The exchange of small molecules, or metabolites, between organisms and their environment gives rise to the complexity of life on Earth1. One of the examples of such complexity is ourselves, our body and the full array of microorganisms (microbiota) that live on and in us, humans.
Just like us, stony corals (Scleractinia) also live in a symbiosis with associated microorganisms. These include bacteria, archea, fungi, viruses, and single-cellular algae called Symbiodinium.
Under normal conditions, these algal cells provide 90 to 95% of the energy required for stony corals to live happily1. The algae provide lipids, carbohydrates, amino acids, and O2 to Scleractinia. In return, the algae get to recycle nitrogen and other inorganic compounds from the coral, that they can use to fuel their own cell metabolism.
Climate change causes a rise in water temperatures; and, this form of environmental heat stress, disrupts the symbiotic relationship between corals and its algae, which results in coral bleaching.
Researchers have now discovered that heat stress destabilizes this basic nutrient exchange between corals and their algae; and, this turn of events happens long before the bleaching process becomes obvious.
In fact, Rädecker and his colleagues2 at the Red Sea Research Centre, discovered that heat stress causes the coral to need more energy, which swings the coral-algae symbiosis from a nitrogen- to a carbon-limited state. This actually ends up reducing the movement and recycling of carbon, and creates an animosity between these life partners.
The coral starts disliking the algae, because the algae it’s not fully doing its work – recycling carbon. As such, the stony coral starts thinking that sheltering such lazy algae is not beneficial anymore. On top of that, the poor coral needs to catabolically degrade more aminoacids, to compensate for the increased energy demands triggered by the warmer waters. Such demanding “cooking tasks” from the coral side, create fury, and actually increase the release of ammonium; which in turn, promote the algae to grow. So, not only does the algae not clean the building properly, but calls its algal friends and they move in.
Under stress, the coral kicks the algae out. But since this marriage is essential to its life support, the Scleractinia cannot feed itself properly anymore. The stony coral goes hungry, and slowly dies out….
1 Williams, A. et al. Metabolomic shifts associated with heat stress in coral holobionts. Science Advances7, eabd4210, doi:doi:10.1126/sciadv.abd4210 (2021).
2 Rädecker, N. et al. Heat stress destabilizes symbiotic nutrient cycling in corals. Proceedings of the National Academy of Sciences118, e2022653118, doi:10.1073/pnas.2022653118 (2021).
Precision medicine is an emerging approach to medical care. It takes into account individual variations in genetic make-up, metabolism and other biological and environmental factors, to better determine which treatment and prevention strategies for a particular disease may work better for which groups of people1.
Today, precision medicine is routinely integrated into the care of cancer patients, and has provided substantial increases in cancer free survival2. For example, translational studies investigating signatures within the tumour that promote disease progression, can predict individual responses to standard and targeted chemotherapy regimens2,3.
In the cardiovascular field, even though the prognosis for people with heart failure has improved in recent decades as research studies demonstrate the effectiveness of various medications, precision medicine is still in its infancy.
Some aspects of precision medicine are routinely used by healthcare providers, like the blood level of the biomarker called B-type natriuretic peptide, which is a sensitive indicator of whether heart failure is worsening or if treatments are helping1,4. This biomarker can also help the doctor determine whether shortness of breath symptoms in an individual are due to heart failure, or another medical problem1.
But as it is now, patients diagnosed with heart failure are still offered essentially identical treatments, regardless of whether their disease was caused by coronary artery disease, genetic mutations, or an autoinflammatory processes2.
Also, historically, clinical trial participants have been predominantly white people with particular genetic variants; but, individuals with different racial and ethnic ancestry have different genetic variants, and therefore, may not have the same response to a certain medication or treatment1.
While this “one-size-fits-all’ approach has led to improvements in clinical outcomes in large populations, the individual response rates continue to vary tremendously; and, it is often difficult to distinguish patients who will achieve a favourable response, from those who will experience disease progression, and ultimately succumb to their illness2.
As such, in the cardiovascular field, it is urgent to personalize heart failure care by identifying groups of patients more likely to develop heart failure, and tailoring which medications and other therapies could be most effective for them1. Currently, many individuals are left poorly treated, and there is substantial room for improvement2.
Key studies demonstrating selective efficacy of certain drugs in patients harbouring specific genetic variants, indicate a direction where treatment responses can be predicted using individual genetic information.
Given the recent cost reductions in exome sequencing, for example, this can now be used routinely to identify genetic variants that predict heart failure prognosis, and specific responses to medical and device-based therapies. Such information can further provide critical insights into new disease mechanisms, like Lamin A mutations that display a molecular phenotype that is dramatically distinct from other forms of dilated cardiomyopathy5.
More and more we come to realize that despite a common surface phenotype or symptomology, certain mutations may actually give rise to distinct diseases that need to be appropriately treated.
As such, researchers need to increase clinical trial diversity, so that optimal treatment approaches can be found for each population group. Also, the power of supercomputing should be used to rapidly predict the outcomes of possible new treatments. And, processes for sharing information across large databases shouldbe put in place with guarantees of patient privacy (e.g., cloud-based platforms), so that clinicians/scientists can quickly collaborate and share data internationally.
Moreover, updated health-wearable devices, artificial intelligence and other deep learning technologies strategies will ultimately be employed to develop testable hypotheses from large datasets, and provide precision-personalized approaches to cardiovascular health care.
Let’s hope Precision will be more than a one night stand on Heart’s Tinder list….
5 Cheedipudi, S. M. et al. Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes Is Associated With Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy. Circ Res. https://pubmed.ncbi.nlm.nih.gov/30739589/124, 1198-1213, doi:10.1161/circresaha.118.314177 (2019).
A healthy lifestyle is the cornerstone of cardiovascular health.
Lifestyle interventions are already a key component of primary prevention in low-risk cardiovascular disease groups, and serve as an important aide to pharmacotherapy in higher-risk groups.
But according to the new guidelines by the American Heart Association (AHA) and the American College of Cardiology (ACC)1, a first line of therapy for mild to moderate–risk groups are lifestyle-only approaches for a proper blood pressure and blood cholesterol management.
As such, the next time you go to the doctor, you might get an exercise prescription instead of an order to visit the pharmacy.
This is a major change in the idea of health, promoted by not taking a pill, but having a look at lifestyle in order to improve health – and avoid the numerous side-effects that certain medications can have.
An exercise prescription is an individualized physical activity program designed using the Frequency (how often?), Intensity (how hard?), Time (how long?), and Type (what kind?), or the FITT principle developed by the American College of Sports Medicine (ACSM).
Although most health care professionals and patients are aware that physical activity is recommended for good health, the abundance of scientific and lay recommendations for activity can be difficult to distil. As such, framing the exercise prescription by the FITT principle provides clinicians with more structured guidance on how to recommend exercise to their patients.
The updated FITT exercise recommendations for adults with elevated blood pressure are the following:
Frequency: in most, preferably all days of the week due to the transient Blood Pressure lowering effects that last for up to 24 hours after an exercise session;
Intensity: Moderate, any intensity of exercise has been shown to lower Blood Pressure;
Time: >20 to 30 minutes per day to total >90 to >150 minutes per week of continuous or accumulated exercise of any duration;
Type: Emphasize aerobic or resistance exercise alone or combined, due to the recent evidence showing the Blood Pressure lowering effects of exercise do not vary by exercise modality2.
The updated FITT exercise prescription recommendations propose more exercise options in less time, that hopefully will translate to better exercise adherence.
Furthermore, long-term exercise produces changes in the availability of receptors that can control the release of monoamines, like the Serotonin-1A receptor of the Raphe Nuclei4, and Dopamine-2 receptor in the Striatum5.
Regular exercise has antidepressant/anxiolytic properties, and results in dramatic alterations in physiological stress responses.
In addition to antidepressant and anxiolytic properties, the Serotonin system (5-HT) has also been linked to cognitive function; since, a distress of the 5-HT system is associated with cognitive syndromes, such as Alzheimer’s disease6.
So, don’t shy away, and take at least a 20 min quick walk today.
It’s free, and it’s good for you!
1 Gibbs, B. B. et al. Physical Activity as a Critical Component of First-Line Treatment for Elevated Blood Pressure or Cholesterol: Who, What, and How?: A Scientific Statement From the American Heart Association. Hypertension0, HYP.0000000000000196, doi:doi:10.1161/HYP.0000000000000196.
2 Pescatello, L. S. et al. Physical Activity to Prevent and Treat Hypertension: A Systematic Review. Med Sci Sports Exerc51, 1314-1323, doi:10.1249/mss.0000000000001943 (2019).
3 Buhr, T. J. et al. The Influence of Moderate Physical Activity on Brain Monoaminergic Responses to Binge-Patterned Alcohol Ingestion in Female Mice. Front Behav Neurosci15, 639790-639790, doi:10.3389/fnbeh.2021.639790 (2021).
4 Greenwood, B. N. et al. Freewheel running prevents learned helplessness/behavioral depression: role of dorsal raphe serotonergic neurons. J Neurosci23, 2889-2898, doi:10.1523/jneurosci.23-07-02889.2003 (2003).
5 Clark, P. J. et al. Wheel running alters patterns of uncontrollable stress-induced cfos mRNA expression in rat dorsal striatum direct and indirect pathways: A possible role for plasticity in adenosine receptors. Behav Brain Res272, 252-263, doi:10.1016/j.bbr.2014.07.006 (2014).
6 Meltzer, C. C. et al. Serotonin in aging, late-life depression, and Alzheimer’s disease: the emerging role of functional imaging. Neuropsychopharmacology18, 407-430, doi:10.1016/s0893-133x(97)00194-2 (1998).
Disrupted sleep is a major feature of Alzheimer’s disease (AD), and it usually appears years before symptoms of cognitive decline emerge.
It seems prolonged wakefulness aggravates the production of amyloid-beta (Aβ) species, which is a major driver of AD progression.
This sleep loss tends to further accelerate AD, with this tendency becoming a vicious cycle of sleepiness and AD advancement.
Unfortunately, the mechanisms by which Aβ affects sleep are still unknown and reason for much research.
Recently, Özcan and team of researchers have shown that in zebrafish, Aβ acutely and reversibly can enhance or suppress sleep in the fish as a function of the length of the oligomer, that is the number of Aβ molecules bounded together.
Genetic disruption analysis has shown that short Aβ oligomers induce acute wakefulness through Adrenergic receptor b2 (Adrb2) and Progesterone membrane receptor component 1 (Pgrmc1). While longer Aβ forms, can actually induce sleep through a pharmacologically tractable Prion Protein (PrP) signalling cascade.
What this data shows, is that Aβ can actually trigger a bi-directional sleep/wake switch in the zebrafish.
And, what this could mean, is that alterations to the brain’s Aβ oligomeric environment, such as during the progression of AD, may lead to disrupt sleep through changes in acute signalling events through similar receptors.
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