Do You Know Tea Tree Oil is Very Useful For Acne and Hair?

You’ve probably heard of the powerful anti-bacterial properties of tea tree oil especially when it comes to our skin. Also known as melaleuca oil, tea tree oil is made from the leaves of the plant Melaleuca alternifolia commonly found in Australia.

Many medical studies have found tea tree oil to kill bacteria, fungi and strains of viruses making it a favourite remedy for decades. These days, tea tree oil has become even more popular with it being an ingredient in face and hair products, massage oils and even detergents.

So, how can we really benefit from this amazing, natural remedy?

The Benefits Of Tea Tree Oil

Don’t just take people’s word for the amazing power of tea tree oil. Many scientific studies 1 have been conducted in order to prove just how beneficial this oil is.

Its exceptional healing properties mean it can have several different uses.

Tea Tree Oil For Acne

This oil can help heal many forms of skin conditions including acne, rashes, eczema, and fungal infections but acne is the most common association with tea tree oil. This is because it contains strong antibacterial and antifungal compounds which penetrates the skin and unblocks sebaceous glands. This has led to studies that have found tea tree oil to be as effective as benzoyl peroxide 2 but without the harshness.

On top of that, it can help against scarring which is a common side effect from continuous acne on the face and body.

Tea tree oil is known for soothing dry scalp and for getting rid of unsightly dandruff 3. It also helps unclog hair follicles and nourishes the roots of the hair which helps your hair to grow more strong and healthy.

For those with kids who are prone to getting head lice, tea tree oil has even been found to kill lice as well as reducing the number of eggs that hatch making it a more natural way to tackle this common problem 4.

Tea Tree Oil For Cuts And Infections

Because tea tree oil is anti-bacterial, it makes an amazing natural way to clean any cuts and tackle any infections found in wounds.

It can also deal with fungal infection such as toenail fungus, ringworm and athlete’s foot as it’s so effective…

A Completely New Kind of Symbiotic Relationship

We’ve seen animals and plants, plants and fungi, animals and bacteria, all with symbiotic relationships that benefit both species. Some combinations even take that relationship to the cellular level. But now scientists have identified algae living in salamander cells through the life of the animal, which is the first time a photosynthetic plant has been found in the cells of a vertebrate.

As a collaborative research team from the American Museum of Natural History and Gettysburg College revealed, the green alga Oophila amblystomatis makes its home inside of cells located across…

How to Deal With Food Poisoning

Image from Mishio.

Food poisoning sucks, but if you do get it, you should know how to figure out which type it is, what you’re in for, and the best way to deal with it so you can feel better.

When you have food poisoning, stay hydrated and do what you can to contain any bacteria you might spread to housemates. Most people don’t realize that not all food poisoning is the same, though. If you have severe symptoms that last for days it might be more than a bad burrito. It might be a more serious type of infection deeper in your digestive symptom. In that case,…

Furry Friends Could Help Prevent Allergies and Obesity in Babies

Two of life’s great joys—dogs and babies—might be even better together. A study published in the journal Microbiome found higher levels of allergy-preventing bacteria in babies who lived with furry pets like dogs and cats.

The relationship between our environments, immune systems, and gut microbes is a tangled one. Studies have found that “dirty behaviors” like thumb-sucking and nail-biting might actually help protect kids against autoimmune conditions, as can living on a farm. So it’s not too much of a stretch to think that our four-legged companions might have a similarly beneficial effect.

To explore the idea further, researchers at the University of Alberta pulled data from the Canadian Healthy Infant Longitudinal Development (CHILD) study, which followed the lives…

CRISPR had a life before it became a gene-editing tool

Bacteria and archaea armed with CRISPR systems have been at war with viruses for eons. Here, hordes of viruses known as phages assault a bacterium to turn it into a virus-making factory.


It is the dazzling star of the biotech world: a powerful new tool that can deftly and precisely alter the structure of DNA. It promises cures for diseases, sturdier crops, malaria-resistant mosquitoes and more. Frenzy over the technique — known as CRISPR/Cas9 — is in full swing. Every week, new CRISPR findings are unfurled in scientific journals. In the courts, universities fight over patents. The media report on the breakthroughs as well as the ethics of this game changer almost daily.

But there is a less sequins-and-glitter side to CRISPR that’s just as alluring to anyone thirsty to understand the natural world. The biology behind CRISPR technology comes from a battle that has been raging for eons, out of sight and yet all around us (and on us, and in us).

The CRISPR editing tool has its origins in microbes — bacteria and archaea that live in obscene numbers everywhere from undersea vents to the snot in the human nose. For billions of years, these single-celled organisms have been at odds with the viruses — known as phages — that attack them, invaders so plentiful that a single drop of seawater can hold 10 million. And natural CRISPR systems (there are many) play a big part in this tussle. They act as gatekeepers, essentially cataloging viruses that get into cells. If a virus shows up again, the cell — and its offspring — can recognize and destroy it. Studying this system will teach biologists much about ecology, disease and the overall workings of life on Earth.

But moving from the simple, textbook story into real life is messy. In the few years since the defensive function of CRISPR systems was first appreciated, microbiologists have busied themselves collecting samples, conducting experiments and crunching reams of DNA data to try to understand what the systems do. From that has come much elegant physiology, a mass of complexity, surprises aplenty — and more than a little mystery.

Spoiled yogurt

The biology is complicated, and its basic nuts and bolts took some figuring out. There are two parts to CRISPR/Cas systems: the CRISPR bit and the Cas bit. The CRISPR bit — or “clustered regularly interspaced short palindromic repeats” — was stumbled on in the late 1980s and 1990s. Scientists then slowly pieced the story together by studying microbes that thrive in animals’ guts and in salt marshes, that cause the plague and that are used to make delicious yogurt and cheese.

None of the scientists knew what they were dealing with at first. They saw stretches of DNA with a characteristic pattern: short lengths of repeated sequence separated by other DNA sequences now known as spacers. Each spacer was unique. Because the roster of spacers could differ from one cell to the next in a given microbe species, an early realization was that these differences could be useful for forensic “typing” — investigators could tell whether food poisoning cases were linked, or if someone had stolen a company’s yogurt starter culture.

Bacteria use CRISPR/Cas as a form of immunity or self-defense against invaders. A bacterium builds a library of genetic material from past invaders so that, if the same invader attacks again, the bacterium and its offspring can disable it.

L. Marraffini/Nature 2015, Adapted by J. Hirshfeld

But curious findings piled up. Some of those spacers, it turned out, matched the DNA of phages. In a flurry of reports in 2005, scientists showed, to name one example, that strains of the lactic acid bacterium Streptococcus thermophilus contained spacers that matched genetic material of phages known to infect Streptococcus. And the more spacers a strain had, the more resistant it was to attack by phages.

This began to look a lot like learned or adaptive immunity, akin to our own antibody system: After exposure to a specific threat, your immune system remembers and you are thereafter resistant to that threat. In a classic experiment published in Science in 2007, researchers at the food company Danisco showed it was so. They could see new spacers added when a phage infected a culture of S. thermophilus. Afterward, the bacterium was immune to the phage. They could artificially engineer a phage spacer into the CRISPR DNA and see resistance emerge; when they took the spacer away, immunity was lost.

This was handy intel for an industry that could find whole vats of yogurt-making bacteria wiped out by phage infestations. It was an exciting time scientifically and commercially, says Rodolphe Barrangou of North Carolina State University in Raleigh, who did a lot of the Danisco work. “It was not just discovering a cool system, but also uncovering a powerful phage-resistance technology for the dairy industry,” he says.

The second part of the CRISPR/Cas system is the Cas bit: a set of genes located near the cluster of CRISPR spacers. The DNA sequences of these genes strongly suggested that they carried instructions for proteins that interact with DNA or RNA in some fashion — sticking to it, cutting it, copying it, unraveling it. When researchers inactivated one Cas gene or another, they saw immunity falter. Clearly, the two bits of the system — CRISPR and Cas — were a team.

It took many more experiments to get to today’s basic model of how CRISPR/Cas systems fight phages — and not just phages. Other types of foreign DNA can get into microbes, including circular rings called plasmids that shuttle from cell to cell and DNA pieces called transposable elements, which jump around within genomes. CRISPRs can fend off these intruders, as well as keep a microbe’s genome in tidy order.

The process works like this: A virus injects its genetic material into the cell. Sensing this danger, the cell selects a little strip of that genetic material and adds it to the spacers in the CRISPR cluster. This step, known as immunization or adaptation, creates a list of encounters a cell has had with viruses, plasmids or other foreign bits of DNA over time — neatly lined up in reverse chronological order, newest to oldest.

Older spacers eventually get shed, but a CRISPR cluster can grow to be long — the record holder to date is 587 spacers in Haliangium ochraceum, a salt-loving microbe isolated from a piece of seaweed. “It’s like looking at the last 600 shots you had in your arm,” says Barrangou. “Think about that.”

New spacer in place, the microbe is now immunized. Later comes targeting. If that same phage enters the cell again, it’s recognized. The cell has made RNA copies of the relevant spacer, which bind to the matching spot on the genome of the invading phage. That “guide RNA” leads Cas proteins to target and snip the phage DNA, defanging the intruder.

Scientists have divided the array of known CRISPR systems into five types and 16 subtypes based on DNA sequence data. The distribution of types differs in archaea and bacteria.

K.S. Makarova et al/Nat. Rev. Microbio. 2015, Adapted by J. Hirshfeld

Researchers now know there are a confetti-storm of different CRISPR systems, and the list continues to grow. Some are simple — such as the CRISPR/Cas9 system that’s been adapted for gene editing in more complex creatures (SN: 4/15/17, p. 16) — and some are elaborate, with many protein workhorses deployed to get the job done.

Those who are sleuthing the evolution of CRISPR systems are deciphering a complex story. The part of the CRISPR toolbox involved in immunity (adding spacers after phages inject their genetic material) seems to have originated from a specific type of transposable element called a casposon. But the part responsible for targeting has multiple origins — in some cases, it’s another type of transposable element. In others, it’s a mystery.

Given the power of CRISPR systems to ward off foes, one might think every respectable microbe out there in the soils, vents, lakes, guts and nostrils of this planet would have one. Not so.

Numbers are far from certain, partly because science hasn’t come close to identifying all the world’s microbes, let alone probe them all for CRISPRs. But the scads of microbial genetic data accrued so far throw up interesting trends.

Tallies suggest that CRISPR systems are far more prevalent in known archaea than in known bacteria — such systems exist in roughly 90 percent of archaea and about…

Antibiotics Raise Mortality Risk for Honeybees, Study Finds

Efforts to protect honeybees may be doing more harm than good. Scientists say the antibiotics routinely administered by beekeepers wipe out beneficial bacteria in the bees’ guts, making them vulnerable to other pathogens. They published their findings in the journal PLOS Biology.

These are hard days for honeybees, and apiarists are doing all they can to keep their charge healthy and safe. Twice a year in North America, Asia, and parts of Europe, many beekeepers dose their hives with preventative antibiotics. The drugs may be dusted on the hive or added to the bees’ food to ensure that each insect gets its medicine.

But, as we’re learning in humans, blanket treatment with antibiotics is not really a great option. The more antibiotics we use, the faster pathogens develop antibiotic resistance, and the drugs kill helpful bacteria along with the harmful stuff they’re meant to treat.

Scientists wondered if the same was true for bees. To find out, they brought about 800 bees from long-established hives into the laboratory and split the bees into two groups: the treatment group, marked with a dot of pink paint, and the control group, marked with a…