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Archive for the ‘Nutrition’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Food is digested by bathing in enzymes that break down its molecules. Those molecular fragments then pass through the gut wall and are absorbed in our intestines. But our bodies make a limited range of enzymes, so that we cannot break down many of the tough compounds in plants. The term “dietary fiber” refers to those indigestible molecules. These dietary fibers are indigestible only to us. The gut is coated with a layer of mucus, on which sits a carpet of hundreds of species of bacteria, part of the human microbiome. Some of these microbes carry the enzymes needed to break down various kinds of dietary fibers.

 

Scientists at the University of Gothenburg in Sweden are running experiments that are yielding some important new clues about fiber’s role in human health. Their research indicates that fiber doesn’t deliver many of its benefits directly to our bodies. Instead, the fiber we eat feeds billions of bacteria in our guts. Keeping them happy means our intestines and immune systems remain in good working order. The scientists have recently reported that the microbes are involved in the benefits obtained from the fruits-and-vegetables diet. Research proved that low fiber diet decreases the gut bacteria population by tenfold.

 

Along with changes to the microbiome there were also rapid changes observed in the experimental mice. Their intestines got smaller, and its mucus layer thinner. As a result, bacteria wound up much closer to the intestinal wall, and that encroachment triggered an immune reaction. After a few days on the low-fiber diet, mouse intestines developed chronic inflammation. After a few weeks, they started putting on fat and developing higher blood sugar levels. Inflammation can help fight infections, but if it becomes chronic, it can harm our bodies. Among other things, chronic inflammation may interfere with how the body uses the calories in food, storing more of it as fat rather than burning it for energy.

 

In a way fiber benefits human health is by giving, indirectly, another source of food. When bacteria finished harvesting the energy in the dietary fiber, they cast off the fragments as waste. That waste — in the form of short-chain fatty acids — is absorbed by intestinal cells, which use it as fuel. But the gut’s microbes do more than just make energy. They also send messages. Intestinal cells rely on chemical signals from the bacteria to work properly. The cells respond to the signals by multiplying and making a healthy supply of mucus. They also release bacteria-killing molecules. By generating these responses, gut bacteria help to maintain a peaceful coexistence with the immune system. They rest on the gut’s mucus layer at a safe distance from the intestinal wall. Any bacteria that wind up too close get wiped out by antimicrobial poisons.

 

A diet of fiber-rich foods, such as fruits and vegetables, reduces the risk of developing diabetes, heart disease and arthritis. Eating more fiber seems to lower people’s mortality rate, whatever be the cause. Researchers hope that they will learn more about how fiber influences the microbiome to use it as a way to treat disorders. Lowering inflammation with fiber may also help in the treatment of immune disorders such as inflammatory bowel disease. Fiber may also help reverse obesity. They found that fiber supplements helped obese people to lose weight. It’s possible that each type of fiber feeds a particular set of bacteria, which send their own important signals to our bodies.

 

References:

 

https://www.nytimes.com/2018/01/01/science/food-fiber-microbiome-inflammation.html

 

 

https://www.ncbi.nlm.nih.gov/pubmed/29276171

 

https://www.ncbi.nlm.nih.gov/pubmed/29276170

 

https://www.ncbi.nlm.nih.gov/pubmed/29486139

 

https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fiber/art-20043983

 

https://nutritiouslife.com/eat-empowered/high-fiber-diet/

 

http://www.eatingwell.com/article/287742/10-amazing-health-benefits-of-eating-more-fiber/

 

http://www.cookinglight.com/eating-smart/nutrition-101/what-is-a-high-fiber-diet

 

https://www.helpguide.org/articles/healthy-eating/high-fiber-foods.htm

 

https://www.gicare.com/diets/high-fiber-diet/

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

The trillions of microbes in the human gut are known to aid the body in synthesizing key vitamins and other nutrients. But this new study suggests that things can sometimes be more adversarial.

 

Choline is a key nutrient in a range of metabolic processes, as well as the production of cell membranes. Researchers identified a strain of choline-metabolizing E. coli that, when transplanted into the guts of germ-free mice, consumed enough of the nutrient to create a choline deficiency in them, even when the animals consumed a choline-rich diet.

 

This new study indicate that choline-utilizing bacteria compete with the host for this nutrient, significantly impacting plasma and hepatic levels of methyl-donor metabolites and recapitulating biochemical signatures of choline deficiency. Mice harboring high levels of choline-consuming bacteria showed increased susceptibility to metabolic disease in the context of a high-fat diet.

 

DNA methylation is essential for normal development and has been linked to everything from aging to carcinogenesis. This study showed changes in DNA methylation across multiple tissues, not just in adult mice with a choline-consuming gut microbiota, but also in the pups of those animals while they developed in utero.

 

Bacterially induced reduction of methyl-donor availability influenced global DNA methylation patterns in both adult mice and their offspring and engendered behavioral alterations. This study reveal an underappreciated effect of bacterial choline metabolism on host metabolism, epigenetics, and behavior.

 

The choline-deficient mice with choline-consuming gut microbes also showed much higher rates of infanticide, and exhibited signs of anxiety, with some mice over-grooming themselves and their cage-mates, sometimes to the point of baldness.

 

Tests have also shown as many as 65 percent of healthy individuals carry genes that encode for the enzyme that metabolizes choline in their gut microbiomes. This work suggests that interpersonal differences in microbial metabolism should be considered when determining optimal nutrient intake requirements.

 

References:

 

https://news.harvard.edu/gazette/story/2017/11/harvard-research-suggests-microbial-menace/

 

http://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30304-9

 

https://www.ncbi.nlm.nih.gov/pubmed/23151509

 

https://www.ncbi.nlm.nih.gov/pubmed/25677519

 

http://mbio.asm.org/content/6/2/e02481-14

 

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“Minerals in Medicine” –  40 Minerals that are crucial to Human Health and Biomedicine: Exhibit by NIH Clinical Center and The Smithsonian Institution National Museum of Natural History

Reporter: Aviva Lev-Ari, PhD, RN

 

Friday, September 9, 2016

NIH Clinical Center and The Smithsonian Institution partner to launch Minerals in Medicine Exhibition

What

The National Institutes of Health Clinical Center, in partnership with The Smithsonian Institution National Museum of Natural History, will open a special exhibition of more than 40 minerals that are crucial to human health and biomedicine. “Minerals in Medicine” is designed to enthrall and enlighten NIH Clinical Center’s patients, their loved ones, and the NIH community. Media are invited into America’s Research Hospital, the NIH Clinical Center, to experience this unique exhibition during a ribbon cutting ceremony on Monday September 12 at 4pm.

Beyond taking in the minerals’ arresting beauty, spectators can learn about their important role in keeping the human body healthy, and in enabling the creation of life-saving medicines and cutting edge medical equipment that is used in the NIH Clinical Center and healthcare facilities worldwide. The exhibition, which is on an eighteen-month loan from the National Museum of Natural History, includes specimens that were handpicked from the museum’s vast collection by NIH physicians in partnership with Smithsonian Institution geologists. Some of the minerals on display were obtained regionally as they are part of the Maryland and Virginia landscape.

Who

  • John I. Gallin, M.D., Director of the NIH Clinical Center
  • Jeffrey E. Post, Ph.D., Smithsonian Institution National Museum of Natural History, Chair of the Department of Mineral Sciences and Curator of the National Gem and Mineral Collection

When

Monday, September 12, 2016, 4:00 – 5:00 p.m.

Where

NIH Clinical Center (Building 10), 10 Center Drive, Bethesda, MD, 20892; 1st Floor near Admissions

How

RSVP encouraged, but not required, to attend in person. NIH Visitors Map: http://www.ors.od.nih.gov/maps/Pages/NIH-Visitor-Map.aspx

About the NIH Clinical Center: The NIH Clinical Center is the clinical research hospital for the National Institutes of Health. Through clinical research, clinician-investigators translate laboratory discoveries into better treatments, therapies and interventions to improve the nation’s health. More information: http://clinicalcenter.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

SOURCE

https://www.nih.gov/news-events/news-releases/nih-clinical-center-smithsonian-institution-partner-launch-minerals-medicine-exhibition

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Nutrition & Aging: Dr. Simin Meydani appointed Vice Provost for Research @Tufts University

Reporter: Aviva Lev-Ari, PhD, RN

 

August 1, 2016

 

Dear Members of the Tufts Community,

It is my great pleasure to announce that Simin Nikbin Meydani, DVM, PhD, will serve as Tufts University’s Vice Provost for Research (VPR). Simin will begin her new responsibilities on a part-time basis on August 15, and assume the office fully on October 1. During this transition period, Simin will continue to serve as Director of the USDA Jean Mayer Human Nutrition Research Center on Aging (HNRCA). As VPR she will remain research active, continuing to serve as Director of the HNRCA Nutritional Immunology Laboratory.

Dr. Meydani’s scientific interests include the basic mechanisms of aging, impact of nutrition on the aging process and age-associated diseases, role of nutrition on immune and inflammatory responses, and predisposition to infectious diseases in developed and less developed countries. Her research is multidisciplinary and expands from cell and molecular to animal and clinical investigations. She is an internationally recognized scholar with more than 300 publications and over $40M of continuous NIH, USDA, industry and foundation research funding as principal investigator or co-investigator and serves/has served on several NIH study sections, industry and foundation grant review committees and advisory boards.

Simin has been associated with Tufts University for more than 30 years, first as a scientist and then as a lab director at HNRCA. Since 2009, she has been the HNRCA Director. Over the past few years, Simin has led the very successful university-wide thematic area working group on Healthy and Active Aging. In addition to her HNRCA appointments, Simin is Professor of Nutrition and Immunology at the Friedman School of Nutrition Science and Policy and the Sackler Graduate Program in Immunology. Throughout her career, she has mentored many students, young scientists and faculty. Simin was President of the American Society of Nutrition in 2014-2015 and President of the American Aging Association in 2005-2006. She is the recipient of both societies’ most prestigious awards.

I wish to thank the deans, administrators, and Office of the Vice Provost (OVPR) staff who participated in this internal search. Please join me in congratulating Simin on her new role at Tufts, and thanking her in advance for the leadership and partnership she will provide.

Sincerely,

 

David Harris

Provost and Senior Vice President

SOURCE

From: announcements-all-request@elist.tufts.edu [mailto:announcements-all-request@elist.tufts.edu] On Behalf Of announcements@tufts.edu
Sent: Monday, August 01, 2016 11:59 AM
To: announcements-all@elist.tufts.edu
Subject: Announcing Dr. Simin Meydani as Vice Provost for Research

 

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Consuming Risk Free Food & Beverages

Author: Debashree Chakrabarti, MSc., Biological Sciences, UMass Lowell (Expected May 2016)

Leading researchers and medical health professionals have raised their concern about the over all declining status of health and well being world wide. A rising trend in childhood obesity, cardiovascular diseases, clinical depression syndrome in young adults is reason enough to try and broaden the scope of plausible agents which result in people making bad health decisions.  As a witness to the emerging dietary trends adopted by children and young adults, it is natural to question the ethics of processed food and beverages industry. Does it seem reasonable the 2L bottles of soda cost $2 USD? There are more people claiming to not like water since it is flavorless. 100% fresh juices are subject to scrutiny for their lack of adequate fiber content and excess presence of sugars. Products with high fructose corn syrups, added preservatives in processed meat, ‘read to eat’ meals are agreeably cost effective and saves a lot of time, however the over riding damage is in the long run with deficient immune system and gain of unnatural toxins which the body finds hard to eliminate. Another marketing frenzy is visible in the neutraceuticals range of instant energy drinks, protein shakes and over the counter pills. The focus is towards having the visibly attractive, muscular body regardless of the compromised health. The companies do their bit of limiting the usage by adding a precaution statement and dosage remarks on the product labels. This is however not translated as useful information to the young consumers who do not foresee the detrimental outcomes in advance.

As the prices of insurance packages and medical aid is negotiated, the same effort needs invested in the regulation of consumer dietary products. We do not want a ban on Colas however, we do not also need them to be sold at prices cheaper than water. Fresh fruits and vegetables need not be price tagged astronomically driving population to adopt a risk driven lifestyle. Taking initiatives to promote urban farming and local gardens, reaching out to the people about their choices and how it impacts the global financial predicament is a need of the hour. We are ok with the attitude of “Don’t tell me how to live my life” in a world relying heavily on subsidized medicines. This has to change. Subsidized medicine is a privilege and should be benefited to those responsible. Researchers and big pharma companies are not the only stake holders in this fight against an exponentially growing illness of misinformed decisions. People need to be brought in and educated. This includes strong arming anyone who feels they have a right to abuse their health or the health of the world.

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Another paradigm to this discussion is the need for more extensive research hubs world wide and making the accessibility of advanced medicines available to the dense population regions in Asia, Africa and Middle East Arab countries which host the majority of the population and have the least of the resources. We need 100 Massachusetts world wide with cutting edge researchers deep diving and venture capitalists backing them up. A vision for 2050 must encompass every individual being aware of what it takes to damage a human body which is a very robust machine. Eating right and being able to afford health must not be difficult. Choices available in the stores must be rational to the level where the most ignorant of the lot is still consuming risk free substances. Given the fantastic evolutionary armaments we have, it takes a lot to be unwell and yet we seem to making it fairly easy to catch cold. Healthy people translate to healthy economy.

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Nutrition: Articles of Note @PharmaceuticalIntelligence.com

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN

 

 

Nutrition and Wellbeing

 

Introduction 

Larry H. Bernstein, MD, FCAP

 

The chapters that follow are divided into three parts, but they are also a summary of 25 years of work with nutritional support research and involvement with nutritional support teams in Connecticut and New York, attendance and presentations at the American Association for Clinical Chemistry and the American Society for Parenteral and Enteral Nutrition, and long term collaborations with the surgeons Walter Pleban and Prof. Stanley Dudrick, and Prof. Yves Ingenbleek at the Laboratory of Nutrition, Department of Pharmacy, University Louis Pasteur, Strasbourg, Fr.   They are presented in the order: malnutrition in childhood; cancer, inflammation, and nutrition; and vegetarian diet and nutrition role in alternative medicines. These are not unrelated as they embrace the role of nutrition throughout the lifespan, the environmental impact of geo-ecological conditions on nutritional wellbeing and human development, and the impact of metabolism and metabolomics on the outcomes of human disease in relationship to severe inflammatory disorders, chronic disease, and cancer. Finally, the discussion emphasizes the negative impact of a vegan diet on long term health, and it reviews the importance of protein sources during phases of the life cycle.

Malnutrition in Childhood

 

Protein Energy Malnutrition and Early Child Development

Curator: Larry H. Bernstein, MD, FCAP

 

The Significant Burden of Childhood Malnutrition and Stunting

Curator: Larry H. Bernstein, MD, FCAP

 

Is Malnutrition the Cost of Civilization?

Curation: Larry H. Bernstein, MD, FCAP

 

Malnutrition in India, High Newborn Death Rate and Stunting of Children Age Under Five Years

Curator: Larry H Bernstein, MD, FCAP

 

Under Nutrition Early in Life may lead to Obesity

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Protein Malnutrition

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Cancer, Inflammation and Nutrition

 

A Second Look at the Transthyretin Nutrition Inflammatory Conundrum

Author and Curator: Larry H. Bernstein, MD, FACP

 

Cancer and Nutrition

Writer and Curator: Larry H. Bernstein, MD, FCAP

 

The history and creators of total parenteral nutrition

Curator: Larry H. Bernstein, MD, FCAP

 

Nutrition Plan

Curator: Larry H. Bernstein, MD, FCAP

 

Nutrition and Aging

Curator: Larry H Bernstein, MD, FCAP

 

Vegetarian Diet and Nutrition Role in Alternative Medicines

 

Plant-based Nutrition, Neutraceuticals and Alternative Medicine: Article Compilation the Journal PharmaceuticalIntelligence.com

Curator: Larry H. Bernstein, MD, FCAP

 

Metabolomics, Metabonomics and Functional Nutrition: the next step in nutritional metabolism and biotherapeutics

Reviewer and Curator: Larry H. Bernstein, MD, FCAP

 

2014 Epidemiology and Prevention, Nutrition, Physical Activity and Metabolism Conference: San Francisco, Ca. Conference Dates: San Francisco, CA 3/18-21, 2014

Reporter: Aviva Lev-Ari, PhD, RN

 

Metabolomics: its Applications in Food and Nutrition Research

Reporter and Curator: Sudipta Saha, Ph.D.

 

Summary

Larry H. Bernstein, MD, FCAP 

The interest in human malnutrition became a major healthcare issue in the 1980’s with the publication of several seminal papers on hospital malnutrition. However, the basis for protein-energy malnutrition that focused on the distinction between kwashiorkor and marasmus was first identified in seminal papers by Ingenbleek and others:

Ingenbleek Y. La malnutrition protein-calorique chez l’enfant en bas age. Repercussions sur la function thyroidienne et les protein vectrices du serum. PhD Thesis. Acco Press. 1997. Univ Louvain.

Ingenbleek Y, Carpentier YA. A prognostic inflammatory and nutrition index scoring critically ill patients. Internat J Vit Nutr Res 1985; 55:91-101.

Ingenbleek Y, Young VR. Transthyretin (prealbumin) in health and disease. Nutritional implications. Ann Rev Nutr 1994; 14:495-533.

Ingenbleek Y, Hardillier E, Jung L. Subclinical protein malnutrition is a determinant of hyperhomocysteinemia. Nutrition 2002; 18:40-46.

It was these early papers that transfixed my attention, and drove me to establish early the transthyretin test by immunodiffusion and later by automated immunoassay at Bridgeport Hospital.

Among the important studies often referred to with respect to hospital malnutrition are:

  1. Hill GL, Blackett RL, Pickford I, Burkinshaw L, Young GA, Warren JV. Malnutrition in surgical patients: An unrecognised problem. Lancet.1977; 310:689–692. [PubMed]
  2. Bistrian BR, Blackburn GL, Vitale J, Cochrane D, Naylor J. Prevalence of malnutrition in general medical patients. JAMA. 1976; 235:1567–1570. [PubMed]
  3. Butterworth CE. The skeleton in the hospital closet. Nutrition Today.1974; 9:4–8.
  4. Buzby GP, Mullen JL, Matthews DC, Hobbs CL, Rosato EF. Prognostic nutritional index in gastrointestinal surgery. Am. J. Surg. 1980; 139:160–167.[PubMed]
  5. Dempsey DT, Mullen JL, Buzby GP. The link between nutritional status and clinical outcomes: can nutritional intervention modify it? Am. J. Clin. Nutr. 1988; 47:352–356. [PubMed]
  6. Detsky AS, Mclaughlin JR, Baker JP, Johnston N, Whittaker S, Mendleson RA, Jeejeebhoy KN. What is subjective global assessment of nutritional status? JPEN J Parenter Enteral Nutr. 1987; 11:8–13. [PubMed]
  7. Scrimshaw NS, DanGiovanni JP. Synergism of nutrition, infection and immunity, an overview. J. Nutr. 1997; 133:S316–S321.
  8. Chandra RK. Nutrition and the immune system: an introduction. Am. J. Clin. Nutr. 1997; 66:460S–463S. [PubMed]
  9. Hill GL. Body composition reserach: Implications for the practice of clinical nutrition. JPEN J. Parenter. Enteral Nutr. 1992; 16:197. [PubMed]
  10. Smith PE, Smith AE. High-quality nutritional interventions reduce costs.Healthc. Financ. Manage. 1997; 5:66–69. [PubMed]
  11. Gallagher-Allred CR, Voss AC, Finn SC, McCamish MA. Malnutrition and clinical outcomes. J. Am. Diet. Assoc. 1996; 96:361–366. [PubMed]
  12. Ferguson M. Uncovering the skeleton in the hoapital closet. What next? Aust. J. Nutr. Diet. 2001; 58:83–84.
  13. Waitzberg DL, Caiaffa WT, Correia MITD. Hospital malnutrition: The Brazilian national survey (IBRANUTRI): a study of 4000 patients. Nutrition.2001; 17:573–580. [PubMed]

The work on hospital (and nursing home) treatment of malnutrition described in this series led to established standards. It first requires identifying a patient at malnutrition risk to be identified via either screening or assessment. This needs to be done on admission, and it has been made mandatory by health care accrediting bodies. In order to achieve this, dietitians need to have the confidence and knowledge to detect malnutrition, which is ideally done using a validated assessment for patient outcomes and financial benefits to be realized.

There is a worldwide relationship between ecological conditions, religious practices, soil conditions, availability of animal food sources, and altitude and river flows has not received the attention that evidence requires. We have seen that the emphasis on the Hindu tradition of not eating beef or having dairy is possibly problematic in the Ganges River basin. There may be other meat sources, but it is questionable that sufficient animal protein is available for the large population. The additional problem of water pollution is an aggravating situation. However, it is this region that is one of the most affected by stunting of children. We have a situation here and in other poor societies where veganism is present, and there is also voluntary veganism in western societies. This is not a practice that leads to any beneficial effect, and it has been shown to lead to a hyperhomocystenemia with the associated risk of arterial vascular disease. For those who voluntarily choose veganism, this is an unexpected result.

Met is implicated in a large spectrum of metabolic and enzyme activities and participates in the conformation of a large number of molecules of survival importance. Due to the fact that plant products are relatively Met-deficient, vegan subjects are more exposed than omnivorous to develop hyperhomocysteinemia – related disorders. Dietary protein restriction may promote supranormal Hcy concentrations which appears as the dark side of adaptive attempts developed by the malnourished and/or stressed body to preserve Met homeostasis.  Summing up, we assume that the low TTR concentrations reported in the blood and CSF of AD or MID patients result in impairment of their normal scavenging capacity and in the excessive accumulation of Hcy in body fluids, hence causing direct harmful damage to the brain and cardiac vasculature.

The content of these discussions has also included nutrition and cancer. This is perhaps least well understood. Reasons for such an association may well include chronic exposure to radiation damage, or persistent focal chronic inflammatory conditions. These would result in a cirumferential and repeated cycle of injury and repair combined with an underlying hypoxia. I have already established a fundamental relationship between inflammation, the cytokine storm, the decreased hepatic synthesis of essential plasma proteins, such as, albumin, transferrin, retinol-binding protein, and transthyretin, and the surge of steroid hormones. This results in an imbalance in the protein and free protein equilibrium of essential vitamins, the retinoids, and other circulating ligands transported. This is discussed in the ‘nutrition-inflammatory conundrum”. As stated, whatever the nutritional status and the disease condition, the actual transthyretin (TTR) plasma level is determined by opposing influences between anabolic and catabolic alterations. Rising TTR values indicate that synthetic processes prevail over tissue breakdown with a nitrogen balance (NB) turning positive as a result of efficient nutritional support and / or anti-inflammatory therapy. Declining TTR values are associated with an effect of maladjusted dietetic management and / or further worsening of the morbid condition.

Inflammatory disorders of any cause are initiated by activated leukocytes releasing a shower of cytokines working as autocrine, paracrine and endocrine molecules. Cytokines regulate the overproduction of acute-phase proteins (APPs), notably that of CRP, 1-acid glycoprotein (AGP), fibrinogen, haptoglobin, 1-antitrypsin and antichymotrypsin. APPs contribute in several ways to defense and repair mechanisms, being characterized by proper kinetic and functional properties. Interleukin-6 (IL-6) is regarded as a key mediator governing both the acute and chronic inflammatory processes, as documented by data recorded on burn, sepsis and AIDS patients. IL-6-NF possesses a high degree of homology with C/EBP-NF1 and competes for the same DNA response element of the IL-6 gene. IL-6-NF is not expressed under normal circumstances, explaining why APP concentrations are kept at baseline levels. In stressful conditions, IL-6-NF causes a dramatic surge in APP values with a concomitant suppressed synthesis of TTR.

Inadequate nutritional management, multiple injuries, occurrence of severe sepsis and metabolic complications result in persistent proteolysis and subnormal TTR concentrations. The evolutionary patterns of urinary N output and of TTR thus appear as mirror images of each other, which supports the view that TTR might well reflect the depletion of TBN in both acute and chronic disease processes. Even in the most complex stressful conditions, the synthesis of visceral proteins is submitted to opposing anabolic or catabolic influences yielding ultimately TTR as an end-product reflecting the prevailing tendency. Whatever the nutritional and/or inflammatory causal factors, the actual TTR plasma level and its course in process of time indicates the exhaustion or restoration of the body N resources, hence its likely (in)ability to assume defense and repair mechanisms.

In westernized societies, elderly persons constitute a growing population group. A substantial proportion of them may develop a syndrome of frailty characterized by weight loss, clumsy gait, impaired memory and sensorial aptitudes, poor physical, mental and social activities, depressive trends. Hallmarks of frailty combine progressive depletion of both structural and metabolic N compartments. Sarcopenia and limitation of muscle strength are naturally involutive events of normal ageing which may nevertheless be accelerated by cytokine-induced underlying inflammatory disorders. Depletion of visceral resources is substantiated by the shrinking of FFM and its partial replacement by FM, mainly in abdominal organs, and by the down-regulation of indices of growth and protein status. Due to reduced tissue reserves and diminished efficiency of immune and repair mechanisms, any stressful condition affecting old age may trigger more severe clinical impact whereas healing processes require longer duration with erratical setbacks. As a result, protein malnutrition is a common finding in most elderly patients with significantly increased morbidity and mortality rates.

TTR has proved to be a useful marker of nutritional alterations with prognostic implications in large bowel cancer, bronchopulmonary carcinoid tumor, ovarian carcinoma and squamous carcinoma of bladder. Many oncologists have observed a rapid TTR fall 2 or 3 months prior to the patient’s death. In cancer patients submitted to surgical intervention, most postoperative complications occurred in subjects with preoperative TTR  180 mg/L. Two independent studies came to the same conclusion that a TTR threshold of 100 mg/L is indicative of extremely weak survival likelihood and that these terminally ill patients better deserve palliative care rather than aggressive therapeutic strategies.

Thyroid hormones and retinoids indeed function in concert through the mediation of common heterodimeric motifs bound to DNA response elements. The data also imply that the provision of thyroid molecules within the CSF works as a relatively stable secretory process, poorly sensitive to extracerebral influences as opposed to the delivery of retinoid molecules whose plasma concentrations are highly dependent on nutritional and/or inflammatory alterations. This last statement is documented by mice experiments and clinical investigations showing that the level of TTR production by the liver operates as a limiting factor for retinol transport. Defective TTR synthesis determines the occurrence of secondary hyporetinolemia which nevertheless results from entirely different kinetic mechanisms in the two quoted studies.

Points to consider:

Protein energy malnutrition has an unlikely causal relationship to carcinogenesis. Perhaps the opposite is true. However, cancer has a relationship to protein energy malnutrition without any doubt. PEM is the consequence of cachexia, whether caused by dietary insufficiency, inflammatory or cancer.

Protein energy malnutrition leads to hyperhomocysteinemia, and by that means, the relationship of dietary insufficiency of methionine has a relationship to heart disease. This is the significant link between veganism and cardiovascular disease, whether voluntary or by unavailability of adequate source.

The last portion of these chapters deals with metabolomics and functional nutrition. This is an emerging and important area of academic interest. There is a significant relationship between these emerging studies and pathways to understanding natural products medicinal chemistry.

 

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Inflammatory Disorders: Articles published @ pharmaceuticalintelligence.com

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN

This is a compilation of articles on Inflammatory Disorders that were published 

@ pharmaceuticalintelligence.com, since 4/2012 to date

There are published works that have not been included.  However, there is a substantial amount of material in the following categories:

  1. The systemic inflammatory response
    https://pharmaceuticalintelligence.com/2014/11/08/introduction-to-impairments-in-pathological-states-endocrine-disorders-stress-hypermetabolism-cancer/
    https://pharmaceuticalintelligence.com/2014/11/09/summary-and-perspectives-impairments-in-pathological-states-endocrine-disorders-stress-hypermetabolism-cancer/
    https://pharmaceuticalintelligence.com/2015/12/19/neutrophil-serine-proteases-in-disease-and-therapeutic-considerations/
    https://pharmaceuticalintelligence.com/2014/03/21/what-is-the-key-method-to-harness-inflammation-to-close-the-doors-for-many-complex-diseases/
    https://pharmaceuticalintelligence.com/2012/08/20/therapeutic-targets-for-diabetes-and-related-metabolic-disorders/
    https://pharmaceuticalintelligence.com/2012/12/03/a-second-look-at-the-transthyretin-nutrition-inflammatory-conundrum/
    https://pharmaceuticalintelligence.com/2012/07/08/zebrafish-provide-insights-into-causes-and-treatment-of-human-diseases/
    https://pharmaceuticalintelligence.com/2016/01/25/ibd-immunomodulatory-effect-of-retinoic-acid-il-23il-17a-axis-correlates-with-the-nitric-oxide-pathway/
    https://pharmaceuticalintelligence.com/2015/11/29/role-of-inflammation-in-disease/
    https://pharmaceuticalintelligence.com/2013/03/06/can-resolvins-suppress-acute-lung-injury/
    https://pharmaceuticalintelligence.com/2015/02/26/acute-lung-injury/
  2. sepsis
    https://pharmaceuticalintelligence.com/2012/10/20/nitric-oxide-and-sepsis-hemodynamic-collapse-and-the-search-for-therapeutic-options/
  3. vasculitis
    https://pharmaceuticalintelligence.com/2015/02/26/acute-lung-injury/
    https://pharmaceuticalintelligence.com/2012/11/26/the-molecular-biology-of-renal-disorders/
    https://pharmaceuticalintelligence.com/2012/11/20/the-potential-for-nitric-oxide-donors-in-renal-function-disorders/
  4. neurodegenerative disease
    https://pharmaceuticalintelligence.com/2013/02/27/ustekinumab-new-drug-therapy-for-cognitive-decline-resulting-from-neuroinflammatory-cytokine-signaling-and-alzheimers-disease/
    https://pharmaceuticalintelligence.com/2016/01/26/amyloid-and-alzheimers-disease/
    https://pharmaceuticalintelligence.com/2016/02/15/alzheimers-disease-tau-art-thou-or-amyloid/
    https://pharmaceuticalintelligence.com/2016/01/26/beyond-tau-and-amyloid/
    https://pharmaceuticalintelligence.com/2015/12/10/remyelination-of-axon-requires-gli1-inhibition/
    https://pharmaceuticalintelligence.com/2015/11/28/neurovascular-pathways-to-neurodegeneration/
    https://pharmaceuticalintelligence.com/2015/11/13/new-alzheimers-protein-aicd-2/
    https://pharmaceuticalintelligence.com/2015/10/31/impairment-of-cognitive-function-and-neurogenesis/
    https://pharmaceuticalintelligence.com/2014/05/06/bwh-researchers-genetic-variations-can-influence-immune-cell-function-risk-factors-for-alzheimers-diseasedm-and-ms-later-in-life/
  5. cancer immunology
    https://pharmaceuticalintelligence.com/2013/04/12/innovations-in-tumor-immunology/
    https://pharmaceuticalintelligence.com/2016/01/09/signaling-of-immune-response-in-colon-cancer/
    https://pharmaceuticalintelligence.com/2015/05/12/vaccines-small-peptides-aptamers-and-immunotherapy-9/
    https://pharmaceuticalintelligence.com/2015/01/30/viruses-vaccines-and-immunotherapy/
    https://pharmaceuticalintelligence.com/2015/10/20/gene-expression-and-adaptive-immune-resistance-mechanisms-in-lymphoma/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
  6. autoimmune diseases: rheumatoid arthritis, colitis, ileitis, …
    https://pharmaceuticalintelligence.com/2016/02/11/intestinal-inflammatory-pharmaceutics/
    https://pharmaceuticalintelligence.com/2016/01/07/two-new-drugs-for-inflammatory-bowel-syndrome-are-giving-patients-hope/
    https://pharmaceuticalintelligence.com/2015/12/16/contribution-to-inflammatory-bowel-disease-ibd-of-bacterial-overgrowth-in-gut-on-a-chip/
    https://pharmaceuticalintelligence.com/2016/02/13/cytokines-in-ibd/
    https://pharmaceuticalintelligence.com/2016/01/23/autoimmune-inflammtory-bowl-diseases-crohns-disease-ulcerative-colitis-potential-roles-for-modulation-of-interleukins-17-and-23-signaling-for-therapeutics/
    https://pharmaceuticalintelligence.com/2014/10/14/autoimmune-disease-single-gene-eliminates-the-immune-protein-isg15-resulting-in-inability-to-resolve-inflammation-and-fight-infections-discovery-rockefeller-university/
    https://pharmaceuticalintelligence.com/2015/03/01/diarrheas-bacterial-and-nonbacterial/
    https://pharmaceuticalintelligence.com/2016/02/11/intestinal-inflammatory-pharmaceutics/
    https://pharmaceuticalintelligence.com/2014/01/28/biologics-for-autoimmune-diseases-cambridge-healthtech-institutes-inaugural-may-5-6-2014-seaport-world-trade-center-boston-ma/
    https://pharmaceuticalintelligence.com/2015/11/19/rheumatoid-arthritis-update/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
    https://pharmaceuticalintelligence.com/2013/07/31/confined-indolamine-2-3-dehydrogenase-controls-the-hemostasis-of-immune-responses-for-good-and-bad/
    https://pharmaceuticalintelligence.com/2012/09/13/tofacitinib-an-oral-janus-kinase-inhibitor-in-active-ulcerative-colitis/
    https://pharmaceuticalintelligence.com/2013/03/05/approach-to-controlling-pathogenic-inflammation-in-arthritis/
    https://pharmaceuticalintelligence.com/2013/03/05/rheumatoid-arthritis-risk/
    https://pharmaceuticalintelligence.com/2012/07/08/the-mechanism-of-action-of-the-drug-acthar-for-systemic-lupus-erythematosus-sle/
  7. T cells in immunity
    https://pharmaceuticalintelligence.com/2015/09/07/t-cell-mediated-immune-responses-signaling-pathways-activated-by-tlrs/
    https://pharmaceuticalintelligence.com/2015/05/14/allogeneic-stem-cell-transplantation-9-2/
    https://pharmaceuticalintelligence.com/2015/02/19/graft-versus-host-disease/
    https://pharmaceuticalintelligence.com/2014/10/14/autoimmune-disease-single-gene-eliminates-the-immune-protein-isg15-resulting-in-inability-to-resolve-inflammation-and-fight-infections-discovery-rockefeller-university/
    https://pharmaceuticalintelligence.com/2014/05/27/immunity-and-host-defense-a-bibliography-of-research-technion/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
    https://pharmaceuticalintelligence.com/2013/07/31/confined-indolamine-2-3-dehydrogenase-controls-the-hemostasis-of-immune-responses-for-good-and-bad/
    https://pharmaceuticalintelligence.com/2013/04/14/immune-regulation-news/

Proteomics, metabolomics and diabetes

https://pharmaceuticalintelligence.com/2015/11/16/reducing-obesity-related-inflammation/

https://pharmaceuticalintelligence.com/2015/10/25/the-relationship-of-stress-hypermetabolism-to-essential-protein-needs/

https://pharmaceuticalintelligence.com/2015/10/24/the-relationship-of-s-amino-acids-to-marasmic-and-kwashiorkor-pem/

https://pharmaceuticalintelligence.com/2015/10/24/the-significant-burden-of-childhood-malnutrition-and-stunting/

https://pharmaceuticalintelligence.com/2015/04/14/protein-binding-protein-protein-interactions-therapeutic-implications-7-3/

https://pharmaceuticalintelligence.com/2015/03/07/transthyretin-and-the-stressful-condition/

https://pharmaceuticalintelligence.com/2015/02/13/neural-activity-regulating-endocrine-response/

https://pharmaceuticalintelligence.com/2015/01/31/proteomics/

https://pharmaceuticalintelligence.com/2015/01/17/proteins-an-evolutionary-record-of-diversity-and-adaptation/

https://pharmaceuticalintelligence.com/2014/11/01/summary-of-signaling-and-signaling-pathways/

https://pharmaceuticalintelligence.com/2014/10/31/complex-models-of-signaling-therapeutic-implications/

https://pharmaceuticalintelligence.com/2014/10/24/diabetes-mellitus/

https://pharmaceuticalintelligence.com/2014/10/16/metabolomics-summary-and-perspective/

https://pharmaceuticalintelligence.com/2014/10/14/metabolic-reactions-need-just-enough/

https://pharmaceuticalintelligence.com/2014/11/03/introduction-to-protein-synthesis-and-degradation/

https://pharmaceuticalintelligence.com/2015/09/25/proceedings-of-the-nyas/

https://pharmaceuticalintelligence.com/2014/10/31/complex-models-of-signaling-therapeutic-implications/

https://pharmaceuticalintelligence.com/2014/03/21/what-is-the-key-method-to-harness-inflammation-to-close-the-doors-for-many-complex-diseases/

https://pharmaceuticalintelligence.com/2013/03/05/irf-1-deficiency-skews-the-differentiation-of-dendritic-cells/

https://pharmaceuticalintelligence.com/2012/11/26/new-insights-on-no-donors/

https://pharmaceuticalintelligence.com/2012/11/20/the-potential-for-nitric-oxide-donors-in-renal-function-disorders/

 

 

 

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