Amplify The Effectiveness Of Chiropractic Care: Weight Loss Tips
Effectiveness: We all know and understand the importance of maintaining a healthy weight. Some individuals do quite nicely at managing their pounds with seemingly little effort, while other struggle constantly.
A recent study by the Center for Disease Control and Prevention (CDC) reports that 78 million American adults suffer from obesity. A person who has sustained an injury or suffers from an illness that affects their back, hips, knees or ankles are especially susceptible to weight gain, because they must deal with limited mobility and the stress of daily pain.
Striving to stay in the ideal weight range for your body type and height provides a variety of health benefits such as adding less pressure on your back and joints, and increasing your range of motion. Patients who receive chiropractic care often enjoy the effectiveness of increased healing by pursuing weight loss.
Successfully fight the battle of the bulge with these four handy weight loss tips to:
Amplify The Effectiveness Of Chiropractic Care
First, Start Small
Replace a couple of negative behaviors with positive ones, and commit to making them stick. Great examples of these are substituting water for soft drinks, eating a high-protein breakfast, or changing out your nightly bowl of ice cream with yogurt.
Simply removing 100 calories a day adds up to a 10 pound weight loss over a year’s time. Small modifications offer the dual benefits of being easier to implement while still showing results.
Next, Keep A Journal
Write down every bite you eat along with the portion size. Listing your food intake provides accountability, which may keep you from noshing on that third slice of pizza or super-sizing those fries.
It also arms you with important intel that will be helpful throughout your weight loss journey. If you hit a plateau, read back through the journal to see what you may have changed over time that caused the scales to stall.
And speaking of scales….
Don’t Live And Cry By The Scales
Often, dieters weigh every day and are elated or depressed based on the number on the scales. That’s a roller coaster way to live, and those emotions can cause calorie laden binges!
Plus, daily weighing is not accurate, as fluctuations in water weight are common. Weigh once a week at the most, at roughly the same time each day. A weekly routine gives you a good idea of your success without the stressful up and down of daily weighing.
Decrease Your Sedentary Ways
Even if you are dealing with an injury or medical condition that limits the ability to exercise, you can still probably be less sedentary than you are now. Again, simplicity is the key.
Walk into the bank instead of using the drive through window, stand up to fold clothes instead of sitting down, and take periodic breaks at your desk to stand for a bit.
Ask your chiropractor about any limitations you need to follow, and request stretching exercises as your personal situation permits. Moving more on a daily basis will aid in shedding those extra pounds and keeping them off long-term.
It’s important for individuals to maintain a normal weight range in order to enjoy a healthy life. Chiropractic patients benefit even more from shedding those extra pounds.
By committing to a healthier lifestyle with fewer pounds to carry around, individuals with back and joint injuries will see greater positive impact from their chiropractic visits. Over time, the combination of a leaner body and chiropractic care will bring greater mobility, less pain, and a decreased chance for re-injury to the patient.
Shea Vaughn Talks “Targeting Obesity”
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Obesity is a complex, multifactorial disease, and better understanding of the mechanisms underlying the interactions between lifestyle, environment, and genetics is critical for developing effective strategies for prevention and treatment [1].
Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into�the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.
(i) Epigenetic Changes In Offspring Associated With Maternal Nutrition During Gestation
Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13�15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes,�especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20�30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic �memory� response that precedes development of the altered phenotype in offspring.
Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31�34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling [35]. Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.
Stable transmission of epigenetic information across multiple generations is well described in plant systems and C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species [31]. The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse [38]. In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation�mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color [41]. One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 [42]; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.
While many studies have identified diet-associated epigenetic changes in animal models using candidate site-specific regions, there have been few genome-wide analyses undertaken. A recent study focussed on determining the direct epigenetic impact of high-fat diets/ diet-induced obesity in adult mice using genome-wide gene expression and DNA methylation analyses [43]. This study identified 232 differentially methylated regions (DMRs) in adipocytes from control and high-fat fed mice. Importantly, the corresponding human regions for the murine DMRs were also differentially methylated in adipose tissue from a population of obese and lean humans, thereby highlighting the remarkable evolutionary conservation of these regions. This result emphasizes the likely importance of the identified DMRs in regulating energy homeostasis in mammals.
(i) Genetic association studies. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential�methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46�48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation [49].
From these studies, altered methylation of PGC1A, HIF3A, ABCG1, and CPT1A and the previously described RXRA [18] have emerged as biomarkers associated with, or perhaps predictive of, metabolic health that are also plausible candidates for a role in development of metabolic disease.
Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20�40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping�with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 [8]. Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice [43] and weight loss in humans [64]. These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.
Prenatal environment: Two recently published studies made use of human populations that experienced �natural� variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants [69]. The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood [68]. The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.
Postnatal environment: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the �mature� epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells [77], and muscle tissue [78] in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver [79] and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat [64]. Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80�82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport [83]. Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss [84].
DNA methylation changes associated with obesity or induced by diet or lifestyle interventions and weight loss are generally modest (<15 %), although this varies depending on the phenotype and tissue studied. For instance, changes greater than 20 % have been reported in adipose tissue after weight loss [64] and associations between HIF3A methylation and BMI in adipose tissue were more pronounced than in blood [52].
Conclusions
The prevalence of obesity in the United States has been increasing for almost 50 years. Currently, more than two-thirds of adults and almost one-third of children and adolescents are 
From 2005 to 2014, there was a 1.4% annual increase in cancers related to overweight and obesity among individuals aged 20 to 49 years and a 0.4% increase in these cancers among individuals aged 50 to 64 years. For example, if cancer rates had stayed the same in 2014 as they were in 2005, there would have been 43?000 fewer cases of colorectal cancer but 33?000 more cases of other cancers related to overweight and obesity. Nearly half of all cancers in people younger than 65 years were associated with overweight and obesity. Overweight and obesity among younger people may exact a toll on individuals� health earlier in their lifetimes.
The 
Implementation of clinical interventions, including screening, counseling, and referral, has major challenges. Since 2011, Medicare has covered behavioral counseling sessions for weight loss in primary care settings. However, the benefit has not been widely utilized.
Achieving sustainable weight loss requires comprehensive strategies that support patients� efforts to make significant lifestyle changes. The availability of clinical and community programs and services to which to refer patients is critically important. Although such programs are available in some communities, there are gaps in availability. Furthermore, even when these programs are available, enhancing linkages between clinical and community care could improve patients� access. Linking community obesity prevention, weight management, and physical activity programs with clinical services can connect people to valuable prevention and intervention resources in the communities where they live, work, and play. Such linkages can give individuals the encouragement they need for the lifestyle changes that maintain or improve their health.
The high prevalence of overweight and obesity in the United States will continue to contribute to increases in health consequences related to obesity, including cancer. Nonetheless, cancer is not inevitable; it is possible that many cancers related to overweight and obesity could be prevented, and physicians have an important responsibility in educating patients and supporting patients� efforts to lead healthy lifestyles. It is important for all health care professionals to emphasize that along with quitting or avoiding tobacco, achieving and maintaining a healthy weight are also important for reducing the risk of cancer.
