Acyclovir interacts with other meds and seniors with cancer

Acyclovir is the generic name for Zovirax, a prescription medication used to treat certain virus infections.

The Food and Drug Administration (FDA) approved acyclovir to treat viral infections from the varicella virus that causes chicken pox and shingles, as well as infections from the virus that causes genital herpes.

Sometimes doctors prescribe acyclovir to treat herpes infections in people with HIV.

The drug works by preventing viruses from dividing and multiplying. The FDA approved acyclovir in the 1980s.

Acyclovir is available as a generic, made by several companies, or under the brand name Zovirax, made by GlaxoSmithKline and available in tablet, capsule, and liquid form.

Acyclovir is one of the oldest drugs used to treat herpes simplex viruses and remains the first line of treatment for these infections.

However, research shows that acyclovir is not as effective as it used to be.

A 2013 study, published in the journal Current Opinion in Infectious Diseases, found that acyclovir-resistant herpes strains could develop over time.

Resistance happens in people with a healthy immune system as well as in those with a weakened immune system.

Acyclovir Warnings

It’s important to know that acyclovir does not cure viral infections. However, it can make infections shorter and less serious for some people.

If you’re taking acyclovir for genital herpes, it can reduce the severity or prevent recurrences of a herpes outbreak.

If you’re taking acyclovir to treat chicken pox or shingles, the drug can reduce the severity of your infection.

It’s important to know that treatment with acyclovir works best when you start taking it as soon as possible after a rash appears.

This means within three days of a shingles rash and within 24 hours of a chicken pox rash.

It’s usually not necessary to treat young, healthy children with chicken pox, but older children or adults who get chicken pox may need treatment.

Drink plenty of fluids when taking this medication. Children younger than 2 should not take acyclovir.

Use acyclovir with caution if you have kidney disease or any condition that weakness your immune system. If you have these conditions, you could be at risk for serious reactions to acyclovir.

Ask your doctor for advice on practicing safe sex if you have a genital herpes infection. Genital herpes spreads through sexual activity, and taking acyclovir alone may not be enough to prevent it.

Acyclovir and Pregnancy

If you’re a woman, let your doctor know if you are or may be pregnant or if you’re breastfeeding.

Researchers have not studied acyclovir use by pregnant women, so there’s not enough evidence to say that it is safe to take during pregnancy.

Acyclovir also may pass into breast milk.

Acyclovir Side Effects

The most common side effects of acyclovir treatment for genital herpes include nausea, vomiting, and diarrhea.

Shingles requires treatment with higher doses of acyclovir, and the most common side effects at higher doses are tiredness and malaise.

Tell your doctor if you have any side effects. Side effects that may be seen in all people using acyclovir include:

  • Nausea
  • Diarrhea
  • Vomiting
  • Headache
  • Dizziness
  • Tiredness
  • Muscle or joint aches
  • Visual changes
  • Fluid retention
  • Hair loss
  • Confusion
  • Changes in behavior

Serious side effects also can occur. If you have any of these side effects, call your doctor right away:

  • Severe rash, hives, or a rash that causes blisters and peeling
  • Yellowing of skin or eyes
  • Unusual bleeding or bruising
  • Seizure
  • Loss of consciousness
  • Swelling of face, lips, or tongue
  • Difficulty breathing
  • Decreased urine output or blood in the urine
  • Extreme sleepiness or confusion
  • Hallucinations
  • Tingling, numbness, or shakiness

Age matters, too. People older than 65 may have more side effects from acyclovir because their kidneys do not get rid of the drug as quickly as younger people’s do.

Acyclovir Interactions

Some drugs may affect the way acyclovir works, and acyclovir may affect other drugs you are taking.

It’s very important to let your doctor know about all drugs you are taking, including any over-the-counter herbs or supplements.

Drugs that may interact with acyclovir include:

Use antimicrobials wisely

STR/AFP/Getty

Antibiotic use in livestock has contributed to drug resistance around the world.

The effectiveness of antibiotics has been waning since they were introduced into modern medicine more than 70 years ago. Today, our inability to treat infections ranks alongside climate change as a global threat1, 2. New classes of antimicrobial drugs are unlikely to become widely available any time soon1; if and when they do, bacteria, viruses and other microbes will again evolve resistance3. In any case, waging war on microbes is not tenable3 — our bodies and planet depend on them4(see Supplementary Information).

Addressing resistance requires global collective action. Like the ozone layer, a stable climate or biodiversity, the global population of susceptible microbes is a common pool resource — one shared by all. But no individual or country has a strong enough incentive to conserve this ‘commons’. It has been depleted by the massive use of antimicrobial compounds and the growing competitive advantage of resistant microbes. It is a classic ‘tragedy of the commons’.

This intimate relationship with microorganisms predates modern humans. It is the result of many millions of years of co-evolution. Our bodies need particular kinds of microbes for digestion, immune function and general health. Equally, microbes support planetary health, for example, through nutrient cycles, including those that maintain soil and water quality4. In other words, microbes sustain human civilization. Yet our understanding of the complex interactions and uncertainties that govern the relationships between humans and microbes is limited.

The 2015 Global Action Plan on Antimicrobial Resistance, drafted by the World Health Organization (WHO) with support from the United Nations Food and Agricultural Organization (FAO) and the World Organisation for Animal Health (OIE), recognizes the need for multisectoral cooperation to address resistance (see go.nature.com/2bbijap). But, in our view, it does not go far enough in recognizing the life support we receive from the global microbiome. Tackling resistance urgently requires the scaling back of the massive overuse of antibiotics to secure the liveability of Earth in the long term.

On 21 September, heads of state will meet to take further action at the United Nations high-level meeting on antimicrobial resistance in New York City. A UN declaration currently under discussion must set global targets, accelerate implementation of the global action plan, plug its gaps and ensure stronger accountability and interagency coordination. It must emphasize the many benefits of microbes.

Parties should aim to build the resilience of society and the microbiome. In our opinion, this is the way to maintain low levels of resistance amid the many surprises of a rapidly changing planet. Advances from studying resilience in other common pool resources such as fisheries and forests5suggest key steps for antimicrobial resistance, which we set out below. Achieving these will require changes to institutions, regulations, education, community norms and expectations, notably in medicine and agriculture.

Boaz Rottem/Alamy

Limited access to quality antimicrobials in the developing world drives unregulated sales.

Educate to learn

Until now, political and financial investments have focused largely on creating incentives to fuel drug innovation and new or faster diagnostics. Currently, such technological fixes appeal to and benefit mainly rich nations in the ‘global north’. Incentives must be targeted to benefit not only large pharmaceutical companies in the north, but also to enlist research and development efforts globally. One of the most important outcomes of the UN meeting should be national commitments to the broadest and most creative participatory education campaigns about resistance2 and the importance of the microbial world.

Why? Because the level of ignorance about the calamity that is antimicrobial resistance is staggering. A 2015 WHO survey across 12 countries found that 64% of the public think that antibiotics also work for, for instance, viral infections such as influenza and colds (see go.nature.com/2c7zvfu). Such basic knowledge gaps lead patients and physicians to reach for antibiotics without appreciating the costs.

Instead, institutions and citizens must understand the central facts, context and risks in a way that allows them to learn more independently. This goal requires awareness campaigns to be revised and scaled up by orders of magnitude2, as well as investment in new communication tools. Initiated in 2007, Thailand’s Antibiotics Smart Use project sets a direction for upscaling. It enables patients in pharmacies to self-diagnose on the basis of the appearance of their sore throat to verify whether they need antibiotic treatment6. For further learning, citizen-science programmes in which participants monitor their own microbiomes should be extended to cover, for example, self-testing for resistance in various parts of the body7.

Such campaigns could engage communities and change norms about how and when to use antibiotics. Campaigns will need to be coordinated internationally for quality and impact, and adapted to suit regional perspectives. Engagement can be spread through schools, mass media and social media.

Join up

Resistance affects animal and environmental health as well as human health, and so requires coordinated action across economic sectors. No single concern exemplifies this better than the high rate of antibiotic use in agriculture (largely as growth promoters or disease prevention). In the United States, 70–80% of all antimicrobials consumed are given to livestock; agricultural use in the BRICS emerging economies (Brazil, Russia, India, China and South Africa) is expected to double by 2030, as compared to 2010 levels8 (see ‘Farm forecast’). As a result, antibiotics and resistance genes enter the food chain, soil and the water table, threatening human health.

Source: Ref. [8]

The European Union has phased out the use of medically important antibiotics for growth promotion in agriculture. Other countries, including Mexico and Taiwan9, have sought to reduce it. In the United States, a directive discourages the use of antibiotics for growth promotion through voluntary measures and stronger veterinary oversight of therapeutic use. However, the powerful industrial farming lobby and a lack of perceived urgency have so far stalled stronger mandates.

Stronger political action to change how we use antibiotics, whether by humans or animals, requires citizens to be better informed. For instance, the public should have online access to surveillance that tracks how human resistance increases in settlements near farms. In the meantime, consumer groups play a crucial part by calling on retail chains to switch where their meat is sourced. For example, US food chains Chipotle, McDonald’s and Chick-fil-A have responded (to varying degrees) to public demands with stricter limits on antibiotic use in the meat they sell.

A particularly worrying issue that is not confined to the use of antimicrobials in food production is the international spread of resistance genes, especially those conferring resistance to many drugs of ‘last resort’. Most recently, a mobile plasmid gene carrying resistance to the last-resort antibiotic colistin has been found in Asia, Europe and North America. Clearly, countries cannot act alone to deal with the problem without jeopardizing the benefits of globalization.

Much better surveillance and containment is needed of the most dangerous multiresistant strains in people and food2. A global routine-surveillance initiative could help to prevent the spread of resistance. It could screen medical tourists or patients returning from hospitals abroad to identify carriers of multiple resistant strains. Hospitals that are centres of international travel for medical treatment must lead the way; funding and learning mechanisms must be increased for other hospitals to follow suit.

The International Health Regulations, revised by WHO member states in 2005, are a legally binding instrument that aims to provide global surveillance and response. Properly financed, they could be effective10. Yet the resources needed to respond to emerging diseases do not flow commensurately to low- and middle-income countries as they do in the global north — a key lesson of the recent Ebola outbreak. All governments have a collective responsibility to improve capacities for rapid response to resistance. Greater support by donor countries to new and existing funding mechanisms such as the Global Fund to Fight AIDS, Tuberculosis and Malaria is needed in low- and middle-income countries.

Extend coalitions

International and national coalitions must be broadened. The global action plan strengthens the established collaboration between the WHO, FAO and OIE. This should be extended to cover other relevant sectors, including trade, development and environment. The model set up by UNAIDS (the Joint United Nations Programme on HIV/AIDS) in 1996 serves as an example of how to intensify collaboration, leverage resources, involve more parties and reduce barriers.

“Building global resilience to resistance is a long game.”

The UN meeting must commit to driving learning between institutions. Global platforms are needed for sharing best practices and the latest data about resistance levels and antibiotic consumption, for instance, among national agencies. Such exchange happens in Europe for resistant human bloodstream infections, and human and veterinary antimicrobial consumption. This must be scaled up to monitor resistance in communities, food industry and the environment. A relevant model for exchange at the global level is the WHO’s Pandemic Influenza Preparedness Framework. To engage the public effectively, more-frequent updating, vivid visualizations and engaging communications are needed.

As in the Paris climate agreement, countries should submit to the UN voluntary but monitored targets on limiting resistance. Parties may go further by making shortfalls subject to potential sanctions. A key priority is to establish measurable indicators at the country level, such as the median yearly consumption of antibiotics per person.

As for the climate issue, non-state actors from business to civil society can be central to societal transformations. Such stakeholders were consulted during the development of the WHO global action plan. But their participation in the long run must become more integral to the global coalition responsible for tackling resistance.

Available governance instruments range from binding treaties to guidelines, with each approach having pros and cons. A first step to holding companies accountable would be an international code on the promotion of antibiotics (promotional spending in the United States in 1998 amounted to US$1.6 billion), akin to that adopted by the WHO in 1981 on the marketing of breast-milk substitutes.

Act now

The complexity and gravity of resistance call for the immediate mass mobilization of society. Maintaining the susceptibility of microbes to drugs for global health is a matter of sustainable development. Improving understanding about humankind’s dependence on the global microbiome should lead to action on many other important issues involving microorganisms. These issues include infectious diseases, food security, natural resources and environmental conservation. Action here could, in turn, lead to more-equitable forms of national progress across the sustainable-development goals3.

Building global resilience to resistance is a long game. But changes can be surprisingly fast when the time is ripe and a plan is ready. This month’s UN high-level meeting is a rare opportunity for global collective action on human interactions with microbes. It must protect both the lifesaving power of antibiotics and the ability to use them when necessary.

http://www.nature.com/news/use-antimicrobials-wisely-1.20534

Inhaled soil bacteria causes AD/brain disease

bacteria.JPGMelioidosis is an infectious disease caused by a gram-negative bacterium, Burkholderia pseudomallei, found in soil and water. It is of public health importance in endemic areas, particularly in Thailand and northern Australia. It exists in acute and chronic forms. Signs and symptoms may include pain in chest, bones, or joints; cough; skin infections, lung nodules and pneumonia.

B. pseudomallei was previously classed as part of the Pseudomonas genus and until 1992, it was known as Pseudomonas pseudomallei. It is phylogenetically related closely to Burkholderia mallei which causes glanders, an infection primarily of horses, donkeys, and mules. The name melioidosis is derived from the Greek melis (μηλις) meaning “a distemper of asses” with the suffixes -oid meaning “similar to” and -osis meaning “a condition”, that is, a condition similar to glanders.[1]


This bacteria from the soil can be inhaled and travels from the nose to the brain. Seek a doctor for an antibiotic treatment when sympoms occur: fever, cough

Acute melioidosis

In the subgroup of patients where an inoculating event was noted, the mean incubation period of acute melioidosis was 9 days (range 1–21 days).[2] Patients with latent melioidosis may be symptom-free for decades; the longest period between presumed exposure and clinical presentation is 62 years.[3] The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the “Vietnam time-bomb”. A wide spectrum of severity exists; in chronic presentations, symptoms may last months, but fulminant infection, particularly associated with near-drowning, may present with severe symptoms over hours.

A patient with active melioidosis usually presents with fever. Pain or other symptoms may be suggestive of a clinical focus, which is found in around 75% of patients. Such symptoms include cough or pleuritic chest pain suggestive of pneumonia, bone or joint pain suggestive of osteomyelitis or septic arthritis, or cellulitis. Intra-abdominal infection (including liver and/or splenic abscesses, or prostatic abscesses) do not usually present with focal pain, and imaging of these organs using ultrasound or CT should be performed routinely. In one series of 214 patients, 27.6% had abscesses in the liver or spleen (95% confidence interval, 22.0% to 33.9%). B. pseudomallei abscesses may have a characteristic “honeycomb” or “swiss cheese” architecture (hypoechoic, multiseptate, multiloculate) on CT.[4][5]

Regional variations in disease presentation are seen: parotid abscesses characteristically occur in Thai children, but this presentation has only been described once in Australia.[6] Conversely, prostatic abscesses are found in up to 20% of Australian males, but are rarely described elsewhere. An encephalomyelitis syndrome is recognised in northern Australia.

Patients with melioidosis usually have risk factors for disease, such as diabetes, thalassemia, hazardous alcohol use, or renal disease, and frequently give a history of occupational or recreational exposure to mud or pooled surface water.[7] However, otherwise healthy patients, including children, may also get melioidosis.

Altering Gut Flora Could Reduce Stroke Risk

Changing the profile of the bacteria in the gut led to a reduction in stroke size, a new study in mice suggests.

“This was a proof-of-concept study,” study author Costantino Iadecola, MD, Weill Cornell Medical College, New York, New York, told Medscape Medical News.

“We have demonstrated two important principles: that changes to the microflora in the gut have an effect on how the brain withstands injury, and that changes to the immune system can have a profound effect on stroke,” he said. “This could eventually lead to new therapies to prevent stroke.”

“The hope is that in future we may be able to reduce an individual’s risks of stroke by changing their microbiota profiles in the gut with use of probiotics and/or antibiotics or maybe just with dietary habits,” he added. “This could be targeted to patients at very high risk of stroke, such as those undergoing cardiac or brain surgery, but may also be applicable to secondary prevention.”

Coauthor Josef Anrather, also from Weill Cornell Medical College, said, “We have shown a new relationship between the intestine and the brain in the setting of stroke. Whatever is going on in the microflora in the gut is contributing to the immune response that controls the damage caused by a stroke. The next step is to address how much of this change is relevant in humans and which bacteria are important.”

The study was published online March 28 in Nature Medicine.

”Our findings shed new light on poorly understood immune mechanisms that have an impact on brain injury and have far-reaching and translationally relevant implications for assessing cerebrovascular risk and predicting stroke severity,” the researchers conclude in their paper.

Dr Iadecola explained that a substantial amount of evidence suggests that immunologic factors have some control over stroke occurring in the brain. “So we figured that if the immune system is geared in a certain way this may protect against stroke. As the intestine is the major reservoir of immune cells, we focused on changing the environment here and whether this would have any affect on stroke.”

For the study, the researchers induced bacteria dysbiosis — changes in the make-up of the bacteria in the gut — by treating mice with antibiotics (amoxicillin and clavulanic acid) for 2 weeks. For controls, they used mice who had been on the same antibiotics for generations, so their flora had become resistant; no bacteria dysbiosis occurred.

When stroke was induced in the mice, the ones that had induced bacterial dysbiosis showed a 60% to 70% reduction in stroke size compared with controls.

As a further verification that it was the dysbiosis rather than the antibiotic itself that was responsible for the reduced stroke, the researchers transplanted the gut contents of the mice with induced bacterial dysbiosis into normal mice and found that these mice also had smaller strokes. “This further suggests that it is the changed composition of the gut flora that is bringing about the benefit on stroke,” Dr Iadecola said.

To address the question of how gut flora can affect the brain in this way, the researchers analyzed the lymphocyte profiles of the mice. They found that the animals with induced dysbiosis and smaller strokes had more protective regulatory T cells and fewer harmful gamma delta T cells. Dr Iadecola commented: “So the change in the gut flora appears to bring about a change in the immune system, which favors smaller stroke injury.”

He explained that these lymphocytes regulate the influx of inflammatory cells, such as neutrophils, into the brain, thereby controlling inflammation in the brain. On further investigation using flow cytometry, the researchers found normal mice had increased neutrophil counts in the brain, whereas the animals with induced dysbiosis had increased neutrophil counts in the meninges but not in the brain itself.

“Our results suggest that the altered gut flora leads to higher amounts of regulatory T cells and fewer gamma delta T cells in the meninges, which somehow causes fewer neutrophils to enter the brain. We believe the gamma delta T cells help neutrophils enter the brain, whereas the regulatory T cells prevent this process,” Dr Iadecola noted.

He added that any clinical application of these findings is still a very long way off. “We need to figure out what is the optimum dysbiotic state in humans. First of all we need to conduct more studies in mice to identify the bacterial species that produce the best changes to the immune system. Then do the same thing in humans.”

 Dr Anrather referred to efforts underway at present to better characterize the human microbiome on a large scale. “We might be able to use this data to analyze how certain microbiome profiles influence stroke risk. Then in certain high-risk populations we could try and change the composition of the gut flora to the profile most suited to producing beneficial immunological changes for the cardiovascular system.”

He agreed with Dr Iadecola that the most obvious target is the prevention of stroke, and it would be more difficult to influence the acute phase of stroke because the immunologic changes take time to come into effect.

“In our current study 1 week of antibiotics did not show any change in stroke risk. The reductions in stroke size only became obvious after 2 weeks of treatment. The changes in the microbiota were there at 1 week but the immune changes did not become apparent until 2 weeks. So this approach does not seem appropriate for use in acute situations. But the immune system also plays a role in regeneration and repair, so there may also be possibilities there,” Dr Anrather said.

By

Nature Med. Published online March 28, 2016. Abstract


From Dr Mercola on Dysbiosis, leaky gut

Dysbiosis, or “leaky gut,” is a bacterial imbalance that leads to inflammation of the intestinal mucosa. Once inflamed, the intestinal lining is compromised and allows undigested food particles and other potential toxins to enter the bloodstream.

  • The most common cause of dysbiosis in today’s dogs and cats is, hands down, antibiotic overuse. Antibiotics, other drugs including vaccines, highly processed diets, and stress all contribute to development of dysbiosis in pets.
  • Typical signs of a leaky gut include gas, bloating and diarrhea. But dysbiosis can also cause or worsen a wide variety of other disorders and diseases – everything from bad breath to certain types of cancer.
  • Every case of dysbiosis is unique, so a customized healing protocol must be designed for each patient based on a specific set of conditions. There is no one-size-fits-all remedy for every leaky gut.
  • In most cases, replacing a highly processed diet with balanced, species-appropriate nutrition, and adding appropriate supplements to address inflammation and support the organs of digestion, will relieve symptoms and resolve the root cause of the leaky gut.

Bacteria in our cells can be our friend and enemy

microbes.JPGMicrobes our enemy and friend

The human body hosts more than ten thousand different kinds of microbes. Most of these bacteria aren’t harmful – in fact, many of them actually aid the immune system.

Microbiota and the healthy brain

Within the first few days of life, humans are colonized by commensal intestinal microbiota.  Review of recent findings show that microbiota are important in normal healthy brain function.  There exists a relation between stress and microbiota, and how alterations in microbiota influence stress-related behaviors.

Bacteria and the CNS

New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems. Ongoing and future animal and clinical studies aimed at understanding the microbiota–gut–brain axis may provide novel approaches for prevention and treatment of mental illness, including anxiety and depression.

The healthy balance of microbial cells in our body is affected by many factors including antibiotics, acidic meds,narcotics,alcohol,sugar and more.

m video.JPG

The new insights into NEC suggest why the microbiome suddenly seems so important to almost everything in the medical and biological worlds, even our understanding of what it means to be human. We tend to think that we are exclusively a product of our own cells, upwards of ten trillion of them. But the microbes we harbor add another 100 trillion cells into the mix.

The creature we admire in the mirror every morning is thus about 10 percent human by cell count. By weight, the picture looks prettier (for once): Altogether an average adult’s commensal microbes weigh about three pounds, roughly as much as the human brain. And while our 21,000 or so human genes help make us who we are, our resident microbes possess another eight million or so genes, many of which collaborate behind the scenes handling food, tinkering with the immune system, turning human genes on and off, and otherwise helping us function. John Donne said “no man is an island,” and Jefferson Airplane said “He’s a peninsula,” but it now looks like he’s actually a metropolis.

***

The modern microbiome era started in the late 1990s, when David Relman, an infectious disease physician at Stanford University, decided to get a sample of the microbes in his own mouth. It’s a simple process: A dentist scrapes a sort of elongated Q-tip across the outer surface of a tooth, or the gums, or the inside of a cheek. These samples typically look like nothing at all. (“You have to have a lot of faith in the invisible,” one dentistry professor advises.)

Stress and the Microbiota

There is now an expanding volume of evidence to support the view that commensal organisms within the gut play a role in early programming and later responsivity of the stress system. The gut is inhabited by 1013–1014 micro-organisms, which is ten times the number of cells in the human body and contains 150 times as many genes as our genome. It has long been recognised that gut pathogens such as Escherichia coli, if they enter the gut can activate the HPA.

However, animals raised in a germ-free environment show exaggerated HPA responses to psychological stress, which normalises with monocolonisation by certain bacterial species including Bifidobacterium infantis. Moreover, increased evidence suggests that animals treated with probiotics have a blunted HPA response.

Stress induces increased permeability of the gut

Stress induces increased permeability of the gut allowing bacteria and bacterial antigens to cross the epithelial barrier and activate a mucosal immune response, which in turn alters the composition of the microbiome and leads to enhanced HPA drive. Increasing data from patients with irritable bowel syndrome and major depression indicate that in these syndromes alteration of the HPA may be induced by increased gut permeability.

In the case of irritable bowel syndrome the increased permeability can respond to probiotic therapy. Detailed prospective studies in patients with mood disorders examining the gut microbiota, immune parameters and HPA activity are required to throw further light on this emerging area. It is however clear that the gut microbiota must be taken into account when considering the factors regulating the HPA.

Antibiotics can cause cell death

Recent studies have revealed that antibiotics can promote the formation of reactive oxygen species which contribute to cell death. In this study, we report that five different antibiotics known to stimulate production of reactive oxygen species inhibited growth ofEscherichia coli biofilm. We demonstrated that supression of biofilm formation was mainly a consequence of the increase in the extracellular concentration of indole, a signal molecule which suppresses growth of bacterial biofilm. Indole production was enhanced under antibiotic-mediated oxidative stress due to overexpression of tryptophanase (TnaA), which catalyzes synthesis of indole. We found that DMSO (dimethyl sulfoxide), a hydrogen peroxide scavenger, or the lack of trypthophanase, which catalyzes production of indole, partly restored formation of E. coli biofilm in the presence of antibiotics. In conclusion, these findings confirmed that antibiotics which promote formation of ROS (reactive oxygen species) can inhibit development of E. colibiofilm in an indole-dependent process.

 

How Gut Bacteria Supports a Healthy Weight and Long Life

Weight and the health of our gut flora

More and more research is emerging that draws a direct link between our weight and the health of our gut flora (including its role in the success of gastric bypass surgery), but this shouldn’t be a surprise. The connection has been known, and manipulated, for years by the agricultural industry.

Antibiotics—which kill the natural bacterial flora in the human body that influences how we break down and absorb the nutrients that help keep us lean and healthy—are known as growth promoters. Farmers have been using antibiotics for more than half a century to fatten cattle, pigs, and chickens. With the use of these medications, animals gain more weight more quickly, on less food. I’ll say that again: antibiotics stimulate growth with less food.

Food craving and weight loss

There is other research on the topic of weight and gut flora as well, two of the more interesting and recent pieces being related to how gut bacteria influence which foods we crave. Here are a few more examples:

Butyrate—one of the fatty acids produced by good gut bacteria—has been suggested to promote feelings of satiety (a feeling of fullness and satisfaction). (Nutr Rev 07;65(2):51–62) (Aliment Pharmacol Ther 08:27(2):104–119) This, obviously, can help prevent overeating.

Fermented milk

A Japanese company gave 87 overweight individuals 100 grams of fermented milk twice a day. The milk consumed by half the group contained the bacteria Lactobacillus gasseri. After 12 weeks, those individuals lost an average of 2.2 pounds—and there was no weight loss in the other group. (Eur J Clin Nutr 2010 March 10. [E-pub ahead of print PMID:20216555] Specifically, the participants lost 4.6 percent of their visceral fat (fat around the stomach) and 3.3 percent of their subcutaneous fat (fat just under the skin). Their hip circumference was reduced by 1.7 cm (almost ¾ of an inch) and their waist went down by 1.5 cm (just over ½ inch). Researchers feel that Lactobacillus gasseri somehow decreases the amount of fat absorbed from the intestines.

Antibiotics and Weight Loss

Researchers evaluated the use of antibiotics in 11,532 children born in Britain’s Avon region in 1991 and 1992. Almost 30 percent of the infants were given antibiotics sometime during the first six months of their life. By age 38 months, the children in the antibiotic group had a 22 percent greater likelihood of being overweight. (Int J Obes (Lond) 21 October 2012 [Epub ahead of print]) Antibiotics. Doing it at such a critical period of development, such as early childhood, has long-lasting effects.

How Gut Bacteria Contributes to Longer Life

The more diverse our bacterial flora is, the more effective it is and the better our overall health tends to be. To see this, you need look no further than a study that examined gut microbes in the elderly.

When researchers looked at the gut bacteria of 178 elderly individuals over the age of 65 (average age 78, none of whom were being treated with antibiotics), they found that the microbes varied extensively depending on where the individual lived and the state of their overall health.

The people who lived independently in the community had the most varied microbacterial flora and were the healthiest. People who lived in long-term assisted living homes had less diverse microbacterial flora and were frailer.

The research team, led by Paul O’Toole of University College Cork in Ireland, tied this difference to the diet of each respective group. Though the foods eaten by people who moved into long-term residential facilities changed immediately upon entry (becoming much more uniform and based on government-issued nutritional data), it took about a year for the profile of their bacteria to change. It was during that transition time when the individuals’ health started declining the most. What makes this study so intriguing to me is the speed at which a person loses his or her health to a decline in the numbers and variety of intestinal bacteria. The clear takeaway from this is that eating a varied diet that includes fermented foods is a key to maintaining gut flora and, by extension, strength and vitality.

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