Category Archives: Diseases

Debunking myths about malaria and its vector, the mosquito

Tabitha Mwangi, Pwani University

Myths about diseases spread like wildfire. Malaria is a case in point. The Conversation Africa’s Health and Medicine Editor Joy Wanja Muraya asked Tabitha Mwangi to help sort out fact from fiction. The Conversation

Mosquitoes only bite at night.

Not entirely true.

There are two types of mosquitoes that bite mostly at night; the Anopheles mosquito that transmits malaria and it’s noisier cousin, the Culex mosquito which spreads lymphatic filariasis, – also known as elephantiasis – that presents as severe swelling in the arms, legs or genitals.

A year-long study in Western Kenya showed that 15% of the mosquitoes bite between 6pm to 9pm while the majority (85%) bite from 9pm till morning. Data from this study puts further emphasis on the value of sleeping under an insecticide treated bednet.

But there are other mosquitoes, such as the Aedes mosquitoes – easily identified by their zebra stripped legs – that are active mostly during the day. They spread viruses that cause dengue, zika, Chikugunya and rift valley fever.

The fact that this mosquito is active during the day makes it harder to control the diseases it spreads because bed nets aren’t an option.

Eating garlic before I sleep will repel mosquitoes.

There’s no scientific evidence to support this.

Garlic does produce a sulphur compound known as allicin which has some anti-bacterial, anti-fungal and anti-parasitic activities. Researchers have looked at it’s impact on mice that have been infected with malaria. In mice, use of allicin leads to a reduction in the number of malaria parasites in the blood, the higher the dose of allicin, the longer the mice survived. But no research has been done on its effect on the human immune system.

Garlic oils are marketed as insect repellents but their efficacy is uncertain.

Mosquitoes like to bite women and children more than men.

This isn’t true, though there’s some evidence that they’re partial to pregnant women.

In The Gambia researchers found that pregnant women are twice as attractive to mosquitoes than non pregnant women.

The research involved 36 pregnant women and 36 women who weren’t pregnant. The two groups slept in separate huts under bed nets. In the morning, researchers collected and counted the mosquitoes found in the separate huts.

Twice as many mosquitoes were found in the huts in which the pregnant women had slept. There were two possible explanations for this. The first is that mosquitoes are attracted to carbon dioxide which pregnant women produce more of. In advanced pregnancy, women exhale 21% greater volumes than non pregnant women.

The second possible explanation is that pregnant women’s tummies are 0.7°C warmer than non pregnant women which could attract mosquitoes.

But there was an additional factor that the researchers suggested could have affected the results. Pregnant women – particularly women in advanced pregnancy – had to leave their huts at night more often than non-pregnant women because they need to urinate frequently.

Mosquitoes die after feeding.

This is not true. Male mosquitoes feed on sugary things while female mosquitoes need blood for their eggs to develop.

After feeding on blood, a female mosquito will rest to digest the blood and wait for the eggs to be ready.

The female mosquito rests for about two to three days then lays her eggs in water. After laying between 50 to 200 eggs, she then searches for another blood meal in order to lay another batch of eggs.

During her lifetime the female tries to lay as many eggs as she can which requires several blood meals.

In a laboratory, female mosquitoes can live for up to one month. But in natural conditions, few survive beyond one to two weeks.

Once you get malaria, you will never get it again.

Researchers have spent years monitoring people in malaria endemic areas to learn the patterns of immunity.

My PhD research involved collecting data on malaria from about 1,000 people in Coastal Kenya for two years. Children under five years had, on average, one clinical attack of malaria every year.

Malaria cases declined steeply after that and it was rare for adults who lived in this malaria endemic areas to have clinical attacks.

Other studies have shown that when highly immune adults spent long periods of time in places where they weren’t being bitten by infected mosquitoes, they could lose some of thatimmunity.

Scientists know that solid immunity to malaria only occurs in people who are constantly challenged. But it’s still not clear how this happens. This is one of the reasons why developing a malaria vaccine that works well has proved so difficult.

Mosquitoes only like the blood of humans.

This is true for some mosquitoes, but because female mosquitoes need a blood meal, most will take it from wherever they can find it. For example, livestock kept outside the homestead can attract mosquitoes. There’s even been a suggestion that cattle should be treated with insecticide as a malaria control strategy.

Tabitha Mwangi, Researcher, Senior Lecturer, Pwani University

This article was originally published on The Conversation. Read the original article.

To fight Zika, let’s genetically modify mosquitoes – the old-fashioned way

The near panic caused by the rapid spread of the Zika virus has brought new urgency to the question of how best to control mosquitoes that transmit human diseases. Aedes aegypti mosquitoes bite people across the globe, spreading three viral diseases: dengue, chikungunya and Zika. There are no proven effective vaccines or specific medications to treat patients after contracting these viruses.

Mosquito control is the only way, at present, to limit them. But that’s no easy task. Classical methods of control such as insecticides are falling out of favor – they can have adverse environmental effects as well as increase insecticide resistance in remaining mosquito populations. New mosquito control methods are needed – now.

The time is ripe, therefore, to explore a long-held dream of vector biologists, including me: to use genetics to stop or limit the spread of mosquito-borne diseases. While gene editing technologies have advanced dramatically in the last few decades, it is my belief that we’ve overlooked older, tried and true methods that could work just as well on these insects. We can accomplish the goal of producing mosquitoes incapable of transmitting human pathogens using the same kinds of selective breeding techniques people have been using for centuries on other animals and plants.

Technicians from Oxitec inspect genetically modified Aedes aegypti mosquitoes in Campinas, Brazil.
Paulo Whitaker/Reuters

Techniques on the table

One classic strategy for reducing insect populations has been to flood populations with sterile males – usually produced using irradiation. When females in the target population mate with these males, they produce no viable offspring – hopefully crashing population numbers.

The modern twist on this method has been to generate transgenic males that carry a dominant lethal gene that essentially makes them sterile; offspring sired by these males die late in the larval stage, eliminating future generations. This method has been promulgated by the biotech company Oxitec and is currently used in Brazil.

Rather than just killing mosquitoes, a more effective and lasting strategy would be to genetically change them so they can no longer transmit a disease-causing microbe.

The powerful new CRISPR gene editing technique could be used to make transgenes (genetic material from another species) take over a wild population. This method works well in mosquitoes and is potentially a way to “drive” transgenes into populations. CRISPR could help quickly spread a gene that confers resistance to transmission of a virus – what scientists call refractoriness.

But CRISPR has been controversial, especially as applied to human beings, because the transgenes it inserts into an individual can be passed on to its offspring. No doubt using CRISPR to create and release genetically modified mosquitoes into nature would stir up controversy. The U.S. Director of National Intelligence, James Clapper, has gone so far as to dub CRISPR a potential weapon of mass destruction.

But are transgenic technologies necessary to genetically modify mosquito populations?

Examples of successful artificial selection of various traits through the years. In the center is a cartoon of the ‘block’ scientists would like to select for in mosquitoes so they can’t pass on the virus.
Jeff Powell, Author provided

Selective breeding the old-fashioned way

Genetic modification of populations has been going on for centuries with great success. This has occurred for almost all commercially useful plants and animals that people use for food or other products, including cotton and wool. Selective breeding can produce immense changes in populations based on naturally occurring variation within the species.

Artificial selection using this natural variation has proven effective over and over again, especially in the agricultural world. By choosing parents with desirable traits (chickens with increased egg production, sheep with softer wool) for several consecutive generations, a “true breeding” strain can be produced that will always have the desired traits. These may look very different from the ancestor – think of all the breeds of dogs derived from an ancestor wolf.

To date, only limited work of this sort has been done on mosquitoes. But it does show that it’s possible to select for mosquitoes with reduced ability to transmit human pathogens. So rather than introducing transgenes from other species, why not use the genetic variation naturally present in mosquito populations?

Deriving strains of mosquitoes through artificial selection has several advantages over transgenic approaches.

  • All the controversy and potential risks surrounding transgenic organisms (GMOs) are avoided. We’re only talking about increasing the prevalence in the population of the naturally occurring mosquito genes we like.
  • Selected mosquitoes derived directly from the target population would likely be more competitive when released back to their corner of the wild. Because the new refractory strain that can’t transmit the virus carries only genes from the target population, it would be specifically adapted to the local environment. Laboratory manipulations to produce transgenic mosquitoes are known to lower their fitness.
  • By starting with the local mosquito population, scientists could select specifically for refractoriness to the virus strain infecting people at the moment in that locality. For example, there are four different “varieties” of the dengue virus called serotypes. To control the disease, the selected mosquitoes would need to be refractory to the serotype active in that place at that time.
  • It may be possible to select for strains of mosquitoes that are unable to transmit multiple viruses. Because the same Aedes aegypti mosquito species transmits dengue, chikungunya and Zika, people living in places that have this mosquito are simultaneously at risk for all three diseases. While it has not yet been demonstrated, there is no reason to think that careful, well-designed selective breeding couldn’t develop mosquitoes unable to spread all medically relevant viruses.

Fortunately, Ae. aegypti is the easiest mosquito to rear in captivity and has a generation time of about 2.5 weeks. So unlike classical plant and animal breeders dealing with organisms with generations in years, 10 generations of selection of this mosquito would take only months.

Researchers are working out mass rearing techniques for Aedes mosquitoes – their generation time is only 2.5 weeks.
IAEA Imagebank, CC BY-NC-ND

This is not to imply there may not be obstacles in using this approach. Perhaps the most important is that the genes that make it hard for these insects to transmit disease may also make individual insects weaker or less healthy than the target natural population. Eventually the lab-bred mosquitoes and their offspring could be out-competed and fade from the wild population. We might need to continuously release refractory mosquitoes – that is, the ones that aren’t good at transmitting the disease in question – to overcome selection against the desirable refractory genes.

And mosquito-borne pathogens themselves evolve. Viruses may mutate to evade any genetically modified mosquito’s block. Any plan to genetically modify mosquito populations needs to have contingency plans in place for when viruses or other pathogens evolve. New strains of mosquitoes can be quickly selected to combat the new version of the virus – no costly transgenic techniques necessary.

Today, plant and animal breeders are increasingly using new gene manipulation techniques to further improve economically important species. But this is only after traditional artificial selection has been taken about as far as it can to improve breeds. Many mosquito biologists are proposing to go directly to the newest fancy transgenic methodologies that have never been shown to actually work in natural populations of mosquitoes. They are skipping over a proven, cheaper and less controversial approach that should at least be given a shot.

The Conversation

Jeffrey Powell, Professor, Yale University

This article was originally published on The Conversation. Read the original article.

Your Body Can Now Be Run With Computer Programming

Scientists have found a new way through which the cells of our body can be controlled through a proprietary programming language, which could help you from falling prey to diseases. This latest innovation comes from a group of biological engineers at MIT, who have developed a programming language capable of designing complex DNA functions that can further be put in a human being’s cell.

How does it work?

Commenting on the functionality of the latest innovation, Christopher Voigt, a biological engineering professor at MIT revealed that it was more of text-based language used to program a computer. Similarly, the program is then compiled into a DNA sequence, which is then inputted into the cell, and its circuit runs within the cell.

How did they do it?

Verilog, a hardware description language has been used by researchers to make this a reality. Sensors that can be programmed into DNA sequences have been used with specially designed computing elements.

The interesting part lies in the way the program works. The DNA sequences are first programmed into a cell to create a circuit. The customizable sensors then detect the amount of glucose, oxygen, and temperature. What wonders science and technology today can put together is completely inspiring.

How Yersinia pestis evolved its ability to kill millions via pneumonic plague

The mere mention of the plague brings to mind the devastating “Black Death” pandemic that spread across Europe in the 1300s. Mass graves were piled high with the corpses of its millions of victims, while the disease rampaged across Europe for many decades. Yersinia pestis, the bacterium responsible for that plague pandemic, still persists in the environment among rodent and flea populations today, and human outbreaks regularly occur around the world. Most recently, an outbreak of plague was confirmed late last year in Madagascar as well as within a prairie dog colony in Colorado just this June.

The various routes of transfer between hosts of Y. pestis bacteria, which are the cause of bubonic plague in the United States.

Y. pestis can cause three different forms of plague: bubonic, pneumonic and septicemic. Pneumonic plague infects the lungs, causing severe pneumonia. It’s the most serious form of the disease, with fatality rates approaching 100% if untreated, although recovery is possible with antibiotics if caught in time. While increased basic hygiene and developments in modern medicine have greatly reduced the severity of plague outbreaks, the symptoms of pneumonic plague are so similar to that of the flu that misdiagnosis or delays in treatment can have fatal consequences.

Y. pestis is known to have evolved from the relatively mild gut pathogen Yersinia pseudotuberculosis sometime within the last 5,000 to 10,000 years – very recently on an evolutionary timescale. Sometime during this evolution Y. pestis developed new modes of transmission and disease manifestations, which allowed it to adapt to new animals and environments. Rather than simply causing an upset stomach, the bacterium became the killer we know from the Middle Ages.

A mother and son, suspected carriers of the pneumonic plague, share a bed in an Indian hospital.
Kamal Kishore / Reuters

One of our lab’s major research goals is to figure out how Y. pestis developed its ability to specifically cause pneumonic plague. Our research, recently published in Nature Communications, offers new insights into how small genetic changes fundamentally affected the emergence of Y. pestis as a severe respiratory pathogen.

Prior to our study, the consensus in the field has been that pneumonic plague was a secondary byproduct of the invasive disease associated with bubonic plague. As pneumonic plague represents only 5%–10% of current plague infections in humans, the field has presumed that pneumonic plague occurs only once Y. pestis reaches the lungs following systemic infection, as might occur during bubonic plague. While this may be the case now, it may not necessarily represent what occurred in the past, especially as Y. pestis was just emerging from its ancestor Y. pseudotuberculosis.

Plague infection in the lungs. Untreated, death results within a week.
CDC/ Dr Jack Poland, CC BY

First, target the lungs

Therefore, we began our study by asking a relatively simple question: “When did Y. pestis develop the ability to infect the lung and cause pneumonic plague?” Remember, it was only recently, evolutionarily speaking, that it started targeting the lungs rather than the gut. Y. pestis is believed to have emerged as a species 5,000–10,000 years ago, but the first known pandemic of plague in humans didn’t occur until the Justinian Plague that afflicted the Byzantine empire about 1,500 years ago.

Excavation of skeletal remains of victims of the Black Death.
Museum of London, Schuenemann et al PNAS vol. 108 no. 38

A recent discovery helped us investigate. Scientists successfully recovered DNA from Y. pestis from human skeletons in a Black Death mass grave in London, England. The genetic material from the historic site is very similar to DNA isolated from recent modern plague outbreaks. The fact that the DNA from then is similar to the DNA from now indicates that today’s Y. pestis has maintained its devastating disease-causing capability.

To answer the question of how Y. pestis made that crucial leap to targeting the lung and therefore being able to cause pneumonic plague, we used strains of both ancestral and modern Y. pestis in our study. These ancestral strains of Y. pestis, isolated from voles in the Transcauscaian highland, carry characteristics of both modern, pandemic Y. pestis and the relatively benign predecessor species Y. pseudotuberculosis that still exists today.

Thus, these ancestral versions can be considered “intermediate” strains, trapped somewhere between the gut Yersiniae and modern, virulent Y. pestis. Indeed, these “intermediate” lineage ancestral strains are as closely related to Y. pseudotuberculosis as we can get while still technically representing species of Y. pestis. Because of their unique genetic characteristics, these ancestral strains can provide crucial insights into how this bacterium may have adapted to new host environments as it evolved from Y. pseudotuberculosis.

Surprisingly, we found that these ancestral strains were able to cause pneumonic plague in a manner indistinguishable from that of modern Y. pestis in mice – but only if the bacteria carried the gene for a single protein called Pla. Pla is unique to Y. pestis and was acquired very early in the evolution of the species.

Almost all ancestral strains of Y. pestis carry the gene for Pla, but there still exist a few that represent ancestral Y. pestis just prior to acquisition of Pla. We were able to test if these pre-Pla strains were able to cause pneumonic plague – and they did not. But as soon as Y. pestis picked up this gene, the bacteria could cause epidemics of pneumonic plague. No further changes were necessary, even though there are dozens of additional differences between these ancestral strains and modern Y. pestis. So Y. pestis was able to cause pneumonic plague much earlier in its history than had previously been thought – as soon as it acquired this single gene for Pla.

Scanning electron micrograph of Yersinia pestis.
Justin Eddy, Lindsay Gielda, et al, CC BY-ND

Second, increase infectiousness

But that’s not where the story ends. It turns out that all modern pandemic strains of Y. pestis contain a single amino acid mutation in Pla compared to ancestral Y. pestis. This change slightly alters the function of the Pla protein. The mutation, however, plays no role in the ability of any Y. pestis isolates to cause pneumonic plague – ancestral or modern.

Quite surprisingly, this modification allowed the Y. pestis to spread deeper into host tissue following a bite from an infected flea or rodent, leading to the development of bubonic plague with its trademark swollen lymph nodes. This suggests that Y. pestis was first a respiratory pathogen before it was able to efficiently cause invasive infections.

This discovery challenges our traditional notion of how plague evolved. Rather than pneumonic plague being a late addition to Y. pestis’s arsenal as commonly believed, its ability to target the lung came before the change that makes it such an infectious pathogen. Our research suggests that the acquisition of Pla and its ability to cause pneumonic plague occurred well before 1,500–5,000 years ago. But the amino acid modification didn’t occur until just prior to 1,500 years ago, allowing Y. pestis to become much more deadly. All strains of Y. pestis from the time of the Justinian Plague and after have the deadly modification of Pla, while strains prior do not.

Physician attire for protection from the Black Death.
Paul Fürst

Our results may explain how, through one small amino acid change, Y. pestis quickly transitioned from causing only localized outbreaks of disease to the pandemic spread of Y. pestis as seen during the Justinian Plague and the Black Death.

And it raises the ominous possibility that other respiratory pathogens could emerge from similar small genetic changes.

The Conversation

Daniel Zimbler is Postdoctoral Fellow in Bacteriology at Northwestern University.
Wyndham Lathem is Assistant Professor of Microbiology-Immunology at Northwestern University.

This article was originally published on The Conversation.
Read the original article.

The science behind sexual orientation

This article is part of a series The Conversation Africa is running on issues related to LGBTI in Africa. You can read the rest of the series here.

People who are attracted to others of the same sex develop their orientation before they are born. This is not a choice. And scientific evidence shows their parents cannot be blamed.

Research proving that there is biological evidence for sexual orientation has been available since the 1980s. The links have been emphasised by new scientific research.

In 2014, researchers confirmed the association between same-sex orientation in men and a specific chromosomal region. This is similar to findings originally published in the 1990s, which, at that time, gave rise to the idea that a “gay gene” must exist. But this argument has never been substantiated, despite the fact that studies have shown that homosexuality is a heritable trait.

Evidence points towards the existence of a complex interaction between genes and environment, which are responsible for the heritable nature of sexual orientation.

These findings are part of a report released by the Academy of Science South Africa. The report is the outcome of work conducted by a panel put together in 2014 to evaluate all research on the subject of sexual orientation done over the last 50 years.

It did this against the backdrop of a growing number of new laws in Africa which discriminate against people attracted to others of the same sex. The work was conducted in conjunction with the Ugandan Academy of Science.

Existing research

The academy looked at several scientific studies with different focus areas that have all provided converging findings. These include family and twin studies. The studies have shown that homosexuality has both a heritable and an environmental component.

Family studies have shown that homosexual men have more older brothers than heterosexual men. Homosexual men are also more likely to have brothers that are also homosexual. Similarly, family studies show that lesbian women have more lesbian sisters than heterosexual women.

Studies on identical twins are important as identical twins inherit the same genes. This can shed light on a possible genetic cause. Studies on twins have established that homosexuality is more common in identical (monozygotic) twins than in non-identical (dizygotic) twins. This proves that homosexuality can be inherited.

However, the extent of the inheritance between twins was lower than expected. These findings contribute to the notion that although homosexuality can be inherited, this does not occur according to the rules of classical genetics. Rather, it occurs through another mechanism, known as epigenetics.

Epigenetics likely to be an important factor

Epigenetics relates to the influence of environmental factors on genes, either in the uterus or after birth. The field of epigenetics was developed after new methods were found that identify the molecular mechanisms (epi-marks) that mediate the effect of the environment on gene expression.

Epi-marks are usually erased from generation to generation. But under certain circumstances, they may be passed on to the next generation.

Normally all females have two X-chromosomes, one of which is inactive or “switched off” in a random manner. Researchers have observed that in some mothers who have homosexual sons there is an extreme “skewing” of inactivation of these X-chromosomes. The process is no longer random and the same X-chromosome is inactivated in these mothers.

This suggests that a region on the X-chromosome may be implicated in determining sexual orientation. The epigenetics hypothesis suggests that one develops a predisposition to homosexuality by inheriting these epi-marks across generations.

External environmental factors such as medicinal drugs, chemicals, toxic compounds, pesticides and substances such as plasticisers can also have an impact on DNA by creating epi-marks.

These environmental factors can also interfere with a pregnant woman’s hormonal system. This affects the levels of sex hormones in the developing foetus and may influence the activity of these hormones.

Future studies will determine whether these factors may have a direct impact on areas of the developing brain associated with the establishment of sexual orientation.

Looking to evolution

From an evolutionary perspective, same-sex relationships are said to constitute a “Darwinian paradox” because they do not contribute to human reproduction. This argument posits that because same-sex relationships do not contribute to the continuation of the species, they would be selected against.

If this suggestion were correct same-sex orientations would decrease and disappear with time. Yet non-heterosexual orientations are consistently maintained in most human populations and in the animal kingdom over time.

There also appear to be compensating factors in what is known as the “balancing selection hypothesis”, which accounts for reproduction and survival of the species. In this context, it has been demonstrated that the female relatives of homosexual men have more children on average than women who do not have homosexual relatives.

Future studies

The academy found that a multitude of scientific studies have shown sexual orientation is biologically determined. There is not a single gene or environmental factor that is responsible for this – but rather a set of complex interactions between the two that determines one’s sexual orientation.

However, more evidence is leading investigators to a specific region on the X-chromosome, and possibly a region on another chromosome.

The identification of these chromosomal regions does not imply that homosexuality is a disorder – nor does it imply that there are mutations in the genes in these regions, which still remain to be identified. Rather, for the first time, it suggests that there is a specific region on a chromosome that determines sexual orientation.

Although research has not yet found what the precise mechanisms are that determine sexual orientation – which may be heterosexual, homosexual, bisexual or asexual – the answers are likely to come to the fore through continued research. These findings will be important for the field of genetics and, more importantly, for those attracted to others of the same sex and society as a whole.

This article draws from the ASSAf report.

The Conversation

Michael Sean Pepper is Director of the Institute for Cellular and Molecular Medicine at University of Pretoria.
Beverley Kramer is Assistant Dean: Research and Postgraduate Support in the Faculty of Health Sciences at University of the Witwatersrand.

This article was originally published on The Conversation.
Read the original article.

The Mystery of Breast Cancer

For most of the common cancers, a major cause has been identified: smoking causes 90% of lung cancer worldwide, hepatitis viruses cause most liver cancer, H pylori bacteria causes stomach cancer, Human papillomavirus causes almost all cases of cervical cancer, colon cancer is largely explained by physical activity, diet and family history.

But for breast cancer, there is no smoking gun. It is almost unique among the common cancers of the world in that there is not a known major cause; there is no consensus among experts that proof of a major cause has been identified.

Yet, breast cancer is the most common form of cancer in women worldwide. The risk is not equally distributed around the globe, though. Women in North America and Northern Europe have long had five times the risk of women in Africa and Asia, though recently risk has been increasing fast in Africa and Asia for unknown reasons.

Was it something I ate?
Supermarket aisle via

Is diet to blame?

Up until about 20 years ago, we thought it was all about diet. As people abandon their local food sources and begin to eat highly processed foods with lots of fats, the hypothesis went, breast cancer was thought to be more likely to develop.

This hypothesis was logical because when researchers analyzed countries’ per capita fat consumption and breast cancer mortality rates, they found a strong correlation. In addition, rats fed a high-fat diet are more prone to breast tumors.

By studying Japanese migrants to California, researchers found that the first generation had low risk like their parents in Japan, but then by the second and third generation, risk was as high as white American women. So, the genetics of race did not account for the stark differences in the breast cancer risk between Asia and America. This was also consistent with the idea that the change in food from the lean Asian diet to the high-fat American diet causes cancer. So it all made sense.

Until it didn’t.

Diet studies find that fat is not the answer

Starting in the mid-1980s, large, well-done prospective studies of diet and breast cancer began to be reported, and they were uniformly negative. Fat in the diet of adult women had no impact on breast cancer risk at all.

This was very surprising – and very disappointing. The evidence for other aspects of diet, like fruits and vegetables, has been mixed, though alcohol consumption does increase risk modestly. It is also clear that heavier women are at higher risk after menopause which might implicate the total amount of calories consumed if not the composition of the diet.

There is a chance that early life dietary fat exposure, even in utero, may be important, but it’s difficult to study in humans, so we don’t know much about how it might relate to breast cancer risk later in life.

If diet is not the major cause of breast cancer, then what else about modernization might be the culprit?

Some risk factors, like exercise, can be modified.
Runner via

Two kinds of risk factors: what we can modify, and what we can’t

The factors shown to affect a woman’s risk for developing breast cancer fall into two categories. First, those that cannot be easily modified: age at menarche, age at birth of first child, family history, genes like BRCA1. And second, those that are modifiable: exercise, body weight, alcohol intake, night-work jobs.

The role of environmental pollution is controversial and also difficult to study. The concern about chemicals, particularly endocrine disruptors, started after the realization that such chemicals could affect cancer risk in rodent models. But in human studies the evidence is mixed.

Because child bearing at a young age and breast feeding reduce risk, the incidence throughout Africa, where birth rates tend to be higher, and where women start their families at younger ages, has been lower.

Death rates, however, from breast cancer in sub-Saharan Africa are now almost as high as in the developed world despite the incidence still being much lower. This is because in Africa, women are diagnosed at a later stage of disease and also because there are far fewer treatment options.

The question is whether the known risk factors differ enough between the high-risk modern societies and the low-risk developing societies to account for the large differences in risk. The answer: probably not. Experts think that less than half the high risk in America is explained by the known risk factors, and that these factors explain very little of the difference in risk with Asia.

A related question is whether the high risk in America and Northern Europe is due to a combination of many known exposures, each of which affects risk a little bit, or mostly due to a major cause that has so far eluded detection. And maybe some of the known risk factors have a common cause which we don’t yet understand.

Are we just finding more cancer?

Since the 1980s, screening by mammography has accounted for some of the increase in incidence in the modern world compared to the developing world, but not nearly enough to explain the entire difference. About 20% of the cancers found by mammography are now believed to be of a type that would never have progressed beyond the very small early stage that mammography can detect. But the problem is that we can’t tell which are the benign ones and which are not.

Electric light and shift work may be factors.
Office worker via

What about electric light?

Electric light is a hallmark of modern life. So, maybe the introduction and increasing use of electricity to light the night accounts for a portion of the worldwide breast cancer burden.

This might be because our circadian rhythm is disrupted, which affects hormones that influence breast cancer development. For example, electric light at night can trick the body into daytime physiology in which the hormone melatonin is suppressed; and melatonin has been shown to have a strong inhibitory effect on human breast tumors growing in rats.

The theory is easy to state but difficult to test in a rigorous manner. Studies have shown that night-working women are at higher risk than day-working women, which was the first prediction of the theory.

Other predictions are that blind women would be at lower risk, short sleepers would be at higher risk, and more highly lighted communities at night would have higher breast cancer incidence. Each of these has some modest support though none are conclusive. What we do know is that electric light in the evening or at night can disrupt our circadian rhythms, and whether this harms our long term health, including risk of breast cancer, is not yet clear.

Whatever is going on, it’s important to find answers because breast cancer has become a scourge that now afflicts women all over the world in very large numbers, at almost two million new cases this year alone.

The Conversation

This article was originally published on The Conversation.
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Many People With Substance Abuse Problems May Find Few To Treat Them

The number of people with insurance coverage for alcohol and drug abuse disorders is about to explode at a time there’s already a severe shortage of trained behavioral health professionals in many states.

Until now, there’s been no data on just how severe the shortage is and where it’s most dire.  Jeff Zornitsky of the health care consulting firm Advocates for Human Potential (AHP) has developed the first measurement of how many behavioral health professionals are available to treat millions of adults with a substance use disorder, or SUD, in all 50 states.

Zornitsky’s “provider availability index” – the number of psychiatrists, psychologists, counselors and social workers available to treat every 1,000 people with SUD – ranges from a high of 70 in Vermont to a low of 11 in Nevada. Nationally, the average is 32 behavioral health specialists for every 1,000 people afflicted with the disorder.  No one has determined what the ideal number of providers should be, but experts agree the current workforce is inadequate in most parts of the country.

“Right now we’re in a severe workforce crisis,” said Becky Vaughn, addictions director for the industry organization National Council for Behavioral Health.  The shortage has consequences, she said. “When people need help for addictions, they need it right away. There’s no such thing as a waiting list. If you put someone on a waiting list, you won’t be able to find them the next day.”

The shortage of specialists threatens to stall a national movement to bring the prevention and treatment of SUD into the mainstream of American medicine at a time when millions of people with addictions have a greater ability to pay for treatment thanks to insurance.

Two Federal Laws

The Affordable Care Act for the first time requires all insurers, including Medicaid, to cover the treatment of drug and alcohol addiction.  In the past, Medicaid covered only pregnant women and adolescents in most states. Private insurance either didn’t pay for treatments or paid so little that most people could not afford to make up the difference.

For anyone with insurance coverage, the Mental Health Parity and Addiction Equity Act ensures that the duration and dollar amount of coverage for substance use disorders is comparable to coverage for medical and surgical care. Together, the two federal laws are expected to make billions of dollars available to the behavioral health care market.

Of the estimated 18 million adults potentially eligible for Medicaid in all 50 states, at least 2.5 million have substance use disorders. Of the 19 million uninsured adults with slightly higher incomes who are eligible for subsidized exchange insurance, an estimated 2.8 million struggle with substance abuse, according to the most recent national survey by the U.S. Substance Abuse and Mental Health Services Administration.

Although the federal government has acknowledged the scarcity of treatment specialists, it has failed to quantify and assess it. Other fields of health care, including mental health and primary care, are tracked by the U.S. Health Resources and Services Administration to determine which communities are “underserved.”  Without this information, it is hard to know where more behavioral health specialists are needed and when the supply of providers is expanding or shrinking in any given region.

That’s where AHP’s Zornitsky steps in. Using data from the U.S. Department of Labor’s Bureau of Labor Statistics on the current size of the labor force and its projected growth, plus Department of Health and Human Services data on the prevalence of SUD among adults, he approximates the relative adequacy of the addiction treatment workforce in each state.

“It is not perfect,” Zornitsky said of the index, “but it’s a consistent, state-based measure that allows for comparisons and tracking over time.”


Poor Pay

According to a 2013 report to Congress from the Substance Abuse and Mental Health Services Administration, the “growing workforce crisis in the addictions field” is due to a variety of factors, including stigma, an aging workforce and inadequate compensation.

The U.S. spent $24 billion on treatment of drug and alcohol disorders in 2009, the most recent year for which comprehensive data are available, according to a new study by the Pew Charitable Trusts (Pew also funds Stateline).  Sixty-nine percent of the spending came from public sources such as state and local governments, Medicaid, Medicare and federal grants. Private sources, including commercial insurance and out-of-pocket spending, made up the balance, according to the report.

Historically, reimbursement rates and consequently salaries for physicians, psychologists, social workers and counselors in the addiction field have been well below salaries for comparable professionals in other health care specialties that require the same level of education and training.

For example, the average salary for social workers in the addiction field is $38,600, compared to $47,230 in the rest of the health care industry, according to the Bureau of Labor Statistics.

As a result, too few health care workers are going into the field and too many are switching to more lucrative specialties. And because the average age of addiction specialists is higher than in other professions, demographers predict a behavioral health retirement boom in the next five years.

Between now and 2020, the addiction services field will need to fill more than 330,000 jobs to keep pace with demand, of which more than half are the result of people retiring and switching to other occupations.


Low Treatment Rates

Of the roughly 23 million Americans who suffer from drug and alcohol disorders, only 11 percent receive treatment at a specialty facility, according to the most recent National Survey on Drug Use and Health.

That compares to U.S. treatment rates as high as 80 percent for diseases such as diabetes and hypertension. Part of the reason for lack of treatment has been inability to pay. With billions in private insurance and Medicaid dollars becoming available, that is expected to change.

But questions remain about how the existing addiction services industry will manage the expansion, whether new businesses will enter the market and how many providers will take Medicaid patients. Today, only 55 percent of addiction practitioners accept Medicaid reimbursements, which tend to be lower than private insurance.

Another reason many substance abusers go without treatment is the social stigma connected with addictions and mental illness. To avoid being labeled, many hide their drug or alcohol use, and refuse to admit they have a problem. With more money available for treatment and increased public concern over the nation’s rising death toll from drug addictions, experts are hopeful the stigma will dissipate and more health care professionals will be drawn to the field.

The Affordable Care Act eventually should spur more competitive salaries for behavioral health professionals. But for now, it is complicating matters, Vaughn said. Both Medicaid and private insurers require levels of professional licensing and credentialing that were not needed when addiction services were funded primarily by federal grants. In addition, many of the mostly small providers in the industry have no business experience negotiating contracts with Medicaid managed care organizations or filing claims for Medicaid and private insurance.

It will be largely up to states to make the changes needed to develop an adequate addiction treatment workforce. The federal government has offered model licensing guidelines that define a so-called “scope of practice” for each job title in the behavioral health profession, but states will have to create licensing laws and regulations. States could also encourage more people to go into the profession by offering to repay student loans and funding local colleges.

In addition, state Medicaid agencies will need to reach out to the existing addiction industry and provide business training to enable them to file claims for the billions in new funding for drug and alcohol treatments. Most important, Vaughn said, Medicaid rates for addiction services need to be raised to provide a reimbursement benchmark that is closer to the fees paid to practitioners in other health care professions.

Is climate change to blame for outbreaks of mosquito-borne disease?

The east coast of Australia is currently experiencing one of its worst outbreaks of mosquito-borne disease in years. Mosquitoes have plagued the summer and now there’s a dramatic increase in disease caused by Ross River virus, spread by the bite of mosquitoes.

Mosquitoes need blood and, unfortunately, they often bite people to get it – some more than others.

Pathogens spread by mosquitoes already kill more than a million people a year across the world, mostly in tropical regions. The increased risk of mosquito-borne disease in a warmer, wetter world is a concern for health authorities internationally.

But more mosquitoes doesn’t guarantee more mosquito-borne disease. If it isn’t the “right” mosquito, there won’t be outbreaks of dengue or malaria.

And while a changing climate may contribute to more mosquito-borne disease, it doesn’t guarantee it: human movement around the world is likely to play just as an important a role.

Not all mozzies are equal

Mosquitoes aren’t like dirty syringes spreading infected blood. They’re diverse and complex creatures that have a special relationship with the parasites and viruses they can spread.

Very few of the thousands of mosquitoes found on earth are able to spread dengue or chikungunya viruses. A different group are involved in the spread of West Nile virus and Japanese encephalitis virus, while a different type of mosquito altogether is involved in spreading malaria parasites.

Human movement

A recent article in the journal Lancet Infectious Diseases reviews the factors contributing to future increases in mosquito-borne disease risk in the United Kingdom. While the authors identify increased temperatures as potentially providing suitable conditions for mosquitoes that spread pathogens, climate change alone wasn’t enough.

The mosquitoes that can spread dengue and chikungunya viruses, particularly the Asian Tiger Mosquito (Aedes albopictus), need to get there in the first place and, most likely, that is with people and their belongings.

The Asian Tiger Mosquito.

It isn’t only the UK that is at risk. Until recently, chikungunya virus was unknown from the Americas but within a year of it being introduced into the Caribbean, it had spread to both North America and South America and is suspected to have infected over 1.2 million people.

As the researchers highlight, even the way authorities respond to the threats of climatic change, such as the construction or rehabilitation of wetlands to create a buffer against increasingly frequent storms and sea level rise, may further increase risk. Mosquitoes that spread West Nile virus could move into these wetlands.

Hitching a ride to Australia

The Asian Tiger Mosquito poses a significant threat to Australia. It was discovered in the Torres Strait in 2005, having thought to have hitchhiked on fishing boats from Indonesia. Its a question of when, not if, this mosquito will make its way to mainland Australia.

The mosquito has already hitchhiked to Europe and North America with eggs attached to used tyres and lucky bamboo. Movement of people, not shifts in climate is the biggest risk.

Should it reach one of our major cities, there is little doubt that mosquito could become a persistent summer pest and possible public health threat. The way we respond to water shortages in our cities, by increasing water storage around our homes, may set the scene for this mozzie to move in.

Aussie mozzie risks

Exotic mosquitoes and viruses are a concern but there are still plenty of ways a local mosquito bite can make you sick.

Ross River virus is the most commonly reported local mosquito-borne disease. Every year about 5,000 fall ill due to this virus. While not fatal, it can cause fever, rash, headache, joint pain and fatigue that may last a few weeks or many months. It can be seriously debilitating.

By the end of March, New South Wales and Queensland will have recorded over 4,700 cases of Ross River virus disease. Those figures already exceed the total number of cases reported in each of the previous three to five years. This may be the biggest outbreak of mosquito-borne disease along the east coast of Australia since the mid-1990s.

Kangaroos and wallabies also carry the Ross River virus.
Thorsten Rinne/Flickr, CC BY-NC-SA

Australia has had major outbreaks of dengue in the past. But the only mosquito in Australia able to spread the virus is restricted to far north Queensland. It is unlikely to spread to southern cities beyond Brisbane based on temperature change alone.

Barmah Forest, Murray Valley encephalitis and Kunjin viruses are all also spread by mosquitoes in Australia too, although they’re generally far less common that Ross River virus.

Could the current outbreak be linked to a changing climate?

Thanks to the warmest spring on record and substantial rainfall associated with tropical cyclones, conditions have been perfect for mosquitoes. If these climatic events become more common, there is little doubt we’ll continue to see outbreaks of Ross River virus disease and other mosquito-borne diseases.

However, outbreaks of Ross River virus are determined by more than mosquitoes. Wildlife play an important role too, as kangaroos and wallabies that carry the virus are increasingly found close to residential areas.

So understanding and predicting outbreaks requires an understanding of wetlands and wildlife, as well as climate and mosquitoes. The way we guide urban development will also be important.

The current outbreak, however, may provide a glimpse of what lays ahead. With warmer weather, we may see an extension of the “mosquito season” each year. Aside from the risks to public health extending well into autumn (or possibly arriving earlier in summer), there is the increased economic burden on local authorities needing to expand mosquito control and disease surveillance programs.

There are still gaps in our understanding of the relationship between climate, mosquitoes and disease. But the current outbreak of Ross River virus disease should serve as a reminder that in the future, more of our “home grown” mosquito-borne disease, and not necessarily the spread of “tropical” disease such as dengue and chikungunya, could be our primary concern.

The Conversation

This article was originally published on The Conversation.
Read the original article.

Why is CRISPR the Science Buzzword of Early 2015?

CRISPR isn’t just the cutting edge of genetic modification – it is re-framing our understanding of evolution.

 What is CRISPR?
CRISPR is a DNA sequence that can do something most other genes can’t. It changes based on the experience of the cell it’s written in.  It works because of a natural ability for cells to rewrite their own genetic code, first discovered in 1987. The name CRISPR was coined in 2002, and it stands for “clustered regularly interspaced short palindromic repeats”. They function as a method of inserting recognizable DNA of questionable or dangerous viruses into DNA strands so that the offspring of the cell can recognize what its ancestors have encountered and defeated in the past. By inserting a CRISPR-associated protein into a cell along with a piece of RNA code the cell didn’t write, DNA can be edited.A 2012 breakthrough  involved, in part, the work of Dr. Jennifer A. Doudna. Doudna and the rest of the team at UC Berkley were the first to edit human DNA using CRISPR.  Recently, in March 2015, she warned this new genome-editing technique comes with dangers and ethical quandaries, as new tech often does. Dr. Doudna in a NYT article, she called for a planet-wide moratorium on human DNA editing, to allow humanity time to better understand the complicated subset of issues we all now face.
CRISPR-related tech insn’t only about editing human genes, though. It affects cloning and the reactivation of otherwise extinct species. It isn’t immediately clear what purpose this type of species revival would have without acknowledging the scary, rapidly increasing list of animals that are going extinct because of human activity. Understanding and utilizing species revival could allow humans to undo or reverse some of our environmental wrongs. The technique may be able to revive the long lost wooly mammoth by editing existing elephant DNA to match the mammoth‘s, for instance. Mammoths likely died out due to an inability to adapt to natural climate change which caused lower temperatures in their era, and are a non-politically controversial choice but the implications for future environmentalism are promising.
Each year, mosquitoes are responsible for the largest planetary human death toll. Editing DNA with CRISPR bio-techniques could help control or even wipe out malaria someday. The goal of this controversial tech is to make the mosquito’s immune system susceptible to malaria or make decisions about their breeding based on how susceptible they are to carrying the disease. The controversy around this approach to pest and disease control involves the relatively young research behind Horizontal Gene Transfer, where DNA is passed from one organism to an unrelated species. A gene that interferes with the ability of mosquitoes to reproduce could end up unintentionally cause other organisms to have trouble reproducing. This info is based on the work of , ,
Even more controversial are the startups claiming they can create new life forms, and own the publishing rights. Austen Heinz’ firm is called Cambrian Genomics which grows genetically-controlled and edited plants. The most amazing example is the creation of a rose species that literally glows in the dark. Cambrian is collaborating with the rose’s designer, a company called Glowing Plant, whose projects were eventually banned from kickstarter for violating a rule about owning lifeforms. Eventually, Heinz wants to let customers request and create creatures:
The final example in an ongoing list of 2015 breakthroughs involving CRISPR is this CRISPR-mediated direct mutation of cancer genes in the mouse liver might be able to combat cancer. It’s the second cancer-related breakthrough in 2015 that affects the immune system, the first was on Cosmos about a week back: Accidental Discovery Could Turn Cancer Cells Into Cancer-Attacking Immune Cells.

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Jonathan Howard
Jonathan is a freelance writer living in Brooklyn, NY