepatic tumor-induced interleukin-6 impairs ketogenesis via PPAR? suppression (Flint et al., 2016). Despite these observations, it is important to note that physiological shifts in Hmgcs2 gene expression have not been mechanistically linked to HMGCS2 protein abundance or to variations of ketogenic rate.

HMGCS2 enzyme activity is regulated through multiple PTMs. HMGCS2 serine phosphorylation enhanced its activity in vitro (Grimsrud et al., 2012). HMGCS2 activity is allosterically inhibited by succinyl-CoA and lysine residue succinylation (Arias et al., 1995; Hegardt, 1999; Lowe and Tubbs, 1985; Quant et al., 1990; Rardin et al., 2013; Reed et al., 1975; Thumelin et al., 1993). Succinylation of HMGCS2, HMGCL, and BDH1 lysine residues in hepatic mitochondria are targets of the NAD+ dependent deacylase sirtuin 5 (SIRT5) (Rardin et al., 2013). HMGCS2 activity is also enhanced by SIRT3 lysine deacetylation, and it is possible that crosstalk between acetylation and succinylation regulates HMGCS2 activity (Rardin et al., 2013; Shimazu et al., 2013). Despite the ability of these PTMs to regulate HMGCS2 Km and Vmax, fluctuations of these PTMs have not yet been carefully mapped and have not been confirmed as mechanistic drivers of ketogenesis in vivo.

SCOT is expressed in all mammalian cells that harbor mitochondria, except those of hepatocytes. The importance of SCOT activity and ketolysis was demonstrated in SCOT-KO mice, which exhibited uniform lethality due to hyperketonemic hypoglycemia within 48h after birth (Cotter et al., 2011). Tissue-specific loss of SCOT in neurons or skeletal myocytes induces metabolic abnormalities during starvation but is not lethal (Cotter et al., 2013b). In humans, SCOT deficiency presents early in life with severe ketoacidosis, causing lethargy, vomiting, and coma (Berry et al., 2001; Fukao et al., 2000; Kassovska-Bratinova et al., 1996; Niezen-Koning et al., 1997; Saudubray et al., 1987; Snyderman et al., 1998; Tildon and Cornblath, 1972). Relatively little is known at the cellular level about SCOT gene and protein expression regulators. Oxct1 mRNA expression and SCOT protein and activity are diminished in ketotic states, possibly through PPAR-dependent mechanisms (Fenselau and Wallis, 1974; Fenselau and Wallis, 1976; Grinblat et al., 1986; Okuda et al., 1991; Turko et al., 2001; Wentz et al., 2010). In diabetic ketoacidosis, the mismatch between hepatic ketogenesis and extrahepatic oxidation becomes exacerbated by impairment of SCOT activity. Overexpression of insulin-independent glucose transporter (GLUT1/SLC2A1) in cardiomyocytes also inhibits Oxct1 gene expression and downregulates ketones terminal oxidation in a non-ketotic state (Yan et al., 2009). In liver, Oxct1 mRNA abundance is suppressed by microRNA-122 and histone methylation H3K27me3 that are evident during the transition from fetal to the neonatal period (Thorrez et al., 2011). However, suppression of hepatic Oxct1 expression in the postnatal period is primarily attributable to the evacuation of Oxct1-expressing hematopoietic progenitors from the liver, rather than a loss of previously existing Oxct1 expression in terminally differentiated hepatocytes. In fact, expression of Oxct1 mRNA and SCOT protein in differentiated hepatocytes are extremely low (Orii et al., 2008).

SCOT is also regulated by PTMs. The enzyme is hyper-acetylated in brains of SIRT3 KO mice, which also exhibit diminished AcAc dependent acetyl-CoA production (Dittenhafer-Reed et al., 2015). Non-enzymatic nitration of tyrosine residues of SCOT also attenuates its activity, which has been reported in hearts of various diabetic mice models (Marcondes et al., 2001; Turko et al., 2001; Wang et al., 2010a). In contrast, tryptophan residue nitration augments SCOT activity (Br�g�re et al., 2010; Rebrin et al., 2007). Molecular mechanisms of residue-specific nitration or de-nitration designed to modulate SCOT activity may exist and require elucidation.

Controversies in Extrahepatic Ketogenesis

In mammals the primary ketogenic organ is liver, and only hepatocytes and gut epithelial cells abundantly express the mitochondrial isoform of HMGCS2 (Cotter et al., 2013a; Cotter et al., 2014; McGarry and Foster, 1980; Robinson and Williamson, 1980). Anaerobic bacterial fermentation of complex polysaccharides yields butyrate, which is absorbed by colonocytes in mammalians for terminal oxidation or ketogenesis (Cherbuy et al., 1995), which may play a role in colonocyte differentiation (Wang et al., 2016). Excluding gut epithelial cells and hepatocytes, HMGCS2 is nearly absent in almost all other mammalian cells, but the prospect of extrahepatic ketogenesis has been raised in tumor cells, astrocytes of the central nervous system, the kidney, pancreatic ? cells, retinal pigment epithelium (RPE), and even in skeletal muscle (Adijanto et al., 2014; Avogaro et al., 1992; El Azzouny et al., 2016; Grabacka et al., 2016; Kang et al., 2015; Le Foll et al., 2014; Nonaka et al., 2016; Takagi et al., 2016a; Thevenet et al., 2016; Zhang et al., 2011). Ectopic HMGCS2 has been observed in tissues that lack net ketogenic capacity (Cook et al., 2016; Wentz et al., 2010), and HMGCS2 exhibits prospective ketogenesis-independent �moonlighting� activities, including within the cell nucleus (Chen et al., 2016; Kostiuk et al., 2010; Meertens et al., 1998).

Any extrahepatic tissue that oxidizes ketone bodies also has the potential to accumulate ketone bodies via HMGCS2 independent mechanisms (Fig. 2A). However, there is no extrahepatic tissue in which a steady state ketone body concentration exceeds that in the circulation (Cotter et al., 2011; Cotter et al., 2013b; Harrison and Long, 1940), underscoring that ketone bodies are transported down a concentration gradient via MCT1/2-dependent mechanisms. One mechanism of apparent extrahepatic ketogenesis may actually reflect relative impairment of ketone oxidation. Additional potential explanations fall within the realm of ketone body formation. First, de novo ketogenesis may occur via reversible enzymatic activity of thiolase and SCOT (Weidemann and Krebs, 1969). When the concentration of acetyl-CoA is relatively high, reactions normally responsible for AcAc oxidation operate in the reverse direction (GOLDMAN, 1954). A second mechanism occurs when ?-oxidation-derived intermediates accumulate due to a TCA cycle bottleneck, AcAc-CoA is converted to l-?OHB-CoA through a reaction catalyzed by mitochondrial 3-hydroxyacyl-CoA dehydrogenase, and further by 3-hydroxybutyryl CoA deacylase to l-?OHB, which is indistinguishable by mass spectrometry or resonance spectroscopy from the physiological enantiomer d-?OHB (Reed and Ozand, 1980). l-?OHB can be chromatographically or enzymatically distinguished from d-?OHB, and is present in extrahepatic tissues, but not in liver or blood (Hsu et al., 2011). Hepatic ketogenesis produces only d-?OHB, the only enantiomer that is a BDH substrate (Ito et al., 1984; Lincoln et al., 1987; Reed and Ozand, 1980; Scofield et al., 1982; Scofield et al., 1982). A third HMGCS2-independent mechanism generates d-?OHB through amino acid catabolism, particularly that of leucine and lysine. A fourth mechanism is only apparent because it is due to a labeling artifact and is thus termed pseudoketogenesis. This phenomenon is attributable to the reversibility of the SCOT and thiolase reactions, and can cause overestimation of ketone body turnover due to the isotopic dilution of ketone body tracer in extrahepatic tissue (Des Rosiers et al., 1990; Fink et al., 1988). Nonetheless, pseudoketogenesis may be negligible in most contexts (Bailey et al., 1990; Keller et al., 1978). A schematic (Fig. 2A) indicates a useful approach to apply while considering elevated tissue steady state concentration of ketones.

� Kidney has recently received attention as a potentially ketogenic organ. In the vast majority of states, the kidney is a net consumer of liver-derived ketone bodies, excreting or reabsorbing ketone bodies from the bloodstream, and kidney is generally not a net ketone body generator or concentrator (Robinson and Williamson, 1980). The authors of a classical study concluded that minimal renal ketogenesis quantified in an artificial experimental system was not physiologically relevant (Weidemann and Krebs, 1969). Recently, renal ketogenesis has been inferred in diabetic and autophagy deficient mouse models, but it is more likely that multi-organ shifts in metabolic homeostasis alter integrative ketone metabolism through inputs on multiple organs (Takagi et al., 2016a; Takagi et al., 2016b; Zhang et al., 2011). One recent publication suggested renal ketogenesis as a protective mechanism against ischemia-reperfusion injury in the kidney (Tran et al., 2016). Absolute steady state concentrations of ?OHB from extracts of mice renal tissue were reported at ~4�12 mM. To test whether this was tenable, we quantified ?OHB concentrations in renal extracts from fed and 24h fasted mice. Serum ?OHB concentrations increased from ~100 �M to 2 mM with 24h fasting (Fig. 2B), while renal steady state ?OHB concentrations approximate 100 �M in the fed state, and only 1 mM in the 24h fasted state (Fig. 2C�E), observations that are consistent with concentrations quantified over 45 years ago (Hems and Brosnan, 1970). It remains possible that in ketotic states, liver-derived ketone bodies could be renoprotective, but evidence for renal ketogenesis requires further substantiation. Compelling evidence that supports true extrahepatic ketogenesis was presented in RPE (Adijanto et al., 2014). This intriguing metabolic transformation was suggested to potentially allow RPE-derived ketones to flow to photoreceptor or M�ller glia cells, which could aid in the regeneration of photoreceptor outer segment.

?OHB as a Signaling Mediator

Although they are energetically rich, ketone bodies exert provocative �non-canonical� signaling roles in cellular homeostasis (Fig. 3) (Newman and Verdin, 2014; Rojas-Morales et al., 2016). For example, ?OHB inhibits Class I HDACs, which increases histone acetylation and thereby induces the expression of genes that curtail oxidative stress (Shimazu et al., 2013). ?OHB itself is a histone covalent modifier at lysine residues in livers of fasted or streptozotocin induced diabetic mice (Xie et al., 2016) (also see below, The integration of ketone body metabolism, post-translational modification, and cell physiology, and Ketone bodies, oxidative stress, and neuroprotection).

?OHB is also an effector via G-protein coupled receptors. Through unclear molecular mechanisms, it suppresses sympathetic nervous system activity and reduces total energy expenditure and heart rate by inhibiting short chain fatty acid signaling through G protein coupled receptor 41 (GPR41) (Kimura et al., 2011). One of the most studied signaling effects of ?OHB proceeds through GPR109A (also known as HCAR2), a member of the hydrocarboxylic acid GPCR sub-family expressed in adipose tissues (white and brown) (Tunaru et al., 2003), and in immune cells (Ahmed et al., 2009). ?OHB is the only known endogenous ligand of GPR109A receptor (EC50 ~770 �M) activated by d-?OHB, l-?OHB, and butyrate, but not AcAc (Taggart et al., 2005). The high concentration threshold for GPR109A activation is achieved through adherence to a ketogenic diet, starvation, or during ketoacidosis, leading to inhibition of adipose tissue lipolysis. The anti-lipolytic effect of GPR109A proceeds through inhibition of adenylyl cyclase and decreased cAMP, inhibiting hormone sensitive triglyceride lipase (Ahmed et al., 2009; Tunaru et al., 2003). This creates a negative feedback loop in which ketosis places a modulatory brake on ketogenesis by diminishing the release of non-esterified fatty acids from adipocytes (Ahmed et al., 2009; Taggart et al., 2005), an effect that can be counterbalanced by the sympathetic drive that stimulates lipolysis. Niacin (vitamin B3, nicotinic acid) is a potent (EC50 ~ 0.1 �M) ligand for GRP109A, effectively employed for decades for dyslipidemias (Benyo et al., 2005; Benyo et al., 2006; Fabbrini et al., 2010a; Lukasova et al., 2011; Tunaru et al., 2003). While niacin enhances reverse cholesterol transport in macrophages and reduces atherosclerotic lesions (Lukasova et al., 2011), the effects of ?OHB on atherosclerotic lesions remain unknown. Although GPR109A receptor exerts protective roles, and intriguing connections exist between ketogenic diet use in stroke and neurodegenerative diseases (Fu et al., 2015; Rahman et al., 2014), a protective role of ?OHB via GPR109A has not been demonstrated in vivo.

Finally, ?OHB may influence appetite and satiety. A meta-analysis of studies that measured the effects of ketogenic and very low energy diets concluded that participants consuming these diets exhibit higher satiety, compared to control diets (Gibson et al., 2015). However, a plausible explanation for this effect is the additional metabolic or hormonal elements that might modulate appetite. For example, mice maintained on a rodent ketogenic diet exhibited increased energy expenditure compared to chow control-fed mice, despite similar caloric intake, and circulating leptin or genes of peptides regulating feeding behavior were not changed (Kennedy et al., 2007). Among proposed mechanisms that suggest appetite suppression by ?OHB includes both signaling and oxidation (Laeger et al., 2010). Hepatocyte specific deletion of circadian rhythm gene (Per2)�and chromatin immunoprecipitation studies revealed that PER2 directly activates the Cpt1a gene, and indirectly regulates Hmgcs2, leading to impaired ketosis in Per2 knockout mice (Chavan et al., 2016). These mice exhibited impaired food anticipation, which was partially restored by systemic ?OHB administration. Future studies will be needed to confirm the central nervous system as a direct ?OHB target, and whether ketone oxidation is required for the observed effects, or whether another signaling mechanism is involved. Other investigators have invoked the possibility of local astrocyte-derived ketogenesis within the ventromedial hypothalamus as a regulator of food intake, but these preliminary observations also will benefit from genetic and flux-based assessments (Le Foll et al., 2014). The relationship between ketosis and nutrient deprivation remains of interest because hunger and satiety are important elements in failed weight loss attempts.

Integration of Ketone Body Metabolism, Post-Translational Modification, and Cell Physiology

Ketone bodies contribute to compartmentalized pools of acetyl-CoA, a key intermediate that exhibits prominent roles in cellular metabolism (Pietrocola et al., 2015). One role of acetyl-CoA is to serve as a substrate for acetylation, an enzymatically-catalyzed histone covalent modification (Choudhary et al., 2014; Dutta et al., 2016; Fan et al., 2015; Menzies et al., 2016). A large number of dynamically acetylated mitochondrial proteins, many of which may occur through non-enzymatic mechanisms, have also emerged from computational proteomics studies (Dittenhafer-Reed et al., 2015; Hebert et al., 2013; Rardin et al., 2013; Shimazu et al., 2010). Lysine deacetylases use a zinc cofactor (e.g., nucleocytosolic HDACs) or NAD+ as co-substrate (sirtuins, SIRTs) (Choudhary et al., 2014; Menzies et al., 2016). The acetylproteome serves as both sensor and effector of the total cellular acetyl-CoA pool, as physiological and genetic manipulations each result in non-enzymatic global variations of acetylation (Weinert et al., 2014). As intracellular metabolites serve as modulators of lysine residue acetylation, it is important to consider the role of ketone bodies, whose abundance is highly dynamic.

?OHB is an epigenetic modifier through at least two mechanisms. Increased ?OHB levels induced by fasting, caloric restriction, direct administration or prolonged exercise provoke HDAC inhibition or histone acetyltransferase activation (Marosi et al., 2016; Sleiman et al., 2016) or to oxidative stress (Shimazu et al., 2013). ?OHB inhibition of HDAC3 could regulate newborn metabolic physiology (Rando et al., 2016). Independently, ?OHB itself directly modifies histone lysine residues (Xie et al., 2016). Prolonged fasting, or steptozotocin-induced diabetic ketoacidosis increased histone ?-hydroxybutyrylation. Although the number of lysine ?-hydroxybutyrylation and acetylation sites was comparable, stoichiometrically greater histone ?-hydroxybutyrylation than acetylation was observed. Distinct genes were impacted by histone lysine ?-hydroxybutyrylation, versus acetylation or methylation, suggesting distinct cellular functions. Whether ?-hydroxybutyrylation is spontaneous or enzymatic is not known, but expands the range of mechanisms through ketone bodies dynamically influence transcription.

Essential cell reprogramming events during caloric restriction and nutrient deprivation may be mediated in SIRT3- and SIRT5-dependent mitochondrial deacetylation and desuccinylation, respectively, regulating ketogenic and ketolytic proteins at post-translational level in liver and extrahepatic tissues (Dittenhafer-Reed et al., 2015; Hebert et al., 2013; Rardin et al., 2013; Shimazu et al., 2010). Even though stoichiometric comparison of occupied sites does not necessarily link directly to shifts in metabolic flux, mitochondrial acetylation is dynamic and may be driven by acetyl-CoA concentration or mitochondrial pH, rather than enzymatic acetyltransferases (Wagner and Payne, 2013). That SIRT3 and SIRT5 modulate activities of ketone body metabolizing enzymes provokes the question of the reciprocal role of ketones in sculpting the acetylproteome, succinylproteome, and other dynamic cellular targets. Indeed, as variations of ketogenesis reflect NAD+ concentrations, ketone production and abundance could regulate sirtuin activity, thereby influencing total acetyl-CoA/succinyl-CoA pools, the acylproteome, and thus mitochondrial and cell physiology. ?-hydroxybutyrylation of enzyme lysine residues could add another layer to cellular reprogramming. In extrahepatic tissues, ketone body oxidation may stimulate analogous changes in cell homeostasis. While compartmentation of acetyl-CoA pools is highly regulated and coordinates a broad spectrum of cellular changes, the ability of ketone bodies to directly shape both mitochondrial and cytoplasmic acetyl-CoA concentrations requires elucidation (Chen et al., 2012; Corbet et al., 2016; Pougovkina et al., 2014; Schwer et al., 2009; Wellen and Thompson, 2012). Because acetyl-CoA concentrations are tightly regulated, and acetyl-CoA is membrane impermeant, it is crucial to consider the driver mechanisms coordinating acetyl-CoA homeostasis, including the rates of production and terminal oxidation in the TCA cycle, conversion into ketone bodies, mitochondrial efflux via carnitine acetyltransferase (CrAT), or acetyl-CoA export to cytosol after conversion to citrate and release by ATP citrate lyase (ACLY). The key roles of these latter mechanisms in cell acetylproteome and homeostasis require matched understanding of the roles of ketogenesis and ketone oxidation (Das et al., 2015; McDonnell et al., 2016; Moussaieff et al., 2015; Overmyer et al., 2015; Seiler et al., 2014; Seiler et al., 2015; Wellen et al., 2009; Wellen and Thompson, 2012). Convergent technologies in metabolomics and acylproteomics in the setting of genetically manipulated models will be required to specify targets and outcomes.

Anti- and Pro-Inflammatory Responses to Ketone Bodies

Ketosis and ketone bodies modulate inflammation and immune cell function, but varied and even discrepant mechanisms have been proposed. Prolonged nutrient deprivation reduces inflammation (Youm et al., 2015), but the chronic ketosis of type 1 diabetes is a pro-inflammatory state (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kurepa et al., 2012). Mechanism-based signaling roles for ?OHB in inflammation emerge because many immune system cells, including macrophages or monocytes, abundantly express GPR109A. While ?OHB exerts a predominantly anti-inflammatory response (Fu et al., 2014; Gambhir et al., 2012; Rahman et al., 2014; Youm et al., 2015), high concentrations of ketone bodies, particularly AcAc, may trigger a pro-inflammatory response (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kurepa et al., 2012).

Anti-inflammatory roles of GPR109A ligands in atherosclerosis, obesity, inflammatory bowel disease, neurological disease, and cancer have been reviewed (Graff et al., 2016). GPR109A expression is augmented in RPE cells of diabetic models, human diabetic patients (Gambhir et al., 2012), and in microglia during neurodegeneration (Fu et al., 2014). Anti-inflammatory effects of ?OHB are enhanced by GPR109A overexpression in RPE cells, and abrogated by pharmacological inhibition or genetic knockout of GPR109A (Gambhir et al., 2012). ?OHB and exogenous nicotinic acid (Taggart et al., 2005), both confer anti-inflammatory effects in TNF? or LPS-induced inflammation by decreasing the levels of pro-inflammatory proteins (iNOS, COX-2), or secreted cytokines (TNF?, IL-1?, IL-6, CCL2/MCP-1), in part through inhibiting NF-?B translocation (Fu et al., 2014; Gambhir et al., 2012). ?OHB decreases ER stress and the NLRP3 inflammasome, activating the antioxidative stress response (Bae et al., 2016; Youm et al., 2015). However, in neurodegenerative inflammation, GPR109A-dependent ?OHB-mediated protection does not involve inflammatory mediators like MAPK pathway signaling (e.g., ERK, JNK, p38) (Fu et al., 2014), but may require COX-1-dependent PGD2 production (Rahman et al., 2014). It is intriguing that macrophage GPR109A is required to exert a neuroprotective effect in an ischemic stroke model (Rahman et al., 2014), but the ability of ?OHB to inhibit the NLRP3 inflammasome in bone marrow derived macrophages is GPR109A independent (Youm et al., 2015). Although most studies link ?OHB to anti-inflammatory effects, ?OHB may be pro-inflammatory and increase markers of lipid peroxidation in calf hepatocytes (Shi et al., 2014). Anti- versus pro-inflammatory effects of ?OHB may thus depend on cell type, ?OHB concentration, exposure duration, and the presence or absence of co-modulators.

Unlike ?OHB, AcAc may activate pro-inflammatory signaling. Elevated AcAc, especially with a high glucose concentration, intensifies endothelial cell injury through an NADPH oxidase/oxidative stress dependent mechanism (Kanikarla-Marie and Jain, 2015). High AcAc concentrations in umbilical cord of diabetic mothers were correlated with higher protein oxidation rate and MCP-1 concentration (Kurepa et al., 2012). High AcAc in diabetic patients was correlated with TNF? expression (Jain et al., 2002), and AcAc, but not ?OHB, induced TNF?, MCP-1 expression, ROS accumulation, and diminished cAMP level in U937 human monocyte cells (Jain et al., 2002; Kurepa et al., 2012).

Ketone body dependent signaling phenomena are frequently triggered only with high ketone body concentrations (> 5 mM), and in the case of many studies linking ketones to pro- or anti-inflammatory effects, through unclear mechanisms. In addition, due to the contradictory effects of ?OHB versus AcAc on inflammation, and the ability of AcAc/?OHB ratio to influence mitochondrial redox potential, the best experiments assessing the roles of ketone bodies on cellular phenotypes compare the effects of AcAc and ?OHB in varying ratios, and at varying cumulative concentrations [e.g., (Saito et al., 2016)]. Finally, AcAc can be purchased commercially only as a lithium salt or as an ethyl ester that requires base hydrolysis before use. Lithium cation independently induces signal transduction cascades (Manji et al., 1995), and AcAc anion is labile. Finally, studies using racemic d/l-?OHB can be confounded, as only the d-?OHB stereoisomer can be oxidized to AcAc, but d-?OHB and l-?OHB can each signal through GPR109A, inhibit the NLRP3 inflammasome, and serve as lipogenic substrates.

Ketone Bodies, Oxidative Stress, and Neuroprotection

Oxidative stress is typically defined as a state in which ROS are presented in excess, due to excessive production and/or impaired elimination. Antioxidant and oxidative stress mitigating roles of ketone bodies have been widely described both in vitro and in vivo, particularly in the context of neuroprotection. As most neurons do not effectively generate high-energy phosphates from fatty acids�but do oxidize ketone bodies when carbohydrates are in short supply, neuroprotective effects of ketone bodies are especially important (Cahill GF Jr, 2006; Edmond et al., 1987; Yang et al., 1987). In oxidative stress models, BDH1 induction and SCOT suppression suggest that ketone body metabolism can be reprogrammed to sustain diverse cell signaling, redox potential, or metabolic requirements (Nagao et al., 2016; Tieu et al., 2003).

Ketone bodies decrease the grades of cellular damage, injury, death and lower apoptosis in neurons and cardiomyocytes (Haces et al., 2008; Maalouf et al., 2007; Nagao et al., 2016; Tieu et al., 2003). Invoked mechanisms are varied and not always linearly related to concentration. Low millimolar concentrations of (d or l)-?OHB scavenge ROS (hydroxyl anion), while AcAc scavenges numerous ROS species, but only at concentrations that exceed the physiological range (IC50 20�67 mM) (Haces et al., 2008). Conversely, a beneficial influence over the electron transport chain�s redox potential is a mechanism commonly linked to d-?OHB. While all three ketone bodies (d/l-?OHB and AcAc) reduced neuronal cell death and ROS accumulation triggered by chemical inhibition of glycolysis, only d-?OHB and AcAc prevented neuronal ATP decline. Conversely, in a hypoglycemic in vivo model, (d or l)-?OHB, but not AcAc prevented hippocampal lipid peroxidation (Haces et al., 2008; Maalouf et al., 2007; Marosi et al., 2016; Murphy, 2009; Tieu et al., 2003). In vivo studies of mice fed a ketogenic diet (87% kcal fat and 13% protein) exhibited neuroanatomical variation of antioxidant capacity (Ziegler et al., 2003), where the most profound changes were observed in hippocampus, with increase glutathione peroxidase and total antioxidant capacities.

Ketogenic diet, ketone esters (also see Therapeutic use of ketogenic diet and exogenous ketone bodies), or ?OHB administration exert neuroprotection in models of ischemic stroke (Rahman et al., 2014); Parkinson�s disease (Tieu et al., 2003); central nervous system oxygen toxicity seizure (D’Agostino et al., 2013); epileptic spasms (Yum et al., 2015); mitochondrial encephalomyopathy, lactic acidosis and stroke-like (MELAS) episodes syndrome (Frey et al., 2016) and Alzheimer�s disease (Cunnane and Crawford, 2003; Yin et al., 2016). Conversely, a recent report demonstrated histopathological evidence of neurodegenerative progression by a ketogenic diet in a transgenic mouse model of abnormal mitochondrial DNA repair, despite increases in mitochondrial biogenesis and antioxidant signatures (Lauritzen et al., 2016). Other conflicting reports suggest that exposure to high ketone body concentrations elicits oxidative stress. High ?OHB or AcAc doses induced nitric oxide secretion, lipid peroxidation, reduced expression of SOD, glutathione peroxidase and catalase in calf hepatocytes, while in rat hepatocytes the MAPK pathway induction was attributed to AcAc but not ?OHB (Abdelmegeed et al., 2004; Shi et al., 2014; Shi et al., 2016).

Taken together, most reports link ?OHB to attenuation of oxidative stress, as its administration inhibits ROS/superoxide production, prevents lipid peroxidation and protein oxidation, increases antioxidant protein levels, and improves mitochondrial respiration and ATP production (Abdelmegeed et al., 2004; Haces et al., 2008; Jain et al., 1998; Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Maalouf et al., 2007; Maalouf and Rho, 2008; Marosi et al., 2016; Tieu et al., 2003; Yin et al., 2016; Ziegler et al., 2003). While AcAc has been more directly correlated than ?OHB with the induction of oxidative stress, these effects are not always easily dissected from prospective pro-inflammatory responses (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kanikarla-Marie and Jain, 2016). Moreover, it is critical to consider that the apparent antioxidative benefit conferred by pleiotropic ketogenic diets may not be transduced by ketone bodies themselves, and neuroprotection conferred by ketone bodies may not entirely be attributable to oxidative stress. For example during glucose deprivation, in a model of glucose deprivation in cortical neurons, ?OHB stimulated autophagic flux and prevented autophagosome accumulation, which was associated with decreased neuronal death (Camberos-Luna et al., 2016). d-?OHB induces also the canonical antioxidant proteins FOXO3a, SOD, MnSOD, and catalase, prospectively through HDAC inhibition (Nagao et al., 2016; Shimazu et al., 2013).

Non-Alcoholic Fatty Liver Disease (NAFLD) and Ketone Body Metabolism

Obesity-associated NAFLD and nonalcoholic steatohepatitis (NASH) are the most common causes of liver disease in Western countries (Rinella and Sanyal, 2016), and NASH-induced liver failure is one of the most common reasons for liver transplantation. While excess storage of triacylglycerols in hepatocytes >5% of liver weight (NAFL) alone does not cause degenerative liver function, the progression to NAFLD in humans correlates with systemic insulin resistance and increased risk of type 2 diabetes, and may contribute to the pathogenesis of cardiovascular disease and chronic kidney disease (Fabbrini et al., 2009; Targher et al., 2010; Targher and Byrne, 2013). The pathogenic mechanisms of NAFLD and NASH are incompletely understood but include abnormalities of hepatocyte metabolism, hepatocyte autophagy and endoplasmic reticulum stress, hepatic immune cell function, adipose tissue inflammation, and systemic inflammatory mediators (Fabbrini et al., 2009; Masuoka and Chalasani, 2013; Targher et al., 2010; Yang et al., 2010). Perturbations of carbohydrate, lipid, and amino acid metabolism occur in and contribute to obesity, diabetes, and NAFLD in humans and in model organisms [reviewed in (Farese et al., 2012; Lin and Accili, 2011; Newgard, 2012; Samuel and Shulman, 2012; Sun and Lazar, 2013)]. While hepatocyte abnormalities in cytoplasmic lipid metabolism are commonly observed in NAFLD (Fabbrini et al., 2010b), the role of mitochondrial metabolism, which governs oxidative disposal of fats is less clear in NAFLD pathogenesis. Abnormalities of mitochondrial metabolism occur in and contribute to NAFLD/NASH pathogenesis (Hyotylainen et al., 2016; Serviddio et al., 2011; Serviddio et al., 2008; Wei et al., 2008). There is general (Felig et al., 1974; Iozzo et al., 2010; Koliaki et al., 2015; Satapati et al., 2015; Satapati et al., 2012; Sunny et al., 2011) but not uniform (Koliaki and Roden, 2013; Perry et al., 2016; Rector et al., 2010) consensus that, prior to the development of bona fide NASH, hepatic mitochondrial oxidation, and in particular fat oxidation, is augmented in obesity, systemic insulin resistance, and NAFLD. It is likely that as NAFLD progresses, oxidative capacity heterogenity, even among individual mitochondria, emerges, and ultimately oxidative function becomes impaired (Koliaki et al., 2015; Rector et al., 2010; Satapati et al., 2008; Satapati et al., 2012).

Ketogenesis is often used as a proxy for hepatic fat oxidation. Impairments of ketogenesis emerge as NAFLD progresses in animal models, and likely in humans. Through incompletely defined mechanisms, hyperinsulinemia suppresses ketogenesis, possibly contributing to hypoketonemia compared to lean controls (Bergman et al., 2007; Bickerton et al., 2008; Satapati et al., 2012; Soeters et al., 2009; Sunny et al., 2011; Vice et al., 2005). Nonetheless, the ability of circulating ketone body concentrations to predict NAFLD is controversial (M�nnist� et al., 2015; Sanyal et al., 2001). Robust quantitative magnetic resonance spectroscopic methods in animal models revealed increased ketone turnover rate with moderate insulin resistance, but decreased rates were evident with more severe insulin resistance (Satapati et al., 2012; Sunny et al., 2010). In obese humans with fatty liver, ketogenic rate is normal (Bickerton et al., 2008; Sunny et al., 2011), and hence, the rates of ketogenesis are diminished relative to the increased fatty acid load within hepatocytes. Consequently, ?-oxidation-derived acetyl-CoA may be directed to terminal oxidation in the TCA cycle, increasing terminal oxidation, phosphoenolpyruvate-driven gluconeogenesis via anaplerosis/cataplerosis, and oxidative stress. Acetyl-CoA also possibly undergoes export from mitochondria as citrate, a precursor substrate for lipogenesis (Fig. 4) (Satapati et al., 2015; Satapati et al., 2012; Solinas et al., 2015). While ketogenesis becomes less responsive to insulin or fasting with prolonged obesity (Satapati et al., 2012), the underlying mechanisms and downstream consequences of this remain incompletely understood. Recent evidence indicates that mTORC1 suppresses ketogenesis in a manner that may be downstream of insulin signaling (Kucejova et al., 2016), which is concordant with the observations that mTORC1 inhibits PPAR?-mediated Hmgcs2 induction (Sengupta et al., 2010) (also see Regulation of HMGCS2 and SCOT/OXCT1).

Preliminary observations from our group suggest adverse hepatic consequences of ketogenic insufficiency (Cotter et al., 2014). To test the hypothesis that impaired ketogenesis, even in carbohydrate-replete and thus �non-ketogenic� states, contributes to abnormal glucose metabolism and provokes steatohepatitis, we generated a mouse model of marked ketogenic insufficiency by administration of antisense oligonucleotides (ASO) targeted to Hmgcs2. Loss of HMGCS2 in standard low-fat chow-fed adult mice caused mild hyperglycemia and markedly increased production of hundreds of hepatic metabolites, a suite of which strongly suggested lipogenesis activation. High-fat diet feeding of mice with insufficient ketogenesis resulted in extensive hepatocyte injury and inflammation. These findings support the central hypotheses that (i) ketogenesis is not a passive overflow pathway but rather a dynamic node in hepatic and integrated physiological homeostasis, and (ii) prudent ketogenic augmentation to mitigate NAFLD/NASH and disordered hepatic glucose metabolism is worthy of exploration.

How might impaired ketogenesis contribute to hepatic injury and altered glucose homeostasis? The first consideration is whether the culprit is deficiency of ketogenic flux, or ketones themselves. A recent report suggests that ketone bodies may mitigate oxidative stress-induced hepatic injury in response to n-3 polyunsaturated fatty acids (Pawlak et al., 2015). Recall that due to lack of SCOT expression in hepatocytes, ketone bodies are not oxidized, but they can contribute to lipogenesis, and serve a variety of signaling roles independent of their oxidation (also see Non-oxidative metabolic fates of ketone bodies and ?OHB as a signaling mediator). It is also possible that hepatocyte-derived ketone bodies may serve as a signal and/or metabolite for neighboring cell types within the hepatic acinus, including stellate cells and Kupffer cell macrophages. While the limited literature available suggests that macrophages are unable to oxidize ketone bodies, this has only been measured using classical methodologies, and only in peritoneal macrophages (Newsholme et al., 1986; Newsholme et al., 1987), indicating that a re-assessment is appropriate given abundant SCOT expression in bone marrow-derived macrophages (Youm et al., 2015).

Hepatocyte ketogenic flux may also be cytoprotective. While salutary mechanisms may not depend on ketogenesis per se, low carbohydrate ketogenic diets have been associated with amelioration of NAFLD (Browning et al., 2011; Foster et al., 2010; Kani et al., 2014; Schugar and Crawford, 2012). Our observations indicate that hepatocyte ketogenesis may feedback and regulate TCA cycle flux, anaplerotic flux, phosphoenolpyruvate-derived gluconeogenesis (Cotter et al., 2014), and even glycogen turnover. Ketogenic impairment directs acetyl-CoA to increase TCA flux, which in liver has been linked to increased ROS-mediated injury (Satapati et al., 2015; Satapati et al., 2012); forces diversion of carbon into de novo synthesized lipid species that could prove cytotoxic; and prevents NADH re-oxidation to NAD+ (Cotter et al., 2014) (Fig. 4). Taken together, future experiments are required to address mechanisms through which relative ketogenic insufficiency may become maladaptive, contribute to hyperglycemia, provoke steatohepatitis, and whether these mechanisms are operant in human NAFLD/NASH. As epidemiological evidence suggests impaired ketogenesis during the progression of steatohepatitis (Embade et al., 2016; Marinou et al., 2011; M�nnist� et al., 2015; Pramfalk et al., 2015; Safaei et al., 2016) therapies that increase hepatic ketogenesis could prove salutary (Degirolamo et al., 2016; Honda et al., 2016).

Ketone Bodies and Heart Failure (HF)

With a metabolic rate exceeding 400 kcal/kg/day, and a turnover of 6�35 kg ATP/day, the heart is the organ with the highest energy expenditure and oxidative demand (Ashrafian et al., 2007; Wang et al., 2010b). The vast majority of myocardial energy turnover resides within mitochondria, and 70% of this supply originates from FAO. The heart is omnivorous and flexible under normal conditions, but the pathologically remodeling heart (e.g., due to hypertension or myocardial infarction) and the diabetic heart each become metabolically inflexible (Balasse and Fery, 1989; BING, 1954; Fukao et al., 2004; Lopaschuk et al., 2010; Taegtmeyer et al., 1980; Taegtmeyer et al., 2002; Young et al., 2002). Indeed, genetically programmed abnormalities of cardiac fuel metabolism in mouse models provoke cardiomyopathy (Carley et al., 2014; Neubauer, 2007). Under physiological conditions normal hearts oxidize ketone bodies in proportion to their delivery, at the expense of fatty acid and glucose oxidation, and myocardium is the highest ketone body consumer per unit mass (BING, 1954; Crawford et al., 2009; GARLAND et al., 1962; Hasselbaink et al., 2003; Jeffrey et al., 1995; Pelletier et al., 2007; Tardif et al., 2001; Yan et al., 2009). Compared to fatty acid oxidation, ketone bodies are more energetically efficient, yielding more energy available for ATP synthesis per molecule of oxygen invested (P/O ratio) (Kashiwaya et al., 2010; Sato et al., 1995; Veech, 2004). Ketone body oxidation also yields potentially higher energy than FAO, keeping ubiquinone oxidized, which raises redox span in the electron transport chain and makes more energy available to synthetize ATP (Sato et al., 1995; Veech, 2004). Oxidation of ketone bodies may also curtail ROS production, and thus oxidative stress (Veech, 2004).

Preliminary interventional and observational studies indicate a potential salutary role of ketone bodies in the heart. In the experimental ischemia/reperfusion injury context, ketone bodies conferred potential cardioprotective effects (Al-Zaid et al., 2007; Wang et al., 2008), possibly due to the increase mitochondrial abundance in heart or up-regulation of crucial oxidative phosphorylation mediators (Snorek et al., 2012; Zou et al., 2002). Recent studies indicate that ketone body utilization is increased in failing hearts of mice (Aubert et al., 2016) and humans (Bedi et al., 2016), supporting prior observations in humans (BING, 1954; Fukao et al., 2000; Janardhan et al., 2011; Longo et al., 2004; Rudolph and Schinz, 1973; Tildon and Cornblath, 1972). Circulating ketone body concentrations are increased in heart failure patients, in direct proportion to filling pressures, observations whose mechanism and significance remains unknown (Kupari et al., 1995; Lommi et al., 1996; Lommi et al., 1997; Neely et al., 1972), but mice with selective SCOT deficiency in cardiomyocytes exhibit accelerated pathological ventricular remodeling and ROS signatures in response to surgically induced pressure overload injury (Schugar et al., 2014).

Recent intriguing observations in diabetes therapy have revealed a potential link between myocardial ketone metabolism and pathological ventricular remodeling (Fig. 5). Inhibition of the renal proximal tubular sodium/glucose co-transporter 2 (SGLT2i) increases circulating ketone body concentrations in humans (Ferrannini et al., 2016a; Inagaki et al., 2015) and mice (Suzuki et al., 2014) via increased hepatic ketogenesis (Ferrannini et al., 2014; Ferrannini et al., 2016a; Katz and Leiter, 2015; Mudaliar et al., 2015). Strikingly, at least one of these agents decreased HF hospitalization (e.g., as revealed by the EMPA-REG OUTCOME trial), and improved cardiovascular mortality (Fitchett et al., 2016; Sonesson et al., 2016; Wu et al., 2016a; Zinman et al., 2015). While the driver mechanisms behind beneficial HF outcomes to linked SGLT2i remain actively debated, the survival benefit is likely multifactorial, prospectively including ketosis but also salutary effects on weight, blood pressure, glucose and uric acid levels, arterial stiffness, the sympathetic nervous system, osmotic diuresis/reduced plasma volume, and increased hematocrit (Raz and Cahn, 2016; Vallon and Thomson, 2016). Taken together, the notion that therapeutically increasing ketonemia either in HF patients, or those at high risk to develop HF, remains controversial but is under active investigation in pre-clinical and clinical studies (Ferrannini et al., 2016b; Kolwicz et al., 2016; Lopaschuk and Verma, 2016; Mudaliar et al., 2016; Taegtmeyer, 2016).

Ketone Bodies in Cancer Biology

Connections between ketone bodies and cancer are rapidly emerging, but studies in both animal models and humans have yielded diverse conclusions. Because ketone metabolism is dynamic and nutrient state responsive, it is enticing to pursue biological connections to cancer because of the potential for precision-guided nutritional therapies. Cancer cells undergo metabolic reprogramming in order to maintain rapid cell proliferation and growth (DeNicola and Cantley, 2015; Pavlova and Thompson, 2016). The classical Warburg effect in cancer cell metabolism arises from the dominant role of glycolysis and lactic acid fermentation to transfer energy and compensate for lower dependence on oxidative phosphorylation and limited mitochondrial respiration (De Feyter et al., 2016; Grabacka et al., 2016; Kang et al., 2015; Poff et al., 2014; Shukla et al., 2014). Glucose carbon is primarily directed through glycolysis, the pentose phosphate pathway, and lipogenesis, which together provide intermediates necessary for tumor biomass expansion (Grabacka et al., 2016; Shukla et al., 2014; Yoshii et al., 2015). Adaptation of cancer cells to glucose deprivation occurs through the ability to exploit alternative fuel sources, including acetate, glutamine, and aspartate (Jaworski et al., 2016; Sullivan et al., 2015). For example, restricted access to pyruvate reveals the ability of cancer cells to convert glutamine into acetyl-CoA by carboxylation, maintaining both energetic and anabolic needs (Yang et al., 2014). An interesting adaptation of cancer cells is the utilization of acetate as a fuel (Comerford et al., 2014; Jaworski et al., 2016; Mashimo et al., 2014; Wright and Simone, 2016; Yoshii et al., 2015). Acetate is also a substrate for lipogenesis, which is critical for tumor cell proliferation, and gain of this lipogenic conduit is associated with shorter patient survival and greater tumor burden (Comerford et al., 2014; Mashimo et al., 2014; Yoshii et al., 2015).

Non-cancer cells easily shift their energy source from glucose to ketone bodies during glucose deprivation. This plasticity may be more variable among cancer cell types, but in vivo implanted brain tumors oxidized [2,4-13C2]-?OHB to a similar degree as surrounding brain tissue (De Feyter et al., 2016). �Reverse Warburg effect� or �two compartment tumor metabolism� models hypothesize that cancer cells induce ?OHB production in adjacent fibroblasts, furnishing the tumor cell�s energy needs (Bonuccelli et al., 2010; Martinez-Outschoorn et al., 2012). In liver, a shift in hepatocytes from ketogenesis to ketone oxidation in hepatocellular carcinoma (hepatoma) cells is consistent with activation of BDH1 and SCOT activities observed in two hepatoma cell lines (Zhang et al., 1989). Indeed, hepatoma cells express OXCT1 and BDH1 and oxidize ketones, but only when serum starved (Huang et al., 2016). Alternatively, tumor cell ketogenesis has also been proposed. Dynamic shifts in ketogenic gene expression are exhibited during cancerous transformation of colonic epithelium, a cell type that normally expresses HMGCS2, and a recent report suggested that HMGCS2 may be a prognostic marker of poor prognosis in colorectal and squamous cell carcinomas (Camarero et al., 2006; Chen et al., 2016). Whether this association requires or involves ketogenesis, or a moonlighting function of HMGCS2, remains to be determined. Conversely, apparent ?OHB production by melanoma and glioblastoma cells, stimulated by the PPAR? agonist fenofibrate, was associated with growth arrest (Grabacka et al., 2016). Further studies are required to characterize roles of HMGCS2/SCOT expression, ketogenesis, and ketone oxidation in cancer cells.

Beyond the realm of fuel metabolism, ketones have recently been implicated in cancer cell biology via a signaling mechanism. Analysis of BRAF-V600E+ melanoma indicated OCT1-dependent induction of HMGCL in an oncogenic BRAF-dependent manner (Kang et al., 2015). HMGCL augmentation was correlated with higher cellular AcAc concentration, which in turn enhanced BRAFV600E-MEK1 interaction, amplifying MEK-ERK signaling in a feed-forward loop that drives tumor cell proliferation and growth. These observations raise the intriguing question of prospective extrahepatic ketogenesis that then supports a signaling mechanism (also see ?OHB as a signaling mediator and Controversies in extrahepatic ketogenesis). It is also important to consider independent effects of AcAc, d-?OHB, and l-?OHB on cancer metabolism, and when considering HMGCL, leucine catabolism may also be deranged.

The effects of ketogenic diets (also see Therapeutic use of ketogenic diet and exogenous ketone bodies) in cancer animal models are varied (De Feyter et al., 2016; Klement et al., 2016; Meidenbauer et al., 2015; Poff et al., 2014; Seyfried et al., 2011; Shukla et al., 2014). While epidemiological associations among obesity, cancer, and ketogenic diets are debated (Liskiewicz et al., 2016; Wright and Simone, 2016), a meta-analysis using ketogenic diets in animal models and in human studies suggested a salutary impact on survival, with benefits prospectively linked to the magnitude of ketosis, time of diet initiation, and tumor location (Klement et al., 2016; Woolf et al., 2016). Treatment of pancreatic cancer cells with ketone bodies (d-?OHB or AcAc) inhibited growth, proliferation and glycolysis, and a ketogenic diet (81% kcal fat, 18% protein, 1% carbohydrate) reduced in vivo tumor weight, glycemia, and increased muscle and body weight in animals with implanted cancer (Shukla et al., 2014). Similar results were observed using a metastatic glioblastoma cell model in mice that received ketone supplementation in the diet (Poff et al., 2014). Conversely, a ketogenic diet (91% kcal fat, 9% protein) increased circulating ?OHB concentration and diminished glycemia�but had no impact on either tumor volume or survival duration in glioma-bearing rats (De Feyter et al., 2016). A glucose ketone index has been proposed as a clinical indicator that improves metabolic management of ketogenic diet-induced brain cancer therapy in humans and mice (Meidenbauer et al., 2015). Taken together, roles of ketone body metabolism and ketone bodies in cancer biology are tantalizing because they each pose tractable therapeutic options, but fundamental aspects remain to be elucidated, with clear influences emerging from a matrix of variables, including (i) differences between exogenous ketone bodies versus ketogenic diet, (ii) cancer cell type, genomic polymorphisms, grade, and stage; and (iii) timing and duration of exposure to the ketotic state.

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Ketogenesis is created by ketone bodies through the breakdown of fatty acids and ketogenic amino acids. This biochemical process provides energy to various organs, specifically the brain, under circumstances of fasting as a response to an unavailability of blood glucose. Ketone bodies are mainly produced in the mitochondria of liver cells. While other cells are capable of carrying out ketogenesis, they are not as effective at doing so as liver cells. Because ketogenesis occurs in the mitochondria, its processes are regulated independently. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Therapeutic Application of Ketogenic Diet and Exogenous Ketone Bodies

The applications of ketogenic diets and ketone bodies as therapeutic tools have also arisen in non-cancerous contexts including obesity and NAFLD/NASH (Browning et al., 2011; Foster et al., 2010; Schugar and Crawford, 2012); heart failure (Huynh, 2016; Kolwicz et al., 2016; Taegtmeyer, 2016); neurological and neurodegenerative disease (Martin et al., 2016; McNally and Hartman, 2012; Rho, 2015; Rogawski et al., 2016; Yang and Cheng, 2010; Yao et al., 2011); inborn errors of metabolism (Scholl-B�rgi et al, 2015); and exercise performance (Cox et al., 2016). The efficacy of ketogenic diets has been especially appreciated in therapy of epileptic seizure, particularly in drug-resistant patients. Most studies have evaluated ketogenic diets in pediatric patients, and reveal up to a ~50% reduction in seizure frequency after 3 months, with improved effectiveness in select syndromes (Wu et al., 2016b). The experience is more limited in adult epilepsy, but a similar reduction is evident, with better response in symptomatic generalized epilepsy patients (Nei et al., 2014). Underlying anti-convulsant mechanisms remain unclear, although postulated hypotheses include reduced glucose utilization/glycolysis, reprogrammed glutamate transport, indirect impact on ATP-sensitive potassium channel or adenosine A1 receptor, alteration of sodium channel isoform expression, or effects on circulating hormones including leptin (Lambrechts et al., 2016; Lin et al., 2017; Lutas and Yellen, 2013). It remains unclear whether the anti-convulsant effect is primarily attributable to ketone bodies, or due to the cascade metabolic consequences of low carbohydrate diets. Nonetheless, ketone esters (see below) appear to elevate the seizure threshold in animal models of provoked seizures (Ciarlone et al., 2016; D’Agostino et al., 2013; Viggiano et al., 2015).

Atkins-style and ketogenic, low carbohydrate diets are often deemed unpleasant, and can cause constipation, hyperuricemia, hypocalcemia, hypomagnesemia, lead to nephrolithiasis, ketoacidosis, cause hyperglycemia, and raise circulating cholesterol and free fatty acid concentrations (Bisschop et al., 2001; Kossoff and Hartman, 2012; Kwiterovich et al., 2003; Suzuki et al., 2002). For these reasons, long-term adherence poses challenges. Rodent studies commonly use a distinctive macronutrient distribution (94% kcal fat, 1% kcal carbohydrate, 5% kcal protein, Bio-Serv F3666), which provokes a robust ketosis. However, increasing the protein content, even to 10% kcal substantially diminishes the ketosis, and 5% kcal protein restriction confers confounding metabolic and physiological effects. This diet formulation is also choline depleted, another variable that influences susceptibility to liver injury, and even ketogenesis (Garbow et al., 2011; Jornayvaz et al., 2010; Kennedy et al., 2007; Pissios et al., 2013; Schugar et al., 2013). Effects of long-term consumption of ketogenic diets in mice remain incompletely defined, but recent studies in mice revealed normal survival and the absence of liver injury markers in mice on ketogenic diets over their lifespan, although amino acid metabolism, energy expenditure, and insulin signaling were markedly reprogrammed (Douris et al., 2015).

Mechanisms increasing ketosis through mechanisms alternative to ketogenic diets include the use of ingestible ketone body precursors. Administration of exogenous ketone bodies could create a unique physiological state not encountered in normal physiology, because circulating glucose and insulin concentrations are relatively normal, while cells might spare glucose uptake and utilization. Ketone bodies themselves have short half-lives, and ingestion or infusion of sodium ?OHB salt to achieve therapeutic ketosis provokes an untoward sodium load. R/S-1,3-butanediol is a non-toxic dialcohol that is readily oxidized in the liver to yield d/l-?OHB (Desrochers et al., 1992). In distinct experimental contexts, this dose has been administered daily to mice or rats for as long as seven weeks, yielding circulating ?OHB concentrations of up to 5 mM within 2 h of administration, which is stable for at least an additional 3h (D’Agostino et al., 2013). Partial suppression of food intake has been observed in rodents given R/S-1,3-butanediol (Carpenter and Grossman, 1983). In addition, three chemically distinct ketone esters (KEs), (i) monoester of R-1,3-butanediol and d-?OHB (R-3-hydroxybutyl R-?OHB); (ii) glyceryl-tris-?OHB; and (iii) R,S-1,3-butanediol acetoacetate diester, have also been extensively studied (Brunengraber, 1997; Clarke et al., 2012a; Clarke et al., 2012b; Desrochers et al., 1995a; Desrochers et al., 1995b; Kashiwaya et al., 2010). An inherent advantage of the former is that 2 moles of physiological d-?OHB are produced per mole of KE, following esterase hydrolysis in the intestine or liver. Safety, pharmacokinetics, and tolerance have been most extensively studied in humans ingesting R-3-hydroxybutyl R-?OHB, at doses up to 714 mg/kg, yielding circulating d-?OHB concentrations up to 6 mM (Clarke et al., 2012a; Cox et al., 2016; Kemper et al., 2015; Shivva et al., 2016). In rodents, this KE decreases caloric intake and plasma total cholesterol, stimulates brown adipose tissue, and improves insulin resistance (Kashiwaya et al., 2010; Kemper et al., 2015; Veech, 2013). Recent findings indicate that during exercise in trained athletes, R-3-hydroxybutyl R-?OHB ingestion decreased skeletal muscle glycolysis and plasma lactate concentrations, increased intramuscular triacylglycerol oxidation, and preserved muscle glycogen content, even when co-ingested carbohydrate stimulated insulin secretion (Cox et al., 2016). Further development of these intriguing results is required, because the improvement in endurance exercise performance was predominantly driven by a robust response to the KE in 2/8 subjects. Nonetheless, these results do support classical studies that indicate a preference for ketone oxidation over other substrates (GARLAND et al., 1962; Hasselbaink et al., 2003; Stanley et al., 2003; Valente-Silva et al., 2015), including during exercise, and that trained athletes may be more primed to utilize ketones (Johnson et al., 1969a; Johnson and Walton, 1972; Winder et al., 1974; Winder et al., 1975). Finally, the mechanisms that might support improved exercise performance following equal caloric intake (differentially distributed among macronutrients) and equal oxygen consumption rates remain to be determined. Clues may emerge from animal studies, as temporary exposure to R-3-hydroxybutyl R-?OHB in rats was associated with increased treadmill time, improved cognitive function, and an apparent energetic benefit in ex vivo perfused hearts (Murray et al., 2016).

Future Perspective

Once largely stigmatized as an overflow pathway capable of accumulating toxic emissions from fat combustion in carbohydrate restricted states (the �ketotoxic� paradigm), recent observations support the notion that ketone body metabolism serves salutary roles even in carbohydrate-laden states, opening a �ketohormetic� hypothesis. While the facile nutritional and pharmacological approaches to manipulate ketone metabolism make it an attractive therapeutic target, aggressively posed but prudent experiments remain in both the basic and translational research laboratories. Unmet needs have emerged in the domains of defining the role of leveraging ketone metabolism in heart failure, obesity, NAFLD/NASH, type 2 diabetes, and cancer. The scope and impact of ‘non-canonical� signaling roles of ketone bodies, including regulation of PTMs that likely feed back and forward into metabolic and signaling pathways, require deeper exploration. Finally, extrahepatic ketogenesis could open intriguing paracrine and autocrine signaling mechanisms and opportunities to influence co-metabolism within the nervous system and tumors to achieve therapeutic ends.



In conclusion, ketone bodies are created by the liver in order to be used as an energy source when there is not enough glucose readily available in the human body. Ketogenesis occurs when there are low glucose levels in the blood, particularly after other cellular carbohydrate stores have been exhausted. The purpose of the article above was to discuss the multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics. 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

Referenced from:�

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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. �

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The Function Of Ketones In Ketosis

The Function Of Ketones In Ketosis

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.

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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

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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. �

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The Ketogenic Diet vs the Modified Ketogenic Diet

The Ketogenic Diet vs the Modified Ketogenic Diet

The ketogenic diet seems to be one of the most popular topics to reach the current diet world. The ketogenic diet, or the keto diet, is characterized as a high fat, low carb dietary regimen. With claims that you can eat all the fat you want while not feeling hungry and considering its belief to reduce your blood sugar when you have type 2 diabetes as well as help improve overall performance, the ketogenic diet appears to be the ideal nutritional standard of the modern world. However, is the ketogenic diet right for everyone? Below, we will discuss what the ketogenic diet is and describe the modified ketogenic diet, their benefits and risks.

What is the Ketogenic Diet?

The “classic” ketogenic diet was created in 1923 by Dr. Russell Wilder for the treatment of epilepsy.�The keto diet is based on the principle that by decreasing the intake of carbohydrates, the human body’s main supply of energy, it is possible to induce the cells to burn fat for fuel, maximizing weight loss. When you eat foods with carbohydrates, the body transforms these into glucose, or blood sugar, which it then uses for energy. Glucose is the easiest type of energy the body can�utilize, however, excess sugar can turn into fat. The objective of the keto diet is to limit carbohydrate intake so the body needs to break down fat instead of glucose for energy.

When this happens, fat is broken down in the liver, thus producing ketones, which can be by-products of your own metabolism. These ketones are subsequently utilized to fuel the body in the absence of sugar. The classic ketogenic diet is characterized by a 4:1 ratio of fat to protein and carbohydrates, where 90 percent of calories come from fats, 6 percent from proteins, and 4 percent from carbohydrates. Although a 4:1 ratio is regarded as the gold standard for the classic keto diet, a modified ketogenic diet can involve a 3:1 ratio. This diet is also regarded as a low glycemic treatment and results in continuous sugar and glucose levels.

What is the Modified Ketogenic Diet?

There are a variety of modifications of the ketogenic diet.The “modified” ketogenic diet is a less restrictive variant of the classic keto diet, which may be helpful for people starting out with the ketogenic diet plan or for those who simply wish to follow a less strict,�long-term�dietary regimen. With a macronutrient ratio between 2:1 -1:1, the modified ketogenic diet was created with versatility in mind to improve compliance and reduce possible gastrointestinal health issues as well as�nutritional deficiencies�which could occur with the long-term�classic ketogenic diet. Nearly all people following a modified keto diet follow the standard ketogenic diet program closely.

Other types of modified ketogenic diets consist of the cyclic ketogenic diets, also called carb cycling, and targeted ketogenic diets, that allow for alterations to carbohydrate consumption around physical activity and exercise. These alterations are generally implemented by athletes seeking to utilize the ketogenic diet to boost endurance and performance rather than by people especially focused on weight loss. As with any ketogenic diet, however, you should plan to eat less than 10 percent of your calories from carbs every day. The rest of the calories must include 20 to 30 percent protein and 60 to 80 percent fat.

How to Follow a Ketogenic Diet

There are many variations of the ketogenic�diet plan, but, to accomplish a state of ketosis, you need to tremendously lower the number of carbohydrates you consume on a regular basis. Research studies have demonstrated that the average American man over the age of 20 intakes approximately 47.4 percent of their daily calories from carbohydrates where the average American woman over the age of 20 intakes approximately 49.6 percent of their daily calories from carbohydrates. In the “classic” ketogenic diet, 80 to 90 percent of calories come from fat, 5 to 15 percent come from proteins, and 5 to 10 percent come from carbohydrates. A common modified variant of the ketogenic diet, permits 20 to 30 percent of calories to come from proteins with the exact same carbohydrate limitation.

Some of the goals of the ketogenic diet are weight loss and improved athletic endurance and performance. The ketogenic diet for weight loss is predicated on the thought that forcing the entire body into ketosis will optimize fat reduction and weight loss. Ketosis is a normal metabolic process which happens when the body doesn’t have enough sugar stores for energy. Whenever these stores are depleted, the body resorts to burning stored fat for energy rather than carbohydrates. This method creates acids called ketones, which build up in the human body and may be used for energy. Ketones are a necessary part of a healthy metabolism.

The ketogenic diet comprises more than just diet. Nutritional supplements, electrolytes, hydration and physical activity or exercise levels will also be a crucial factor in the nutritional program. Those that suffer from digestive problems normally require extra support. This is where a ketogenic expert can be greatly beneficial. Tracking ketosis is another important element of therapy. Ketosis can be quantified by three distinct approaches: Blood, urine and breath. Blood readings would be the most precise and reliable way of testing, even though it’s also the most expensive. Urine strips give a reasonable alternative, though readings may vary widely according to hydration. Though technology is advancing, breath screens have likewise varying consequences and also a higher initial cost.

Dr Jimenez White Coat
The ketogenic diet, or keto diet, is a low-carbohydrate, high-fat diet which has been demonstrated to have a wide variety of health benefits. As a matter of fact, many research studies have shown how the keto diet can help with weight loss, improving overall health and wellness. Modified versions of the ketogenic diet may also be utilized to accommodate to different needs. Ketogenic diets may even provide benefits against type-2 diabetes, epilepsy, Alzheimer’s disease and cancer.� By drastically reducing carbohydrate intake and replacing it with fat, the human body enters a metabolic state called ketosis, which efficiently burns fat and turns it into energy. Dr. Alex Jimenez D.C., C.C.S.T. Insight

What are the Advantages of Ketosis?

Reaching a state of ketosis may have many advantages from treating chronic ailments to maximizing functionality. While the advantages are well documented, the underlying mechanism of activity isn’t completely known. The ketogenic diet appears to boost the capability of mitochondria, the energy plants of our cells, to provide our own bodies’ with the energy it needs in a manner that reduces inflammation and oxidative stress. Through optimizing how our body uses energy we reinforce our bodies’ capacity to undertake the ever-growing temptations of the contemporary method of living, improving overall health and wellness.

What to Expect with the Ketogenic Diet

Although the ketogenic diet may result in rapid weight loss through ketosis, the dietary program includes some health risks, such as nutrient deficiencies, heart problems, gastrointestinal health issues, such as constipation, and much more. As a result of health risks involved, specialists advise some people, like those with cardiovascular disease or even people that are at a greater risk for this, to�be careful with the ketogenic diet. Individuals with type 2 diabetes should consult their healthcare professionals. Due to the severe limitations and removal of certain food groups, such as carbohydrates, the strategy might also be hard to stick to in the long term.

If you’re planning to try out the ketogenic diet, make sure you speak with a healthcare professional to be sure to meet your nutritional requirements with the nutritional regimen. Working with an expert can help you figure out if you need to make modifications or stop using the ketogenic diet in the event that complications may occu. 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

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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. �

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EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor


Analyzing the Ketogenic Diet

Analyzing the Ketogenic Diet

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.




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EXTRA IMPORTANT TOPIC: Low Back Pain Management


MORE TOPICS: EXTRA EXTRA:�Chronic Pain & Treatments


Keto Diet: Ketones vs Glucose for Brain Function | Advanced Nutrition

Keto Diet: Ketones vs Glucose for Brain Function | Advanced Nutrition

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.

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10 Common Ketogenic Diet Mistakes for Athletes | Advanced Fitness

10 Common Ketogenic Diet Mistakes for Athletes | Advanced Fitness

Since ketones are a preferred fuel for the heart and the diaphragm, and because a state of ketosis may provide extreme focus and cognitive performance during difficult mental activities, a ketogenic diet can be extremely useful for endurance athletes such as triathletes, distance swimmers, cyclists, marathoners, ultra-runners, etc..


Problem is, there are not a ton of tools out there about how highly active people can really get into a state of ketosis.


In this guide, author, triathlete, and ketogenic expert extraordinaire Patricia Daly explains how to do things the ideal way. Patricia just finished writing an amazing publication called “Practical Keto Meal Plans For Endurance Athletes: Tips, Tricks And How To’s For Optimizing Performance Using A High Fat, Low Carb Meal Plan”, and she has a wealth of information on this topic.�So in this article, you’re going to get the top 10 mistakes low-carb athletes make.


Mistake #1: Being Scared of Fat


The ketogenic diet is quite different from other typical diets. The objective of your lifestyle is to teach the body to utilize ketone bodies rather than glucose as the primary source of energy. That is why the quantity is about 75 to 85+ percent of daily caloric consumption.


Quite simply, if you operate out quite a bit you probably eat about 2,900 calories a day, of which about 2,300 will come from fat should you follow a ketogenic diet. Fat contains 9 calories per gram, and you will eat 256g of fat daily, based on how much you train of course. To simplify this further: all your intake will be approximately 18 tablespoons, one tablespoon of olive oil, for example, weighs approximately 14g.


Mistake #2: Eating Too Much Protein


Another mistake novices make is to substitute most of the carbs they used to consume with protein instead of fat. This happen all of the time. The problem is that excess protein intake can result in gluconeogenesis, which is the conversion of amino acids to glucose. This is not what we need on a ketogenic diet, to the contrary, promote the creation of ketone bodies from fatty acids to keep glucose levels low.


A lot of men and women are amazed when they start weighing their food according to the proper meal plans and realize how small protein they actually must consume on a ketogenic dietplan. But fat is protein sparing, meaning that a high fat consumption is decreased with by your need for protein.


Mistake #3: Carbs Creeping In


Carbohydrates can quickly add up if you’re eager to get your veggies, herbs and spices in. They can in fact be found in products that you’d never think contained carbs.


Good examples are any processed foods, shop bought salad dressings, milk replacements (many almond and coconut milks have added sugar), tomato sauce, a few meats, such as duck confit, starchy vegetables and even herbal tea, to name only a few. Eating out can be challenging because most restaurants prefer to use dressings, sauces and dips that have added alternative or honey sources of sugar. It tastes nice but is not keto-friendly. Having strong, reliable information is key to carb restriction, especially in the first stages when metabolic alterations occur.


Mistake #4: Giving Up Too Early


The faster you enter nutritional ketosis, the more side effects you could suffer from initially. The metabolic changes may be striking because every single cell in the body wants to do the change from glucose. Insulin is influenced: Amounts return because of reduced consumption. Insulin allows the kidneys to hold on to sodium. If insulin is at a lower level, the body starts getting rid of excess sodium and also water.


This is why it’s so important to guarantee you add sufficient sodium to your diet and keep well hydrated, especially in the first few days of beginning to reduce carbohydrates. This will make certain that you don’t suffer from some of the symptoms of the dreaded “keto flu”: shivers, foggy mind, headaches or nausea are some of the possible symptoms. It is probably more appropriate to call them “carbohydrate withdrawal symptoms” because of the effects on hormonal and electrolyte balance.


Things that help to get over these initial obstacles are strong bone broth with good quality salt, a great deal of rest, no extreme exercise and plenty of mineral-rich water, e.g. San Pellegrino. However, the best advice I could give is to take things slowly and not to give up when you are feeling a bit off in the initial phases, provided you’ve done all of the suggested blood tests to exclude any underlying health issues before starting a ketogenic diet.


Mistake #5: Scared of the New; Eating the Same


Many people feel overwhelmed from the first phases of executing a low carb and ketogenic diet. And because they have very little experience with certain new foods, they still keep eating the same “safe” low-carb stuff. For instance bacon and eggs for breakfast and nuts for snacks.


Of course this means that you’re eating low carbohydrate but its often a first priority to always improve their wellness. And this is only possible using a healthy diet. Eating the same things over and over again is dull, it may set you up for having deficiencies and growing food intolerances. This happens quite frequently especially if you’re somewhat worried, your gut function is not optimal or if you’re using medications.


Food intolerances may have an effect not only on your stomach health by causing nausea, bloating, diarrhea, constipation or other symptoms, but also in your immune system. The best advice is to continue experimenting with new foods, even if they seem completely strange to you, such as (for example) chicken liver, that is way easier to find and prepare than you’d think. There is a wonderful recipe for each and every food.


Mistake #6: Eating Processed Foods


This is particularly common for people who have read about the Atkins diet and noticed the products that are sold online and in stores. Yes, they keep you inside the limits that you select and may make life easier but they are also full of artificial flavors, polydextrose, odor, sucralose and other artificial sweeteners that can mess with your psychological and physical health.


A rule of thumb: if you wouldn’t have the ability to bake or cook a meal depending on the components list (because you don’t recognize half of them or wouldn’t know where to buy them), then you should stay away from it. Hopefully, with a growing amount of research to verify the advantages of low carb and ketogenic diets there will be plenty of incentives for companies to create snacks based on real foods.


Mistake #7: Deficiency Of Planning (And Obsessing)


Both absence of preparation and obsessing too much could be stumbling stone. If you don’t plan you’re much more likely to “fail” and give up in your lifestyle modifications. You see, the challenge is that if you realize you haven’t got all you might not find them.


Some of the goods that are staples on a low carb or ketogenic diet like olive oil, olives, fatty fish or ghee can only be bought in health stores or on the internet. More and more supermarkets start to inventory them but this depends where you live. Planning makes it more easy to cook in bulk and save cash and time.


Evidently, it’s a different story for somebody who follows a ketogenic diet for medical reasons, for instance in the case of epilepsy, no mistakes could be made without a consequence and where the diet has to be nicely calculated. But occasionally people become stressed out about dietary modifications that they wake in the middle of the night and can not go back to sleep. They fear what their next meal could look like ketones could be further increased by them or what to eat on a vacation In cases like this, it’s time to choose a (big) step back, relax, try some recipes without weighing and counting and possibly give it another go after a couple of weeks with a great deal of preparation and support. Stressing about meals can cancel the positive effects of good nutrition out.


Mistake #8: Ignoring the Body’s Warning Signs


Trainers who obsess over dietary modifications can get caught up in measuring blood sugar and ketones, weighing their meals all the time, producing exact meal programs and they are able to get really scared of eating out where items are out of their hands. In experience, they are also likely candidates to ignore the warning signs of their body.


Please remember that you just know your body best and that no meal or instruction program can conquer your innate wisdom and intuition. Take warning signs since you have it in your head to adhere to a specific regime, and do not override them. Low carb and ketogenic diets are not for everybody and if you are feeling worse than before, even after getting over the first symptoms talked about before, then it is probably time to stop and reconsider.


Mistake #9: Social Pressure


Even years into following a ketogenic diet, many people get opinions from close friends and family regarding this specific nutritional plan and it can sometimes be difficult for individuals to follow their keto diet close when social pressure pushes them to eat a variety of foods outside of their meal plan.


Ketogenic diets are still very poorly known even by the medical profession. People don’t understand where a few treats are allowed in moderate quantities, that you can not follow the famous 80/20 rule. You are either in ketosis or you’re not.


Mistake #10: Bad Timing


And lastly, lets discuss when to start lowering your carbs or attempting to go into ketosis. Please don’t do it a week before your competition of the season or during a period when you’re super busy at the office.


The best period of the year to make key adjustments to lifestyle and diet is when you are “off season”. Another fantastic time is before a few preparatory competitions to build towards the most important race. That’s when you see how your body responds to intensity and if the diet doesn’t suit you, you have loads of time to make changes.


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.

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