New research suggests that the physiological ‘wear and tear’ of stress may affect a woman’s fecundability, ie her ability to fall pregnant within a menstrual cycle. The study was published in Acta Obstetricia et Gynecologica Scandinavica.
Allostatic load reflects multi-system physiological changes which occur in response to chronic psychosocial stress, reflecting a kind of ‘wear and tear’. The study investigated the link between female pre-pregnancy allostatic and time to pregnancy.
Reduced human fecundability not only results in infertility, it also creates social aging problems. Female fecundability is a complicated topic that can be influenced in many ways, including physical factors and psychological factors. Prior research tended to focus on the impact of chronic diseases, such as hypertension, diabetes and obesity. However, mental factors, including psychological pressure, anxiety and depression, could also potentially exert impact on female fecundability. Evidence supports that infertility may cause stress in many ways, but it is unclear whether stress causes infertility, or how stress and human fecundability interact.
The study assessed AL in 444 women who were trying to become pregnant. Women with higher allostatic load scores – based on nine indicators such as blood pressure, blood sugar, cortisol, noradrenaline, and cholesterol – were less likely to become pregnant within a year. For example, the women with an allostatic load score of 5–6 would have a 59% reduction of fecundability compared with those with scores of 0.
“What we found provides a new idea for preconception counselling. But obviously, how to objectively assess the stress is a complex scientific question, and how to intervene and reduce the impact of chronic stress is a burning problem, which are all things we need to study further,” said senior author Bei Wang, PhD, of Southeast University in Jiangsu, China.
The Treatment Action Campaign (TAC) has called on former president Thabo Mbeki to offer an apology to the public for the “dissident” views he expressed about HIV/AIDS while delivering a speech at the University of South Africa (UNISA) last week Wednesday.
In a scathing statement published by the TAC on Tuesday, the organisation said the “repetition of his scientifically erroneous views with such insensitive arrogance is an insult to the 8 million people living with HIV in SA and the families of 4 million South Africans who have died from HIV over the last three decades”.
Mbeki, who is also the Chancellor at UNISA, was speaking to students, diplomats and members of the media at an event which takes place twice each year and allows students to interact with him on pertinent issues that affect Africans.
The TAC accuses Mbeki of misleading the public when he questions the cause of AIDS. The organisation also goes on to say that they were stunned again by Mbeki’s support of the views of the late former Minister of Health, Manto Tshabalala-Msimang “who was ridiculed for promoting garlic and beetroot as the essential ingredient to manage AIDS, giving it a higher premium than antiretroviral (ARV) treatment”.
“Whilst there may be benefits in all healthy foods, the idea that these vegetables are what are most required in the management of AIDS has no basis in fact and is misleading to the public,” said the statement.
Speaking about HIV/AIDS after a question was raised in the event, Mbeki said the questions that he raised then, he would still raise today. He emphasized that AIDS was a syndrome and not a disease.
“Now this syndrome in medical terms is a group of diseases. So all of these diseases which fall under this syndrome, meningitis, TB, they’re in the syndrome.”
“Causes of Tuberculosis are known and historical, but it’s part of the syndrome. So you can’t say one virus causes all of these illnesses, what you can say is this virus impacts negatively on the immune system, it’s that weakened immune system which results in a syndrome.”
“But there’s a consequence to that kind of thinking which is when you go to test and that test says HIV positive… it does not necessarily mean you’ve got the virus. What it means is that the immune system is responding to something that is threatening the body, and therefore you need a clinical analysis in order to determine what is this thing that the immune system is rejecting. It’s in all the medical documents that go about it, and it’s correct, because then you have to go and do this clinical examination in order to determine which of these illnesses in the syndrome is the one that’s affecting this person. And then you treat the person for that particular disease,” said Mbeki.
Mentioning the views of Tshabalala-Msimang, Mbeki started off by saying as government they had to respond in an effective manner to the HIV/AIDS pandemic and various interventions were needed to do this.
“Which is why the question was raised by the then Minister of Health in a very dramatic fashion. Nutrition. Nutrition is very very critical to solving this problem and that’s why she was saying that we must take garlic and beetroot and so on. She was not saying that with those things you’re going to be cured.”
“She was raising the matter about the importance of nutrition. And those particular types of foods even today have been raised in the context of this Covid-19,” said Mbeki.
The TAC, which successfully campaigned in the 2000s for Mbeki’s government to roll out life-saving medicines, was not impressed.
“There is much ongoing stigma and denial when it comes to HIV and we call on Mr Mbeki to desist from statements about HIV that have no basis in fact,” said the TAC statement.
It said: “The former president’s statements remind us that his unscientific views led to a delay in the rollout of the ARV programme during his presidency.”
The TAC’s General Secretary, Anele Yawa, said that if Mbeki was not prepared to apologise, the organisation would make sure that his HIV denialism and the thousands of deaths that resulted, would be the only thing that he would be remembered for.
These are the facts when it comes to HIV/AIDS under Thabo Mbeki’s presidency
By Nathan Geffen, GroundUp Editor
It’s seldom clear what Thabo Mbeki means when it comes to HIV/AIDS. There is much obfuscation. But the key facts are this:
HIV destroys immune system cells in infected people.
Usually over a period of several years, if left untreated, the immune system collapses, causing the person to become ill with life-threatening infections. This is known as AIDS.
Only antiretroviral medicines can halt this process. They have been so effective that the life-expectancy for people with HIV who take them is brought back to almost normal.
HIV tests are reliable. If proper protocols are followed the odds of an incorrect result are extremely small.
Mbeki’s government delayed the rollout of antiretroviral treatment in the public sector until 2004, even though an effective combination of antiretroviral medicines was available from the mid to late 1990s.
It was only due to pressure from the TAC and its allies that Mbeki’s government made antiretrovirals available in the public sector.
The prices of these medicines also became affordable because of the TAC’s (and its allies) campaigning against pharmaceutical companies. Mbeki’s government was largely AWOL in these efforts, despite Mbeki’s rhetoric about these companies.
Two different studies have estimated that the delayed rollout of antiretrovirals resulted in well over 300 000 avoidable deaths. These estimates are conservative.
These estimates also exclude those who died because they were convinced by Mbeki, Tshabalala-Msimang and their acolytes to try treatments promoted by as alternatives to antiretroviral medicines. The promotion of these nonsense remedies by Mbeki and his health minister continued long after the antiretroviral treatment rollout began.
Geffen was involved with the TAC from 2000 to 2013.
Intravenous treatment with omega-3 fatty acids in elderly hospitalised patients in intensive care due to COVID seems to help the immune system’s ability to cope with the virus, according to a study published in the journal Clinical and Translational Medicine. These findings could lead to a complementary, cost-effective treatment for COVID.
In COVID patients, the immune system and the body’s activation of white blood cells are over-activated. It can lead to a so-called systemic inflammatory storm, which worsens the disease state and can cause complications such as sepsis and heart failure.
Researchers at Karolinska Institutet, among others, have now shown that omega-3 fatty acids can stimulate active healing of inflammation, without inhibiting the immune response. By accelerating the healing of the inflammation without compromising the body’s immune system, it could be possible to counteract the most serious complications of COVID, researchers believe.
Stimulated inflammation-healing molecules
The treatment effect was found by mapping inflammatory biomarkers and immunological reactions.
“First, we showed that fatty acid metabolism to inflammation-healing molecules was stimulated in those patients treated with omega-3 fatty acids. By isolating immune cells before, during, and after treatment, we were able to show that immune function improved,” said corresponding author Magnus Bäck, senior consultant in cardiology and professor at Karolinska Institutet.
Planning further studies
Researchers are now planning for larger clinical studies, which will be needed to show whether the course of the disease in severe COVID is improved through treatment with omega-3 fatty acids.
“It is important that even our weakest and frailest patients have the opportunity to participate in studies when the enemy, in this case, COVID, is on the attack and that they can fight the disease with the help of the medicine,” said Dorota Religa, senior consultant and professor in geriatrics at Karolinska Institutet.
“Stimulating the healing of inflammation with omega-3 fatty acids has the potential to lead to a new, cost-effective low-risk treatment for COVID-19, as a complement to existing treatment,” said Prof Magnus Bäck.
The neurohormone oxytocin has a number of functions involved in pleasure and social bonding, and plays a role in both female and male reproductive functions. Now, researchers have shown that in zebrafish and human cell cultures, oxytocin has yet another, unsuspected, function: it stimulates stem cells derived from the heart’s epicardium (the outer layer) to migrate into its myocardium (middle layer) and there develop into cardiomyocytes, cardiac muscle cells. This discovery could one day be used to promote the regeneration of the human heart after a heart attack. The results are published in Frontiers in Cell and Developmental Biology.
“Here we show that oxytocin, a neuropeptide also known as the love hormone, is capable of activating heart repair mechanisms in injured hearts in zebrafish and human cell cultures, opening the door to potential new therapies for heart regeneration in humans,” said senior author Dr Aitor Aguirre, an assistant professor at Michigan State University.
Stem-like cells can replenish cardiomyocytes
Cardiomyocetes typically die off in great numbers after a heart attack. Because they are highly specialised cells, they can’t replenish themselves. But previous studies have shown that a subset of cells in the epicardium can undergo reprogramming to become stem-like cells, called Epicardium-derived Progenitor Cells (EpiPCs), which can regenerate not only cardiomyocytes, but also other types of heart cells.
“Think of the EpiPCs as the stonemasons that repaired cathedrals in Europe in the Middle Ages,” explained A/Prof Aguirre.
Unfortunately for us, the production of EpiPCs is inefficient for heart regeneration in humans under natural conditions.
Zebrafish could teach us how to regenerate hearts more efficiently
Zebrafish are famous for their extraordinary capacity for regenerating organs. They don’t suffer heart attacks, but its many predators are happy to take a bite out of any organ, including the heart – so zebrafish can regrow their heart when as much as a quarter of it has been lost. This is done partly by proliferation of cardiomyocytes, but also by EpiPCs. How the EpiPCs so efficiently repair the heart, and whether they could be boosted in humans remained a mystery.
The authors argued that this was possible.
To reach this conclusion, the authors found that in zebrafish, within three days after cryoinjury – injury due to freezing – to the heart, the expression of the messenger RNA for oxytocin increases up to 20-fold in the brain. They further showed that this oxytocin then travels to the zebrafish epicardium and binds to the oxytocin receptor, triggering a molecular cascade that stimulates local cells to expand and develop into EpiPCs. These new EpiPCs then migrate to the zebrafish myocardium to develop into cardiomyocytes, blood vessels, and other important heart cells, to replace those which had been lost.
Similar effect on human tissue cultures
Crucially, the authors showed that oxytocin has a similar effect on human tissue in vitro. Of the 15 neurohormones tested, only oxytocin stimulates cultures of human Induced Pluripotent Stem Cells (hIPSCs) to become EpiPCs, at up to twice the basal rate: a much stronger effect than other molecules previously shown to stimulate EpiPC production in mice. Conversely, genetic knock-down of the oxytocin receptor prevented the the regenerative activation of human EpiPCs in culture. The authors also showed that the link between oxytocin and the stimulation of EpiPCs is the important ‘TGF-β signaling pathway’, known to regulate the growth, differentiation, and migration of cells.
A/Prof Aguirre said: “These results show that it is likely that the stimulation by oxytocin of EpiPC production is evolutionary conserved in humans to a significant extent. Oxytocin is widely used in the clinic for other reasons, so repurposing for patients after heart damage is not a long stretch of the imagination. Even if heart regeneration is only partial, the benefits for patients could be enormous.”
A/Prof Aguirre concluded: “Next, we need to look at oxytocin in humans after cardiac injury. Oxytocin itself is short-lived in the circulation, so its effects in humans might be hindered by that. Drugs specifically designed with a longer half-life or more potency might be useful in this setting. Overall, pre-clinical trials in animals and clinical trials in humans are necessary to move forward.”
Analysing decades of environmental data associated with Lassa virus outbreaks, researchers projected that areas hospitable to Lassa virus spread may extend from West Africa into Central and East Africa in the next several decades. With this expansion and expected African population growth, the human population living in the areas where the virus should theoretically be able to circulate may rise by more than 600 million.
“Our analysis shows how climate, land use, and population changes in the next 50 years could dramatically increase the risk of Lassa fever in Africa,” says first author Raphaëlle Klitting, PhD, a postdoctoral researcher at Scripps Research during the study, which is published in Nature Communications.
Lassa virus is a zoonotic pathogen found in the Natal multimammate rat (Mastomys natalensis), most likely transmitted to humans via its droppings. While an estimated 80% of infections are mild or asymptomatic, the remaining cases are more severe, with signs and symptoms that can include haemorrhaging from the mouth and gut, hypotension, and potentially permanent hearing loss. Mortality rate in hospitalised patients can be up to 80%.
An estimated several hundred thousand infections occur each year, chiefly in Nigeria and several other West African countries. So far there is no approved vaccine or highly effective drug treatment.
Although the primary animal reservoir for Lassa virus is known, the virus spreads in only a subset of the areas where the animal is found. Thus, it is possible that environmental factors also help determine whether and where significant viral transmission can occur. In the study, the researchers developed an ‘ecological niche’ model of Lassa virus transmission, using environmental data at sites of known spread.
Combining the model with projections of climate and land-use changes in Africa in the next several decades, as well as the known range of the Natal multimammate rat, the researchers estimated the areas of Africa that could support Lassa virus transmission currently, and in the years 2030, 2050, and 2070. The projected current areas corresponded well to known endemic areas in West Africa, but the estimates for future decades suggested a vast expansion within and beyond West Africa.
“We found that several regions will likely become ecologically suitable for virus spread in Central Africa, including in Cameroon and the Democratic Republic of the Congo, and even in East Africa, in Uganda,” Klitting said.
Currently Africa’s population is undergoing rapid growth; the researchers therefore considered projections of this population growth for the areas of current and potential future Lassa virus circulation. They found that the number of people potentially exposed to the virus could increase from about 92 million today to 453 million by 2050, and 700 million by 2070 – an increase of over 600%.
More hopefully, the researchers examined the dynamics of the spread of Lassa virus using data on sequenced viral genomes sampled at various locations in West Africa and found that virus dispersal appeared to be slow. They concluded that, unless transmission dynamics change drastically in the new location where the virus circulates, the virus’s spread into new ecologically suitable areas in the coming decades may also be slow.
The authors say that the findings should inform African public health policies, for example, by encouraging officials to add Lassa virus to lists of viruses under epidemiologic surveillance in parts of Central and East Africa.
“With the ongoing climate change and increasing impact of human activities on the environment, further comprehensive studies of the ecology and spread of zoonotic and vector-borne diseases are needed to anticipate possible future changes in their distribution as well as their impact on public health,” said senior author Simon Dellicour, PhD, of the University of Brussels.
A new, safer drug has been developed that could revolutionise the way clinicians treat some of the most common gynaecologic diseases including fibroids and endometriosis. A clinical trial published in the Lancet found that linzagolix, an oral drug that hinders oestrogen production, is an effective and customisable treatment for fibroids. Not only does linzagolix ease symptoms but also shrinks the fibroids themselves.
Professor Hugh S. Taylor, MD, co-author of the paper, said: “No treatments to date for fibroid growth are something I would ever want my patients to take for a prolonged period of time, as they did not treat the underlying cause of the problem. This is an extremely well tolerated class of drugs that can control fibroid growth. We’ve never had anything like that before.”
The suffering and inconvenience caused by uterine fibroids can have a serious impact on quality of life. “This can be an impediment to getting a good night’s sleep and being socially active, and it can even affect job performance,” said Prof Taylor.
As fibroids grow larger, they may begin putting pressure on other organs, resulting in a range of unpleasant symptoms including diarrhoea or constipation and frequent urination. Fibroids can also lead to difficulty in getting pregnant and increased risk of miscarriage. They are more common and aggressive in black patients.
Most drugs commonly used for uterine fibroids, including birth control pills, do not treat the fibroids themselves and just lighten or stop periods. And more aggressive drugs, although they treat the root of the problem are “overkill” Prof Taylor said. For example, leuprolide is an injectable drug that puts patients into a menopausal state by initially overstimulating hormonal receptors, which eventually shuts them down and completely blocks oestrogen production. Although the treatment addresses the fibroids, it also can initially exacerbate symptoms and cause harsh side effects. In more extreme cases, patients may opt for hysterectomy.
Promising clinical trial results
Linzagolix is an oral medication that works similarly to leuprolide by hindering hormone production. However, unlike its predecessor, it works by directly blocking the receptors instead of overstimulating them. The drug is also titratable, allowing reduction of oestrogen production without initiating menopause.
The new drug may however cause menopause symptoms such as hot flashes, with hormonal add-back therapy an option for mitigating these symptoms. For some patients, however, including patients with obesity, hypertension, or diabetes, this therapy has risks and may not be a suitable option. These conditions also tend to be more prevalent in Black patients. In this group, a lower dose of linzagolix without add-back therapy might be preferable.
To test the effectiveness of the drug, Prof Taylor’s team ran two large prospective, randomised, double-blind, placebo-controlled clinical trials known as PRIMROSE 1 and PRIMROSE 2. The studies enrolled patients suffering from substantial bleeding who were randomised to placebo or one of several different doses of the drug: 100mg alone, 100 mg with add-back therapy, 200mg alone, or 200mg with add-back therapy. Patients were followed for one year. The researchers considered the therapy successful if the patient’s bleeding was reduced by half and also stayed in what is considered the normal range.
Patients in all four treatment groups experienced a significant reduction in menstrual bleeding. The 200 mg with add-back therapy group worked with “amazing efficacy,” said Prof Taylor: the clinical trials showed a 75.5% response rate in PRIMROSE 1 and a 93.9% rate in PRIMROSE 2. Even the lower dose of the drug still showed promising results. There were greater than 60% response rates in both trials for the 100mg group with add-back therapy, and the 100mg group without add-back showed better than 50% response rates.
“What is interesting and unique about our trials, that has not been done with other drugs in this class, is that we used a low dose with or without hormones,” said Prof Taylor. “This is a great option for patients who experience severe menopause symptoms from the high dose or have a medical problem where they can’t tolerate hormonal add-back therapy.”
Changing the treatment of gynaecologic disease
Linzagolix is one of several in this new class of drugs in development for the treatment for common gynaecologic diseases. Prof Taylor was also involved in the 2017 clinical trial for elagolix, a medication designed to suppress endometriosis that has recently become available for patients.
Linzagolix has so far been approved in Europe. Taylor says drugs in this class will radically change how clinicians treat fibroids, and he hopes linzagolix will lead to a reduction in future hysterectomies once it becomes available.
“A good medical therapy is finally here for fibroids, and I predict that what was a very common operation will dramatically decrease within the next few years,” he says. “Reducing the need for hysterectomy is very important for patients who don’t want to undergo a major surgery, especially for younger people who may still want to preserve the potential of having children in the future.”
While endocrine-metabolic disorders and depression are known to co-occur, genetic and environmental factors are known to underlie both. In a study examining the link, published in the American Journal of Psychiatry, analysis revealed the balance of genetic and environmental influences underlying the co-occurrence of depression for a range of endocrine-metabolic disorders.
It is known that there is elevated co-occurrence between endocrine-metabolic disorders and depression, but the relationship between them is still not well understood.
The authors identified 2.2 million individuals born in Sweden between 1973 and 1996, as well as their full and half siblings, and followed them up to age 40. A number of medical conditions were studied; depression and various endocrine-metabolic disorders, including three autoimmune diseases (autoimmune hypothyroidism, Graves’ disease, and type 1 diabetes) and three non-autoimmune disorders (type 2 diabetes, obesity, and polycystic ovary syndrome).
Individuals with endocrine-metabolic disorders had 1.4 to 3.5 times the risk of depression compared to people without these diagnoses. Full and half siblings of these individuals also showed some elevated risk for depression, suggesting that genetic and/or environmental risk factors shared between family members play a role in the co-occurrence of these mental and physical disorders.
Genetic and environmental contributions
By comparing pairs of full sibling (who share about half of their genes) to pairs of half siblings (who share about a quarter of their genes), it was possible to calculate the relative contribution of genetic and environmental factors to the co-occurrence of depression and various endocrine-metabolic disorders.
The results were a mix of these possibilities; the overlap between depression and non-autoimmune conditions was mainly explained by shared genetic influences, while environmental factors were predominantly involved in the association between depression and autoimmune disorders, particularly type 1 diabetes.
This indicates that the link between depression and different endocrine-metabolic disorders may be driven by different mechanisms. For example, shared biological mechanisms, such as immuno-inflammatory and metabolic dysregulations, may underlie the co-occurrence of depression and type 2 diabetes, obesity, and polycystic ovarian syndrome. In contrast, the absence of shared genetics in the association between type 1 diabetes and depression may reflect the existence of environmental factors influencing the risk of both conditions and/or a direct link between these conditions through mediating factors – eg, biological and psychosocial mechanisms connected to type 1 diabetes, including inflammation, cerebral damage, as well as stress of this lifelong condition that is often diagnosed early in life and that requires a complex management regime for both patients and their families.
“Our results underscore that clinicians should be aware of increased risks of depression in individuals with endocrine-metabolic disorders, and vice versa, and be vigilant for shared symptoms. This study also provides a useful foundation for future research aimed at identifying and targeting the biological mechanisms and modifiable risk factors underlying the co-presentation of endocrine-metabolic disorders and depression”, said Marica Leone, first author for the study.
Guar gum is derived from guar beans, and is a common food additive and dietary fibre. Surprisingly, limited inflammation and delayed the onset of multiple sclerosis (MS) symptoms in mice, according to new research published in Cell Reports.
“The rapid increase of autoimmune and inflammatory disorders in industrialised countries in the last few decades indicates dietary choices are one environmental factor contributing to incidence,” said Dr Lisa Osborne, senior study researcher on the study.
“Dietary fibres are potent modulators of immune responses and can control inflammation in multiple diseases, but they’re a very biochemically diverse family. Our study gives us a clearer window into the potential of several sources of fibre in maintaining immune health.”
Dr Osborne and colleagues exposed groups of mice to a variety of diets: a control diet with 5% cellulose fibre, a no-fibre diet, or diets enriched (30%) with fibre in either resistant starch, inulin, pectin, or guar gum. Guar gum was the only fibre type that significantly limited the MS-like symptoms.
Guar gum (guaran) is extracted from guar beans, and is often used as an additive to thicken and stabilise food and animal feed, and in industrial applications.
“Guar beans aren’t that common in western diets, and the gum isn’t used at these high levels as an additive in the west,” says Naomi Fettig, first author on the study and a PhD student with the Department of Microbiology and Immunology at UBC.
“Experts have consistently been saying fibre is good for you – and a variety of fibre sources is important to immune health – but there hasn’t been very much critical work into identifying how the body responds to different fibre types. It’s fascinating that this particular source has such an impact.”
In the US and Canada, the average daily intake of fibre is 15g – current recommendations are 30g, with no regard to specific fibre type. “Incorporating guar beans might be challenging to achieve at the doses we gave to mice,” says Dr Osborne. “But a guar gum derivative, partially hydrolysed guar gum, is commercially available as a prebiotic.”
After the gum is broken down by the gut microbiota of mice, the resulting molecules appeared to reduce the activity and proliferation of a type of CD4+ T cells, Th1 cells, which have a key role in triggering the autoimmune response, which can lead to MS-like symptoms in mice. The effects of fibre on Th1 cells remained largely unknown prior to this study, and these findings suggest that the biochemical differences in fibre structures can influence diverse immune pathways.
Dr Osborne and her lab now want to explore the potential benefits in humans – including developing a more detailed understanding of the molecular picture, which might help design therapeutics that offer the benefits of such high guar gum diets in a more practical form.
Conventional wisdom holds that men run 10–12% faster than women regardless of the distance raced. But new research published in theJournal of Applied Physiology suggests that the performance gap narrows at shorter sprint distances.
Speed over short distances is determined by different factors – specifically, the magnitude of the ground forces athletes can apply in relation to their body mass. Muscular force to body mass ratios are greater in smaller individuals.
PhD candidate Emily McClelland, working with Peter Weyand, the Director of SMU’s Locomotor Performance Lab, quantified sex performance differences using data from sanctioned international athletic competitions such as the Olympics and World Championships. An accomplished athlete, McClelland has always had a natural interest in the scientific basis of human performance. The researchers hypothesised that these data would reveal smaller male-female performance differences at shorter distances.
The understanding of comparative strength, speed and endurance capabilities of male and female athletes has been a contentious issue for modern sport. Yet, prior to the new SMU study, quantitative understanding of sex performance differences for short sprint events had received little attention. McClelland’s background, male-female differences in force/mass capabilities, and existing data trends led her to hypothesise that sex differences in sprint running performance might be relatively small and increase with distance.
Her analysis of race data from sanctioned international competitions between 2003 and 2018 supported her initial hypothesis. These data revealed that the difference between male and female performance time increased with event distance from 8.6% to 11% from shortest to longest sprint events (60 to 400m). Additionally, within-race analysis of each 10-meter segment of the 100m event revealed a more pronounced pattern across distance: sex differences rose from 5.6% for the first segment to 14.2% in the last segment.
Why then are women potentially less disadvantaged versus men at shorter sprint distances?
Unlike other running species like horses and dogs, there is significant variation in body size between human males and females. Holding all other factors equal, body size differences result in muscular force to body mass ratios that are greater in relatively smaller individuals. Since sprinting velocities are directly dependent on the mass-specific forces runners can apply during the foot-to-ground contact phase of the stride, greater force/mass ratios of smaller individuals provide a theoretical relative advantage. A female runner’s shorter legs may confer the advantage of more steps and pushing cycles per unit time during the acceleration phase of a race. These factors offset male advantages (longer legs and greater muscularity) that become more influential over longer distances.
Since the introduction of the first antiretroviral therapy (ART) drug for HIV/AIDS treatment 35 years ago, life expectancy in Sub-Saharan Africa has steadily increased. ART medications are specifically designed to help an individual’s immune system fight HIV and in turn suppress HIV replication. However, there is a limited understanding of the combined effects of HIV and ART on disability and healthy longevity for individuals with the disease.
In a study published in The Lancet HIV, investigators from the Brigham and Women’s Hospital collaborated alongside international partners in South Africa to compare people with both virally suppressed and unsuppressed HIV, with people who were uninfected with HIV. The team used data they collected in an observational, longitudinal, population-based cohort study that included baseline interviews and blood collection, as well as subsequent follow-up interviews and blood collection about four years later. Their modelling analysis found that those receiving ART medication were predicted to live considerably longer and with less disability than those with unsuppressed HIV.
This research demonstrates the role of ART in healthy aging, as well as the continued importance for international global health organisations to provide HIV treatment to those all over the world, including in Africa.
“It was exciting for us to find that – at the population level – achieving high rates of viral suppression among people with HIV will not only lead to increases in life expectancy but also to healthier aging,” said senior author Jennifer Manne-Goehler, MD of the Division of Infectious Diseases. “This confirms the critical importance of maintaining support for antiretroviral programs as a way to ensure the best long-term health outcomes for people growing older with HIV.”