Guts Mind & Soul

Guts

Mind

&

Soul

Oscar Pallotta

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All material in this book belongs to the author solely. No part of this book may be used or reproduced by any means, graphic, electronic, or mechanical, including photocopying, recording, taping, or by any information storage and retrieval system, without permission in writing from the author.

Disclaimer

The material contained in this book is not intended to provide medical advice, diagnosis, or treatment, the author of this book does not prescribe the use of any product or technique as a form of treatment for physical, emotional, or medical problems. All the material in this book is for your information only.

TABLE OF CONTENT

INTRODUCTION

THE MICROBIOTA

SMALL INTESTINE BACTERIAL OVERGROWTH (SIBO)

INTERVENTIONS

DISORDERS AND DISEASES

THE STANDARD AMERICAN DIET

THE GOVERNMENT

THE EVIL CORPORATIONS

FINAL THOUGHTS

REFERENCES

INTRODUCTION

Validity and proof of causality are the main goals of every scientist to ensure that a group of their peers will accept the results of their research. The only way to accomplish these goals is through a robust and well-designed experiment that includes a large enough number of subjects or samples, sufficient experiment length, detectable effect, and precise control of variables, these are some of the challenges that researchers face complete a successful investigation.

In general terms, research is inspired by the recognition of patterns that occur with regularity, then a correlation is discovered and a hypothesis is enunciated, the next step, and driving force to experimentation and conclusions, is cause and effect.

Cause and effect may be tricky, sometimes we can mistake causation with correlation. A correlation is a connection between two variables while causation is the absolute certainty that one variable directly affects another variable. For instance, in the infamous 7 Countries Study conducted by Dr. Ancel Keys in 1953, data showed a link between high consumption of saturated fat and cholesterol with a high incidence of cardiovascular mortality. In this case, we could say there is a positive correlation between the variables saturated fat and cholesterol consumption and mortality due to coronary heart disease (CHD) but we can’t say that dietary fat causes CHD. I need to remind you that Dr. Keys had data available from 22 countries but he chose to ignore the data from 15 countries because it didn’t fit his hypothesis. This hypothesis, therefore, should have been discarded then, however, the belief that a low-fat diet prevents the dreaded clogged arteries by cholesterol or a high cholesterol diet is the cause of heart attack has been reinforced by subsequent flawed studies and persists today despite numerous clinical studies confirming the absence of a link between the consumption of saturated fat and cardiovascular death.

Let’s redefine the hypothesis, an abnormally high level of cholesterol in the bloodstream may result in cholesterol deposits in the arteries which increases the probability of heart disease.

In the previous brief account, we observed a pattern, enunciated a hypothesis, and defined correlation and effect. We can now proceed to design and carry on an experiment or study available data to find out a positive correlation or even better, a cause.

Does the high cholesterol that circulates in your vascular system come from dietary cholesterol? First of all, 75 percent of your cholesterol is produced by your liver so dietary cholesterol accounts for only 25 percent. Second, a study from 2015 [1] established a positive correlation between the consumption of high-fructose corn syrup (HFCS) and the liver production of cholesterol, triglycerides, uric acid, and other risk factors for cardiovascular disease (CVD). Indeed, a large percentage of dietary fructose is converted by the liver into known CVD risk factors. Cholesterol and triglycerides, for instance, flow with the blood and can damage artery walls increasing the risk for stroke and coronary artery disease, accordingly, if you control your consumption of added sugar you reduce the risk of CVD mortality. Again, a positive correlation is not causation, a significant number of heart attacks occur in people with low or normal cholesterol levels.

Oftentimes politicians twist scientific conclusions to fit their policies. Scientists working for interest groups leak their results to the media before the scientific community can comment on their research and validate their work. And then there is the alternative explanation to scientific results which, more often than not, are pure speculation from marketing groups to influence perception and sell their products. It’s very difficult for the general public to sort out the voice of science from the voice of professional lobbyists and marketers hidden behind writers and bloggers.

Another problem with causality is to isolate a variable as the only cause responsible for the effect. In a complex medical experiment, it is often difficult to control overlapping variables, hence, research with mice in the controlled conditions of a lab is much easier than research with humans living a normal life, moreover, scientists can’t perform an autopsy on humans at the end of an experiment.

In another example, Parkinson’s disease (PD) patients suffer from constipation years before the disease is diagnosed, in this case, we can say there is a positive correlation between constipation and Parkinson’s but we can’t say constipation causes PD. Intuitively we know that constipation is an effect, not a cause so researchers look into the cause of constipation to connect it with PD. Many researchers believe that microbes are at the root of all diseases, consequently, proof of causality between components of the microbiota and specific diseases such as Parkinson’s, Alzheimer’s, and depression is a fundamental objective in the medical field.

Two recurrent questions should pop up in your mind as you read this book, the first one is Is it cause or effect? and the second is Is it a bug? For instance, it remains unclear whether inflammation damages the intestinal mucosal barrier and thus allows penetration of toxins and other foreign substances (antigen) or whether antigens damage the mucosal barrier and trigger the inflammatory response. In other words, which one is the cause and which one is the effect?

Correlation doesn’t prove causation, true. Scientists are very clear in the concept, they design and carry on experiments, obtain results, and reach conclusions that are peer-reviewed before publication. Peers look for these two fallacies: 1) two events occurring together don’t establish necessarily cause and effect (cum hoc ergo propter hoc) and 2) an event that follows another does not necessarily cause and effect (post hoc ergo propter hoc). Usually, lobbyists, marketers, and politicians are the ones using these fallacies, not scientists.

As you go through the interventions, your microbiota will change and so will the symptoms or the symptoms’ intensity. If at some point you feel you are not getting any better or even regressing, stay the course and don’t get discouraged you are not relapsing, you are progressing, you are establishing the conditions for your body to heal itself, to go back to the time when your guts were healthy and strong. Let me say this again, I am not offering a cure, I am suggesting a plan to create optimal conditions so your guts can heal themselves.

Medical breakthroughs will continue at a faster pace than ever before, indeed, we may see more advances in medicine in the next ten years than in the past century. But, healing is different than curing a disease, for healing to happen you must actively and consciously participate in the process. Ideally, we need to cure and heal, if your life has been broken and your health is failing, you need to put yourself together, you can be whole again starting with the guts.

THE MICROBIOTA

If you adapt to your illness by dieting, avoiding certain activities, or soothing the symptoms, you are not healing, you are giving in to your ailment.

The intestinal microbiota is a complex ecosystem of interacting organisms mainly bacteria, but also archaea, yeasts, parasites, viruses, and protozoa living in a steady balance in our digestive tract. Our gastrointestinal (GI) tract contains more than 1000 bacterial species and 100 trillion bacteria, about 4.4 pounds, many of which are vital for breaking down food, excreting toxins, making vitamins, and training our immune systems to recognize harmful from commensal bacteria. The diverse and interdependent ecosystem of bacteria in the human gut is very Darwinian, the microorganisms best adapted to their environment will survive and proliferate while others will extinct.

Two principles need to be discussed to understand changes in the gut’s ecosystem balance. 1) Competition. Two different species competing for the same limited resources cannot occupy the same ecological niche, this is the competitive exclusion principle; two species competing for the same space and limited resources cannot coexist, eventually, one species -the fittest species- will drive out the other. 2) Empty niches. Although the fittest species survive, evidence shows that competition is not the driving force, instead, an expansion into empty ecological niches is the real reason for survival and proliferation. While direct competition is observed between individuals, the factor determining survival is often not the superiority of one species competing with another but the ability to survive in new environmental conditions. Accordingly, the access to new empty ecological niches, like an impaired small intestine, results in the opportunistic expansion of the most adaptable species. Likewise, the massive extinction of a species due to drastic shifts in the abiotic environment, for example, creates empty ecological niches which are then filled by the invasion and colonization of a better-adapted species.

The number, type, and function of microbes vary along the length of the GI tract, from mouth to large bowel we can identify five well-defined ecosystems performing specific functions.

More than 625 different kinds of bacteria are found in the mouth. The waste products from these bacteria contribute to bad breath and cavities, while the accumulation of bacteria on the surface of the teeth causes gingivitis. The mouth is in itself an ecosystem with microorganisms forming complex, beneficial biofilms that preclude pathogens from colonizing the oral cavity.

The esophageal mucosa hosts over 100 species of bacteria only found in the esophagus but not the mouth or stomach, this complex microbial ecosystem plays a fundamental role in defense against the establishment of microbial pathogens.

The acid of the stomach acts as a barrier by destroying most of the bacteria that enter the body from food and drink. However, some bacteria can live in the inhospitable conditions of the stomach, the best-known stomach bacteria is Helicobacter pylori, responsible for ulcers in the duodenum.

The small intestine is a 22-foot long muscular tube that takes up most of the space in the abdominal cavity. After passing through the small intestine, 90% of all nutrients contained in food have been extracted and absorbed. The absorption of nutrients is greatly enhanced by the presence of millions of finger-like structures called villi. Once the nutrients have been absorbed through the intestine’s walls, the watery leftover food moves on to the large intestine.

The colon is home to the highest number of bacteria (in the order of 1,000,000,000 bacteria per ml of fluid) and much lower in the small intestine (less than 10,000 bacteria per ml of fluid). Accordingly, within the GI tract, the colon is the only substantial contributor to the total bacterial population, while the stomach and small intestine account for a negligible amount. The large number of bacteria found within the large bowel convert undigested food coming from the small intestine into fecal bulk upon fermentation and other reactions, synthesize various vitamins, and protect against harmful bacteria.

For people with normal gastric acid secretion, the stomach and the upper small intestine are virtually free from bacteria before breakfast. For up to 1 hr. after a meal, numerous bacteria can be found and these bacteria present in the upper small intestine are removed in time by the intestine’s involuntary contraction and relaxation of the muscles. Therefore, the presence of bacteria in the intestine varies throughout the day, the bacteria being replenished after each meal. In people with low stomach acid (hypochlorhydria) the presence of bacteria in the stomach and upper small intestine is remarkably higher. This is important and we will come back to the sterile small intestine model. We are not concerned with the transient bacteria from food and drinks that