Smoking , alcohol, meds/drugs and poor lifestyle (absence of exercise, clean water, air and whole foods) contributed to poor health in the southern part of the United States.
Smoking , alcohol, meds/drugs and poor lifestyle (absence of exercise, clean water, air and whole foods) contributed to poor health in the southern part of the United States.
By JJ Virgin
I often talk about how important it is to be a fat burner instead of a sugar burner, but what does that really mean? Instead of diving straight into the science, let’s keep this simple: do any of these apply to you?
You know you’re a sugar burner if…
… you rarely feel completely full and satisfied after a meal. Stuffed, maybe. Bloated and uncomfortable, yes. But ready to go another 4-6 hours without anything else to eat? No way.
… you snack regularly. You typically graze throughout the day, even when you’ve resolved to stop eating so much between meals. If you don’t snack, you feel lethargic and moody.
… you often get “hangry.” You’re no stranger to apologizing for being irritable because you were hungry. Your friends and family know that a bad attitude = hand you some food.
… you crave carbs and sugar. A meal isn’t complete without potatoes, rolls, or pasta. Dessert is a must. And when you try to eat less sugar, you find yourself cranky and unable to focus.
… you have a hard time losing weight, especially around your middle. You’ve tried multiple diets, and even when you manage to lose a few pounds, your belly never seems to shrink.
Being a sugar burner is just what it sounds like: your primary source of fuel is glucose, which gives your body no reason to access your fat stores for fuel. Why should it, since your body runs on a steady supply of carbs?
The more carbohydrates you eat, the higher your blood sugar goes. The higher your blood sugar levels, the more insulin your body is forced to produce in order to return those levels to normal.
All that insulin comes with several major drawbacks, including blocking leptin production. Leptin is your appetite-control hormone. Without it, your brain never gets that signal that says you’re full. That’s why sugar burners are often hungry and overweight.1
Anytime you diet and lose weight without losing waist, you’re actually making things worse.
It’s a vicious cycle. Being a sugar burner means your body needs more insulin and hangs on to fat; in turn, high body fat makes you less responsive to insulin.2 That insulin resistance causes its own set of problems, including increased risk of heart disease, type 2 diabetes, and other inflammatory disease.3,4 As a result, sugar burners often suffer from joint pain, headaches, skin trouble, and other uncomfortable issues.5-7Even when sugar burners lose weight, they seldom lose fat. And anytime you diet and lose weight without losing waist, you’re actually making things worse. You’re training your body to store your fat even more stubbornly.
The results can be miserable: sugar burners often suffer from anxiety or depression, constant cravings, and obesity. With time, they develop symptoms ranging from high blood pressure to elevated cholesterol.8,9
The goal is to be a fat burner. By eating fewer carbs and more clean, lean protein and healthy fats, you train your body to burn fat for fuel.
As a fat burner, your system still burns carbs as fuel first and will use the small amount of sugar you get from slow-low carbs like vegetables, quinoa, or legumes. Then your metabolism quickly turns to your fat stores for energy.
Because fat burns more slowly and steadily, fat burners can easily go 4-6 hours between meals and don’t suffer from sugar or carb cravings.10 They also lose fat easily and experience more steady energy.
If you recognize yourself as a sugar burner, the WORST thing you can do is go sugar-free. Suddenly cutting off that supply of glucose and carbs will make you feel awful and set you up for a cycle of yo-yo dieting and further health issues.
Instead, gradually lower your sugar impact by eliminating the most harmful sugars and replacing high-sugar impact foods with healthier options.Click to tweet
The Sugar Impact Diet walks you through that process of shifting from sugar burner to fat burner.If you think you’d benefit from more resources and hands-on support, I recommend the Sugar Impact Diet Online Program. It’s got a private Facebook community and dozens of videos, guides, menus, recipes, and assessment tools to help you customize the Sugar Impact Diet so it fits your body and lifestyle. While I call it a “diet,” the goal is actually a permanent change in how you live, feel, and think. (Not bad for less than the cost of a single visit to a nutritionist…)
You can find out more about the Sugar Impact Diet Online Program here. If you’re a sugar burner, it’s not too late to stop the cycle of mood swings, hunger, energy crashes, and brain fog. Your body and your loved ones will thank you!
Our results suggest that relative abundance data from the human gut microbiome differentiates individuals with healthy colons from those with adenomas and carcinomas. Most importantly, there was a significant difference in the gut microbiome of people with colonic adenomas compared with those with healthy colons. This has considerable importance in secondary prevention because screening for early-stage colorectal cancer hinges on the ability to detect early pathologic changes. In this regard, we found that failure to detect at least 1 of the 5 OTUs served as a signal of the presence of adenoma. The probability of having an adenoma rose more than 50-fold with this added information about microbiome. Taken with the existing literature about the importance of the gut microbiome in health and disease, our study further suggests that the microbiome may play a crucial role in the etiology of colorectal cancer.
A strength of our study design was that we collected samples from 3 clinical groups that represented the multistage progression in colorectal cancer (healthy, adenoma, and carcinoma). This allowed us to identify a panel of bacterial populations that could indicate both the progression from healthy tissue to adenoma and the progression from adenoma to carcinoma. Interestingly, when we looked at each patient, we rarely observed significant enrichment of every bacterial population among the OTUs incorporated in the logit models. For example, 11 of the 30 carcinoma patients had no detectable levels of Fusobacterium. However using the relative abundance data for the remaining panel of microbial biomarkers, such as Porphyromonas, Bacteroides, and Enterobacteriaceae, we were able to accurately classify these subjects. This strongly suggests that there may be multiple underlying mechanisms by which the microbiome is involved in colorectal cancer and that colorectal cancer is likely a polymicrobial disease.
Our findings are supported by previous evidence. Three research groups reported that Fusobacterium spp. were enriched on the surface of tumors compared with adjacent healthy tissue (22, 37, 38). Building upon these clinical studies, animal and tissue culture-based studies have provided evidence that Fusobacterium may contribute to tumor multiplicity through the recruitment of immune cells to tumors (22, 37). These mechanistic studies agree with our findings that Fusobacterium may be a marker for the presence of tumors. In addition, enterotoxigenic Bacteroides fragilis (ETBF), a pathogenic variant of a common commensal, has been shown to directly influence the development of colorectal cancer in murine genetic models through the production of a metalloprotease toxin (39). In our samples, subjects with carcinomas showed an increase in the relative abundance of one Bacteroides population (OTU 1882) compared with subjects with adenomas. However, PCR-based screens for the toxin producing genes did not reveal the presence of ETBF. In addition, we observed a significant decrease in the relative abundance of Bacteroides populations (OTUs 1889 and 1913) associated with the advancement of tumorigenesis. Finally, a polyketide synthetase operon from Escherichia coli was shown to influence the progression of tumors using a murine model of inflammation-derived tumorigenesis (21, 23). Although we did see an enrichment for non–E. coli Enterobacteriaceae in the carcinoma subjects relative to the healthy subjects, we were unable to detect significant differences in the relative abundance of E. coli across the 3 clinical groups.
It is tempting to speculate on the enrichment of Fusobacterium and Porphyromonas spp. in subjects with colorectal cancer. Both of these bacterial taxa are common commensals of the mouth and a wealth of literature has linked them to chronic inflammation and periodontal disease (40, 41). It is possible that the mouth is a reservoir for these pathogens, allowing for colonization of the gastrointestinal tract under abnormal environmental conditions. During colorectal carcinogenesis, dramatic physiologic changes occur in the microenvironment of colonic lesions (42). Tumor-associated fluxes in nutrients and shifts in inflammatory mediators may favor colonization by opportunistic pathogens such as Fusobacterium and Porphyromonas. As demonstrated by Kostic and colleagues, colonization by such pathogens can support the development and progression of colorectal cancer (22, 37). We were unable to detect a significant association between either population and carcinoma severity or location. Additional studies are needed to examine how and at what stage these bacterial populations are affecting the development of colorectal cancer and how they may be linked to the oral microbiome and related to oral disease.
As highlighted above, there is a clear association with the enrichment of pathogenic bacterial populations and colon tumorigenesis; however, in this study we emphasize that the depletion of potentially protective bacteria likely plays a similar role colorectal cancer pathology. We identified several bacterial populations that were significantly depleted in colorectal cancer. Individuals with both adenomas and carcinomas showed a dramatic loss in OTUs associated with the genera Clostridium and Bacteroides, and the family Lachnospiraceae (43–45). Each of these bacterial taxa are well known producers of short chain fatty acids (SCFA) in the colon. SCFAs are important microbial metabolites that supply nutrients to colonocytes and help maintain epithelial health and homeostasis. Specifically, the SCFA, butyrate, has been shown to have substantial antitumorigenenic properties, including the ability to inhibit tumor cell proliferation, initiate apoptosis in tumor cells (46), and mediate T-regulatory cell homeostasis (44). Loss of these important bacterial populations in concert with an enrichment of pathogenic populations likely plays a synergistic role in potentiating tumorigenesis.
Summary: A lack of REM sleep may lead to an increased desire to consume unhealthy foods, a new study reports.
Source: University of Tsukuba.
It is not well understood what role sleep loss plays in affecting areas of the brain that control the desire to consume unhealthy foods. A new paper published on December 6 in the journal eLife finds that rapid eye movement (REM) sleep loss leads to increased consumption of unhealthy foods, specifically sucrose and fat.
The researchers at the University of Tsukuba’s International Institute for Integrative Sleep Medicine (IIIS) used a new method to produce REM sleep loss in mice along with a chemical-genetic technique to block prefrontal cortex neurons and the behaviors they mediate. As a result, the IIIS researchers discovered that inhibiting these neurons reversed the effect of REM sleep loss on sucrose consumption while having no effect on fat consumption.
REM sleep is a unique phase of sleep in mammals that is closely associated with dreaming and characterized by random eye movement and almost complete paralysis of the body.
The prefrontal cortex plays a role in judging the palatability of foods through taste, smell and texture. Moreover, persons who are obese tend to have increased activity in the prefrontal cortex when exposed to high calorie foods.
“Our results suggest that the medial prefrontal cortex may play a direct role in controlling our desire to consume weight promoting foods, high in sucrose content, when we are lacking sleep,” says Kristopher McEown, the lead author on this project.
IIIS was launched by the Ministry of Education, Culture, Sports, Science and Technology of Japan with the aim of building globally visible research centers. At IIIS gather globally prominent scientists from multiple research fields contributing to elucidate the fundamental principles of sleep/wake regulation, and develop new strategies to assess and treat sleep diseases as well as the closely associated metabolic and mental disorders.
Funding: The research was funded by the Japan Society for the Promotion of Science.
Source: Masataka Sasabe – University of Tsukuba
Image Source: NeuroscienceNews.com image is credited to University of Tsukuba.
Original Research: Full open access research for “Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption” by Kristopher McEown, Yohko Takata, Yoan Cherasse, Nanae Nagata, Kosuke Aritake, and Michael Lazarus in eLife. Published online December 6 2016 doi:10.7554/eLife.20269
Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption
Rapid eye movement (REM) sleep loss is associated with increased consumption of weight-promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25–48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption.
“Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption” by Kristopher McEown, Yohko Takata, Yoan Cherasse, Nanae Nagata, Kosuke Aritake, and Michael Lazarus in eLife. Published online December 6 2016 doi:10.7554/eLife.20269
20:80 is my guess. Our genes affect us 20% of the time while our environment and lifestyle affects us 80% of the time (epigenetics).
Each person metabolize glucose or drugs or food in the liver differently. Pharmacogenetic tests classified these into 4 groups of people.
We have to choose good carbohydrates from whole foods (colored greens, fibrous whole foods) and avoid toxins (alcohol, soda, aspartame, processed foods, burned BBQ meat, etc). We sleep before 10pm and exercise 30min every day. We destress and be proactive with our own health.
In mammals the response to dietary glucose is more complex because it combines effects related to glucose metabolism itself and effects secondary to glucose-dependent hormonal modifications, mainly pancreatic stimulation of insulin secretion and inhibition of glucagon secretion. In the pancreatic β cells, glucose is the primary physiological stimulus for the regulation of insulin synthesis and secretion. In the liver, glucose, in the presence of insulin, induces expression of genes encoding glucose transporters and glycolytic and lipogenic enzymes.
Although insulin and glucagon were long known as critical in regulating gene expression, it is only recently that carbohydrates also have been shown to play a key role in transcriptional regulation. DNA sequences and DNA binding complexes involved in the glucose-regulated gene expression have been characterized recently in liver and β cells.
Regulation of gene expression by nutrients in mammals is an important mechanism allowing them to adapt to the nutritional environment.
In-vivo and in-vitro experiments have demonstrated that the transcription of genes coding for lipogenic and glycolytic enzymes in liver and/or adipose tissue is upregulated by glucose.
In order for glucose to act as a gene inducer, it must be metabolized.
Diffuse large B-cell lymphoma (DLBCL or DLBL) is a cancer of B cells, a type of white blood cell responsible for producing antibodies. It is the most common type of non-Hodgkin lymphoma among adults, with an annual incidence of 7–8 cases per 100,000 people per year. This cancer occurs primarily in older individuals, with a median age of diagnosis at approximately 70 years of age, though it can also occur in children and young adults in rare cases. DLBCL is an aggressive tumor which can arise in virtually any part of the body, and the first sign of this illness is typically the observation of a rapidly growing mass, sometimes associated with B symptoms—fever, weight loss, and night sweats.
The causes of diffuse large B-cell lymphoma are not well understood. Usually DLBCL arises from normal B cells, but it can also represent a malignant transformation of other types of lymphoma or leukemia. An underlying immunodeficiency is a significant risk factor. Infection with Epstein–Barr virus has also been found to contribute to the development of some subgroups of DLBCL.
Diagnosis of DLBCL is made by removing a portion of the tumor through a biopsy, and then examining this tissue using a microscope. Usually a hematopathologist makes this diagnosis. Several subtypes of DLBCL have been identified, each having a different clinical presentation and prognosis. However, the usual treatment for each of these is chemotherapy, often in combination with an antibody targeted at the tumor cells. Through these treatments, more than half of patients with DLBCL can be cured, and the overall five-year survival rate for older adults is around 58%.
A number of animal studies have clearly documented the association between aspartame and cancer, as the study points out. But what most researchers do not appreciate is that humans are the only animals that do NOT have the protective mechanism to compensate for methanol toxicity. So evaluating methanol toxicity in animals is a flawed model for testing human toxicity.
This is due to alcohol dehydrogenase (ADH). In humans, methanol is allowed to be transported in the body to susceptible tissues where this enzyme, ADH, then converts it to formaldehyde, which damages protein and DNA that lead to the increased risk of cancer and autoimmune disease.
Interestingly, the previous AARP Diet and Health Study, which did not find an association with aspartame and cancer, used fruit juice as the control. Most are unaware that canned or bottled fruit juice is loaded with methanol that dissociates from the pectin over time and can actually cause similar problems as aspartame. This does not occur in freshly consumed fruits and vegetables, only ones that are bottled or canned. Hence no major difference could be discerned between the aspartame and the control group.
The safety of aspartame has been the subject of several political and medical controversies, United States congressional hearings and Internet hoaxes since its initial approval for use in food products by the U.S. Food and Drug Administration (FDA) in 1981.:2 The European Food Safety Authority concluded in its 2013 re-evaluation that aspartame and its breakdown products are safe for human consumption at current levels of exposure, corroborating other medical reviews. However, because its breakdown products include phenylalanine, aspartame must be avoided by people with the genetic condition phenylketonuria (PKU).