Harvard scientists just cracked the code to hair regeneration.

 

By 35, 60% of men experience hair loss (& its not genetics). Here are 7 proven ways to prevent hair loss and even regrow your hair: 1. Harvard study: “You don’t lose hair because follicles die.”

Harvard’s 2021 study proved this. They found that balding scalps still have hair follicle stem cells. They don’t disappear. They go inactive. Hair grows when stimulated, nourished, and oxygenated.

By 35, over 60% of men and 40% of women experience hair thinning. But fortunately, scientists discovered 5 protocols that fixes this. Here’s the protocol to train your scalp for thicker, stronger hair: The myth: “You lose hair because follicles die.” Harvard’s 2021 study proved otherwise. They found that balding scalps still have hair follicle stem cells. They don’t disappear. They go inactive. The key is reactivating them.

Fix #1: Microneedling (1–2x/week) Tiny needles = micro-injuries → healing response. It stimulates stem cells and increases growth factor signaling. Use 1.0–1.5 mm rollers or pens. In one study, men using microneedling + minoxidil saw 4x more hair growth than minoxidil alone. Fix #3: DHT Blockers (Internal + Topical) DHT is a hormone that shrinks follicles. Proven blockers include: • Finasteride (Rx, oral) • Pumpkin seed oil (natural, oral/topical) • Saw palmetto • Green tea extract Less DHT = less miniaturization. 4. Minoxidil (Rogaine) Results take 3–6 months. • Increases blood flow • Extends anagen (growth) phase • Works even better with microneedling It works with patience, but the side effects are also real. Beware and be careful. Fix #5: Ancient Botanicals (Fo-Ti) Used in Traditional Chinese Medicine for centuries. Fo-Ti may: • Promote hair pigmentation • Extend the growth cycle • Improve scalp circulation Now backed by animal and early human studies. Best used as a supplement or a topical. Hair growth is not a gimmick. It’s a multi-system protocol based on: • Biology • Circulation • Hormones • Inflammation • Energy metabolism You’re not “losing” your hair. Train your follicles properly, and they can come back.

2. Scalp massage (5–10 min/day)

Gentle daily massage increases blood flow, delivers oxygen, and removes tension from the scalp.

A 2016 study showed that massage led to thicker hair after 24 weeks.

Add nourishing oil (rosemary, pumpkin seed, or peppermint) for extra benefit.

3. Hydration

Your scalp is 10–13% water by weight.

When you’re dehydrated, blood volume drops → less oxygen & nutrients reach your follicles → hair grows slower and sheds easier.

Aim for:

• 2.5–3.5L water/day

• 1–2 glasses first thing in the morning

4. Red light therapy (3–5x/week)

Low-Level Laser Therapy (LLLT) uses 630–680 nm light to increase ATP in follicle mitochondria.

More ATP = more energy for hair regeneration.

A 2017 meta-analysis showed consistent red light increases hair density and count within 24 weeks.

5. DHT Blockers

DHT is a hormone that shrinks follicles.

Proven blockers include:

• Finasteride (Rx, oral)

• Pumpkin seed oil (natural, oral/topical)

• Saw palmetto

• Green tea extract

Less DHT = less miniaturization.

6. Lower your stress

Stress hormones block Gas6, a key protein that activates hair follicle stem cells.

• Less Gas6 → stem cells shut down

• More Gas6 → stem cells reawaken

Restore this cycle, and you restore hair growth.

Start with 7-8 hours of sleep.

7. Whole-food nutrition

Hair growth depends on protein, minerals, and antioxidants.

Focus on:

• High-quality protein (eggs, fish, legumes)

• Iron + zinc-rich foods (pumpkin seeds, beef, lentils)

• Vitamin C-rich produce for collagen production

Warning: Don't overwash your scalp

Overwashing strips the scalp’s natural lipid layer, which protects hair shafts and keeps follicles hydrated.

Aim to:

• Wash 2–4×/week depending on hair type

• Use mild, sulfate-free shampoo

https://tinyurl.com/52d66tz4

8 best acupressure points to treat body pains and ashes

 

Have you ever tried acupressure techniques?

Acupressure is a non-invasive, natural therapy that involves applying steady pressure to specific points on the body—called meridians—that correspond to vital energy channels through which *qi* (life force) flows. When this energy is disrupted, physical or emotional imbalances can emerge.

Originating in ancient China, acupressure predates acupuncture and relies solely on the healing power of human touch. What's truly remarkable is how this traditional practice has found relevance in modern science and global healthcare. For instance, NASA has explored acupressure wristbands to combat motion sickness in astronauts, targeting the P6 (Nei Guan) point on the wrist—a technique also widely used to ease nausea during pregnancy or chemotherapy.

Scientifically, acupressure has been shown to stimulate the release of endorphins, serotonin, and dopamine—natural chemicals in the brain that relieve pain and elevate mood. Some wellness practitioners even use the term "Acu-nap" to describe the deeply relaxing effects of a short acupressure session, known to restore mental clarity and energy. What’s more, many of the body’s powerful healing points are located on the hands, feet, and face, making it an incredibly accessible and travel-friendly self-care tool.

Acupressure helps release these blockages, activating the body’s natural healing responses. Research supports its efficacy: a 2019 study published in Pain Management Nursing found that acupressure significantly reduced chronic pain and improved physical function in patients with lower back pain.

Another randomized clinical trial in Sleep Medicine Reviews (2021) concluded that acupressure improved sleep quality in individuals suffering from insomnia.

Studies in Evidence-Based Complementary and Alternative Medicine have demonstrated its role in reducing stress-related hormones, such as cortisol, thereby enhancing emotional well-being.

Acupressure has also shown promise in boosting immune responses and improving digestion by modulating the autonomic nervous system.

In a world often quick to medicate, acupressure offers a gentle yet scientifically grounded alternative—reminding us that healing can come not from adding more, but from pressing into the intelligence our bodies already possess.

⚠️While self-acupressure can be helpful for minor issues, chronic conditions should be addressed under the guidance of a trained practitioner or a healthcare provider familiar with integrative medicine.

⚠️Avoid if Pregnant (Without Medical Advice): Certain acupressure points—particularly those on the abdomen, lower back, and hands—are believed to potentially stimulate uterine contractions. Always consult a healthcare provider before using acupressure during pregnancy.

⚠️If you have heart disease, osteoporosis, bleeding disorders, or are taking blood-thinning medications, consult a doctor before starting acupressure. Some techniques may pose risks in these cases.

https://tinyurl.com/yrzkt5wj

A New Therapeutic Target for the Treatment of Melanoma

GPER. Penn Medicine


By PENN STATE UNIVERSITY

Researchers in the Perelman School of Medicine at the University of Pennsylvania have identified a new therapeutic target for the treatment of melanoma. For decades, research has associated female sex and a history of previous pregnancy with better outcomes after a melanoma diagnosis. Now, a research team from Perelman School of Medicine at the University of Pennsylvania says it may have determined the reason for the melanoma-protective effect. The mechanism is related to a cellular protein called the G protein-coupled estrogen receptor (GPER). When GPER was activated and combined with anti PD-1 inhibitor drugs in mouse cancer models, the therapy dramatically extended survival in all animals and completely eliminated the tumor in 50 percent of the mice. Researchers published their findings in the journal eLife today.

Melanoma is the deadliest form of skin cancer, despite accounting for only about one percent of skin cancers overall. Rates of melanoma have been rising for 30 years, and the American Cancer Society estimates there were more than 87,000 new cases in the United States in 2017. Even with recent advances in immunotherapy, the majority of patients with metastatic forms of melanoma will die from their disease.

“In melanoma and many other types of cancer, women have a better prognosis than men, and women with a history of pregnancy seem to have a better prognosis than those women that have never been pregnant” said the study’s senior author Todd W. Ridky, MD, PhD, an assistant professor of Dermatology at Penn. “Decades of research certainly suggests that there is something about female sex and pregnancy hormones that helps protect against melanoma, but no one really understood how that might work.”

Researchers say the key is GPER, a receptor found on melanocytes, which are pigment-producing cells in the skin. The receptor is normally activated by estrogen, which is higher in females, especially during pregnancy. Activation of GPER likely explains why many women notice that many areas of their skin gets darker during pregnancy. Previous research from the Ridky lab has shown the effects of GPER activation are totally different than the effects of classical estrogen receptor signaling, which is important in breast cancer. The team discovered that melanocytes do not even express the classical estrogen receptor, and that all estrogen effects were the result of GPER.

In melanoma specifically, once GPER is activated, the cancer cell becomes more differentiated. This means it divides less frequently, makes more pigment, and becomes more visible and vulnerable to the natural immune system. This makes it harder for the cancer to become resistant to immunotherapies.

No drugs specifically target GPER, but Ridky and his team used a lab compound called G-1, originally developed by Eric Prossnitz, PhD, at the University of New Mexico Comprehensive Cancer Center, to stimulate GPER in mice, and then used anti-PD-1 inhibitors to treat the melanoma. The approach eliminated the tumors in half of all mice. The authors note that anti-PD-1 inhibitors, when used alone in mice with melanoma, extend survival modestly, but do not completely eliminate tumors, and no animals survive long-term.

“We hope this work inspires other researchers to revisit old ideas of differentiation-based cancer therapies now that immune therapies are available,” said the study’s lead author Christopher A. Natale, a researcher in Ridky’s lab. “It is clear that the future of cancer therapy lies in combination treatments, and differentiation drivers may be a very useful component in future cancer therapy regimens.”

As Ridky points out, this represents a unique approach to immunotherapy and cancer therapy in general.

“So much of the cancer field is focused on inhibitors, but in this new treatment approach, we’re actually activating something rather than blocking it,” Ridky said. “We used a synthetic compound to mimic part of what happens naturally during pregnancy, and as a result, the GPER activator is very well tolerated without any obvious toxic side effects that are common with most cancer drugs.”

Ridky also said this approach could be promising beyond melanoma.

“This is a receptor that is expressed in many organs, so there’s a reasonable expectation that this may work in other tumor types too,” Ridky said.

Although researchers did not observe any toxicities from the compound in mice, though they say they plan further toxicity studies before hopefully moving on to human trials.

Publication: Christopher A Natale,et al., “Activation of G protein-coupled estrogen receptor signaling inhibits melanoma and improves response to immune checkpoint blockade,” eLife, 2018; DOI: 10.7554/eLife.31770

On the front lines of Parkinson’s research

Charles River and The Michael J. Fox Foundation team up to fight Parkinson’s disease

It starts simply. A slight tremor in a hand or a change in posture. However, as Parkinson’s disease (PD) progresses, patients have increasing mobility problems and neurological changes. PD is the second most common neurodegenerative disease in the world, with around 60,000 new cases each year in the United States alone. According to a 2018 CDC report, complications from PD are the 14th most likely cause of death in the US.

In PD research, there are several key targets researchers consider when looking for ways to treat the disease. The first is the aggregation of alpha-synuclein in Lewy bodies. The second is a mutation in LRRK2 (Leucine-rich repeat Kinase 2), a gene that encodes enzymes. Common consensus among researchers is that developing compounds that target alpha-synuclein and its aggregation, or compounds that inhibit LRRK2 could offer huge potential to treat PD.

In collaboration with The Michael J. Fox Foundation for Parkinson’s Research, Charles River has worked across multiple sites to better understand the pathophysiology of PD and to develop imaging agents to use as biomarkers in clinical studies. Many compounds from different chemical classes have been synthesized and tested in cell-based models as potential agents to interact with aggregated alpha-synuclein. Promising compounds are then radio-labelled and evaluated in PD animal models. These tracers could potentially be used as imaging agents in patients to help visualize the development alpha-synuclein enriched Lewy bodies.

Cell-based models are a useful tool to test the efficacy of disease-modifying therapies, since they develop the pathological hallmarks of PD quickly, do not require approval, and are cost-effective. Robust cell-based models are useful to rapidly screen compounds, which can then be further validated in research models of PD. Cell-based models are also used to identify and optimize compounds that inhibit LRRK2. Before any compound can go into research models, researchers need to see clear target engagement, and the right drug-like characteristics to be effective in PD patients.

In a project commissioned by The Michael J. Fox Foundation, scientists at Charles River have developed a high content analysis-based assay to measure alpha-synuclein aggregation in a terminally differentiated neuron cell-based model. This neuronal cell model effectively overexpresses alpha-synuclein, which then forms the standard protein aggregates. The aggregates are then detected using a conformation-specific antibody that binds with very high affinity to alpha-synuclein.

This model can facilitate high throughput, fully automated testing of therapeutic agents that reduce alpha-synuclein aggregation. Similarly, cell-based assays can be used to optimize compounds focused on inhibiting LRRK2. In collaboration with The Michael J. Fox Foundation and other organizations, Charles River has worked to understand how the LRRK2 inhibitors, identified from cell-based assays, influence function in models of PD. With the support of their partners, Charles River has used both normal healthy mice and mice with the human LRRK2-mutation to assess clinically relevant measures of PD.

Using these models, Charles River was able to demonstrate dose-related inhibition of LRRK2 activity in the brain. Models then received an infusion that led to an overproduction of alpha-synuclein. Models receiving the infusion displayed some of the classic signs of PD, including loss of dopaminergic function, reduction in dopamine cells, and clear motor impairment. Using the technique of push-pull microdialysis, researchers were also able to measure extracellular alpha-synuclein levels. These assays are now being used to identify novel compounds that could be progressed to the clinic.

A number of promising compounds have been identified that inhibit LRRK2 or alpha-synuclein aggregation in cell-based assays, which lead to meaningful effects in research models. Charles River developed a procedure called fine motor kinematic analysis that uses detailed video monitoring and proprietary analysis software to look at very subtle changes in motor function. Kinematic analysis allows researchers to see how compounds affect dopaminergic function at the very early stages, hopefully leading to the development of compounds that not only treat the symptoms of PD, but also slow or prevent the progression of the disease.

The examples above highlight the value of collaboration between contract research organizations like Charles River, industry and foundations to develop novel therapies focused on promising targets, with the ultimate goal of developing a cure for patients.

Improve Patient-Physician Communication and Increase Treatment Adherence

The Serotonin Syndrome

Today we”ll go over two  sometimes fatal syndromes that can occur from the use of the SSRI antidepressants. The first one is called the Serotonin Syndrome which can occur when the patient experiences too much serotonin effect in the brain. The second syndrome called Serotonin Withdrawal Syndrome occurs during the exact opposite of the first when a patient misses her dose or deliberately tries to quit on her own without the proper guidance. Both can be deadly in the extreme, both can also cause mania and appalling behavior such as we have been discussing here at length in other articles. Let’s look at the first one shall we:

The symptoms of the serotonin syndrome are (from The Serotonin Syndrome, AM J PSYCHIATRY, June 1991):

1. Euphoria

2. Drowsiness

3. Sustained rapid eye movement

4. Overreaction of the reflexes

5. Rapid muscle contraction and relaxation in the ankle causing abnormal movements of the foot

6. Clumsiness

7. Restlessness

8. Feeling drunk and dizzy

9. Muscle contraction and relaxation in the jaw

10. Sweating

11. Intoxication

12. Muscle twitching

13. Rigidity

14. High body temperature

15. Mental status changes were frequent (including confusion and hypomania – a “happy drunk” state)

16. Shivering

17. Diarrhea

18. Loss of consciousness and death.

There is an additional and unique 19th symptom in which the patient experiences intense, deep, brain pain which is not like a headache either it’s a totally different type of pain.

I have made this diagnosis before and it isn’t pretty. In fact I see it as yet another form of malpractice. Why malpractice? Because it usually takes a deliberate attempt to induce this syndrome by adding in one serotonergic drug after another like you would to a lab rat. In the case where I saw it, this person (see below the case of Poor Jimmy) was slowly being driven mad. It could have easily been prevented if his psychiatrist hadn’t been so apathetic. Jimmy would describe his psychiatric appointments like this: in and out in less than five minutes. How on earth can anyone tell anything in five minutes? Every time he had a complaint (side effect) he was given another serotonergic drug. Until finally he had 5 serotonergic agents on board, five! Had I not been there I fear he would have died in the next day or two before anyone could figure out what was happening. This is the same psychiatrist that was writing for speed, amphetamine, in a patient that had already suffered sudden death but was successfully revived. Recall amphetamine has a Black Box warning that includes sudden death as a consequence of chronic amphetamine exposure.

Dr Tracy continues:

The serotonin syndrome is generally caused by a combination of two or more drugs, one of which is often a selective serotonergic medication. The drugs which we know most frequently contribute to this condition are the combining of MAOIs with Prozac (this should also include the other SSRIs) or other drugs that have a powerful effect upon serotonin, ie., clomipramine (Anafranil), trazadone (Deseryl), etc. The combination of lithium with these selective serotonergic agents has been implicated in enhancing the serotonin syndrome. The tricyclic antidepressants, lithium, MAOIs, SSRIs, ECT (electric shock treatment), tryptophan, and the serotonin agonists (fenfluramine) all enhance serotonin neurotransmission and can contribute to this syndrome. Anything which will raise the level of serotonin can bring on this hyperserotonergic condition. The optimal treatment for the serotonin syndrome is discontinuation of the offending medication or medications, offer supportive measures, and wait for the symptoms to resolve. If the offending medication is discontinued, the condition will often resolve on its own within a 24 hour period. If the medication is not discontinued the condition can progress rapidly to a more serious state and become fatal. It should be apparent that the greater the enhancement of serotonin levels, the greater the chances of producing the serotonin syndrome. Therefore it is recommended that Zoloft, Prozac, Paxil, Luvox, Serzone, etc. not be used concurrently with each other or any other serotonergic drugs and that these serious adverse reactions should be expected with these combinations (Callahan, 1993). [PROZAC: PANACEA OR PANDORA?, p. 88.]

Yet the combining of these drugs is exactly what doctors do all of the time in direct contradistinction to recommended safe prescribing methods.

Serotonin Withdrawal Syndrome (SWS) On top of that, the antidepressants produce serious withdrawal reactions, making it difficult and at times life-threatening to withdraw from them, even with the recommended clinical supervision and slow taper.

Up to 60% of SSRI treated patients will have some form of serotonin withdrawal syndrome if they abruptly stop their antidepressant. There are five core systems affected:

I.            Dysequilibrium leading to ataxia (unable to walk a straight line)

II.            GI symptoms such as nausea and vomiting, or diarrhea

III.            Flu like symptoms

IV.           Sensory disturbances such as electrical shocks, and paresthesias

V.            Sleep disturbances such as insomnia and vivid dreams

The psychological symptoms include anxiety, agitation, crying spells, irritability. The afflicted patient may experience the feeling of “going postal” wanting to jump out of a car at 80 mph.

FINISH Mnemonic for Recognition of Antidepressant Discontinuation Syndrome[1]

Flu-like symptoms

Fatigue

Lethargy

General malaise

Muscle aches/headaches

Diarrhea

Insomnia

Nausea

Imbalance

Gait instability

Dizziness/lightheadedness

Vertigo

Sensory disturbances

Paresthesia

“Electric shock” sensations

Visual disturbance

Hyperarousal

Anxiety

Agitation

Keep in mind that withdrawal is not to be taken lightly as patients can die from this or have a psychotic break such as full blown mania. Dr Tracy provides a CD on her website titled Help I can’t Get Off My Antidepressant for any patient or physician interested in learning a way to wean yourself off of these powerfully addicting psychotropics.

Dr Breggin just published a book devoted to weaning one off of these mind melding materials: Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients and their Families by Peter Roger Breggin (Jul 19, 2012)

Recently a study came out (2011) that confirmed how difficult to near impossible it is to conventionally stop taking an antidepressant. The result of the study, Published in the journal, Frontiers of Evolutionary Psychology, was expressed by the lead author, Paul W. Andrews in Science Daily:

“We found that the more these drugs affect serotonin and other neurotransmitters in your brain—and that’s what they’re supposed to do—the greater your risk of relapse once you stop taking them…Our results suggest that when you try to go off the drugs, depression will bounce back. This can leave people stuck in a cycle where they need to keep taking anti-depressants to prevent a return of symptoms.”

I received this information from Dr Ann Blake Tracy’s newsletter. It only confirms what we already know. The only way to be rid of these drugs is to slowly, and I mean slowly, reduce your dose over 6 months or more. Of course, when you break through and develop anxiety or depression from weaning too fast your psychiatric Doc in the Box (P-DIB) will automatically conclude that it is your native disease that’s manifesting and give you another SSRI or up your original dose.

Christopher Rasmussen MD, MS

[1] Christopher H. Warner  Antidepressant Discontinuation Syndrome Am Fam Physician. 2006 Aug 1;74(3):449-456. (http://www.aafp.org/afp/2006/0801/p449.html) 04/30/2012

Exactly How Bad Is Antibiotic Resistance Right Now?

David Dorward; Ph.D.; National Institute of Allergy and Infectious Diseases (NIAID)

Klebsiella pneumoniae are a normal part of the human gut’s bacterial community, but they can cause dangerous infections for people in hospitals and nursing homes. A woman recently died from a strain that no antibiotics could treat.

A WOMAN IN THE US RECENTLY DIED FROM A SUPERBUG THAT NO ANTIBIOTICS COULD TREAT

By Kate Baggaley

We are starting to see the kind of incurable infection that scientists have warned us about for years. In January, the Centers for Disease Control and Prevention announced that a woman in Nevada had died from an infection resistant to every available antibiotic.

The woman picked up a virulent germ from a group of microbes called carbapenem-resistant Enterobacteriaceae (CRE). After breaking her leg, she’d been hospitalized repeatedly over the course of several years in India. Tests showed that none of the 26 antibiotics typically used to treat the type of infection she’d developed would have cured her.

People in the United States have been infected by pan-resistant bacteria before. “It’s not the first time that there has been an untreatable bacterial infection in the US,” says James Hughes, co-director of the Emory Antibiotic Resistance Center in Atlanta. “This particular case…is an extreme example of how bad it can get.”

Thankfully, these cases are still rare. But they’re also just one piece of a much bigger problem. Antibiotic resistance is stealthily creeping closer, spreading among disease-causing bacteria, sickening people, and making life-saving drugs less effective.

“It doesn’t spread easily from person to person and terrify people to the extent that something like Ebola does,” Hughes says. But “it’s a serious problem and it’s getting worse, and we don’t have the tools that we need to fully confront it.”

So how bad is antibiotic resistance? Here’s what we know:

It’s all over the place

Antibiotic resistance has been found in many different bacteria, some of which cause common problems like pneumonia, sexually transmitted infections, or food poisoning. Some bacteria aren’t vulnerable to a particular drug to begin with. Germs can also mutate to become resistant to a given antibiotic, or pick up resistance-granting genes from other species.

In some cases, bacteria become impervious to the antibiotics that doctors commonly use to treat them. This forces doctors to prescribe more powerful drugs, some of which cause additional problems like kidney damage. And some bacteria carry genes that allow them to fight off these last-ditch antibiotics.

“We are seeing an increasing number of accounts of resistance to top-shelf antibiotics (like colistin and the carbapenem class), which are our last lines of defense against these bugs,” Keeve Nachman, an assistant professor at the Johns Hopkins Bloomberg School of Public Health in Baltimore, said in an email. “We are also learning more and more that some of the most worrisome genes that allow bacteria to resist our most powerful antibiotics are being exchanged more readily between different types of bacteria.”

Bacteria that could defeat the last-resort drug colistin were first ID’d in China in 2015. The resistance-granting gene, called mcr -1, has shown up a handful of times in the United States. This gene is worrying because it’s carried on plasmids—rings of self-replicating DNA—that could be swapped between different species of bacteria.

This past December, researchers reported bacteria on a pig farm in the United States resistant to carbapenems, a class of drugs also used against bugs that are already impervious to other treatments. The genes were also harbored on plasmids, although fortunately none of the bacteria appear to have contaminated pork from the farm.

Even if a bug can fight off our most formidable drugs, it isn’t necessarily resistant to everything in our arsenal. Some of these germs can still be felled by less powerful antibiotics. The fear is that some superbugs will cobble together resistance to everything that we can throw at them, as was the case for the woman in Nevada.

“There are people dying of infections that we once were able to treat with antibiotics,” says Jean Patel, the CDC Antibiotic Resistance Laboratory Network Lead. “Those occurrences are rare, but…it means that in other cases where we have resistance to just a few drugs, we can anticipate that those bacteria will also become resistant to all drugs.”

It’s already making people sick

A bacterium doesn’t have to be resistant to everything to be dangerous. At least 2 million people come down with antibiotic resistant infections in America ever year, and 23,000 of these people die. These infections may be adding $20 billion to healthcare costs in the United States each year, and dragging out people’s recovery from illnesses.

“Resistance limits the number of options we have to treat infections, which can mean that someone…may take longer or require more expensive (and possibly invasive) interventions to treat,” says Nachman.

Sometimes, doctors do not realize that the bacteria making a person sick happen to be resistant to the antibiotics they’d normally prescribe. “You’re put on antibiotics that are not effective, and then by the time you figure out that those antibiotics are not going to work the infection has had two or three days to progress,” says Henry Chambers, chief of the Division of Infectious Diseases at San Francisco General Hospital.

Superbugs most often spread through hospitals, targeting people who are already sick or have compromised immune systems. But these infections do strike and even kill people who are otherwise perfectly healthy, too. “Anybody can become infected with a resistant bacteria,” Patel says.

And some people carry superbugs within their bodies without even realizing it. In one case last year, a rare strain of E. coli that was resistant to many drugs, including colistin, was discovered in an apparently healthy woman in Pennsylvania.

These bugs might not have the opportunity to cause problems until a person becomes weakened, or spreads the germs to someone else (most likely while in a hospital). But because these hosts show no symptoms, we don’t really know how many of them there are.

We’re going to have to step up our tracking

It’s hard to predict how much worse antibiotic resistance will get in the next few years. We do have a long-term forecast though, and it’s pretty grim. If we don’t make a dent in antibiotic resistance, superbugs could kill more people per year than cancer by 2050. Minor injuries and common medical procedures like C-sections, hip replacements, or chemotherapy will become a lot more dangerous. Maladies we think of as being under control in modern times, like tuberculosis or gonorrhea, could become untreatable.

Scientists are tracking which bacteria develop tricks to become resistant over time, and identifying the most dangerous strains. “What’s been really challenging is being able to test all the isolates that people are concerned with,” Patel says. The CDC has recently expanded its capacity to investigate potential superbugs by creating a network of labs across the United States.

“Once you have the bacteria in hand, you’re able to detect get new information…that wasn’t collected at the hospital,” Patel says. “All that information is going to help epidemiologists respond to antibiotic resistance outbreaks.”

And when an outbreak does crop up, there’s an investigation to find out how widely the bug spread. In the case of the Nevada woman who recently died, the superbug does not appear to have jumped to exposed caregivers. But “just because there is a single case, I would not take great comfort in that fact,” Chambers says. “When you identify one case there are often very many that have not yet been recognized but soon will be. It’s kind of a tip of the iceberg problem.”

That’s why we’re going to have to work harder to thwart antibiotic resistance. Some prevention efforts are as simple as basic hygiene. But we’ll also need to use antibiotics more responsibly and curtail their use in farm animals. We must come up with incentives for drug companies to develop new antibiotics, dream up alternative treatments, and devise tools to diagnose infections more quickly.

“We’ll never totally eliminate the problem of antibiotic resistance,” Hughes says. “But we can do a heck of a lot better in terms of being prepared to detect it, respond to it, treat it effectively and prevent much of the…potential future increases in the problem.”