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Med Clin North Am. Author manuscript; available in PMC 2019 Jan 1.

Published in final edited form as:

PMCID: PMC5764193

NIHMSID: NIHMS904015

1National Institute of Diabetes & Digestive & Kidney Diseases

2Johns Hopkins Bloomberg School of Public Health

3George Washington University School of Medicine

1National Institute of Diabetes & Digestive & Kidney Diseases

2Johns Hopkins Bloomberg School of Public Health

3George Washington University School of Medicine

Weight loss can be achieved through a variety of modalities, but long-term maintenance of lost weight is much more challenging. Obesity interventions typically result in early rapid weight loss followed by a weight plateau and progressive regain. This review describes our current understanding of the biological, behavioral, and environmental factors driving this near-ubiquitous body weight trajectory and the implications for long-term weight management. Treatment of obesity requires ongoing clinical attention and weight maintenance-specific counseling to support sustainable healthful behaviors and positive weight regulation.

Keywords: obesity treatment, weight loss, weight maintenance, behavioral counseling, appetite, physiology

Robert is a 47 year old patient who initially weighed 270 pounds. He lost 85 pounds three years ago by carefully following your guidance to decrease his caloric intake to 1500 calories per day and exercise six days weekly. Today he comes in for his annual physical examination. You were excited to hear about his continued progress and see how much more hes lost, but you felt immediately dejected to see that he had regained almost 60 pounds. I dont know what to dothe weight keeps coming back on. I keep trying, but there must be something wrong. Im sure my metabolism is in the dumps. It feels like every moment of the day I cant help but think about food it was never like this before I lost the weight. And no matter how hard I try to stop eating after one serving, I just cant seem to do it anymore. Feeling defeated, he says I dont even know whats the point of doing this anymore!

Frustrated, you remind him that he was able to do it just fine when he was losing weight initially, and he just needs to keep working hard at it. I know its not easy, but I cant help you unless youre willing to help yourself. You just need to work harder and take control of this again. You feel for him, but you know that you need to be stern to get him past this backsliding. Hoping to motivate him, you remind him how bad he will feel if he regains more weight, and you tell him to make a follow-up appointment for six months and warn him that if he doesnt turn things around quickly he will have to restart his blood pressure medications.

Substantial weight loss is possible across a range of treatment modalities, but long-term sustenance of lost weight is much more challenging, and weight regain is typical13. In a meta-analysis of 29 long-term weight loss studies, more than half of the lost weight was regained within two years, and by five years more than 80% of lost weight was regained ()4. Indeed, previous failed attempts at achieving durable weight loss may have contributed to the recent decrease in the percentage of people with obesity who are trying to lose weight5 and many now believe that weight loss is a futile endeavor6.

Average time course of weight regain after a weight loss intervention.

Data from Anderson JW, Konz EC, Frederich RC, et al. Long-term weight-loss maintenance: a meta-analysis of US studies. Am J Clin Nutr 2001;74(5):579584.

Here, we describe our current understanding of the factors contributing to weight gain, physiological responses that resist weight loss, behavioral correlates of successful maintenance of lost weight, as well as the implications and recommendations for long-term clinical management of patients with obesity.

Long term weight management is extremely challenging due to interactions between our biology, behavior, and the obesogenic environment. The rise in obesity prevalence over the past several decades has been mirrored by industrialization of the food system7 involving increased production and marketing of inexpensive, highly-processed foods810 with supernormal appetitive properties11,12. Ultraprocessed foods13 now contribute the majority of calories consumed in America14 and their overconsumption has been implicated as a causative factor in weight gain15. Such foods are typically more calorically dense and far less healthy than unprocessed foods such as fruits, vegetables, and fish16. Food has progressively become cheaper17, fewer people prepare meals at home18,19, and more food is consumed in restaurants18. In addition, changes in the physical activity environment have made it more challenging to be active throughout the day. Occupations have become more sedentary20 and suburban sprawl necessitates vehicular transportation rather than walking to work or school as had been common in the past. Taken together, changes in the food and physical activity environments tend to drive individuals towards increased intake, decreased activity, and ultimately weight gain.

Outdated guidance to physicians and their patients gives the mistaken impression that relatively modest diet changes will consistently and progressively result in substantial weight loss at rate of one pound for every 3500 kcal of accumulated dietary calorie deficit2124. For example, cutting just a couple of cans of soda (~300 kcal) from ones daily diet was thought to lead to about 30 pounds of weight loss in a year, 60 pounds in 2 years, etc. Failure to achieve and maintain substantial weight loss over the long term is then simply attributed to poor adherence to the prescribed lifestyle changes, thereby potentially further stigmatizing the patient as lacking in willpower, motivation, or fortitude to lose weight25.

We now know that the simple calculations underlying the old weight loss guidelines are fatally flawed because they fail to consider declining energy expenditure with weight loss26. More realistic calculations of expected weight loss for a given change in energy intake or physical activity are provided by a web-based tool called NIH Body Weight Planner (http://BWplanner.niddk.nih.gov) that uses a mathematical model to account for dynamic changes in human energy balance27.

In addition to adaptations in energy expenditure with weight loss, body weight is regulated by negative feedback circuits that influence food intake28,29. Weight loss is accompanied by persistent endocrine adaptations30 that increase appetite and decrease satiety31 thereby resisting continued weight loss and conspiring against long-term weight maintenance.

The overlapping physiological changes that occur with weight loss help explain the near-ubiquitous weight loss time course: early rapid weight loss that stalls after several months, followed by progressive weight regain32. Different interventions result in varying degrees of weight loss and regain, but the overall time courses are similar. As people progressively lose more and more weight, they fight an increasing battle against the biological responses that oppose further weight loss.

Appetite changes likely play a more important role than slowing metabolism in explaining the weight loss plateau since the feedback circuit controlling long-term calorie intake has greater overall strength than the feedback circuit controlling calorie expenditure. Specifically, it has been estimated that for each kilogram of lost weight, calorie expenditure decreases by about 2030 kcal/d whereas appetite increases by about 100 kcal/d above the baseline level prior to weight loss31. Despite these predictable physiologic phenomena, the typical response of the patient is to blame themselves as lazy or lacking in willpower, sentiments that are often reinforced by healthcare providers, as in the example of Robert, above.

Using a validated mathematical model of human energy balance dynamics27,31, illustrates the energy balance dynamics underlying the weight loss time courses of two example 90 kg women who either regain (blue curves) or maintain (orange curves) much of their lost weight after reaching a plateau within the first year of a diet intervention. In both women, large decreases in calorie intake at the start of the intervention result in rapid loss of weight and body fat leading to a modest decrease in calorie expenditure that contributes to slowing weight loss. However, the exponential rise in calorie intake from its initially reduced value is the primary factor that halts weight loss within the first year. In contrast to the modest drop in calorie expenditure of less than 200 kcal/d at the weight plateau, appetite has risen by 400600 kcal/d and energy intake has increased by 600700 kcal/d since the start of the intervention.

Mathematical model simulations of body weight, fat mass, energy intake, energy expenditure, appetite, and effort for two hypothetical women participating in a weight loss program. The curves in blue depict the typical weight loss, plateau and regain trajectory whereas the orange curves show successful weight loss maintenance.

These mathematical model results contrast with patients reports of eating approximately the same diet after the weight plateau that was previously successful during the initial phases of weight loss33. While self-reported diet measurements are notoriously inaccurate and imprecise3436, it may be possible to reconcile such data with objectively quantified increases in calorie intake. It is entirely possible that patients truly believe they are sticking with their diet despite not losing any more weight or even regaining weight.

The patients perception of ongoing diet maintenance despite no further weight loss may arise because the physiological regulation of appetite occurs in brain regions that operate below the patients conscious awareness37. Thus, signals to the brain that increase appetite with weight loss could introduce subconscious biases such as portion sizes creeping upwards over time. Such a slow drift upwards in energy intake would be difficult to detect given the large 2030% fluctuations in energy intake from day to day38,39. Furthermore, a relatively persistent effort is required to avoid overeating to match the increased appetite that grows in proportion to the weight lost31. For example, the model-calculated intervention effort for the simulated patient who experiences the weight plateau at six months followed by weight regain (, blue curves) maintains more than ~70% of their initial intervention effort until the plateau. Perhaps self-reported diet maintenance before and after the weight plateau is more representative of the patients relatively persistent effort to avoid overeating in response to their increased appetite31. New technologies using repeated weight monitoring can be used calculate changes in calorie intake and effort over time40 and help guide individuals participating in a weight loss intervention4144.

From a purely calorie balance perspective, a patient who maintains lost weight after the first year of an intervention (, orange curves) may be eating only about 100 kcal/d fewer than a patient who experiences long-term weight regain (, blue curves). However, such a small difference in food intake behavior is somewhat misleading considering that prevention of weight regain requires about 300500 kcal/d of increased persistent effort to counter the ongoing slowing of metabolism and increased appetite associated with the lost weight. The more typical pattern of long-term weight regain is characterized by a waning effort to sustain the intervention.

There are likely many factors that account for the ability of some patients to achieve and maintain large weight losses over the long term whereas others experience substantial weight regain. Unravelling the biological, psychosocial, educational, and environmental determinants of such individual variability will be an active area of obesity research for the foreseeable future45.

The laws of thermodynamics dictate that the energy derived from macronutrients being oxidized via the intricate biochemical pathways of oxidative phosphorylation inside cells can be equated to the values measured by combusting these fuels in a bomb calorimeter. However, this equivalence does not necessarily imply that a calorie is a calorie when it comes to diets with different macronutrient proportions differentially impacting weight loss.

Altering dietary macronutrient composition could theoretically influence overall calorie intake or expenditure resulting in a corresponding change in body weight. Alternatively, manipulation of diet composition can result in differences in the endocrine status in a way that could theoretically influence the propensity to accumulate body fat or affect subjective hunger or satiety. These possibilities do not necessarily violate the laws of thermodynamics since any change in the bodys overall energy stores (i.e. fat mass) must be accompanied by changes in calorie intake or expenditure. Therefore, it is theoretically possible that a particular diet could result in an advantageous endocrine or metabolic state that promotes weight loss. This promise provides fodder for the diet industry and false hope to the patient with obesity since it implies that if they simply choose the right diet then weight loss can be easily achieved.

In recent years, there has been a reemergence of low-carbohydrate, high-fat diets as popular weight loss interventions. Such diets have been claimed to reverse the metabolic and endocrine derangements resulting from following advice to consume low-fat, high-carbohydrate diets that allegedly caused the obesity epidemic. Specifically, the so-called carbohydrate-insulin model of obesity posits that diets high in carbohydrates are particularly fattening because they increase the secretion insulin and thereby drive fat accumulation in adipose tissue and away from oxidation by metabolically active tissues, and this altered fat partitioning results in a state of cellular starvation leading to adaptive increases in hunger, and suppression of energy expenditure46. Therefore, the carbohydrate-insulin model implies that reversing these processes by eating a low-carbohydrate, high-fat diet should result in effortless weight loss47. Unfortunately, important aspects of the carbohydrate-insulin model have failed experimental interrogation48 and, for all practical purposes, a calorie is a calorie when it comes to body fat and energy expenditure differences between controlled isocaloric diets varying in the ratio of carbohydrate to fat49. Nevertheless, low-carbohydrate, high-fat diets may lead to spontaneous reduction in calorie reduction and increased weight loss, especially over the short term5052. Meta-analyses of long-term weight loss have suggested that low-fat weight loss diets are slightly, if statistically, inferior to low-carbohydrate diets53, but the average differences between diets is too small to be clinically significant54. Furthermore, the similarity of the mean weight loss patterns between diet groups in randomized weight loss trials strongly suggests that there is no generalizable advantage of one diet over another when it comes to long-term calorie intake or expenditure33.

In contrast to the near equivalency of dietary carbohydrate and fat, dietary protein is known to positively influence body composition during weight loss55,56 and has a small positive effect on resting metabolism57. Diets with higher protein may also offer benefits for maintaining weight loss58, particularly when the overall diet has a low glycemic index59. This might be partially mediated by dietary proteins greater effect on satiety compared to carbohydrate and fat55,56 along with the possibility of increased overall energy expenditure60. More research is needed to better understand whether these potentially positive attributes of higher protein diets outweigh concerns that such diets mitigate improvements in insulin sensitivity that are typically achieved with weight loss using lower protein diets61.

Whereas long-term diet trails have not resulted in clear superiority of one diet over another with respect to average weight loss, within each diet group there is a high degree of individual variability and anecdotal success stories abound for a wide range of weight loss diets33. Some of this variability may be due to interactions between diet type and patient genetics62,63 or baseline physiology such as insulin sensitivity6467. Such interactions offer the promise of personalized diets that optimize the patients chances for long-term weight loss success45,63. Unfortunately, diet-biology interactions for weight loss have not always been reproducible68,69 and likely explain only a fraction of the individual variability.

It is certainly possible that the patients who successfully lost weight on one diet would have been equally successful had they been assigned to an alternative diet. In other words, long-term success with a weight loss diet may have less to do with biology than factors such as the patients food environment, socioeconomics, medical comorbidities, and social support, as well as practical factors, such as developing cooking skills and managing job requirements. Such non-biological factors likely play a strong role in determining whether diet adherence is sustainable.

Given the physiologic and environmental obstacles to long-term maintenance of lost weight described above, we offer the following recommendations for clinical practice and then present an alternative preferable depiction of the opening case example.

Long term behavioral changes and obesity management require ongoing attention. Even the highest quality short-term interventions are unlikely to yield continued positive outcomes without persisting intervention and support. Several studies show that ongoing interaction with healthcare providers or in group settings significantly improves weight maintenance and long-term outcomes, compared with treatments that end after a short period of time ()70,71. The importance of long-term intervention has been codified in the obesity treatment guidelines, which state that weight loss interventions should include long term comprehensive weight loss maintenance programs that continue for at least 1 year72.

Weight management programs with a focus on maintenance of lost weight demonstrate improved long-term weight loss (red curve) compared to programs without maintenance visits (blue curve).

Adapted from Perri MG, McAllister DA, Gange JJ, et al. Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol 1988;56(4):529534; with permission.

With respect to the case study at the start of this paper, the physician should not expect ongoing weight loss without ongoing support and interaction. Rather than asking Robert to turn things around on his own, the physician has an opportunity to reengage with Robert to offer guidance and support in a more intensive and regular manner than sending him off on his own for six months, or if this is not realistic in a busy primary care practice, he could refer Robert to an obesity medicine specialist, registered dietitian, comprehensive weight management clinic, or recommend that he engage in a community weight management group, such as the Diabetes Prevention Program (now covered by Medicare for patients with prediabetes), or a commercial program, such as Weight Watchers.

Behavioral strategies for initiation of weight loss are described elsewhere in this volume []. Weight-loss specific behaviors associated with long term success include: frequent self-monitoring and self-weighing, reduced calorie intake, smaller and more frequent meals/snacks throughout the day, increased physical activity, consistently eating breakfast, more frequent at-home meals compared with restaurant and fast-food meals, reducing screen time, and use of portion-controlled meals or meal substitutes2,7375. Weight maintenance-specific behavioral skills and strategies help patients to build insight for long-term management, anticipate struggles and prepare contingency plans, moderate behavioral fatigue, and put into perspective the inevitable lapses and relapses of any long-term engagement.

Although the research is mixed, several studies show improved weight loss outcomes in patients receiving weight maintenance-specific training, compared with those who only receive traditional weight loss training7679. Strategies are discussed below for weight maintenance-specific counseling.

People tend to focus on what they havent achieved, rather than what theyve already accomplished. Unlike with weight loss, during which the external reward of watching the scale decrease and clinical measures (e.g., lipid levels) improve can increase motivation, the extended period of weight maintenance has fewer of these explicit rewards. To support motivation and make salient satisfaction with outcomes, call attention to patients progress, which often becomes overlooked. Providers can point to the magnitude of weight that has been kept off, putting it into context in terms of average expected weight loss (described below), as well as clinical improvements in risk factors, such as blood pressure and glycemic control. Additionally, showing patients before and after photographs of themselves and other tangible evidence of progress helps them to build awareness of and appreciate the benefits they have already achieved, which may improve long-term persistence with weight maintenance efforts.

Anticipating and managing high-risk situations for slips and lapses helps patients minimize lapses, get back on track, and avoid giving up. This counseling often includes self-weighing and identifying weight thresholds that signal the need for reengaging with a support team or initiating contingency strategies; proactively developing plans and practicing strategies for managing and coping with lapses; problem solving to identify challenges, formulate solutions, and evaluate options; and building strategies for non-food activities and coping mechanisms, such as engaging in hobbies or mindfulness activities, to minimize counterproductive coping mechanisms, such as emotional eating.

Cycles of negative and maladaptive thoughts (e.g., Whats the pointI failed again and Ill never lose weight!) and coping patterns (e.g., binge eating in response to gaining a few pounds) are counterproductive and demotivating. Helping patients to recognize and restructure the core beliefs and thought processes that underlie these patterns helps minimize behavioral fatigue and prevent or productively manage slips and lapses.

Many tendencies that promote initial weight loss are unrealistic over the long term. For example, many patients aim to make large, absolute changes in an all-or-none fashion via rigid rules, such as aiming for no carbs or very restrictive intake. Much as a sprinter can run all-out for a short race, but not for the entirety of a marathon, expecting strict, all-out efforts and clear-cut, black-and-white outcomes over the lifelong management of obesity is a recipe for frustration and failure. Instead, learning to accept that rigid expectations and perfect adherence to behavioral goals is unrealistic and building cognitive flexibility to take in stride when ones plans do not go according to plan is a core competency for long term sustainable behavioral changes and weight management.

External, superficial rewards are unlikely to support the long term endurance needed for weight maintenance. For example, studies of financial rewards to incentivize behavioral changes, such as weight loss or tobacco cessation, yield initial benefits that invariably wane precipitously over time80,81. Whereas white knuckling and external, controlled motivations, such as directives from a spouse or healthcare provider, may lead to short-term weight loss, longer term sustained motivation is more likely when patients take ownership of their behavioral changes and goals, and engage in them because they are deeply meaningful or enjoyable80,81. As an example, compared with difficulty of sticking to a strict low-fat or low-carb diet, which are often arbitrarily prescribed and of little personal significance to the patient, and therefore difficult to maintain, countless millions throughout the world rigorously stick to comparably strict kosher, halal, or vegan eating patterns, which are aligned with their religious, ethical, or other deeply held beliefs and values. Similarly, prescribing daily gym visits to someone who hates the gym environment or gym activities is unlikely to be fruitful, whereas supporting patients to find more enjoyable physical activities, such as sports or group dance-exercise classes, increases the likelihood of continuing over time.

Both patients and healthcare providers have wildly unrealistic expectations for weight loss outcomes. In one study, patients entering a diet and exercise program expected to lose 2040% of their starting body weight - amounts that can only realistically be achieved by bariatric surgery82. Physician expectations are similarly inflated: in a survey of primary care physicians, acceptable behavioral weight loss was considered to be a loss of 21% of initial body weight83. In contrast, numerous studies show that diet, exercise, and behavioral counseling, in the best of cases, only leads to 510% average weight loss, and few patients with significantly elevated initial weights achieve and maintain an ideal body weight. From a cognitive psychology perspective, a waning intervention effort may be due to disappointment in the degree of weight loss actually achieved82 leading the patient to conclude that the effort is not worth the achieved benefits84.

Although the published data is mixed on whether unrealistic outcomes will deter weight loss success, it stands to reason that excessive discrepancies between expectations and actual outcomes would be demoralizing and increase negative thoughts and self-blame (which itself is associated with numerous negative health outcomes85), and may diminish long term persistence for continued behavioral change and weight loss maintenance. We recommend advising patients about the physiologic challenges of long term weight loss and the degree of weight loss that can be realistically expected from behavioral interventions. At minimum, theres no known harm of offering this insight and being frank with patients about expectations, and it may help them navigate the minefield of unscrupulous diet programs and promises that promise miraculous outcomes.

Nonetheless, positive outcomes of behavioral counseling extend beyond weight loss. Despite the modest weight losses associated with behavioral interventions, small weight losses can lead to impressive health improvements and risk factor reductions. In the Diabetes Prevention Program, 7% weight loss over six months led to 58% reduction in development of diabetes, despite half the weight being regained over three years86. In the Look Ahead trial, 6% weight loss over eight years yielded improvements in a range of cardiovascular risk factors, including glycemic control and lipids, as well as less medication usage, and reduced hospitalizations and healthcare costs87,88.

While losing weight is important for improved health, peoples motivations for seeing the scale go down is all-too-often driven by cultural norms for thinness and healthcare provider-imposed weight loss directives. These external motivations can move the weight loss needle in the short-run, but they rarely lead to long-lasting determination. As described in the section above, long term management is improved when motivations are aligned with personal values and preferences. Helping patients shift their locus of motivation from weight loss alone to intrinsically meaningful areas, such as health improvement, can improve long term weight and behavioral outcomes89.

For patients that do not achieve sufficient weight loss or health improvements with basic counseling in primary care settings, there are several opportunities to intensify therapy. Consider referral to a registered dietitian, obesity medicine physician, or comprehensive weight management clinic, as well as targeted specialists (such as a behavioral psychologist for patients with binge eating disorder or body dysmorphia). For patients with BMI greater than 30 kg/m2 (or 2730 kg/m2 with obesity-related comorbid conditions), obesity pharmacotherapy leads to as much as 15% weight loss in responders, with weight loss being maintained in several studies for several years9092. For patients with BMI greater than 40 kg/m2 (or 3540 kg/m2 with comorbidities), bariatric surgery is a well-studied and valuable option that leads to large, sustainable weight losses in most patients93.

Using the principles discussed above, a more productive encounter in response to Roberts presentation might go like this:

Physician: I understand, and I know its challenging. It sounds like youre feeling frustrated because youve worked so hard and you feel like youve got nothing to show for it.

He nods and says, Exactly. Whats the point of doing this anymore.

Physician: From my view, the evidence we have shows something different: Youre actually doing quite well in the scheme of things. I actually see quite a lot of progress for your efforts. Youre down 25 lbs, right? Thats almost 10% down from where you startedthats impressive. Few people lose that much weight and keep it off for three years. Studies show that even under the best of circumstances with aggressive counseling, average weight loss is between 510% of starting body weight so youre doing better than most! Youve been able to get off several blood pressure medications and you no longer take the pain medicine for your back and knees. And, we know from studies that losing just 7%, even if part of it is regained over the years, lowers the risk of diabetes by 60%! His eyes widen. Weight goes up and down, and our bodies fight back against weight loss, so this is never easy. Some regain and relapse is inevitable just like in other areas of life. He takes a deep breath and clearly seems more engaged and hopeful. So lets figure out how we can move forward and keep getting the benefits, and Ill be here with you to help along the way. Lets agree on a couple of next steps, and well meet again in a few weeks to see how its going. If we need, we can also consider additional strategies or treatments.

The degree of weight loss and its maintenance should not be the sole metric of obesity treatment success. Rather, physicians should support and encourage patients to make sustainable improvements in their diet quality and physical activities if these behaviors fail to meet national guidelines94,95. Such lifestyle changes over the long-term will likely improve the health of patients even in the absence of major weight loss96.

Key points

Long-term maintenance of lost weight is the primary challenge of obesity treatment.

Biological, behavioral, and environmental factors conspire to resist weight loss and promote regain.

Treatment of obesity requires ongoing attention and support, and weight maintenance-specific counseling, to improve long-term weight management.

Realistic long-term weight loss magnitude is significantly lower than patient and healthcare provider expectations. However, even small amounts of sustained weight loss lead to clinical health improvements and risk factor reductions.

Funding: This research was supported by the Intramural Research Program of the NIH, National Institute of Diabetes & Digestive & Kidney Diseases.

KDH has received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure. KDH also has a patent on a method of personalized dynamic feedback control of body weight (US Patent No 9,569,483; assigned to the National Institutes of Health).

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Conflicts of Interest: SK has no relevant disclosures.

42. Hall KD Inventor; National Institutes of Health, assignee. Personalized dynamic feedback control of body weight. 9,569,483. [02/14/2017];US patent. 2013

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Maintenance of lost weight and long-term management of obesity

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The ketogenic diet (or keto diet, for short) is a low carb, high fat diet that offers many health benefits.

In fact, many studies show that this type of diet can help you lose weight and improve your health (1).

Ketogenic diets may even have benefits against diabetes, cancer, epilepsy, and Alzheimers disease (2, 3, 4, 5).

Here is a detailed beginners guide to the keto diet.

The ketogenic diet is a very low carb, high fat diet that shares many similarities with the Atkins and low carb diets.

It involves drastically reducing carbohydrate intake and replacing it with fat. This reduction in carbs puts your body into a metabolic state called ketosis.

When this happens, your body becomes incredibly efficient at burning fat for energy. It also turns fat into ketones in the liver, which can supply energy for the brain (6).

Ketogenic diets can cause significant reductions in blood sugar and insulin levels. This, along with the increased ketones, has some health benefits (6, 7, 8).

The keto diet is a low carb, high fat diet. It lowers blood sugar and insulin levels and shifts the bodys metabolism away from carbs and toward fat and ketones.

There are several versions of the ketogenic diet, including:

However, only the standard and high protein ketogenic diets have been studied extensively. Cyclical or targeted ketogenic diets are more advanced methods and primarily used by bodybuilders or athletes.

The information in this article mostly applies to the standard ketogenic diet (SKD), although many of the same principles also apply to the other versions.

There are several versions of the keto diet. The standard (SKD) version is the most researched and most recommended.

Ketosis is a metabolic state in which your body uses fat for fuel instead of carbs.

It occurs when you significantly reduce your consumption of carbohydrates, limiting your bodys supply of glucose (sugar), which is the main source of energy for the cells.

Following a ketogenic diet is the most effective way to enter ketosis. Generally, this involves limiting carb consumption to around 20 to 50 grams per day and filling up on fats, such as meat, fish, eggs, nuts, and healthy oils (6).

Its also important to moderate your protein consumption. This is because protein can be converted into glucose if consumed in high amounts, which may slow your transition into ketosis (10).

Practicing intermittent fasting could also help you enter ketosis faster. There are many different forms of intermittent fasting, but the most common method involves limiting food intake to around 8 hours per day and fasting for the remaining 16 hours (11).

Blood, urine, and breath tests are available, which can help determine whether youve entered ketosis by measuring the amount of ketones produced by your body.

Certain symptoms may also indicate that youve entered ketosis, including increased thirst, dry mouth, frequent urination, and decreased hunger or appetite (12).

Ketosis is a metabolic state in which your body uses fat for fuel instead of carbs. Modifying your diet and practicing intermittent fasting can help you enter ketosis faster. Certain tests and symptoms can also help determine whether youve entered ketosis.

A ketogenic diet is an effective way to lose weight and lower risk factors for disease (1, 2, 3, 4, 5).

In fact, research shows that the ketogenic diet may be as effective for weight loss as a low fat diet (13, 14, 15).

Whats more, the diet is so filling that you can lose weight without counting calories or tracking your food intake (16).

One review of 13 studies found that following a very low carb, ketogenic diet was slightly more effective for long-term weight loss than a low fat diet. People who followed the keto diet lost an average of 2 pounds (0.9 kg) more than the group that followed a low fat diet (13).

Whats more, it also led to reductions in diastolic blood pressure and triglyceride levels (13).

Another study in 34 older adults found that those who followed a ketogenic diet for 8 weeks lost nearly five times as much total body fat as those who followed a low fat diet (17).

The increased ketones, lower blood sugar levels, and improved insulin sensitivity may also play a key role (18, 19).

For more details on the weight loss effects of a ketogenic diet, read this article.

A ketogenic diet can help you lose slightly more weight than a low fat diet. This often happens with less hunger.

Diabetes is characterized by changes in metabolism, high blood sugar, and impaired insulin function (20).

The ketogenic diet can help you lose excess fat, which is closely linked to type 2 diabetes, prediabetes, and metabolic syndrome (21, 22, 23, 24).

One older study found that the ketogenic diet improved insulin sensitivity by a whopping 75% (25).

A small study in women with type 2 diabetes also found that following a ketogenic diet for 90 days significantly reduced levels of hemoglobin A1C, which is a measure of long-term blood sugar management (26).

Another study in 349 people with type 2 diabetes found that those who followed a ketogenic diet lost an average of 26.2 pounds (11.9 kg) over a 2-year period. This is an important benefit when considering the link between weight and type 2 diabetes (24, 27).

Whats more, they also experienced improved blood sugar management, and the use of certain blood sugar medications decreased among participants throughout the course of the study (27).

For more information, check out this article on the benefits of low carb diets for people with diabetes.

The ketogenic diet can boost insulin sensitivity and cause fat loss, leading to significant health benefits for people with type 2 diabetes or prediabetes.

The ketogenic diet actually originated as a tool for treating neurological diseases such as epilepsy.

Studies have now shown that the diet can have benefits for a wide variety of different health conditions:

However, keep in mind that research into many of these areas is far from conclusive.

A ketogenic diet may provide many health benefits, especially with metabolic, neurological, or insulin-related diseases.

Any food thats high in carbs should be limited.

Heres a list of foods that need to be reduced or eliminated on a ketogenic diet:

Avoid carb-based foods like grains, sugars, legumes, rice, potatoes, candy, juice, and even most fruits.

You should base the majority of your meals around these foods:

Its best to base your diet mostly on whole, single-ingredient foods. Heres a list of 44 healthy low carb foods.

Base the majority of your diet on foods such as meat, fish, eggs, butter, nuts, healthy oils, avocados, and plenty of low carb veggies.

To help get you started, heres a sample ketogenic diet meal plan for one week:

Always try to rotate the vegetables and meat over the long term, as each type provides different nutrients and health benefits.

For tons of recipes, check out these 101 healthy low carb recipes and this keto shopping list.

You can eat a wide variety of tasty and nutritious meals on a ketogenic diet. Its not all meats and fats. Vegetables are an important part of the diet.

In case you get hungry between meals, here are some healthy, keto-approved snacks:

Great snacks for a keto diet include pieces of meat, cheese, olives, boiled eggs, nuts, raw veggies, and dark chocolate.

Although getting started on the ketogenic diet can be challenging, there are several tips and tricks that you can use to make it easier.

Reading food labels, planning your meals ahead, and bringing your own foods when visiting family and friends can make it much easier to stick to the ketogenic diet.

Many restaurant meals can be made keto-friendly.

Most restaurants offer some kind of meat or fish-based dish. Order this and replace any high carb food with extra vegetables.

Egg-based meals are also a great option, such as an omelet or eggs and bacon.

Another favorite is bun-less burgers. You could also swap the fries for vegetables instead. Add extra avocado, cheese, bacon, or eggs.

At Mexican restaurants, you can enjoy any type of meat with extra cheese, guacamole, salsa, and sour cream.

For dessert, ask for a mixed cheese board or berries with cream.

When eating out, select a meat-, fish-, or egg-based dish. Order extra veggies instead of carbs or starches, and have cheese for dessert.

Although the ketogenic diet is usually safe for most healthy people, there may be some initial side effects while your body adapts.

Theres some anecdotal evidence of these effects often referred to as the keto flu (38). Based on reports from some on the eating plan, its usually over within a few days.

Reported keto flu symptoms include diarrhea, constipation, and vomiting (39). Other less common symptoms include:

To minimize this, you can try a regular low carb diet for the first few weeks. This may teach your body to burn more fat before you completely eliminate carbs.

A ketogenic diet can also change the water and mineral balance of your body, so adding extra salt to your meals or taking mineral supplements may help. Talk to your doctor about your nutritional needs.

At least in the beginning, its important to eat until youre full and avoid restricting calories too much. Usually, a ketogenic diet causes weight loss without intentional calorie restriction.

Many of the side effects of starting a ketogenic diet can be limited. Easing into the diet and taking mineral supplements can help.

Staying on the keto diet in the long term may have some negative effects, including risks of the following:

A type of medication called sodium-glucose cotransporter 2 (SGLT2) inhibitors for type 2 diabetes can increase the risk for diabetic ketoacidosis, a dangerous condition that increases blood acidity. Anyone taking this medication should avoid the keto diet (40, 41).

More research is being done to determine the safety of the keto diet in the long term. Keep your doctor informed of your eating plan to guide your choices.

There are some side effects to the keto diet about which you should speak to your doctor if you plan to stay on the diet long term.

Although no supplements are required, some can be useful.

Certain supplements can be beneficial on a ketogenic diet. These include exogenous ketones, MCT oil, and minerals.

Here are answers to some of the most common questions about the ketogenic diet.

1. Can I ever eat carbs again?

Yes. However, its important to significantly reduce your carb intake initially. After the first 2 to 3 months, you can eat carbs on special occasions just return to the diet immediately after.

2. Will I lose muscle?

Theres a risk of losing some muscle on any diet. However, protein intake and high ketone levels may help minimize muscle loss, especially if you lift weights (50, 51).

3. Can I build muscle on a ketogenic diet?

Yes, but it may not work as well as on a moderate carb diet (52, 53). For more details about low carb or keto diets and exercise performance, read this article.

4. How much protein can I eat?

Protein should be moderate, as a very high intake can spike insulin levels and lower ketones. Around 35% of total calorie intake is probably the upper limit.

5. What if I am constantly tired, weak, or fatigued?

You may not be in full ketosis or be utilizing fats and ketones efficiently. To counter this, lower your carb intake and revisit the points above. A supplement like MCT oil or ketones may also help (42, 43).

6. My urine smells fruity. Why is this?

Dont be alarmed. This is simply due to the excretion of by-products created during ketosis (54).

7. My breath smells. What can I do?

This is a common side effect. Try drinking naturally flavored water or chewing sugar-free gum.

8. I heard ketosis was extremely dangerous. Is this true?

People often confuse ketosis with ketoacidosis. Ketoacidosis is dangerous, but the ketosis on a ketogenic diet is usually fine for healthy people. Speak to your doctor before starting any new diet.

9. I have digestion issues and diarrhea. What can I do?

This common side effect usually passes after 3 to 4 weeks. If it persists, try eating more high fiber veggies (55, 56).

A ketogenic diet can be great for people who:

It may be less suitable for elite athletes or those wishing to add large amounts of muscle or weight.

It may also not be sustainable for some peoples lifestyles and preferences. Speak with your doctor about your eating plan and goals to decide if a keto eating plan right for you.

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The Ketogenic Diet: A Detailed Beginners Guide to Keto - Healthline

Summary of findings

Overall, vegans in this study had higher risks of total and some site-specific fractures (hip, leg, vertebra) than meat eaters. The strongest associations were observed for hip fractures, for which fish eaters, vegetarians, and vegans all had higher risks. These risk differences might be partially explained by the lower average BMI, and lower average intakes of calcium and protein in the non-meat eaters. However, because the differences remained, especially in vegans, after accounting for these factors, other unaccounted for factors may be important.

Few previous studies have examined the associations of vegetarian diets with fracture risk. In previous EPIC-Oxford analyses of self-reported fractures with short follow-up, vegans, but not fish eaters or vegetarians, were reported to have 30% (HR 1.30; 1.02, 1.66) higher risks of total fractures, but in contrast to the current findings, the association attenuated completely when restricted to participants who reported consuming at least 525mg/day of calcium [16]. This apparent inconsistency might be explained by several differences between the current and previous analysis; while the current analysis included close to 4000 hospital-admitted cases over more than 17years of average follow-up on around 55,000 participants, the previous study included under 2000 self-reported fracture cases over 5years of follow-up on around 35,000 participants. Given the difference in case ascertainment method, the current analysis is less prone to reporting error and is not susceptible to selective drop-out. It is also possible that there was insufficient power to detect a difference after stratifying by calcium intake status in the previous analysis, which also did not examine site-specific fractures.

The only other studies which reported on risks of fractures by diet groups were one small prospective study in Vietnam of 210 women (105 vegans) which found no significant difference in fracture incidence (10 cases in total) between vegans and omnivores over 2years [17], and one prospective study in India which reported a higher crude rate of stress fractures (604 cases in total) among 2131 vegetarian than 6439 non-vegetarian army recruits [18]. Separately, previous findings from the Adventist Health Study 2, which has a large proportion of vegetarians, showed that participants who ate meat more than three times a week had lower risks of hip fractures (HR 0.60; 0.41, 0.87) than participants who ate meat less than once a week [32], while combined analyses of peri- and postmenopausal women from Adventist Health Study 1 and 2 found that participants who ate meat more than four times a week had lower risks of wrist fractures (HR 0.44; 0.23, 0.84) than participants who never ate meat [33], but these results cannot be used to infer risks in fish eaters, vegetarians, or vegans as separate diet groups.

The higher observed risks of fractures in non-meat eaters were usually stronger before BMI adjustment, which suggests that the risk differences were likely partially due to differences in BMI. Vegetarians and vegans generally have lower BMI than meat eaters [2, 8], and previous studies have reported an inverse association between BMI and some fractures, particularly hip fractures, possibly due to reasons including the cushioning against impact force during a fall, enhanced oestrogen production with increased adiposity, or stronger bones from increased weight-bearing [14, 34]. However, a positive association between BMI and fracture risk has been observed for some other sites, including ankle fractures, possibly as a result of higher torques from twisting of the ankle in people with higher BMI [14]. No significant differences in the risks of ankle fractures by diet group were observed in our study, but the point estimates were directionally consistent with a lower risk in all non-meat eaters before BMI adjustment, and the results might reflect a counterbalance between a protective effect from lower BMI but higher risk due to lower intakes of nutrients related to bone health in the non-meat eaters.

In our stratified analyses, there is limited evidence of heterogeneity in fracture risk by BMI categories. Although a statistically significant higher risk of total and hip fractures was only observed in vegans in the lower BMI category (<22.5kg/m2), our interpretation is limited by the small numbers of cases in each stratum in these analyses, especially because of the strong correlation between diet group and BMI, which results in very few vegans in the higher BMI category, and vice versa comparatively small numbers of meat eaters with a low BMI. In addition to BMI, previous studies have reported that muscle strength is an important risk factor which is protective against fall risk and subsequently fractures in older adults [35]. A previous study in the UK found lower lean mass and grip strength in vegetarians and vegans compared to meat eaters [2]; therefore, the possible influences of muscle strength and fall risk in addition to bone health on fracture risk in vegetarian and vegan populations should be further investigated. Fractures at some sites, especially at the hip, may also be more related to osteoporosis than fractures at some other sites, which might be more likely to be the result of violent impacts in accidents [36, 37]. We were unable to differentiate fragility and traumatic fractures in this study, since data were not available on the causes of the fractures.

In this study and previous studies, vegans had substantially lower intakes of calcium than other diet groups since they do not consume dairy, a major source of dietary calcium [4, 5], while both vegetarians and vegans had lower protein intakes on average [6, 7]. In the human body, 99% of calcium is present in bones and teeth in the form of hydroxyapatite, which in cases of calcium deficiency gets resorbed to maintain the metabolic calcium balance, and thus, osteoporosis could occur if the calcium was not restored [38,39,40]. A recent meta-analysis reported that increasing calcium intake from either dietary sources or supplements resulted in small increases in BMD [9], but the evidence on fracture risk has been less consistent. Previous analyses in EPIC-Oxford found a higher risk of self-reported fractures in women, but not men, with calcium intakes below 525mg/day compared with over 1200mg/day [41]. A recent meta-analysis of both randomised trials and prospective studies concluded that there was no evidence of an association between calcium intake from diet and fracture risk, but a possible weak protective association between calcium supplement use and some fractures [10]. More recently however, a separate meta-analysis showed a protective effect against fractures of combined vitamin D and calcium supplements, but not vitamin D supplements alone [11].

For protein, some older studies suggested that excessive protein intake would lead to an increased metabolic acid load, subsequently buffered by bone resorption and calciuria, and thus poorer bone health [12, 42]. However, more recent experimental evidence has shown that high protein intake also increases intestinal calcium absorption [43], and stimulates the production of insulin-like growth factor (IGF)-I [44], which in turn is associated with better bone health [45, 46]. Two meta-analyses, which included different studies, both reported a possible protective effect of higher protein intake on lumbar spine BMD [13, 47]; several epidemiological studies have reported inverse associations between protein intake and fracture risks [48,49,50], though a recent meta-analysis found no significant association between protein intake and osteoporotic fractures [51].

The higher risks of fractures especially in the vegans remained significant after adjustment for dietary calcium and protein, which suggests that these factors may at most only partly explain the differences in fracture risks by diet group, and other factors may also contribute. However, estimation of intakes of these nutrients by questionnaires has substantial error, and we were only able to account for differences in dietary calcium but not differences in calcium supplement use, since data on the latter were not available. A detailed analysis of the associations of specific foods, such as meat or dairy, with fracture risk is beyond the scope of the current study, but should be explored in further studies. Future research should also focus on possible effects of other nutrients or biological markers on fracture risks, for example circulating vitamin D, vitamin B12, or IGF-I, which may vary by degree of animal-sourced food intake [52,53,54]. The value of incorporating habitual dietary habits in addition to established parameters for predicting fracture risks in clinical settings should also be further explored.

The strengths of this study were that it included a large number of non-meat eaters with a long follow-up, and studied both total and site-specific fractures, after accounting for a range of confounders. We updated diet group and relevant confounders where possible, to account for changes over the period of follow-up. There was little evidence of reverse causality, as results were similar after excluding the first 5years of follow-up. The outcome data were ascertained based on hospital records, which reduced misreporting and selective loss to follow-up, although a possible limitation of this approach was that less serious fractures that did not require hospitalisation would not have been captured.

Of other limitations, while we excluded known cases of fractures before baseline based on hospital records, this may not be a complete exclusion, since no questions on previous diagnosis of fractures (prior to the earliest available hospital data) or osteoporosis were asked at baseline, and no data on the use of anti-osteoporosis medication were available. Repeat measures of diet were not available in all participants, and the exact date of dietary change during follow-up was also not recorded, but considering the good agreement of diet group in participants who did provide a repeat measure, and the fact that a dietary change may only influence fracture risk after a period of time, we do not expect substantial misclassification. As with all observational studies, residual confounding from both dietary and non-dietary factors may be present; for example, the role of calcium might have been underestimated due to measurement error. As the study predominantly includes white European participants, generalisability to other populations or ethnicities may be limited, which could be important considering previously observed differences in BMD [2, 55] and fracture risks [56] by ethnicity. We also observed only a small number of cases in many subgroup analyses, and thus, it is likely we had insufficient power to reliably assess whether there might be any heterogeneity by these subgroups including age, sex, menopausal status, or BMI; additional data are therefore needed to confirm or refute possible differences. In particular, because the EPIC-Oxford cohort consists predominantly of women (77%), further work should be conducted in cohorts with a larger proportion of men to explore heterogeneity by sex and to derive reliable sex-specific estimates.

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Vegetarian and vegan diets and risks of total and site-specific ...

Medical condition

Chronic myelogenous leukemia (CML), also known as chronic myeloid leukemia, is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which a proliferation of mature granulocytes (neutrophils, eosinophils and basophils) and their precursors is found. It is a type of myeloproliferative neoplasm associated with a characteristic chromosomal translocation called the Philadelphia chromosome.

CML is largely treated with targeted drugs called tyrosine-kinase inhibitors (TKIs) which have led to dramatically improved long-term survival rates since 2001. These drugs have revolutionized treatment of this disease and allow most patients to have a good quality of life when compared to the former chemotherapy drugs. In Western countries, CML accounts for 1525% of all adult leukemias and 14% of leukemias overall (including the pediatric population, where CML is less common).[3]

The way CML presents depends on the stage of the disease at diagnosis as it has been known to skip stages in some cases.[4]

Most patients (~90%) are diagnosed during the chronic stage which is most often asymptomatic. In these cases, it may be diagnosed incidentally with an elevated white blood cell count on a routine laboratory test. It can also present with symptoms indicative of hepatosplenomegaly and the resulting left upper quadrant pain this causes. The enlarged spleen may put pressure on the stomach causing a loss of appetite and resulting weight loss. It may also present with mild fever and night sweats due to an elevated basal level of metabolism.[4]

Some (<10%) are diagnosed during the accelerated stage which most often presents bleeding, petechiae and ecchymosis.[4] In these patients fevers are most commonly the result of opportunistic infections.[4]

Some patients are initially diagnosed in the blast phase in which the symptoms are most likely fever, bone pain and an increase in bone marrow fibrosis.[4]

In most cases, no obvious cause for CML can be isolated.[5]

CML is more common in males than in females (male to female ratio of 1.4:1) and appears more commonly in the elderly with a median age at diagnosis of 65 years.[5] Exposure to ionising radiation appears to be a risk factor, based on a 50 fold higher incidence of CML in Hiroshima and Nagasaki nuclear bombing survivors.[5] The rate of CML in these individuals seems to peak about 10 years after the exposure.[5]

CML was the first cancer to be linked to a clear genetic abnormality, the chromosomal translocation known as the Philadelphia chromosome. This chromosomal abnormality is so named because it was first discovered and described in 1960 by two scientists from Philadelphia, Pennsylvania, USA: Peter Nowell of the University of Pennsylvania and David Hungerford of Fox Chase Cancer Center.[6]

In this translocation, parts of two chromosomes (the 9th and 22nd) switch places. As a result, part of the BCR ("breakpoint cluster region") gene from chromosome 22 is fused with the ABL gene on chromosome 9. This abnormal "fusion" gene generates a protein of p210 or sometimes p185 weight (p210 is short for 210 kDa protein, a shorthand used for characterizing proteins based solely on size). Because abl carries a domain that can add phosphate groups to tyrosine residues (a tyrosine kinase), the bcr-abl fusion gene product is also a tyrosine kinase.[7][8]

The fused BCR-ABL protein interacts with the interleukin 3beta(c) receptor subunit. The BCR-ABL transcript is continuously active and does not require activation by other cellular messaging proteins. In turn, BCR-ABL activates a cascade of proteins that control the cell cycle, speeding up cell division. Moreover, the BCR-ABL protein inhibits DNA repair, causing genomic instability and making the cell more susceptible to developing further genetic abnormalities. The action of the BCR-ABL protein is the pathophysiologic cause of chronic myelogenous leukemia. With improved understanding of the nature of the BCR-ABL protein and its action as a tyrosine kinase, targeted therapies (the first of which was imatinib) that specifically inhibit the activity of the BCR-ABL protein have been developed. These tyrosine kinase inhibitors can induce complete remissions in CML, confirming the central importance of bcr-abl as the cause of CML.[8]

CML is often suspected on the basis of a complete blood count, which shows increased granulocytes of all types, typically including mature myeloid cells. Basophils and eosinophils are almost universally increased; this feature may help differentiate CML from a leukemoid reaction. A bone marrow biopsy is often performed as part of the evaluation for CML, and CML is diagnosed by cytogenetics that detects the translocation t(9;22)(q34;q11.2) which involves the ABL1 gene in chromosome 9 and the BCR gene in chromosome 22.[9] As a result of this translocation, the chromosome looks smaller than its homologue chromosome, and this appearance is known as the Philadelphia chromosome chromosomal abnormality. Thus, this abnormality can be detected by routine cytogenetics, and the involved genes BCR-ABL1 can be detected by fluorescent in situ hybridization, as well as by PCR.[10]

Controversy exists over so-called Ph-negative CML, or cases of suspected CML in which the Philadelphia chromosome cannot be detected. Many such patients in fact have complex chromosomal abnormalities that mask the (9;22) translocation, or have evidence of the translocation by FISH or RT-PCR in spite of normal routine karyotyping.[11] The small subset of patients without detectable molecular evidence of BCR-ABL1 fusion may be better classified as having an undifferentiated myelodysplastic/myeloproliferative disorder, as their clinical course tends to be different from patients with CML.[12]

CML must be distinguished from a leukemoid reaction, which can have a similar appearance on a blood smear.[10]

CML is often divided into three phases based on clinical characteristics and laboratory findings. In the absence of intervention, CML typically begins in the chronic phase, and over the course of several years progresses to an accelerated phase and ultimately to a blast crisis. Blast crisis is the terminal phase of CML and clinically behaves like an acute leukemia. Drug treatment will usually stop this progression if started early. One of the drivers of the progression from chronic phase through acceleration and blast crisis is the acquisition of new chromosomal abnormalities (in addition to the Philadelphia chromosome).[7] Some patients may already be in the accelerated phase or blast crisis by the time they are diagnosed.[10]

Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis. During this phase, patients are usually asymptomatic or have only mild symptoms of fatigue, left side pain, joint and/or hip pain, or abdominal fullness. The duration of chronic phase is variable and depends on how early the disease was diagnosed as well as the therapies used. In the absence of treatment, the disease progresses to an accelerated phase.[10] Precise patient staging based on clinical markers and personal genomic profile will likely prove beneficial in the assessment of disease history with respect to progression risk.[13]

Criteria for diagnosing transition into the accelerated phase are somewhat variable; the most widely used criteria are those put forward by investigators at M.D. Anderson Cancer Center,[14] by Sokal et al.,[15] and the World Health Organization.[12][16] The WHO criteria[17] are perhaps most widely used, and define the accelerated phase by the presence of 1 of the following haematological/cytogenetic criteria or provisional criteria concerning response to tyrosine kinase inhibitor (TKI) therapy

The patient is considered to be in the accelerated phase if any of the above are present. The accelerated phase is significant because it signals that the disease is progressing and transformation to blast crisis is imminent. Drug treatment often becomes less effective in the advanced stages.[12]

Blast crisis is the final phase in the evolution of CML, and behaves like an acute leukemia, with rapid progression and short survival.[10] Blast crisis is diagnosed if any of the following are present in a patient with CML:[18]

The only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant.[19] Other than this there are four major mainstays of treatment in CML: treatment with tyrosine kinase inhibitors, myelosuppressive or leukopheresis therapy (to counteract the leukocytosis during early treatment), splenectomy and interferon alfa-2b treatment.[19] Due to the high median age of patients with CML it is relatively rare for CML to be seen in pregnant women, despite this, however, chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with the cytokine Interferon-alpha.[20]

In the past, antimetabolites (e.g., cytarabine, hydroxyurea), alkylating agents, interferon alfa 2b, and steroids were used as treatments of CML in the chronic phase, but since the 2000s have been replaced by Bcr-Abl tyrosine-kinase inhibitors[21] drugs that specifically target BCR-ABL, the constitutively activated tyrosine kinase fusion protein caused by the Philadelphia chromosome translocation. Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes hydroxyurea is still used to counteract the high leukocyte counts encountered during treatment with tyrosine kinase inhibitors like imatinib; in these situations it may be the preferred myelosuppressive agent due to its relative lack of leukemogenic effects and hence the relative lack of potential for secondary haematologic malignancies to result from treatment.[22] IRIS, an international study that compared interferon/cytarabine combination and the first of these new drugs imatinib, with long-term follow up, demonstrated the clear superiority of tyrosine-kinase-targeted inhibition over existing treatments.[23]

The first of this new class of drugs was imatinib mesylate (marketed as Gleevec or Glivec), approved by the US Food and Drug Administration (FDA) in 2001. Imatinib was found to inhibit the progression of CML in the majority of patients (6575%) sufficiently to achieve regrowth of their normal bone marrow stem cell population (a cytogenetic response) with stable proportions of maturing white blood cells. Because some leukemic cells (as evaluated by RT-PCR) persist in nearly all patients, the treatment has to be continued indefinitely. Since the advent of imatinib, CML has become the first cancer in which a standard medical treatment may give to the patient a normal life expectancy.[24]

To overcome imatinib resistance and to increase responsiveness to TK inhibitors, four novel agents were later developed. The first, dasatinib, blocks several further oncogenic proteins, in addition to more potent inhibition of the BCR-ABL protein, and was approved in 2007, by the U.S. Food and Drug Administration (FDA) to treat CML in people who were either resistant to or intolerant of imatinib. A second TK inhibitor, nilotinib, was approved by the FDA for the same indication. In 2010, nilotinib and dasatinib were also approved for first-line therapy, making three drugs in this class available for treatment of newly diagnosed CML. In 2012, radotinib joined the class of novel agents in the inhibition of the BCR-ABL protein and was approved in South Korea for people resistant to or intolerant of imatinib. Bosutinib received US FDA and EU European Medicines Agency approval on 4 September 2012, and 27 March 2013, respectively for the treatment of adults with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy.[citation needed]

Asciminib (Scemblix) was approved for medical use in the United States in October 2021.[25]

While capable of producing significantly improved responses compared with the action of imatinib, neither dasatinib nor nilotinib could overcome drug resistance caused by one particular mutation found to occur in the structure of BCR-ABL1 known as the T315I mutation (in other words, where the 315th amino acid is mutated from a threonine residue to an isoleucine residue).[citation needed] Two approaches were developed to the treatment of CML as a result:

In 2007, Chemgenex released results of an open-label Phase 2/3 study (CGX-635-CML-202) that investigated the use of a non BCR-ABL targeted agent omacetaxine, administered subcutaneously (under the skin) in patients who had failed with imatinib and exhibited T315I kinase domain mutation.[26][27] This is a study which is ongoing through 2014.[28] In September 2012, the FDA approved omacetaxine for the treatment of CML in the case of resistance to other chemotherapeutic agents.[29][30]

Independently, ARIAD pharmaceuticals, adapting the chemical structures from first and second-generation TK inhibitors, arrived at a new pan-BCR-ABL1 inhibitor which showed (for the first time) efficacy against T315I, as well as all other known mutations of the oncoprotein. The drug, ponatinib, gained FDA approval in December 2012 for treatment of patients with resistant or intolerant CML. Just as with second-generation TK inhibitors, early approval is being sought to extend the use of ponatinib to newly diagnosed CML also.[citation needed]

In 2005, encouraging but mixed results of vaccination were reported with the BCR/ABL1 p210 fusion protein in patients with stable disease, with GM-CSF as an adjuvant.[31]

Before the advent of tyrosine kinase inhibitors, the median survival time for CML patients had been about 35 years from time of diagnosis.[3]

With the use of tyrosine kinase inhibitors, survival rates have improved dramatically. A 2006 follow-up of 553 patients using imatinib (Gleevec) found an overall survival rate of 89% after five years.[32]

A 2011 followup of 832 patients using imatinib who achieved a stable cytogenetic response found an overall survival rate of 95.2% after 8 years, which is similar to the rate in the general population. Fewer than 1% of patients died because of leukemia progression.[24]

CML accounts for 8% of all leukaemias in the UK, and around 680 people were diagnosed with the disease in 2011.[33]

The American Cancer Society estimates that in 2014, about 5,980 new cases of chronic myeloid leukemia were diagnosed, and about 810 people died of the disease. This means that a little over 10% of all newly diagnosed leukemia cases will be chronic myeloid leukemia. The average risk of a person getting this disease is 1 in 588. The disease is more common in men than women, and more common in whites than African-Americans. The average age at diagnosis is 64 years, and this disease is rarely seen in children.[34]

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Chronic myelogenous leukemia - Wikipedia

Low carb foods are products that are low in carbohydrate content and high in protein, healthy fats, fiber, and essential nutrients. They are satisfying, nutritionally dense, and healthy and help dieters to lose extra weight.

Some food groups are low in carbohydrates, including lean meat, dairies, fish, and vegetables. Fish meat contains omega-3, phosphorus, vitamin B6, and other nutrients. The group of lean meats is also an integral component of any low-carb diet. Some fruits and vegetables are also allowed, for example:

Good or complex carbohydrates get absorbed gradually while bad carbs cause blood sugar level spikes. Hamburger buns, pretzels, potatoes, corn, and white rice are products to avoid. There are healthy foods to consume, including whole wheat products, sunflower and sesame seeds, nuts, soybeans, cheese and cream, and others.

The Glycemic Index assigns values to different foods to measure their effect on blood sugar or glucose. This index is important in that some foods trigger spikes in blood glucose while others help maintain steady blood sugar levels. Examples of foods with high GI include branflakes, bagels, scones, and donuts. Foods with a low glycemic index value are healthy and safe, including yam, nuts, chick peas, butter beans, and hummus.

The list of low carb foods is quite long and depends on the your choice. Some popular plans exclude fruits during the initial phase while others are more restrictive. The list generally includes meat, shellfish, and fish such as:Lamb, Bacon, Venison, Lobster, Crabmeat, Peasant, Cornish hen, Sole, Sardines

Dieters also consume cheese, milk, eggs, and oils such as safflower, grapeseed, extra virgin olive oil. Salad garnishes and vegetables such as okra, leeks, bamboo shoots, and asparagus are also on the allowed list. People are encouraged to drink water and herbal teas.

Low carb bars include ingredients such as apple, coconut, cinnamon, berries, and others. Retailers advertise high protein bars and offer meal replacements with a high nutritional value. Opponents point to the fact that they are highly processed and contain artificial flavors and other ingredients. Some ingredients, for example, rolled oats are rich in carbohydrates. Another problem is that high protein bars are very sweet and contain sweeteners such as inulin, acesulfame potassium, sucralose, and glycerin. They are also packed with sugar alcohols, soy-derived products, and processed ingredients.

Some diets allow sugar substitutes such as xylitol, stevia, mannitol, erythritol, and others.

Carbohydrate reduced menus feature protein sources, plenty of vegetables, and other unprocessed, healthy foods. Basically, a balanced menu includes products such as: non-gluten grains, healthy oils and fats, dairies, seeds and nuts, eggs, fish, lean meat, some vegetables, some fruits

There are plenty of healthy and filling breakfast ideas for your menu, for example:

Dieters use flour substitutes such as soy flour, almond flour, coconut flour, protein powder, and pumpkin puree.

Snacks are an important component of many diets, and there are many recipes to try. People can choose from delicious and nutrient-rich snacks such as:

Low carb plans emphasize the importance of filling and healthy meals, and many dishes are easy to prepare. Dieters can choose from fish-based and meat-based meals, soups, and vegetarian options. Recipes to try include:

Diet-friendly desserts are delicious and quick to make and are low on simple carbohydrates and sugar content. You can make:

and many other desserts.

Popular plans such as South Beach and Atkins emphasize a healthy and balanced approach to eating and weight loss. A low carb diet is a nutritional approach based on reduced carbohydrate consumption that focuses on healthy foods such as monounsaturated fats, protein, and vegetables rich in fiber.

Reduced-carbohydrate plans often go through several stages, and the initial stage is more restrictive. Different foods and food groups are gradually added to the daily menu. The menu and carbohydrate consumption depends on the plan of choice - Go Lower, Dukan, Ketogenic, Hollywood, High Protein, Scarsdale, and others. These plans are based on the assumption that the body burns fat deposits for energy when carbohydrate consumption is more limited.

There are popular reduced-carbohydrate plans such as:

Some plans are based on a healthy protein, carbohydrate, and fat ratio while others recommend eating foods with low GI (the Low GI Diet). Semi-vegetarian and vegetarian plans and the Mediterranean Diet are also popular choices. Crash diets such as the Beverly Hills Diet are extreme and should be avoided.

According to healthcare professionals, foods high in carbs are associated with health risks such as:

Vitamin deficiency is also a source of concern because vitamin E, K, and A are found in foods that are high in healthy fats. Some studies also suggest that high carb foods may increase the risk for chronic and serious conditions such as Alzheimer's and heart disease. The consumption of foods that contain bad carbs also increases the risk for diabetes and heart problems. Foods such as whole-grain breads, dark breads, and high-protein products are healthier choices. A healthy diet based on protein-rich foods, complex carbohydrates, and fats lowers LDL cholesterol and blood pressure and thus reduces the risk for stroke, heart attack, and other heart problems.

Reduced-carbohydrate plans offer plenty of benefits such as steady weight loss, lower triglyceride levels, lower insulin and blood sugar levels, and many others. There are other benefits to low carbing, including positive effect on diseases and conditions such as Parkinson's, seizures and epilepsy, high fasting blood sugar, and abdominal obesity. According to a study at Duke University, low carb plans also improve glycemic control and have a beneficial effect on type 2 diabetes.

Many studies indicate that low carb diets result in more significant health improvements compared to low fat plans. For example, the Duke University study followed patients on a low glycemic and ketogenic plan and found out that the second group lost more weight within a period of 6 months. Following the ketogenic diet resulted in a more drastic reduction in hemoglobin A1 levels, and more patients stopped taking diabetes medications. Another study followed Swedish patients suffering from type 2 diabetes, prediabetes, and ischemic heart disease. Some of the patients followed the Mediterranean Diet while the second group ate foods such as nuts, eggs, vegetables and fruit, fish, and meat. The second group saw significant improvement in weight and glycemic levels. Other studies also prove the beneficial effects of low carb diets. One study published in the New England Journal of Medicine followed people on a low carb and low fat diets. The low carb group lost 2.8 percent more weight on average. Another study focused on patients with severe obesity. Many of the participants were diagnosed with type 2 diabetes and metabolic syndrome. The low carbers lost more weight compared to the low fat group. Other studies have also shown significant improvement in LDL particle size and cholesterol levels.

Some critics point to the fact that reduced-carbohydrate plans are hard to follow and lead to diet boredom. While these plans ban simple carbohydrates, there is a wealth of products and recipes to try, from gourmet foods to snacks you can have on the go. Critics also point out that some popular plans exclude foods that supply essential nutrients. Supporters claim that sugary and starchy foods are packed with simple carbohydrates and are empty of nutritional value. Finally, critics claim that low carb plans encourage the consumption of saturated fat. While people consume some foods that are high in saturated fats, many products contain omega-3 and monounsaturated fat.

Crash diets involve a drastic reduction of calories and are harmful for human health. Diets such as the Junk Food, Cabbage Soup, and Subway Diet pose health risks associated with nutritional deficiency which can result in tiredness, irritability, food cravings, and depression. In the long term, crash dieting increases the risk for kidney and liver problems, calcium deficiency, osteoporosis, bulimia and anorexia, and other serious problems. Low carb plans, on the other hand, emphasize a balanced approach to dieting and include all major food groups, the only exception being bad carbohydrates. A low carb diet is a lifestyle change because it is an effective weight loss approach with long term results. Plans such as the Atkins Diet go through an initial phase of quick weight loss followed by a lifetime maintenance phase. Once dieters have found their carb tolerance level, they try to stay within that range to maintain healthy weight throughout life. In this sense, the eating habits developed during earlier stages help dieters to control their weight and are a lifestyle change.

People find support in low-carb forums, message boards, and different online networks. Popular plans also offer nutritional advice, recipes, and weight loss tools to help dieters stay on track. Some plans also offer diet-friendly products such as cereals, bread, and cheese, as well as magazines, books, scales, and other products. Newsletters and interactive tools are also available, and some plans offer the option to get professional advice from a weight-loss mentor. Videos, cheat sheets, and apps that offer a database of foods and diet-friendly restaurants are also available.

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Low Carb Foods and Diets Guide

"Boundaries are not about telling someone else what they can or cannot do," says Urban. "A boundary is not designed to control someone else. A boundary is designed to let other people know what actions we are going to take to keep ourselves safe and healthy." For example, let's say you'd like to set boundaries with family members around diet culture conversations. "The boundary in this situation is not to tell your family, 'You can't talk about your diets anymore,'" says Urban. Rather, frame the boundary around how you participate in those conversations and offer an actionable solution.

You could say, "Just so you know, it makes me really uncomfortable when we talk about the food that's on our plate while we are eating. Can we not bring that subject of conversation up?" Or perhaps, "I'm not in a great place with my mental health when it comes to my body, so it would really be helpful for me if we chose not to talk about our bodies or our weight when we get together. Is that something you're willing to do?"

If that person is unwilling to respect the boundary after that, then you may need to set stricter boundaries in place. For example, if a family member keeps talking about diet culture, you could say, "It seems like we just can't eat together without this being a subject of conversation. So I'll come by after dinner." As Urban reminds us, "You're always focused on the actions that you are going to take on behalf of yourself (and perhaps your younger children) to keep you safe and healthy."

Originally posted here:
3 Tips To Set Healthy Boundaries With Yourself & Others - mindbodygreen

Dieters have long been warned to avoid eating late at night. Some research, like this study from 2019, provides scientific support for that conventional wisdom by associating eating later in the day with a higher risk of obesity and losing less weight after completing weight loss surgery.

However, little research has been conducted on how the timing of eating impacts physiological mechanisms, according to the researchers from Brigham and Womens Hospital who published the results of a new randomized, controlled, crossover trial in the journal Cell Metabolism.

We wanted to test the mechanisms that may explain why late eating increases obesity risk, notes senior author Dr. Frank A. J. L. Scheer, director of the Medical Chronobiology Program in Brighams Division of Sleep and Circadian Disorders.

The current buzz surrounding intermittent fasting, an eating pattern that involves fasting for a period each day, makes this study particularly timely, according to Prof. Kelly C. Allison, a professor of psychology at the Perelman School of Medicine at the University of Pennsylvania, and director of the Center for Weight and Eating Disorders, who was not involved with this study.

This study really does a nice job of targeting [] the impact of the timing of eating, she told Medical News Today, and it did so in a tightly controlled way within a laboratory experiment.

The study featured 16 participants with a body mass index (BMI) in the overweight or obesity range. They ranged in age from 25 to 59, with a mean age of 37. Five women and 11 men participated. The paper notes five participants were Black, three were Asian and one was Hispanic.

To be selected for the study, participants had to be in good health. They also reported habitually eating breakfast, and stable levels of physical activity.

None had worked shift work in the prior 12 months. For 2 weeks before each testing visit, the participants did not drink caffeine or alcohol, use tobacco in any form, or take drugs, either recreational drugs or medicinal, except for birth control and one participant took antihypertensive medication throughout the study.

No women in perimenopause took part in this study. Pre-menopausal women were scheduled to participate during specific times of their menstrual cycles to avoid hormone surges around ovulation.

For the study, participants spent 9 days in laboratory suites at the Brigham and Womens Hospital Center for Clinical Investigation on two separate occasions. They took 3 to 12 weeks off between each laboratory stay.

Additionally, in the 2 to 3 weeks prior to arriving at the laboratory for the first stay, participants prepared for the study by going to sleep and waking up on the same schedule. Researchers monitored that participants spent a fixed, 8-hour period in bed by having them wear a wrist actigraphy.

Participants also kept a sleep diary and called into a time-stamped voicemail prior to going to sleep and after waking up.

Their effort here was to try to get people to conform to a regular sleep-wake cycle before they came into the lab, Prof. Allison explained.

In the 3 days prior to arriving at the laboratory, participants were also instructed to strictly follow identical diets and meal schedules.

At the facility, light levels and temperature were strictly controlled. Participants did not have phones, radios, or access to the internet, and they were not allowed visitors. They did not exercise. A video camera in each room monitored compliance.

During each stint at the laboratory, participants ate controlled nutrient diets on a firm schedule. Participants on the early meal schedule had their first meal 1 hour after waking and ate again every 250 minutes.

For the late meal schedule, every meal was scheduled for 4 hours later. A researcher timed participants as they ate and no meal lasted longer than 30 minutes.

On test days, participants reported their perceived hunger and appetite using a series of computerized visual analog scales 18 times a day.

Researchers looked at the impact of late eating on the hormones ghrelin, which tells the brain that the body needs food, and leptin, which tells the brain that the stomach is full. Researchers tested these hormones hourly over the course of 24 hours on every test day.

Additionally, researchers measured participants energy expenditure using indirect calorimetry 12 times over the 16 hours participants were awake on test days. They also measured the participants core body temperature continuously for each test day to examine energy expenditure.

To measure how the timing of meals affected molecular pathways involved in how the body stores fat, researchers collected a biopsy of subcutaneous white adipose tissue, the fat stored between skin and muscles, from seven participants during both the early eating stage and late eating stage.

Late eating doubled the odds of being hungry compared to early eating. Late eating also significantly increased the odds of a high rating on a scale of how much a participant would like to eat as well as a high rating on a scale measuring desire to eat starchy foods and meat.

Eating late decreased levels of the hormone leptin by 16% during the 16 hours participants were awake. Additionally, eating late increased the ghrelin-to-leptin ratio, which has been correlated with hunger, by 34% during that time.

Participants who ate later also had significantly lower energy expenditure. Late eating also significantly reduced the participants average core body temperature over 24 hours.

The subset of participants who allowed a biopsy to be collected exhibited adipose tissue gene expression towards increased adipogenesis and decreased lipolysis, which promotes fat growth, when on the late-eating schedule.

I think what [the study] basically is telling us is that it probably really is beneficial to stop eating late into the night.

Prof. Kelly C. Allison

Prof. Allison acknowledged that this study had a small sample size.

These laboratory studies are [] just difficult to do, she told MNT. And Im sure this was done during the time of COVID, which made it even more difficult to find participants.

Of particular concern: The study only had five female participants, which Prof. Allison said limits the generalizability of the research.

And theres only certain kinds of people who can stay in an inpatient unit for 6 days, she said. There are definitely limitations for doing a lab study. There are pros and cons, like the pros are that [] you know exactly what theyre doing, what theyre eating [] when theyre sleeping, you can measure them really frequently. But the cons are that they [] dont represent everybody.

DJ Mazzoni, a registered dietitian based in New York and a medical reviewer for Illuminate Labs, said that even after reading this study his main recommendation continues to be that people should eat nutritious diets free of processed foods.

What a person eats, he told MNT, is more important than time of eating.

Reading the study, Mazzoni wondered whether it was highlighting the benefits of intermittent fasting. I wondered whether the issue was simply that late eating extends the eating window which reduces the time that the body can regenerate and heal without actively digesting food, he explained.

Mazzoni provided an example where two people eat breakfast at 10 a.m. One of those two individuals eats their final meal of the day at 6 p.m. while the other eats their final meal at 11 p.m.

The first individual has an eating window thats 5 hours shorter in duration which may have metabolic benefits, he said. I would be curious to see a study where individuals tried intermittent fasting late in the day, as this could potentially disprove some of the supposed health risks of late eating suggested by the study authors.

Continue reading here:
Eating time and weight gain: Why might late meals increase risk? - Medical News Today

On September 27, the Biden-Harris administration announced its Nutrition, Hunger, and Health Strategy, revealed at the first White House conference to address health and hunger in 50 years. The plan includes initiatives spread across 25 different agencies and commissions, all aimed at ending hunger in America by 2030 and reducing rates of diet-related disease. The five pillars of the new strategy are food access, nutrition, consumer empowerment, physical activity and research.

The plan is massive in scope and has a lot to offer, especially in the area of food access, but ultimately it falls short. The strategy relies heavily on donations from industrial agriculture, but makes scarce mention of the kinds of plant-based dietary interventions that could substantially address food insecurity without the environmental damage caused by the meat and dairy industries.

The new plan relies on a collaborative strategy of working with historically marginalized groups, including Indigenous communities and individuals living in food deserts. The strategy recognizes the importance of sustained dietary change to improve health outcomes, as well as the undeniable reality that many Americans are disadvantaged in terms of health and food access

The initiatives within include boosting physical activity programs, connecting more people to national parks and creating multilingual educational content that covers nutrition.

The White House also wants the FDA to update the requirements for food companies using the term healthy on their labels, a move that would address a longtime concern of public health advocates that the food industrys misleading use of the term is detrimental to public health.

The campaign incorporates a food is medicine approach in seven of their corporate collaborations. Research is beginning to show this to be a highly effective strategy for improving health outcomes.

Yet the plan will undoubtedly face an uphill legislative battle, reports NPR, as much of the strategy will require funding and approval from Congress. The final form of the plan may ultimately end up neutered by compromises made with the Republican Party.

There is barely any mention of plant-based meals or diets in the plan, and just a few proposals focused on fresh fruits and vegetables, despite the many health benefits from boosting consumption of plant-rich meals.

Diets that feature mostly or entirely plant-based whole foods are linked with many positive health outcomes, including lower risk of heart disease, cancer and Type-2 diabetes. Despite these benefits, the vast majority of people in the U.S. do not eat enough fruits and vegetables, according to a 2019 study from the CDC. Getting more people to meet their daily recommendations would improve immune health and decrease disease rates.

Despite these many benefits, the White House is only suggesting a few programs. One proposal seeks to expand SNAP discounts for fruits and vegetables, which would boost access to produce for lower-income individuals. Another would work with the James Beard Foundation to encourage chefs, restaurant owners, and operators to offer at least one plant-based or vegetarian option on their dinner menus. The plan also references a Boston-based program to grow produce and healthy meals for patients too, but doesnt mention expanding this practice nationwide.

Increasing plant-rich diets and decreasing consumption of meat and dairy wouldnt just be a boon for public health, but a clear win for planetary health too, and at a critical time for climate action. Even if the world managed to cut all other emissions to zero, research shows we would still not meet the Paris Accord goals without changing our food systems to reduce red meat consumption.

Meat is also highly inefficient. 77 percent of all agricultural land is used for meat, despite it only providing 17 percent of our food. Calorie-for-calorie, animal products are frighteningly inefficient; for every 1000 calories of feed invested into beef production for example, consumers can only consume 19 calories.

Research suggests that widespread adoption of a vegan diet would allow the U.S. to reduce its agricultural land use 8 times over. This would free up farmland for rewilding efforts and conservation reserves but, when combined with effective distribution channels, would also give the U.S. enough resources to wipe out food insecurity entirely. Despite all of these upsides, the White House strategy doesnt offer much to boost plant-based food production.

What the administrations plan does feature is donations and initiatives from meat and dairy companies, including Tyson, Chobani and Danone. The proposal includes $4 billion in donations from corporations and nonprofits as compared to $2.5 billion for research

The strategy perpetuates the industrys outsize role in crafting federal food policy despite its environmental track record. Over the last 25 years, the U.S. government has given meat and dairy companies subsidies worth 50 billion, not including 160 billion in subsidies for animal feed, a policy that shows no signs of stopping. By comparison, plant-based proteins received less than 20 million in the same period. These subsidies are partly responsible for keeping the price of animal products artificially low and increasing the land use of animal agriculture. Their donations to the White House strategy are modest by comparison.

The agenda mentions climate change once, in the final prong of the final paragraph of the legislation. It doesnt offer much in the way of specifics, simply to research the effects of climate change on food quality and nutrition security.

There is no mention of the consensus on foods impact on climate that already exists: Study after study after study shows that in virtually every area land use, water use, carbon emissions, pollution animal agriculture is significantly more damaging to the Earth than plant-based agriculture.

This is an anathema to the administrations stated climate goals. President Biden campaigned on climate change, while Vice President Kamala Harris is herself a flexitarian and has advocated against the environmental destruction of Big Meat in the past. And while their flagship Inflation Reduction Act is a significant step forward for emissions reduction, possibly the biggest step forward of the century, less than 5 percent of that act goes towards farming, and 0 percent goes towards plant-based solutions.

The Biden-Harris strategy could have done so much more to address hunger and environmental health, in what could have been a food system overhaul to truly address food inequities. This latest proposed federal policy lags behind many local initiatives already working to address food-related emissions, including the New York City School District, which offers Vegan Fridays, and the Washington DC School District, which has mandated plant-based options. The new national strategy could have expanded these initiatives or implemented policies in line with Universal Meals, a plan backed by the Physicians Committee for Responsible Medicine that aims to create whole-foods plant-based options in hospitals, prisons, schools, and other federal facilities. But for now, the Biden-Harris administration appears unwilling, or perhaps unable, to tackle the climate damage caused by our food system..

Read More

What Are the Environmental Impacts of Dairy Farming?

Making Plant-Based More Accessible Through Universal School Meals

Plant-Based Meats Are Better for Your Health and the Environment

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The New White House Nutrition Strategy Barely Mentions Plant-based Diets, and That's a Problem - Sentient Media

Sustainable Diet: A sustainable diet must be economical, available, nutrient-dense, and devoid of hazardous substances like food-borne viruses in order to maintain humans in the short term.

Sustainable Diet: It requires eating foods that are not harmful for the environment

You might be wondering about a sustainable diet if you want to reduce your environmental impact or connect to your local ecology via the foods you eat.

Even while the topic of sustainability in relation to food is frequently discussed, its definition is rarely touched upon. Diets that are fully plant-based or organic are frequently thought of as being sustainable, however, sustainability is far more complicated.

Environmental aspects including resource utilisation and greenhouse gas emissions are crucial. A truly sustainable diet, however, considers labour, food availability, and land management.

How does a sustainable diet work?

There are several recommendations on what constitutes a sustainable diet. A sustainable diet, however, typically takes into account the sort of food we eat, how it is cultivated, delivered, and packaged, as well as the impact this has on the environment.

For instance, a sustainable diet would include a wide range of fruits and vegetables, whole grains, legumes, nuts, dairy, eggs, poultry, fish, and modest amounts of red meat can all be included.

Along with this minimises the use of plastics and other derivatives in food packaging minimises the use of antibiotics and hormones in food production minimises food loss and waste.

How to follow a sustainable diet?

Our diets should become more flexitarian, which means we should consume a greater variety of vegetarian meals together with little portions of fish and meat, such as one huge steak per month or one beef burger per week. Concerns about the lack of protein in a diet that is primarily plant-based are common.

Even while you can consume some meat in a sustainable way, it's vital to think about how much you consume, cut back on your red meat intake, and determine whether you can offset the effects of your meat consumption through other aspects of your diet or consumer behaviour.

Plant-based foods should dominate sustainable diets. You do not have to completely avoid meat or dairy, though. Any diet heavy in plant-based foods fruits, vegetables, grains, legumes, nuts, seeds, and anything made from these sources and low in animal foods is linked to greater health for both people and the environment.

What is the impact of a sustainable diet on us?

A sustainable diet must be economical, available, nutrient-dense, and devoid of hazardous substances like food-borne viruses in order to maintain humans in the short term.

In addition, it's critical that those employed in all facets of the food system from farming and packing to transport, retail, and cooking earn a liveable income, have sufficient health benefits, and work in environments that are secure.

A sustainable diet should reduce the risk of diet-related diseases such as type 2 diabetes, heart disease, and cancer in order to maintain people over the long run.

What is the impact of a sustainable diet on the planet?

A sustainable diet should reduce greenhouse gas emissions, water usage, soil erosion, and pollution, promote animal welfare, and encourage biodiversity in order to preserve the environment for both the short and long term, which also benefits people.

On a personal level, this entails adopting adjustments like cutting back on meat consumption and selecting fruit cultivated without poisonous chemicals and fertilisers. It includes spending money on agricultural systems that replenish rather than degrade the ecosystems to which they belong on a bigger scale.

A sustainable diet emphasises consuming more entire plant foods. Though in far smaller amounts, people may still opt to consume animal products. If you areconsidering changing to a more sustainable diet, youshould think about what diet would be most likely easyto follow and start by taking baby steps.

Disclaimer: This content including advice provides generic information only. It is in no way a substitute for a qualified medical opinion. Always consult a specialist or your own doctor for more information. NDTV does not claim responsibility for this information.

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Diet: Here's What A Sustainable Diet Means And How To Follow It - NDTV Doctor

By Monica Saumoy, MD

Millions of people across the United States struggle with obesity. This common and serious disease increases the risk for a variety of other health conditions, such as diabetes, high blood pressure, and infertility, and it can negatively impact body image and self-esteem.

Treating obesity, however, has been shown to decrease the risk for many of these conditions and to help people overcome the damaging physical and emotional effects of being overweight.

A Complex Disease

Obesity is a complex disease influenced by a range of factors, including:

In addition, obesity itself can cause hormonal and other chemical changes in your body that contribute to the disease and make it difficult to lose weight solely through diet and exercise.

More than 42% of U.S. adults have obesity, which is defined as having a body mass index (BMI) of 30 or above, according to the Centers for Disease Control and Prevention (CDC).

Diet and Exercise Often Not Enough

Many people who have obesity have struggled for years or even decades to lose weight on their own, trying various diets and or exercise programs that promise rapid results.

Diet and exercise alone are often not enough to treat obesity.

This is in part because when your body notices a calorie deficit it starts to get nervous, afraid it could be starving to death. Your brain and your gut then work together to fight the perceived threat, conserving calories to keep your body alive.

A Minimally Invasive Treatment Approach

Endoscopic sleeve gastrectomy is a minimally invasive procedure for weight loss that reduces the size of the stomach so the patient will eat less and lose weight.

With endoscopic sleeve gastroplasty, doctors insert an endoscope equipped with a suturing device into your throat and down to your stomach. The doctor then sutures the stomach to create a smaller, tube-shaped pouch, which effectively restricts the amount of food you can eat.

The procedure is available through the Center for Digestive Health at Penn Medicine Princeton Medical Center, in consultation with the Center for Bariatric Surgery & Metabolic Medicine at Princeton Medical Center. It takes about an hour to 90 minutes to perform and does not require any incisions. Most patients go home the same day.

Following endoscopic sleeve gastroplasty, a liquid diet is temporarily prescribed in order to allow for healing and to jumpstart the weight-loss process. There generally are no other restrictions beyond diet following the procedure. Patients usually return to work within a few days after the procedure and begin to integrate a diet and exercise routine to help lose weight and keep it off.

Studies show that the endoscopic sleeve gastroplasty can result in rapid weight loss, and the average patient can expect to lose 15-18% of their body weight within one year. For example, if you weigh 250 pounds, you could lose up to 45 pounds over time.

Obesity-related medical problems will likely improve with a modest degree of weight loss following the procedure. With steady weight loss, patients often require lower doses of medications for diabetes and high blood pressure, and in some cases, they may no longer need medication at all.

Candidates for endoscopic sleeve gastroplasty include patients with obesity who have a BMI greater than 30 and have not had success with weight loss through diet and exercise.

One Piece of the Puzzle

Successful weight loss is a process, and a procedure like endoscopic sleeve gastrectomy is just one piece of the puzzle. Patients who undergo endoscopic sleeve gastrectomy are encouraged to follow these eight tips to help ensure long-term weight loss success:

1. Attend each and every follow-up visit with the doctors and support staff.2. Eat smaller portions and listen to your fullness signals.3. Choose healthier foods for better nutrition.4. Exercise regularly doing the physical activities you enjoy most.5. Participate in support groups both in person and online.6. Join a bariatric exercise program for support and motivation.7. Get into the habit of monitoring your weight.8. Celebrate your weight loss success with friends and family.

When it comes to weight loss, there is no such thing as a quick fix. Endoscopic sleeve gastrectomy, however, is an effective treatment for obesity that can help jump start your weight loss and give you the leverage you need to build lifelong healthy habits. Coverage for the procedure varies by insurance plan. Check with your plan to see if it is covered.

To find a gastroenterologist with Penn Medicine Princeton Health or for more information about the Center for Bariatric Surgery & Metabolic Medicine at Princeton Medical Center, call 888-742-7496 or visit http://www.princetonhcs.org.

Monica Saumoy, MD, is board certified in gastroenterology and internal medicine and specializes in obesity medicine. She is a member of the Medical Staff at Penn Medicine Princeton Health.

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Health Matters: A Minimally Invasive Approach to Treating Obesity - centraljersey.com

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