Sara Gottfried reveals the hormone cure that can help you reboot your metabolism.
Your body is equipped with a thermostat that can help you burn off extra fat. The adipostat located in the hypothalamus, or control center of your brain — that also receives metabolic messages from the body — that dial down hunger when fat stores are sufficient and turn up hunger when fat stores are deficient.
Although obesity and its associated metabolic dysregulation are established risk factors for many cancers, the biologic mechanisms underlying this relationship are also not well understood. Furthermore, the results from a systematic literature review by Himbert et al of human clinical studies exploring the crosstalk between adipose tissue and cancer-prone cells may help researchers gain a better understanding of the biologic mechanisms linking obesity to cancer. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742583/
Overweight and obesity are health problems of epidemic proportions, increasing the risk not only of cardiovascular disease and type 2 diabetes mellitus but also of various types of cancer. Obesity is strongly associated with changes in the physiological function of adipose tissue, leading to insulin resistance, chronic inflammation, and also altered the secretion of adipokines.
Several of the factors, such as insulin resistance, increased levels of leptin, plasminogen activator inhibitor-1, and endogenous sex steroids, decreased levels of adiponectin, and chronic inflammation, are involved in carcinogenesis and cancer progression.
This article reviews these mechanisms, focusing also on adipose tissue dysfunction as a unifying causal factor. Although understanding the link between obesity and cancer might provide therapeutic targets, preventing overweight and obesity still remains number one priority.
Findings from the clinical studies reviewed have found that adipose stromal cells can infiltrate cancer lesions and promote tumor growth. In addition, visceral white adipose tissue is more bioenergetically active and is associated with a more procancer secretome than subcutaneous adipose tissue. Efforts to “eavesdrop” and ultimately interfere with cancer-enhancing crosstalk between adipose tissue and carcinomas may lead to new targets and strategies for decreasing the burden of obesity-related cancers, according to the study. The study was published in Cancer Prevention Research.
Study Methodology
The researchers conducted a systematic literature search in PubMed/Medline covering publications from January 1946 to March 2017 to identify study literature characterizing crosstalk between adipose tissue and carcinomas. They ultimately found twenty primary research publications of human clinical studies directly relevant. . .in describing adipose tissue/tumor interactions. The different cancer types studied included breast, colorectal, esophageal, endometrial, prostate, and ear/nose/throat.
Study Findings
The researchers found that their analysis of the clinical studies reinforce the preclinical data and suggest organ – dependent crosstalk between adipose tissue and carcinomas via vascular endothelial growth factor, interleukein-6, tumor necrosis factor alpha, and other mechanisms. Moreover, they found that visceral white adipose tissue plays a more central role, as it is more bioenergetically active and is associated with a more procancer secretome than subcutaneous adipose tissue.
The problem is: inflammation can damage the adipostat, making it unable to receive signals from our metabolic messengers.Inflammation in the brain can be triggered by stress, toxins and sugary carbs that abound in the Standard American Diet. . Making the adipostat unable to hear the metabolic messages unable hear.
When this communication breaks down, the brain defaults into crisis mode. And because the brain’s job is to protect you by stocking up om fuel reserves in case of emergency, crisis mode means fat-storage mode. So basically, your brain is telling your hungry all the time even though you’re not. What’s more, we are also told to slash excess pounds by slashing carbs, but by doing so weight loss becomes almost impossible. Dr. Gottfried points out, a multi enter study published in JAMA found that extreme card restriction. Lowered these participants thyroid hormone levels 22% within 4 weeks while upping the levels of the fat storing stress hormone cortisol by 21%.
By restricting the beneficial “complex carbohydrates” to much it deprives the brain and body of the essential vitamins, minerals and compounds needed to operate at their peak.
Fortunately, Dr. Gottfried has discovered the carbohydrate combination that stems brain inflammation and reboots your metabolic thermostat. Plant based carbs are also rich in nutrients that defend the hypothalamus against inflammatory damage: plus supply ample prebiotic fiber, which feeds friendly flora in the gut.
This is crucial since good gut bacteria helps restore the adipostat’s sensitivity to insulin, so the body can produce less of the fat-storage hormone. Also, the healthy protein and friendly good “omega” fat that round out her formula rebalance hunger hormones and dial down appetite while boosting levels of fat burning hormones by 32%.
Chronic inflammation, not only, causes brain fog, depression and anxiety, but also, diseases like Alzheimer’s, Cancer and heart disease. What’s also exciting is people that follow this plan report improvements in energy levels, mental clarity and mood swings.
The Deadly Cycle: Inflammation & Cancer!!!
When you have chronic inflammation, the inflammatory process may begin even if there is no injury, and it does not end when it should. Why inflammation continues is not always known. Chronic inflammation may be caused by infections. . .that don’t go away, abnormal immune reactions to normal tissues, or conditions such as obesity.
Over time, chronic inflammation can cause DNA damage and lead to cancer.
For example, people with chronic inflammatory bowel diseases, such as ulcerative colitis and Crohn disease, have an increased risk of colon cancer. Also the functional relationship between inflammation and cancer is not new. In 1863, Rudolf Virchow hypothesized the origin of cancer was at sites of chronic inflammation, in part based on his hypothesis: that some classes of irritants, together with the tissue injury and ensuing inflammation they cause, enhance cell proliferation. Although it is now clear that proliferation of cells alone does not cause cancer, sustained cell proliferation in an environment rich in inflammatory growth factor cells, activated stroma & DNA-damage-promoting agents, certainly potentiates and/or promotes neoplastic risk.
During tissue injury associated with wounding, cell proliferation is enhanced while the tissue regenerates; proliferation and inflammation subside after the assaulting agent is removed or the repair is completed. In contrast, proliferating cells sustain DNA damage and/or mutagenic assault (for example, initiated cells) also continue to proliferate micro-environments rich in inflammatory cells and growth/survival factors that support their growth.
How Is balance Working Out For You!!!
In a sense, tumors act as wounds that fails to heal.
Today, the causal relationship between inflammation, innate immunity and cancer is more widely accepted; however, many of the molecular and cellular mechanisms mediating this relationship remain unresolved — these are the focus of this review. Furthermore, tumor cells also may usurp key mechanisms by which inflammation interfaces with cancers, to further their colonization of the host.
Although the acquired immune response to cancer is intimately related to the inflammatory response, this topic is beyond the scope of this article, but readers are referred to several excellent reviews. Wound healing versus invasive tumor growth. a, Normal tissues have a highly organized and segregated architecture.
Epithelial cells sit atop a basement membrane separated from the vascularized stromal (dermis) compartment. Upon wounding or tissue assault, platelets are activated and form a haemostatic plug where they release vasoactive mediators that regulate vascular permeability, influx of serum fibrinogen, and formation of the fibrin clot. Chemotactic factors such as transforming growth factor-β and platelet-derived growth factor, derived from activated platelets & also initiated granulation tissue formation, activation of fibroblasts, induction and activation of proteolytic enzymes necessary for remodeling of the extracellular matrix (for example, matrix metalloproteinases and urokinase-type plasminogen activator).
In combination, granulocytes, monocytes and fibroblasts are recruited, the venous network restored, and re-epithelialization across the wound occurs. Epithelial and stromal cell types engage in a reciprocal signaling dialogue to also facilitate healing. Once the wound is healed, the reciprocal signaling subsides. Invasive carcinomas are less organized.
Neoplasia-associated angiogenesis and lymphangiogenesis produces a chaotic vascular organization of blood vessels and lymphatics where neoplastic cells interact with other cell types (mesenchymal, haematopoietic and lymphoid) and a remodelled extracellular matrix. Although the vascular network isn’t disrupted in the same way during neoplastic progression as it is during wounding, many reciprocal interactions occur in parallel.
Peyton Rous was first to recognize that cancers develop from “subthreshold neoplastic states” caused by viral or chemical carcinogens induce somatic changes. These states, now known as ‘initiation’, involve DNA alterations, are irreversible and can persist in otherwise normal tissue indefinitely until occurrence of a second type of stimulation (now referred to as ‘promotion’). Promotion can result from exposure of initiated cells to chemical irritants, such as phorbol esters, factors released at the site of wounding, partial organ resection, hormones or chronic irritation and inflammation (Fig.1)
Functionally, many promoters, whether directly or indirectly, induce cell proliferation, recruit inflammatory cells, increase production of reactive oxygen species that lead to oxidative DNA damage, and reduce DNA repair. Subversion of cell death and/or repair programmes occurs in chronically inflamed tissues, thus resulting in DNA replication and proliferation of cells – that have lost normal growth control. Normal inflammation is self-limiting, because the production of anti-inflammatory cytokines follows the pro-inflammatory cytokines closely (Fig. 2).
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803035/
However, chronic inflammation seems to be due to persistence of the initiating factors or a failure of mechanisms required for resolving the inflammatory response. Why does the inflammatory response to tumors persist?