Intestinal Microbiota

* Studies in mice, which also have large numbers of microbes living in their guts, have shown that there may be a link between storing energy as fat and microbial activity.

The sheer diversity of the microbiota means that bodily disorders associated with the gut region (encompassing the stomach and intestines) are difficult to diagnose, and even harder to find the source of the disorder. Intestinal Bowel Disease (IBD) is a large category of bodily disorders associated with the gut. IBD most commonly manifests itself in two forms – Crohn’s Disease, and Ulcerative Colitis [1]. Crohn’s disease is arguably a more severe form of the disease, as the diseased tissue tends to go deeper into the intestines. Ulcerative Colitis, while still very detrimental and pain causing, causes inflammation of tissue at more of the surface level. The diseases affects a significant portion of the population, with a high rate of new cases discovered - between 20,000 and 100,000 people are diagnosed with types of IBD annually in North America [1]. The role of the microbiota in inducing intestinal diseases has been suspected.

Unique microbiota could suggest a human’s current health or if there is any forthcoming chronic disease (Ley, 2006). Families with shared healthy microbes may be able to help relatives who suffer from gastrointestinal disease; but the extant to which the microbiome is shared across generations is not readily known and more research is needed. The core trends for current research revolve around control of obesity, treatment of gastrointestinal diseases such as Crohn’s, and hormonal manipulation in cases of depression. It is imperative to learn to eat for optimal health, to evolve along with the commensals (Turner et al., 2013) as human diets influence diversity of microbes present (Ley et al., 2008). This is a relatively new field with exciting prospects of positive outcomes for some of society’s more chronic

The study intended to look at the gut microbiome that is naturally present within the gut. The research team of the Louisiana State University designed an experiment with lab rats to predict how the manipulation of the gut microbiome with a high fat diet would affect their brain

The Oxford English Dictionary defines a drug as, “a substance which has a physiological effect when ingested or otherwise introduced into the body” (“Drug,” 2016). Most would consider this definition too broad since simply ingesting food causes physiological changes in the body. However, most do not consider the multifarious ways in which the food that we eat affects our epigenetic gene expression, or the bi-directional signaling between our gut and our brains. The food that we eat is metabolized in the gut by micro-organisms which collectively form our microbiota. The 100 trillion prokaryotic cells that make up our microbiota, constitute 90% of the cells in our bodies, and are derived from more than 40,000 bacterial strains (Forsythe & Kunze, 2012). Increasingly, research is showing the importance of host microbiota composition and the bidirectional signaling pathways between the brain and the gut: some of which are epigenetic. These studies elucidate the profound impacts that signaling pathways, such as short-chain fatty acid mediated effects, nucleomodulins, and other bacterial metabolites, can have on health, behavior and cognition (Sommer & Backhed, 2013). It is now clear that diet-mediated epigenetic effects are important mechanisms in the etiology of numerous diseases (Choi & Friso, 2010). Furthermore, artificial drugs that can act on these epigenetic pathways could

As the leading cause for dementia, Alzheimer’s disease –AD-, effects more than 25 million people in the world (Perrone & Grant, 2015, p. 1).The neurodegenerative disorder, results in behavioral changes, as well as cognitive including, loss of memory and language skills ( Mayo Clinic Staff, 2014). Researchers have tracked two leading abnormalities resulting in Alzheimer’s. These two are, amyloid plaques-clumps of protein which form in and around the neurons- and neurofibrillary tangles- insoluble fibers made up mostly of tau protein- (Mayo Clinic Staff, 2014). Although both are a prevalent indication of AD, scientist have not been able to indicate whether these are merely a byproduct or a cause. Hence, call for epidemiological research is ongoing. Earlier studies have suggested a link between diabetes- specifically, Type 2 diabetes mellitus- and AD (Paddock, 2015). These observations suggest the metabolic processing of glucose is abnormal, and this plays a role in AD pathogenesis (Macauley et al., 2015).Recently, studies have linked, a dietary relevance of advanced glycogen end products, or AGEs, to the incidence of AD (Perrone & Grant, 2015, p. 2). AGEs are also called glycotoxins, because they increase the risk of diseases such as diabetes, cardiovascular disease, and several other aging related-diseases, such as AD (Perrone & Grant, 2015, p. 2). More on, as with diabetes and AGEs , researchers have directly linked high blood sugar to the production of beta-amyloid, in

The hippocampus, in the limbic system of the brain, controls long-term memory and emotions. With the high sugar diets, inflammation markers within the hippocampus increased, but the immunomodulatory gene expression decreased. The inflammation markers directly correlate with the decrease in memory on these high sugar diets. Memory deficiency happened within short term exposures of sugar to the diet. Rats tested showed lower exploration ratios than control rats. These animals fed "sugar for less than 2 weeks (showed) impaired hippocampal-dependent place recognition memory compared to control and PUFA fed rats." (Beilharz, Kaakoush, Maniam, and Morris, 2016, p. 309). Place recognition tests confirmed the effects on memory with the sugar fed group being considerably lower in their scores. Sugar was the factor that proved to be "crucial for the memory deficits." (Beilharz et al., 2016, p. 309). The gut microbiome also has significant effects on emotions. Depression and anxiety, including anhedonic-like behaviors were found in direct relation to the sugar intake.

To understand how microbes may be involved in AD, we first must look at what physically happens to the brain with this disease. There are two distinct aspects involved in Alzheimer’s disease; beta-amyloid plaques and tau tangles. Beta-amyloid plaques are formed when the amyloid precursor protein (APP) which is present in the membrane of neurons (alz.org) is cleaved off by beta and gamma-secretases (Chen et al., 2001). In a normal brain, alpha-secretase does the cleaving and the body processes APP on its own (Chen, et al., 2001). In AD, the small pieces join to form beta-amyloid plaques but as smaller individual pieces they can interfere with nerve signaling

Several possible mechanisms through which the changes in gut microbiota can influence the pathophysiology of metabolic syndrome have been proposed. Dysbiosis of the gut microbiota due to triggers such us a high fat diet can alter the distribution gut junction proteins leading to the translocation of the colonic contents such as LPS to the blood. This increased gut permeability and leakage of contents referred to as Endotoxemia contributes to low grade inflammation. In gut dysbiosis the gut microbiota become more efficient at energy extraction and the SCFA produced may act as signaling molecules and stimulate a cascade od signaling that increases fat storage and energy production. Gut microbiota regulates expression of fasting induced adipose factor (FIFA) proteins which suppress expression of LPL thus fat storage is

Research was conducted comparing the intestinal bacteria of obese and thin people, which showed that microbes in the thin individuals intestines where much more diverse than that of an obese individuals. Studies showed that thin individuals

The Paleolithic diet, also knows as the cave man diet, the Stone Age Diet or the Hunter-Gatherer Diet, has been suggested as the way to eat to reduce many western diseases including type 2 diabetes mellitus (T2D) (Masharani et. Al 2015). People with T2D often have a number of metabolic anomalies, one being insulin resistance (Masharani et. Al. 2015). Below we report of studies conducted on the metabolic effects of this modern Paleolithic diet on T2D and the results from these studies.

According to the hot lens, Yong’s article, “Gut bacteria in Japanese people borrowed sushi-digesting genes from ocean bacteria” is a quite decent article. However, in just the second paragraph of the article it seems a little exaggerated from him because he says that, “The genes are wielded by the hordes of bacteria lurking in the guts of every Japanese person, but not by those in American intestines.” (p. 1), he claims that “every” Japanese person has this type of organism. This is a pretty strong statement he makes about all Japanese people having this complex breaking down organism.

The first was that glial cells, under situations that are comparable to environmental, aggregate in the lamina propria during early stages of development after birth. The second finding was that this population of glial cells undergoes a regenerative cycle throughout the life of the organism. This occurs in a specific region of the gut. The final finding was that this early stage development and subsequent regeneration throughout the life of the organism depends on the microbiota presented to the gut. The Microbiota, as they are referred to in the article, are part of an enormous array of microbes which colonize the body (Baily, Gur, Worly, 2015). Therefore it can be understood that the gut microbiota are the microbes of the body that inhabit the gut. These seem to be part of the primary focus in the article.

Function: The function of brain-gut axis is to monitor and integrate gastrointestinal functions and to mediate impact of stress and emotions on gut. Many emotions are reflected in terms of changes in gut physiology. It has been known that a symbiotic relationship between resident gut flora, nutrient absorption and other aspects of digestion exists. In addition, it is now clear that gut flora helps with other functions, including homeostasis of the immune system and neuro-hormonal signaling along the brain-gut axis [1, 2]. It also serves the host against pathogens, metabolism of certain drugs, modulation of intestinal pain and some elements of fat absorption.

Maintenance HFHS diet can also negatively affect learning and memory by promoting hippocampal inflammation. Evidently, sugar-fed rats that performed poorly in hippocampally dependent spatial task exhibited increased hippocampal inflammation and oxidative stress markers (Beilharz, Maniam, & Morris, 2014). Similarly, consumption HFHS diets by healthy juvenile rats worsened performance on spatial tasks and increased expression of inflammatory markers in the